Download risks of exercise

1
RISKS OF EXERCISE
In recent years, regular exercise and increased lifestyle activity have been widely
popularized and promoted by the medical community and others because of the associated health
and fitness benefits. Although considerable epidemiologic evidence suggests that regular
physical activity may help to protect against and treat aging-related chronic diseases, the risk of
cardiovascular, pulmonary, musculoskeletal and metabolic complications appear to increase
transiently during strenuous physical activity compared with the risk at other times. This seems
particularly true when concomitant chronic diseases/medical conditions and/or superimposed
environmental stressors are involved, especially among habitually sedentary persons performing
unaccustomed, vigorous physical activity.
Pathophysiological Basis for Exertion-Related Cardiovascular Events
Cardiovascular events associated with exercise have been reported in the medical
literature and the lay press, suggesting that strenuous physical activity may actually precipitate
acute myocardial infarction (AMI) or sudden cardiac death (SCD) in selected individuals
(Thompson, Franklin et al. 2007). Pathophysiologic evidence suggests that acute exercise, by
increasing sympathetic activity, catecholamine excretion, and sodium potassium imbalance, may
evoke irritability and a transient oxygen deficiency at the subendocardial level, which is
exacerbated by decreased venous return and coronary perfusion, secondary to abrupt cessation
activity (Fig. 1) (Franklin 1983). Ischemia can alter depolarization, repolarization, and
conduction velocity, triggering threatening ventricular arrhythmias which, in extreme cases, may
be the harbingers of ventricular tachycardia or fibrillation. Moreover, strenuous physical
exertion can provoke plaque rupture and acute coronary thrombosis by several triggering
mechanisms (Table 1) (Kestin, Ellis et al. 1993; Thompson 1996).
2
In middle-aged and older adults, exercise-related deaths are generally due to plaque
rupture and thrombosis formation, leading to AMI, or to malignant ventricular arrhythmias. In
apparently healthy individuals with no prior history of cardiovascular disease, the presentation is
generally AMI rather than SCD, by a nearly 7:1 ratio (Foster and Porcari 2001). However, in
patients with documented cardiovascular disease, sudden arrhythmogenic death is the more
common presentation, by a 5:1 ratio over AMI (Haskell 1978; Hossack 1982; Siscovick, Weiss
et al. 1984). Structural cardiovascular abnormalities, including ruptured aorta, anomalous origin
of the left coronary artery, hypertrophic and/or right ventricular cardiomyopathy, mural left
anterior descending coronary artery, mitral valve prolapse, and irregularities of the conduction
system, have also been implicated as potential causes of SCD, particularly in adolescents and
young adults (≤ 35 years of age) (Corrado, Basso et al. 2003). Thus, the combination of exercise
and a diseased or susceptible heart, rather than the exercise itself, seems to pose the major acute
cardiovascular risk of physical activity.
Relative Risk of Exercise-Related Cardiovascular Events
At least 7 independent studies have documented that AMI and SCD can be triggered by
unaccustomed moderate-to-vigorous physical exertion (≥ 5 metabolic equivalents [METs; 1
MET = 3.5 mL O2/kg/min]), especially among habitually sedentary men and women with occult
or known coronary artery disease (CAD), and that the risk decreases with increasing levels of
regular exercise (Siscovick, Weiss et al. 1984; Willich, Lewis et al. 1993; Giri, Thompson et al.
1999; Albert, Mittleman et al. 2000; Hallqvist, Moller et al. 2000; Whang, Manson et al. 2006).
Overall, these studies showed that the “relative risk” of a cardiovascular event during or soon
after physical exertion (ie, within 1 hour) was at least two times greater than the risk during
periods of lesser or no exertion (Mittleman 2002). However, the relative risk varied inversely
3
with the patient’s usual frequency of physical activity. For example, the Onset study (Mittleman,
Maclure et al. 1993) estimated that the risk of AMI associated with vigorous exertion was 107
(95% confidence interval: 67, 171) among patients who exercised < 1 time per week, and
decreased progressively with increasing levels of habitual physical exertion. In fact, the relative
risk was only 2.4 for the most active cohort in this study, that is, those exercising ≥ 5 times per
week.
Using the ongoing Nurses’ Health Study database, investigators recently reported that the
relative risk of SCD during moderate-to-vigorous exertion was modestly elevated at 2.38 (95%
confidence interval: 1.23 – 4.60; p = 0.01) compared with risk at other times (Whang, Manson et
al. 2006). In contrast, the relative risk during a bout of vigorous exertion was approximately 19fold higher (relative risk, 44.9; 95% confidence interval, 26.7 – 75.4) among men enrolled in the
Physicians’ Health Study (Albert, Mittleman et al. 2000). Although this difference may be
attributed, at least in part, to the inclusion of moderate exertion in the Nurses’ Health Study
cohort, a similar gender difference has been reported in smaller retrospective studies (Vuori
1986; Siscovick 1997).
Absolute Risk of Exercise-Related Cardiovascular Events
The absolute risk that an acute cardiovascular event will occur within 1 hour of vigorous
exertion has been estimated to be between 1 in 500,000 to 1 in 1.5 million hours of exercise
(Mittleman, Maclure et al. 1993; Albert, Mittleman et al. 2000; Hallqvist, Moller et al. 2000).
On the other hand, prospective data suggest that exertion-related SCD is an extremely rare event
in women, corresponding to 1 fatality per 36.5 million hours of exertion (Whang, Manson et al.
2006). Thus, although discrete episodes of strenuous physical activity may transiently increase
4
the risk of cardiovascular complications, even among fit individuals, the absolute risk associated
with each bout of exercise remains extremely low (Mittleman 2002).
The incidence of non-fatal and fatal cardiovascular events during and soon after exercise
is considerably greater among persons with known CAD than among presumably healthy adults.
Since 1980, an analysis of 4 reports (Van Camp and Peterson 1986; Digenio, Sim et al. 1991;
Vongvanich, Paul-Labrador et al. 1996; Franklin, Bonzheim et al. 1998) estimates 1 cardiac
arrest per 116,906 patient-hours, 1 AMI per 219,970 patient-hours, 1 fatality per 752,365 patienthours, and 1 major complication per 81,670 patient-hours of exercise-based cardiac
rehabilitation. More recently, the French Registry of complications during cardiac rehabilitation
reported no fatalities and an event rate of 1 per 49,565 patient-hours of exercise training; the
cardiac arrest rate was 1.3 per million patient-hours of exercise (Pavy, Iliou et al. 2006). Thus,
most exercise-related cardiac arrests that occur in contemporary, medically supervised, cardiac
rehabilitation programs are successfully reversed, without residual adverse sequelae (Franklin
2005).
Potential Risk Modulators
The rarity of exercise-related cardiovascular events makes evaluation of time of day and
“high risk” activities difficult because of small sample sizes and methodological limitations,
primarily from observational studies and anecdotal reports (Thompson, Franklin et al. 2007).
Time of Day. During the early morning hours a variety of pathophysiologic mechanisms for
coronary artery plaque rupture and thrombosis are more likely to be operative (Muller 1989).
Accordingly, superimposed physical stresses (eg, vigorous exercise) may serve to accentuate
these responses, and heighten the risk of AMI and SCD. To date, two studies (Murray,
Herrington et al. 1993; Franklin, Bonzheim et al. 1998) have reported that time of day had little
5
or no influence on the rate of cardiovascular complications during exercise-based cardiac
rehabilitation. Given the cardioprotective benefits of regular physical activity, and the low
incidence of exercise-related events, these data suggest that exercise training need not be
restricted to afternoon/evening hours in individuals at increased risk (Thompson, Franklin et al.
2007).
High-Risk Activities. Few data are available regarding the cardiovascular event rates of varied
occupational and recreational activities. Nevertheless, it appears that the incidence of exertionrelated cardiovascular complications across a variety of activities, performed at light-to-moderate
intensities, is similar to that expected by chance alone (Fletcher, Balady et al. 2001). In subjects
with known or occult CAD, strenuous physical exertion, especially when it is sudden,
unaccustomed, or involving competition, reliance on anaerobic metabolism, combined arm and
leg activity, or high-tension muscle contractions, may increase the risk of cardiovascular
complications (Friedewald and Spence 1990). For example, running, racquet sports, and
strenuous sports activity seem to be associated with a greater incidence of SCD than other
activities (Fletcher, Balady et al. 2001). Recreational and domestic activities that are associated
with an increased incidence of cardiovascular events include deer hunting (Haapaniemi, Franklin
et al. 2007) and snow removal (Chowdhury, Franklin et al. 2003), presumably due to
superimposed physical, cognitive, and environmental stresses. Snow shoveling is associated
with increased cardiovascular events, probably because it can elicit disproportionate cardiac
demands and a coronary vasoconstrictor response, and because it is often performed out of
necessity by at risk, habitually sedentary individuals (Thompson, Franklin et al. 2007).
Does the Benefit Outweigh the Risk?
6
Clearly, the risk of exertion-related cardiovascular complications is transiently increased,
even in habitually active persons, compared with that at other times. This appears to be
particularly true among persons with latent or known CAD who were performing unaccustomed
vigorous physical exertion. The “critical question,” however, is whether the cardiovascular
benefits of regular exercise outweigh the risk.
To clarify this issue, researchers examined the incidence of SCD during vigorous
physical exertion. The relative risk of cardiac arrest during exercise compared with that at other
times was 56 times greater among men with low levels of habitual activity and only 5 times
greater among men with high levels (Siscovick, Weiss et al. 1984). However, the total risk of
cardiac arrest among habitually active men was only 40% of that for their sedentary counterparts.
Similarly, a follow-up study demonstrated that habitual exercise strongly decreased the risk that
vigorous exertion would trigger SCD (Albert, Mittleman et al. 2000). Collectively, these
findings and previous reports (Mittleman, Maclure et al. 1993; Willich, Lewis et al. 1993)
support the hypothesis that physical activity is a double-edged sword, that is, it can protect
against and provoke acute cardiovascular events (Raum, Rothenbacher et al. 2007).
To clarify the risk: benefit ratio of physical activity, consider that the risk of AMI
associated with each bout of vigorous exercise is approximately doubled for an individual who
exercises 1 hour, 5 or more days per week (Mittleman, Maclure et al. 1993; Mittleman 2002).
However, two meta-analyses now suggest that regular exercise can reduce the overall risk of
cardiovascular events by up to 50% (Powell, Thompson et al. 1987; Berlin and Colditz 1990).
Thus, during exercise training his or her risk will double and approximate that at all times if he
or she were habitually sedentary. However, over the remaining 23 hours of the day, his or her
risk would be up to 50% lower, highlighting the clear net benefit of regular exercise.
7
Recent epidemiologic studies have shown that each 1-MET increase in exercise capacity
confers an 8% to 17% reduction in cardiovascular and all-cause mortality (Franklin 2007). One
possible mechanism by which regular physical activity, improved aerobic fitness, or both, may
provide cardioprotective benefits might be through adaptations in autonomic control, specifically
reduced sympathetic drive at rest and increased vagal tone. However, recent animal studies have
challenged the notion that exercise-induced protection from ventricular fibrillation is due solely
to enhanced cardiac vagal regulation (Billman and Kukielka 2006). It appears that the
association between higher levels of physical activity and lower rates of cardiovascular events
can be explained in large part by the favorable modification of known risk factors, with
inflammatory/hemostatic biomarkers making the largest contribution to lowered risk, followed
by blood pressure, lipids, and body mass index (Mora, Cook et al. 2007).
Identifying the Individual “At Risk” for Exercise-Related Cardiovascular Complications
Rogosta and associates (Ragosta, Crabtree et al. 1984) reported that 88% of exertionrelated deaths were attributed to underlying atherosclerotic CAD, and that only 7% of the deaths
were in individuals with no known history of or risk factors for atherosclerotic heart disease.
This suggests that a significant proportion of these exertion-related deaths may have been
prevented if appropriate counseling and preliminary screening had been employed.
Population studies have shown that exercise-related cardiovascular events are often
preceded by forewarning signs or symptoms (Thompson, Stern et al. 1979; Northcote, Flannigan
et al. 1986). On the other hand, coronary patients with impaired left ventricular function,
exercise-induced ST-segment depression and/or angina pectoris, threatening ventricular
arrhythmias, and those who have a very low or relatively high exercise capacity (≤ 4 METs or ≥
10 METs, respectively) appear to be at increased risk for exercise-related cardiovascular events
8
(Franklin 2005). Moreover, heart failure patients at increased risk for exercise-related cardiac
events are characterized by a significantly higher prevalence of pacemaker/implantable
cardioverter-defibrillators, larger left ventricular end-diastolic diameter, lower exercise tolerance,
greater ventilation drive, and higher plasma brain natriuretic peptide concentration at baseline
(Nishi, Noguchi et al. 2007). In addition, multivariate analysis indicated that a large left
ventricular end-diastolic diameter was an independent predictor of cardiac events during
exercise.
Although exercise testing may be helpful in identifying silent ischemia and malignant
ventricular arrhythmias, a truly positive exercise test requires a hemodynamically significant
coronary lesion (eg, > 75% stenosis), whereas nearly 90% of AMIs occur at the site of previously
non-obstructive, angiographically documented plaques (Falk, Shah et al. 1995). These findings,
coupled with the extremely low absolute rate of cardiovascular complications among persons
who exercise, the high costs of mass stress testing, and the uncertainties associated with
abnormal electrocardiograms (ECG) in persons with a low pre-test risk of CAD, suggest that it is
impractical to use routine exercise testing to prevent untoward events in all asymptomatic
persons who exercise (2004; Thompson, Franklin et al. 2007). Perhaps one alternative to mass
exercise testing lies in using a well-designed health assessment or medical history questionnaire
(eg, Physical Activity Readiness Questionnaire) to identify conditions, symptoms, and risk
factors that are predictive of future cardiovascular events (Physiology 1994). Individuals
categorized at “increased risk” would need to consult a physician before becoming more
physically active, especially if vigorous exercise is contemplated.
Other Risk Conditions
9
In selected individuals, exercise may also increase the likelihood of musculoskeletal
injuries, metabolic complications (eg, marked fluctuations in blood glucose), and pulmonary
symptoms.
Musculoskeletal Injuries. Moderate intensity physical activity, as recommended by the
American College of Sports Medicine and the American Heart Association, is associated with a
very low risk of orthopedic and cardiovascular complications (Haskell, Lee et al. 2007). On the
other hand, the most common risk of vigorous physical activity is musculoskeletal injury, which
can exceed 50% among participants involved in jogging programs (Hootman, Macera et al.
2002) and US Army basic training (Jones and Knapik 1999).
Inordinate exercise demands, especially during the initial weeks of a physical
conditioning regimen, often result in muscle soreness, orthopedic injury, and attrition. Excessive
frequency (≥ 5 days/week) and/or duration (≥ 45 minutes/session) of training offer the
participant little additional again in aerobic capacity, whereas the incidence of orthopedic injury
increases disproportionately (Pollock, Gettman et al. 1977). Similarly, very-hard training
intensities (≥ 85% heart rate reserve) provide little additional improvement in cardiorespiratory
fitness, and are associated with an injury rate of 50% (Mann, Garrett et al. 1969).
Diabetes. For the diabetic, a lack of sufficient insulin before exercise may impair glucose
transport into the muscles, and lead to a cascade of potentially adverse metabolic responses,
including ketosis and hyperglycemia. On the other hand, because exercise has an insulin-like
effect, hypoglycemia is the most common complication experienced by exercising diabetics who
take exogenous insulin or, to a lesser extent, oral hypoglycemic agents. Other recommendations
and precautionary measures to reduce the likelihood of complications in exercising diabetics are
listed in Table 2.
10
Asthma or Chronic Obstructive Pulmonary Disease. Many patients with pulmonary
problems may experience an exacerbation of symptoms during exercise due to ventilatory
limitations, oxygen desaturation, or both. Accordingly, such patients should be instructed in
pursed-lip breathing during exercise, as well as the use of supplemental oxygen. Intermittent
exercise, that is, brief repetitive exercise-rest periods on alternate days, may also be employed
during the initial training sessions, until the patient can achieve 20 to 30 minutes of continuous
exercise.
Recommendations to Reduce the Incidence of Exercise-Related Complications
Recommendations to potentially reduce the incidence and severity of exercise-related
cardiopulmonary, musculoskeletal, and metabolic complications include (Foster and Porcari
2001; Franklin 2005; Thompson, Franklin et al. 2007): ensure medical clearance of “high risk”
adults and patients with diabetes and/or cardiovascular disease, especially when vigorous
exercise is contemplated; conduct regular emergency drills and establish an emergency plan;
encourage novice exercisers to improve their cardiorespiratory fitness through participation in a
moderate intensity exercise program, to move them out of the least fit, least active, “high risk”
cohort (Friedewald and Spence 1990); counsel habitually sedentary individuals to avoid
unaccustomed, vigorous physical activity (eg, racquet sports, squash, snow shoveling)
(Thompson, Franklin et al. 2007); advocate appropriate warm-up and cool-down procedures
(Haskell 1978; Dimsdale, Hartley et al. 1984); promote eduction of warning signs/symptoms (eg,
anginal equivalents, lightheadedness, abnormal heart rhythms); minimize competition and
modify recreational game rules to decrease the energy cost and heart rate response to play
(Franklin 2005); and, reduce the exercise intensity in settings with superimposed environmental
stressors (eg, heat/humidity, cold, altitude) (Friedewald and Spence 1990). Because automated
11
external defibrillators have become easier to use, safer, relatively inexpensive, and more
effective at improving survival from SCD, it seems that in addition to enhancing their screening
procedures and emergency preparedness, health clubs (McInnis, Herbert et al. 2001) and
university-based fitness facilities (Herbert, Herbert et al. 2007) should be equipped with these
life-saving devices.
Börjesson et al. (Borjesson, Assanelli et al. 2006) and others (Meyer, Samek et al. 1995)
have recommended that patients with CAD exercise at more moderate intensities, that is, below
the anaerobic or ventilatory threshold, because exercise above this level is associated with signs
or symptoms of myocardial ischemia during exercise testing, and an increased risk of
cardiovascular complications. Because symptomatic or silent myocardial ischemia may be highly
arrhythmogenic in patients with obstructive atherosclerotic CAD (Hoberg, Schuler et al. 1990),
the prescribed heart rate for endurance exercise should be set safely below (≥ 10 beats/minute)
the ischemic ECG or anginal threshold (Medicine 2005).
Recent guidelines have also
addressed recommendations for safe exercise training and sports participation in patients with
hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular
dysplasia/cardiomyopathy, myocarditis and pericarditis (Pelliccia, Corrado et al. 2006).
12
REFERENCES
1.
THOMPSON, P. D., B. A. FRANKLIN, G. J. BALADY, S. N. BLAIR, D. CORRADO,
M. ESTES III, J. E. FULTON, N. F. GORDON, W. L. HASKELL, M S. LINK, B. J.
MARON, M. A. MITTLEMAN, A. PELLICCIA, N. K. WENGER, S. N. WILLICH, and
F. COSTA. Exercise and acute cardiovascular events. Placing the risks into perspective.
A Scientific Statement from the American Heart Association Council on Nutrition,
Physical Activity, and Metabolism and the Council on Clinical Cardiology. In
collaboration with the American College of Sports Medicine. Circulation 115:23582368, 2007.
2.
FRANKLIN, B. A. The role of electrocardiographic monitoring in cardiac exercise
programs. J Cardiopulm Rehabil 3:806-810, 1983.
3.
THOMPSON, P. D. The cardiovascular complications of vigorous physical activity.
Arch Intern Med 156:2297-2302, 1996.
4.
KESTIN, A. S., P. A. ELLIS, M. R. BARNARD, A. ERRICHETTI, B. A. ROSNER, and
A. D. MICHELSON. Effect of strenuous exercise on platelet activation state and
reactivity. Circulation 88:1502-1511, 1993.
5.
FOSTER, C., and J. P. PORCARI. The risks of exercise training. J Cardiopulm Rehabil
21:347-352, 2001.
6.
SISCOVICK, D., S. L. G. EKELUND, J. L. JOHNSON, Y. TRUONG, and A. ADLER.
Sensitivity of exercise electrocardiography for acute cardiac events during moderate and
strenuous physical activity. Arch Intern Med 151:325-330, 1991.
7.
HOSSACK, K. F., and R. HARTWIG. Cardiac arrest associated with supervised cardiac
rehabilitation. J Cardiac Rehabil 2:402-408, 1982.
13
8.
HASKELL, W. L. Cardiovascular complications during exercise training in cardiac
patients. Circulation 57:920-925, 1978.
9.
CORRADO, D., C. BASSO, G. RIZZOLI, M. SCHIAVON, and G. THIENE. Does
sports activity enhance the risk of sudden death in adolescents and young adults? J Am
Coll Cardiol 42:1959-1963, 2003.
10.
SISCOVICK, D. S., N. S. WEISS, R. H. FLETCHER, and T. LASKY. The incidence of
primary cardiac arrest during vigorous exercise. N Engl J Med 311:874-877, 1984.
11.
MITTLEMAN, M. A., M. MACLURE, G. H. TOFLER, J. B. SHERWOOD, R. J.
GOLDBERG, and J. E. MULLER. Triggering of acute myocardial infarction by heavy
physical exertion. Protection against triggering by regular exertion: Determinants of
Myocardial Infarction Onset Study Investigators. N Engl J Med 329:1677-1683, 1993.
12.
WILLICH, S. N., M. LEWIS, H. LOWELL, H. R. ARNTZ, F. SCHUBERT, and R.
SCHRODER. Physical exertion as a trigger of acute myocardial infarction: Triggers and
Mechanisms of Myocardial Infarction Study Group. N Engl J Med 329:1684-1690, 1993.
13.
GIRI, S., P. D. THOMPSON, F. J. KIERNAN, J. CLIVE, D. B. FRAM, J. F. MITCHEL,
J. A. HIRST, R. G. MCKAY, and D. D. WATERS. Clinical and angiographic
characteristics of exertion-related acute myocardial infarction. JAMA 282:1731-1736,
1999.
14.
HALLQVIST, J., J. MOLLER, A. AHLBOM, F. DIDERICHSEN, C. REUTERWALL,
and U. DE FAIRE. Does heavy physical exertion trigger myocardial infarction? A casecrossover analysis nested in a population-based case-referent study. Am J Epidemiol
151:459-467, 2000.
14
15.
ALBERT, C. M., M. A. MITTLEMAN, C. U. CHAE, I. M. LEE, C. H. HENNEKENS,
and J. E. MANSON. Triggering of sudden death from cardiac causes by vigorous
exertion. N Engl J Med 343:1355-1361, 2000.
16.
WHANG, W., J. E. MANSON, F. B. HU, C. U. CHAE, K. M. REXRODE, W. C.
WILLETT, M. J. STAMPFER, and C. M. ALBERT. Physical exertion, exercise, and
sudden cardiac death in women. JAMA 295:1399-1403, 2006.
17.
MITTLEMAN, M. A. Triggers of acute cardiac events: new insights. Am J Med Sports
4:99-102, 2002.
18.
VUORI, I. The cardiovascular risks of physical activity. Acta Med Scand Suppl.
711:204-214, 1986.
19.
SISCOVICK, D. S. Exercise and its role in sudden cardiac death. Cardiol Clin 15:467472, 1997.
20.
VAN CAMP, S. P., and R. A. PETERSON. Cardiovascular complications of outpatient
cardiac rehabilitation programs. JAMA 256:1160-1163, 1986.
21.
DIGENIO, A. G., J. G. SIM, R. J. DOWDESELL, and R. MORRIS. Exercise-related
cardiac arrest in cardiac rehabilitation: the Johannesburg experience. S Afr Med J 79:188191, 1991.
22.
FRANKLIN, B. A., K. BONZHEIM, S. GORDON, and G. C. TIMMIS. Safety of
medically supervised outpatient cardiac rehabilitation exercise therapy: a 16-year followup. Chest 114:902-906, 1998.
23.
VONGVANICH P., M. J. PAUL-LABRADOR, and C. N. MERZ. Safety of medially
supervised exercise in a cardiac rehabilitation center. Am J Cardiol 77:1383-1385, 1996.
15
24.
PAVY, B., M. C. ILIOU, P. MEURIN, J-Y. TABET, and S. CORONE; for the Functional
Evaluation and Cardiac Rehabilitation Working Group of the French Society of
Cardiology. Safety of exercise training for cardiac patients. Results of the French
Registry of Complications During Cardiac Rehabilitation. Arch Intern Med 166:23292334, 2006.
25.
FRANKLIN, B. A. Cardiovascular events associated with exercise. The risk-protection
paradox. J Cardiopulm Rehabil 25:189-195, 2005.
26.
MULLER, J. E. Morning increase of onset of myocardial infarction. Implications
concerning triggering events. Cardiology 76:96-104, 1989.
27.
MURRAY, P. M., D. M. HERRINGTON, C. W. PETTUS, H. S. MILLER, J. D.
CANTWELL, and W. C. LITTLE. Should patients with heart disease exercise in the
morning or afternoon? Arch Intern Med 153:833-836, 1993.
28.
FLETCHER, G. F., G. J. BALADY, E. A. AMSTERDAM, B. CHAITMAN, R. ECKEL,
J. FLEG, V. F. FROELICHER, A. S. LEON, I. L. PIÑA, R. RODNEY, D. G. SIMONSMORTON, M. A. WILLIAMS, and T. BAZZARRE. Exercise standards for testing and
training: a statement for healthcare professionals from the American Heart Association.
Circulation 104:1694-1740, 2001.
29.
FRIEDEWALD, V. E., and D. W. SPENCE. Sudden cardiac death associated with
exercise: the risk-benefit issue. Am J Cardiol 66:183-188, 1990.
30.
HAAPANIEMI, S., B. A. FRANKLIN, J. H. WEGNER, S. HAMAR, S. GORDON, G.
C. TIMMIS, and W.W. O’NEILL. Electrocardiographic responses to deer hunting
activities in men with and without coronary artery disease. Am J Cardiol 100:175-179,
2007.
16
31.
CHOWDHURY, P. S., B. A. FRANKLIN, J. A. BOURA, L. J. DRAGOVIC, S.
KANLUEN, W. SPITZ, J. HODAK, and W. W. O’NEILL. Sudden cardiac death after
manual or automated snow removal. Am J Cardiol 92:833-835, 2003.
32.
RAUM, E., D. ROTHENBACHER, H. ZIEGLER, and H. BRENNER. Heavy physical
activity: Risk or protective factor for cardiovascular disease? A life course perspective.
Ann Epidemiol 17:417-424, 2007.
33.
POWELL, K. E., P. D. THOMPSON, C. J. CASPERSEN, and J. S. KENDRICK.
Physical activity and the incidence of coronary heart disease. Annu Rev Public Health
8:253-287, 1987.
34.
BERLIN, J. A., and G. A. COLDITZ. A meta-analysis of physical activity in the
prevention of coronary heart disease. Am J Epidemiol 134:232-234, 1991.
35.
FRANKLIN, B. A., and N. F. GORDON. Contemporary Diagnosis and Management in
Cardiovascular Exercise. 1st ed., Newton, PA: Handbooks in Health Care Co., 2007.
36.
BILLMAN, G. E., and M. KUKIELKA. Effects of endurance exercise training on heart
rate variability and susceptibility to sudden cardiac death: protection is not due to
enhanced cardiac vagal regulation. J Appl Physiol 100:896-906, 2006.
37.
MORA, S., N. COOK, J. E. BURING, P. M. RIDKER, and I-M. LEE. Physical activity
and reduced risk of cardiovascular events. Potential mediating mechanisms. Circulation
116:2110-2118, 2007.
38.
RAGOSTA, M., J. CRABTREE, W. Q. STURNER, and P. D. THOMPSON. Death
during recreational exercise in the State of Rhode Island. Med Sci Sports Exerc 16:339342, 1984.
17
39.
THOMPSON, P. D., M. P. STERN, P. WILLIAMS, K. DUNCAN, W. L. HASKELL,
and P. D. WOOD. Death during jogging or running: a study of 18 cases. JAMA
242:1265-1267, 1979.
40.
NORTHCOTE, R. J., C. FLANNINGAN, and D. BALLANTYNE. Sudden death and
vigorous exercise: a study of 60 deaths associated with squash. Br Heart J 55:198-203,
1986.
41.
NISHI, I., T. NOGUCHI, S. FURUICHI, Y. IWANAGA, J. KIM, H. OHYA, N.
AIHARA, H. TAKAKI, and Y. GOTO. Are cardiac events during exercise therapy for
heart failure predictable from the baseline variables? Circ J 71:1035-1039, 2007.
42.
FALK, E., P. K. SHAH, and V. FUSTER. Coronary plaque disruption. Circulation
92:657-671, 1995.
43.
US PREVENTIVE SERVICES TASK FORCE. Screening for coronary heart disease:
recommendation statement. Ann Intern Med 140:569-572, 2004.
44.
CANADIAN SOCIETY FOR EXERCISE PHYSIOLOGY. PAR-Q and You.
Gloucester, Ontario: 1-2, 1994.
45.
HASKELL, W. L., I-M LEE, R. R. PATE, K. E. POWELL, S. N. BLAIR, B. A.
FRANKLIN, C. A. MACERA, G. W. HEATH, P. D. THOMPSON, and A. BAUMAN.
Physical activity and public health: Updated recommendation for adults from the
American College of Sports Medicine and the American Heart Association. Circulation
116:1081-1093, 2007.
46.
HOOTMAN, J. M., C. A. MACERA, B. E. AINSWORTH, C. L. ADDY, M. MARTIN,
and S. N. BLAIR. Epidemiology of musculoskeletal injuries among sedentary and
physically active adults. Med Sci Sports Exerc 34:838-844, 2002.
18
47.
JONES, B.H., and J. J. KNAPIK. Physical training and exercise-related injuries:
surveillance, research and injury prevention in military populations. Sports Med 27:111125, 1999.
48.
POLLOCK, M. L., L. R. GETTMAN, C. A. MILESIS, M. D. BAH, L. DURSTINE, and
R. B. JOHNSON. Effects of frequency and duration of training on attrition and incidence
of injury. Med Sci Sports Exerc 9:31-36, 1977.
49.
MANN, G. V., H. L. GARRETT, A. FARHI, H. MURRAY, F. T. BILLINGS, E.
SHUTE, and W. E. SCHWARTEEN. Exercise to prevent coronary heart disease: An
experimental study of the effects of training on risk factors for coronary disease in men.
Am J Med 46:12-27, 1969.
50.
DIMSDALE, J. E., L. H. HARTLEY, T. GUINEY, J. N. RUSKIN, and D.
GREENBLATT. Post exercise peril. Plasma catecholamines and exercise. JAMA
251:630-632, 1984.
51.
McINNIS, K., W. HERBERT, D. HERBERT, J. HERBERT, P. RIBISL, and B.
FRANKLIN. Low compliance with national standards for cardiovascular emergency
preparedness at health clubs. Chest 120:283-288, 2001.
52.
HERBERT, W. G., D. L. HERBERT, K. J. McINNIS, P. M. RIBISL, B. A. FRANKLIN,
M. CALLAHAN, and A. W. HOOD. Cardiovascular emergency preparedness in
recreation facilities at major US universities: College fitness center emergency readiness.
Prev Cardiol 10:128-133, 2007.
53.
BÖRJESSON, M., D. ASSANELLI, F. CARRE, D. DUGMORE, N. PANHUYZENGOEDKOOP, C. SEILER, J. SENDEN, and E. E. SOLBERG. Recommendations for
19
participation in leisure time physical activity and competitive sports for patients with
ischemic heart disease. Eur J Cardiovasc Prev Rehabi13:133-136, 2006.
54.
MEYER, K., L. SAMEK, A. PINCHAS, M. BAIER, P. BETZ, and H. ROSKAMM.
Relationship between ventilatory threshold and onset of ischaemia in ECG during stress
testing. Eur Heart J 16:623-630, 1995.
55.
HOBERG, E., G. SCHULER, B. KUNZE, A. L. OBERMOSER, K. HAUER, H. P.
MAUTNER, G. SCHLIERF, and W. KUBLER. Silent myocardial ischemia as a
potential link between lack of premonitoring symptoms and increased risk of cardiac
arrest during physical stress. Am J Cardiol 65:583-589, 1990.
56.
AMERICAN COLLEGE OF SPORTS MEDICINE. Guidelines for Exercise Testing and
Prescription, 7th ed, Baltimore, MD: Lippincott Williams & Wilkins, 2005.
57.
PELLICCIA, A., D. CORRADO, H. H. BJØRNSTAD, N. PANHUYZEN-GOEDKOOP,
A. URHAUSEN, F. CARRE, A. ANASTASAKIS, L. VANHEES, E. ARBUSTINI, and
S. PRIORI. Recommendations for participation in competitive sport and leisure-time
physical activity in individuals with cardiomyopathies, myocarditis and pericarditis. Eur
J Cardiovasc Prev Rehabil 13:876-885, 2006.
20
TABLE 1. Potential triggering mechanisms of acute myocardial infarction by strenuous
physical exertion.*
____________________________________________________________________________
● Coronary artery spasm in diseased segments → plaque rupture
● Changes in cardiac dimensions → twisting of the epicardial coronaries → plaque rupture
● Increased heart rate and blood pressure (shear forces ) → plaque disruption
● Increased catecholamine-induced platelet aggregation and hyperreactivity† → coronary
thrombosis
*Adapted from references # 3 and 4. †This potential triggering mechanism has been reported in
habitually sedentary individuals who engaged in sporadic high-intensity exercise, but not in
physically trained individuals (4).
_____________________________________________________________________________
21
TABLE 2. Recommendations and precautionary measures to reduce the likelihood of
complications in exercising diabetics.
___________________________________________________________________________
● Wear proper footwear and practice good foot hygiene.
● Monitor blood glucose before, during, and after physical activity when starting an exercise
program.
● Inject insulin in body areas that are not engaged by exercise (eg, abdomen).
● Avoid exercising during periods of peak insulin action.
● Avoid exercise if the glucose level is < 100 mg/dL or > 300 mg/dL (or > 240 mg/dL with
urinary ketone bodies).
● Know the signs and symptoms of hypoglycemia. These include heart palpitations, confusion,
weakness, and visual disturbances which, if left untreated, could lead to unconsciousness or
convulsions. To reduce the likelihood of such adverse sequelae, exercising diabetics should be
instructed to always carry a form of fast-acting carbohydrate.
● Monitor for symptoms of hyperglycemia. These include excessive thirst, frequent urination,
blurred vision, itchy, dry skin or a fruity odor or breath, which can lead to ketoacidosis,
commonly called diabetic coma.
● Recognize that diabetic neuropathies can alter cardiovascular, skin blood flow, and sweating
responses to exercise in hot/humid environments, increasing the risk of heat injury. As a general
rule, diabetics should curtail outdoor exercise when the temperature is > 32oC (90oF), when the
relative humidity is > 60%, or both.
______________________________________________________________________________
22
Figure 1. Physiologic alterations accompanying acute exercise and recovery and their possible
sequelae. HR = heart rate, SBP = systolic blood pressure, MVO2 = myocardial oxygen uptake,
CHD = coronary artery disease, ↑ = increase, ↓ = decrease.
(2004). "Screening for coronary heart disease: recommendation statement." Ann Intern Med
140(7): 569-72.
This statement summarizes the current U.S. Preventive Services Task Force (USPSTF)
recommendations on screening for coronary heart disease and the supporting scientific
evidence and updates the 1996 recommendations on this topic. The complete information
on which this statement is based, including evidence tables and references, is available in
the background article and the systematic evidence review, available through the
USPSTF Web site (http://www.preventiveservices.ahrq.gov) and through the National
Guideline Clearinghouse (http://www.guideline.gov). The article and the
recommendation statement are also available in print through the Agency for Healthcare
Research and Quality Publications Clearinghouse (telephone, 800-358-9295; e-mail,
[email protected]).
Albert, C. M., M. A. Mittleman, et al. (2000). "Triggering of sudden death from cardiac causes
by vigorous exertion." N Engl J Med 343(19): 1355-61.
BACKGROUND: Retrospective and cross-sectional data suggest that vigorous exertion
can trigger cardiac arrest or sudden death and that habitual exercise may diminish this
risk. However, the role of physical activity in precipitating or preventing sudden death
has not been assessed prospectively in a large number of subjects. METHODS: We used
a prospective, nested case-crossover design within the Physicians' Health Study to
compare the risk of sudden death during and up to 30 minutes after an episode of
vigorous exertion with that during periods of lighter exertion or none. We then evaluated
whether habitual vigorous exercise modified the risk of sudden death that was associated
with vigorous exertion. In addition, the relation of vigorous exercise to the overall risk of
sudden death and nonsudden death from coronary heart disease was assessed. RESULTS:
During 12 years of follow-up, 122 sudden deaths were confirmed among the 21,481 male
physicians who were initially free of self-reported cardiovascular disease and who
provided information on their habitual level of exercise at base line. The relative risk ofsudden death during and up to 30 minutes after vigorous exertion was 16.9 (95 percent
confidence interval, 10.5 to 27.0; P<0.001). However, the absolute risk of sudden death
during any particular episode of vigorous exertion was extremely low (1 sudden death per
1.51 million episodes of exertion). Habitual vigorous exercise attenuated the relative risk
of sudden death that was associated with an episode of vigorous exertion (P value for
trend=0.006). The base-line level of exercise was not associated with the overall risk of
subsequent sudden death. CONCLUSIONS: These prospective data from a study of U.S.
male physicians suggest that habitual vigorous exercise diminishes the risk of sudden
death during vigorous exertion.
23
Berlin, J. A. and G. A. Colditz (1990). "A meta-analysis of physical activity in the prevention of
coronary heart disease." Am J Epidemiol 132(4): 612-28.
Evidence for an independent role of increased physical activity in the primary prevention
of coronary heart disease has grown in recent years. The authors apply the techniques of
meta-analysis to data extracted from the published literature by Powell et al. (Ann Rev
Public Health 1987;8:253-87), as well as more recent studies addressing this relation, in
order to make formal quantitative statements and to explore features of study design that
influence the observed relation between physical activity and coronary heart disease risk.
They find, for example, a summary relative risk of death from coronary heart disease of
1.9 (95% confidence interval 1.6-2.2) for sedentary compared with active occupations.
The authors also find that methodologically stronger studies tend to show a larger benefit
of physical activity than less well-designed studies.
Billman, G. E. and M. Kukielka (2006). "Effects of endurance exercise training on heart rate
variability and susceptibility to sudden cardiac death: protection is not due to enhanced cardiac
vagal regulation." J Appl Physiol 100(3): 896-906.
Low heart rate variability (HRV) is associated with an increased susceptibility to
ventricular fibrillation (VF). Exercise training can increase HRV (an index of cardiac
vagal regulation) and could, thereby, decrease the risk for VF. To test this hypothesis, a
2-min coronary occlusion was made during the last min of a 18-min submaximal exercise
test in dogs with healed myocardial infarctions; 20 had VF (susceptible), and 13 did not
(resistant). The dogs then received either a 10-wk exercise program (susceptible, n=9;
resistant, n=8) or an equivalent sedentary period (susceptible, n=11; resistant, n=5). HRV
was evaluated at rest, during exercise, and during a 2-min occlusion at rest and before
and after the 10-wk period. Pretraining, the occlusion provoked significantly (P<0.01)
greater increases in HR (susceptible, 54.9+/-8.3 vs. resistant, 25.0+/-6.1 beats/min) and
greater reductions in HRV (susceptible, -6.3+/-0.3 vs. resistant, -2.8+/-0.8 ln ms2) in the
susceptible dogs compared with the resistant animals. Similar response differences
between susceptible and resistant dogs were noted during submaximal exercise. Training
significantly reduced the HR and HRV responses to the occlusion (HR, 17.9+/-11.5
beats/min; HRV, -1.2+/-0.8, ln ms2) in the susceptible dogs; similar response reductions
were noted during exercise. In contrast, these variables were not altered in the sedentary
susceptible dogs. Posttraining, VF could no longer be induced in the susceptible dogs,
whereas four sedentary susceptible dogs died during the 10-wk control period, and the
remaining seven animals still had VF when tested. Atropine decreased HRV but only
induced VF in one of eight trained susceptible dogs. Thus exercise training increased
cardiac vagal activity, which was not solely responsible for the training-induced VF
protection.
Borjesson, M., D. Assanelli, et al. (2006). "ESC Study Group of Sports Cardiology:
recommendations for participation in leisure-time physical activity and competitive sports for
patients with ischaemic heart disease." Eur J Cardiovasc Prev Rehabil 13(2): 137-49.
BACKGROUND: Evidence for the proper management of ischemic heart disease (IHD)
in the general population is well established, but recommendations for physical activity
and competitive sports in these patients are scarce. The aim of the present paper was to
provide such recommendations to complement existing ESC and international guidelines
24
on rehabilitation and primary/secondary prevention. DESIGN AND METHODS: Due to
the lack of studies in this field, the current recommendations are the result of consensus
among experts. Sports are classified into low/moderate/high dynamic and
low/moderate/high static, respectively. RESULTS: Patients with a definitive IHD and
higher probability of cardiac events are not eligible for competitive sports (CS) but for
individually designed leisure time physical activity (LPA); patients with definitive IHD
and lower probability of cardiac events as well as those with no IHD but with a positive
exercise test and high risk profile (SCORE > 5%) are eligible for low/moderate static and
low dynamic (IA-IIA) sports and individually designed LPA. Patients without IHD and a
high risk profile+ a negative exercise-test and those with a low risk profile (SCORE <
5%) are allowed all LPA and competitive sports with a few exceptions.
CONCLUSIONS: Individually designed LPA is possible and encouraged in patients with
and without established IHD. Competitive sports may be restricted for patients with IHD,
depending on the probability of cardiac events and the demands of the sport according to
the current classification.
Chowdhury, P. S., B. A. Franklin, et al. (2003). "Sudden cardiac death after manual or automated
snow removal." Am J Cardiol 92(7): 833-5.
To examine the proximate circumstances of sudden cardiac death (SCD) in the setting of
major snowstorms, we reviewed records from the medical examiners' offices of 3
counties in the weeks before, during, and after 2 heavy snowfalls that occurred in the
greater metropolitan Detroit area. Of those who experienced SCD due to atherosclerotic
cardiovascular disease (n = 271), 36 (33 men, 3 women) were engaged in snow removal,
representing the largest number of exertion-related deaths after heavy snowfalls reported
to date.
Corrado, D., C. Basso, et al. (2003). "Does sports activity enhance the risk of sudden death in
adolescents and young adults?" J Am Coll Cardiol 42(11): 1959-63.
OBJECTIVES: We sought to assess the risk of sudden death (SD) in both male and
female athletes age 12 to 35 years. BACKGROUND: Little is known about the risk of SD
in adolescents and young adults engaged in sports. METHODS: We did a 21-year
prospective cohort study of all young people of the Veneto Region of Italy. From 1979 to
1999, the total population of adolescents and young adults averaged 1,386,600 (692,100
males and 694,500 females), of which 112,790 (90,690 males and 22,100 females) were
competitive athletes. An analysis by gender of risk of SD and underlying pathologic
substrates was performed in the athletic and non-athletic populations. RESULTS: There
were 300 cases of SD, producing an overall cohort incidence rate of 1 in 100,000 persons
per year. Fifty-five SDs occurred among athletes (2.3 in 100,000 per year) and 245
among non-athletes (0.9 in 100,000 per year), with an estimated relative risk (RR) of 2.5
(95% confidence interval [CI] 1.8 to 3.4; p < 0.0001). The RR of SD among athletes
versus non-athletes was 1.95 (CI 1.3 to 2.6; p = 0.0001) for males and 2.00 (CI 0.6 to 4.9;
p = 0.15) for females. The higher risk of SD in athletes was strongly related to underlying
cardiovascular diseases such as congenital coronary artery anomaly (RR 79, CI 10 to
3,564; p < 0.0001), arrhythmogenic right ventricular cardiomyopathy (RR 5.4, CI 2.5 to
11.2; p < 0.0001), and premature coronary artery disease (RR 2.6, CI 1.2 to 5.1; p =
0.008). CONCLUSIONS: Sports activity in adolescents and young adults was associated
25
with an increased risk of SD, both in males and females. Sports, per se, was not a cause
of the enhanced mortality, but it triggered SD in those athletes who were affected by
cardiovascular conditions predisposing to life-threatening ventricular arrhythmias during
physical exercise.
Digenio, A. G., J. G. Sim, et al. (1991). "Exercise-related cardiac arrest in cardiac rehabilitation.
The Johannesburg experience." S Afr Med J 79(4): 188-91.
Prescribed physical activity plays a major role in the rehabilitation of patients with
coronary artery disease, and as with any other form of treatment its benefits must be
weighed against its possible risks. This study attempted to establish the safety of cardiac
rehabilitation as a medical intervention at the Johannesburg Cardiac Rehabilitation Centre
from its inception in September 1982 to July 1988, and analyses the medical status of
patients who suffered a cardiac arrest (CA) in order to determine possible factors
predictive of sudden death. Between September 1982 and July 1988, 1,574 patients were
admitted to the unit; 480,000 man-hours of exercises were accumulated with 4 episodes
of CA, giving an incidence of CA of 1/120,000 patient-hours. Three of the 4 episodes
were fatal, giving an incidence of fatal CA of 1/160,000 patient-hours. This incidence is
acceptably low and comparable with other cardiac rehabilitation programmes, making
exercise as prescribed at the Johannesburg Cardiac Rehabilitation Centre a safe form of
medical intervention. Patients at risk of CA during exercise were essentially not
identifiable, since they did not come from a group currently recognised as at particularly
high risk. A combination of inferior infarction with occluded dominant right coronary
artery, good collateralisation and asymptomatic ischaemia was present in all CA patients.
The likelihood of these pathological features being predictors of exercise-related sudden
death requires further investigation.
Dimsdale, J. E., L. H. Hartley, et al. (1984). "Postexercise peril. Plasma catecholamines and
exercise." JAMA 251(5): 630-2.
Postexercise cardiac morbidity is noted both in the exercise testing laboratory and in the
field, but the physiology of this phenomenon has been unclear. Plasma catecholamine
levels were studied in ten healthy men at each work load during exercise testing and
during the recovery period after exercise. Both norepinephrine and epinephrine levels
increased in response to exercise, although the response was much more noteworthy for
norepinephrine. In the recovery period after exercise, both catecholamine levels
continued to increase, with the norepinephrine level increasing tenfold over baseline.
Such increases may have profound effects, particularly for subjects with preexisting
coronary disease.
Falk, E., P. K. Shah, et al. (1995). "Coronary plaque disruption." Circulation 92(3): 657-71.
Fletcher, G. F., G. J. Balady, et al. (2001). "Exercise standards for testing and training: a
statement for healthcare professionals from the American Heart Association." Circulation
104(14): 1694-740.
Foster, C. and J. P. Porcari (2001). "The risks of exercise training." J Cardiopulm Rehabil 21(6):
347-52.
26
Franklin, B. (1983). "The role of electrocardiographic monitoring in cardiac exercise programs."
J Cardiopulm Rehabil 3: 806-810.
Franklin, B. A. (2005). "Cardiovascular events associated with exercise. The risk-protection
paradox." J Cardiopulm Rehabil 25(4): 189-95; quiz 196-7.
Franklin, B. A., and N.F. Gordon (2007). Contemporary Diagnosis and Management in
Cardiovascular Exercise. Newton, PA, Handbooks in Health Care Co.
Franklin, B. A., K. Bonzheim, et al. (1998). "Safety of medically supervised outpatient cardiac
rehabilitation exercise therapy: a 16-year follow-up." Chest 114(3): 902-6.
Friedewald, V. E., Jr. and D. W. Spence (1990). "Sudden cardiac death associated with exercise:
the risk-benefit issue." Am J Cardiol 66(2): 183-8.
Although there is an overall increased risk of sudden cardiac death associated with
physical exertion, the risk is small. Yet it warrants consideration by physicians and their
adult patients who pursue exercise because, in any individual patient, the risk may be
high. To advise patients properly on the risks and benefits of exercise, physicians should
have an understanding of the risks of exercise, a strategy for patient evaluation that
effectively identifies patients at risk, and a knowledge of appropriate exercise procedures
that minimize risk. Patients should also know proper exercise procedures, be aware that
there is some degree of risk in exercise, know their exercise tolerance, understand selfmonitoring procedures, and be sensitive to prodromal symptoms. The essential feature of
prudent exercise is a gradual progression during which an individual remains well within
the limits of his/her exercise tolerance.
Giri, S., P. D. Thompson, et al. (1999). "Clinical and angiographic characteristics of exertionrelated acute myocardial infarction." JAMA 282(18): 1731-6.
CONTEXT: Vigorous physical exertion transiently increases the risk of acute myocardial
infarction (MI), but little is known about the clinical characteristics of exertion-related
MI. OBJECTIVE: To compare the clinical and angiographic characteristics of patients
who had an exertion-related acute MI vs those who experienced an MI not related to
exertion. DESIGN AND SETTING: Prospective observational cohort study of patients
with an acute MI referred to a tertiary care hospital for primary angioplasty. PATIENTS:
Of 1048 patients with acute MI, 640 (64 who experienced an exertion-related MI and 576
who did not) were selected for treatment with primary angioplasty and admitted between
August 1995 and November 1998. MAIN OUTCOME MEASURES: Clinical
characteristics of the patients, including their habitual physical activity (determined by
the Framingham Physical Activity Index and the Lipid Research Clinic Physical Activity
Questionnaire), angiographic findings during coronary angiography, and the relative risk
(RR) of MI during exertion. RESULTS: Patients who experienced exertion-related MI
were more frequently men (86% vs 68%), hyperlipidemic (62% vs 40%), and smokers
(59% vs 37%), were more likely to present with ventricular fibrillation (20% vs 11%),
Killip classification III or IV heart failure (44% vs 22%), single-vessel disease (50% vs
28%), and a large thrombus in the infarct artery (64% vs 35%) and were more likely to be
27
classified as having very low or low activity (84% vs 66%). The RR of experiencing an
MI during exertion was 10.1 times greater than the risk at other times (95% confidence
interval [CI], 1.6-65.6), with the highest risk among patients classified as very low active
(RR, 30.5; 95% CI, 4.4-209.9) and low active (RR, 20.9; 95% CI, 3.1-142.1).
CONCLUSION: These results show that exertion-related MIs occur in habitually inactive
people with multiple cardiac risk factors. These individuals may benefit from modest
exercise training and aggressive risk-factor modification before they perform vigorous
physical activity.
Haapaniemi, S., B. A. Franklin, et al. (2007). "Electrocardiographic responses to deer hunting
activities in men with and without coronary artery disease." Am J Cardiol 100(2): 175-9.
To evaluate the cardiac demands of hunting deer, continuous ambulatory
electrocardiograms were obtained in men with and without coronary artery disease
(CAD) and compared with their responses to maximal treadmill testing. A volunteer
sample of 25 middle-aged men (mean +/- SD 55 +/- 7 years of age), 17 of whom had
known CAD, completed the study. Peak heart rate (HR) during 7 different deer hunting
activities was expressed as the mean percentage of the maximal HR (HRmax) attained
during treadmill testing. Periods of sustained sinus tachycardia were identified.
Arrhythmias and ST-segment depression during deer hunting that were not apparent
during treadmill testing were documented. Overall, 22 of 25 subjects demonstrated HR
responses >85% HRmax for 1 to 65 minutes. Ten subjects exceeded the HRmax achieved
during treadmill testing for 1 to 5 minutes. The relative HR response during ambulatory
activity in the field was inversely related to cardiorespiratory fitness, expressed as METs
(r = -0.59; p = 0.0020). Three subjects had ischemic electrocardiograms during deer
hunting, but not during treadmill testing. Complex arrhythmias in the field not detected
by treadmill testing included ventricular bi-trigeminy, ventricular couplets, and 8 runs of
ventricular tachycardia (3 to 28 beats) in 3 subjects with documented CAD. In
conclusion, deer hunting can evoke sustained HRs, ischemic ST-segment depression, and
threatening ventricular arrhythmias in excess of those documented during maximal
treadmill testing. The strenuous nature of deer hunting coupled with presumed
hyperadrenergia and superimposed environmental stresses may contribute to the
excessive cardiac demands associated with this activity.
Hallqvist, J., J. Moller, et al. (2000). "Does heavy physical exertion trigger myocardial
infarction? A case-crossover analysis nested in a population-based case-referent study." Am J
Epidemiol 151(5): 459-67.
To study possible triggering of first events of acute myocardial infarction by heavy
physical exertion, the authors conducted a case-crossover analysis (1993-1994) within a
population-based case-referent study in Stockholm County, Sweden (the Stockholm
Heart Epidemiology Program). Interviews were carried out with 699 myocardial
infarction patients after onset of the disease. These cases represented 47 percent of all
cases in the study base, and 70 percent of all nonfatal cases. The relative risk from
vigorous exertion was 6.1 (95% confidence interval: 4.2, 9.0). The rate difference was 1.5
per million person-hours, and the attributable proportion was 5.7 percent. The risk was
modified by physical fitness, with an increased risk being seen among sedentary subjects
as in earlier studies, but the data also suggested a U-shaped association. In addition, the
28
trigger effect was modified by socioeconomic status. Premonitory symptoms were
common, and this implies risks of reverse causation bias and misclassification of case
exposure information that require methodological consideration. Different techniques
(the use of the usual-frequency type of control information, a pair-matched analysis, and
a standard case-referent analysis) were applied to overcome the threat of misclassification
of control exposure information. A case-crossover analysis in a random sample of healthy
subjects resulted in a relative risk close to unity, as expected.
Haskell, W. L. (1978). "Cardiovascular complications during exercise training of cardiac
patients." Circulation 57(5): 920-4.
The occurrence of major cardiovascular complications during exercise training of cardiac
patients in 30 cardiac rehabilitation programs in North America was determined by
questionnaire. These programs conducted medically supervised cardiac exercise classes
in 103 locations and reported information on 13,570 participants who accumulated a total
of 1,629,634 patient hours of supervised exercise. Cardiovascular complications were
reported as nonfatal or fatal and included cardiac arrest, myocardial infarction and other.
A total of 50 cardiac arrests were observed during exercise, 42 of which were
successfully resuscitated while eight were fatal. Seven myocardial infarctions were
reported; five were nonfatal and two were fatal. Four other fatalities were reported due to
acute cardiopulmonary disorders. The average complication rate for all programs was one
nonfatal and one fatal event every 34,673 and 116,402 patient hours of participation,
respectively. Complication rates are lower in programs which continuously monitor the
electrocardiogram during exercise and are lower when only the experience since 1970 is
evaluated. These data support the recommendation that medically prescribed and
supervised exercise can be performed reasonably safely by medically selected cardiac
patients.
Haskell, W. L., I. M. Lee, et al. (2007). "Physical activity and public health: updated
recommendation for adults from the American College of Sports Medicine and the American
Heart Association." Med Sci Sports Exerc 39(8): 1423-34.
SUMMARY: In 1995 the American College of Sports Medicine and the Centers for
Disease Control and Prevention published national guidelines on Physical Activity and
Public Health. The Committee on Exercise and Cardiac Rehabilitation of the American
Heart Association endorsed and supported these recommendations. The purpose of the
present report is to update and clarify the 1995 recommendations on the types and
amounts of physical activity needed by healthy adults to improve and maintain health.
Development of this document was by an expert panel of scientists, including physicians,
epidemiologists, exercise scientists, and public health specialists. This panel reviewed
advances in pertinent physiologic, epidemiologic, and clinical scientific data, including
primary research articles and reviews published since the original recommendation was
issued in 1995. Issues considered by the panel included new scientific evidence relating
physical activity to health, physical activity recommendations by various organizations in
the interim, and communications issues. Key points related to updating the physical
activity recommendation were outlined and writing groups were formed. A draft
manuscript was prepared and circulated for review to the expert panel as well as to
outside experts. Comments were integrated into the final recommendation. PRIMARY
29
RECOMMENDATION: To promote and maintain health, all healthy adults aged 18 to 65
yr need moderate-intensity aerobic (endurance) physical activity for a minimum of 30
min on five days each week or vigorous-intensity aerobic physical activity for a
minimum of 20 min on three days each week. [I (A)] Combinations of moderate- and
vigorous-intensity activity can be performed to meet this recommendation. [IIa (B)] For
example, a person can meet the recommendation by walking briskly for 30 min twice
during the week and then jogging for 20 min on two other days. Moderate-intensity
aerobic activity, which is generally equivalent to a brisk walk and noticeably accelerates
the heart rate, can be accumulated toward the 30-min minimum by performing bouts each
lasting 10 or more minutes. [I (B)] Vigorous-intensity activity is exemplified by jogging,
and causes rapid breathing and a substantial increase in heart rate. In addition, every adult
should perform activities that maintain or increase muscular strength and endurance a
minimum of two days each week. [IIa (A)] Because of the dose-response relation
between physical activity and health, persons who wish to further improve their personal
fitness, reduce their risk for chronic diseases and disabilities or prevent unhealthy weight
gain may benefit by exceeding the minimum recommended amounts of physical activity.
[I (A)].
Herbert, W. G., D. L. Herbert, et al. (2007). "Cardiovascular emergency preparedness in
recreation facilities at major US universities: college fitness center emergency readiness." Prev
Cardiol 10(3): 128-33.
Recent American Heart Association/American College of Sports Medicine
(AHA/ACSM) guidelines advocate preparticipation screening, planning, and rehearsal for
emergencies and automated external defibrillators in all health/fitness facilities. The
authors evaluated adherence to these recommendations at 158 recreational service
departments in major US universities (51% response rate for 313 institutions queried).
Many made their facilities available to unaffiliated residents, with 39% offering programs
for those with special medical conditions. Only 18% performed universal preparticipation
screening. Twenty-seven percent reported having 1 or more exercise-related instances of
cardiac arrest or sudden cardiac death within the past 5 years. Seventy-three percent had
an automated external defibrillator, but only 6% reported using it in an emergency.
Almost all had written emergency plans, but only 50% posted their plans, and only 27%
performed the recommended quarterly emergency drills. The authors' findings suggest
low awareness of and adherence to the AHA/ACSM recommendations for identifying
individuals at risk for exercise-related cardiovascular complications and for handling
such emergencies in university-based fitness facilities. (
Hoberg, E., G. Schuler, et al. (1990). "Silent myocardial ischemia as a potential link between
lack of premonitoring symptoms and increased risk of cardiac arrest during physical stress." Am
J Cardiol 65(9): 583-9.
The risk of cardiac arrest is increased during strenuous physical exercise in patients with
stable coronary artery disease (CAD). Because premonitoring symptoms are rarely
observed, silent myocardial ischemia may represent the pathophysiological basis for the
induction of malignant ventricular arrhythmias. Holter monitoring was, therefore,
performed in 40 consecutive patients entering a randomized intervention trial on
progression of CAD. In 20 of 21 participants (95%) in the intervention program greater
30
than or equal to 1 episode of silent myocardial ischemia was observed during the initial
training session. The mean duration of silent myocardial ischemia per patient was 25 +/13 min/hr of training session. During normal daily activity only 5 patients (24%)
experienced greater than or equal to 1 episode of silent myocardial ischemia (p less than
0.001) yielding a mean duration of 0.6 +/- 1.3 minutes of silent myocardial ischemia/hr of
ordinary activity per patient (p less than 0.001 vs training session). During a control
period of 24 hours without exercise training the incidence (33%) and mean duration of
silent myocardial ischemia (0.8 +/- 2.1 min/hr/patient) were similar to those during
normal daily activity on the day of the training session. During the training session the
occurrence of frequent or repetitive ventricular arrhythmias was related to 10 silent
myocardial ischemia episodes detected in 5 patients. During normal daily activity in 1
patient only was the onset of malignant ventricular arrhythmias associated with silent
myocardial ischemia (p less than 0.05). Conditions and results of the Holter studies in the
control group patients were comparable to those of the patients in the intervention group
on the day without physical exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Hootman, J. M., C. A. Macera, et al. (2002). "Epidemiology of musculoskeletal injuries among
sedentary and physically active adults." Med Sci Sports Exerc 34(5): 838-44.
PURPOSE: This study describes the types and frequencies of musculoskeletal injuries
among a cohort of adults with above average activity levels who were enrolled in the
Aerobics Center Longitudinal Study (Dallas, TX). METHODS: Participants were adults
aged 20-85 yr who completed a baseline clinical examination (1970-1982) and returned a
mailed follow-up survey in 1986. Participants (5,028 men, 1,285 women) were measured
for aerobic fitness, height, and body weight during the baseline examination. They
reported detailed information about their physical activity levels and injury experiences
on the follow-up survey (1986). An injury was defined as any self-reported soft tissue or
bone injury that occurred within the previous 12 months. Activity-related injuries were
those injuries participants attributed to participation in a formal exercise program.
RESULTS: A quarter of all participants reported a musculoskeletal injury. Of these, 83%
were activity-related. More than 66% of activity-related injuries occurred in the lower
extremity; the knee was listed as the joint most often affected. There were no significant
sex differences in the prevalence of injury, regardless of cause. Sport participants had the
highest proportion of all-cause and activity-related musculoskeletal injuries among both
men and women. Self-perceived severe injuries had a significant negative impact on
physical activity levels since almost 1/3 of subjects reported permanently stopping their
exercise program after injury. CONCLUSION: These results suggest the need for
developing and implementing injury prevention programs targeted toward moderately
active adults.
Hossack, R. F., and R. Hartwig (1982). "Cardiac arrest associated with supervised cardiac
rehabilitation." J Cardiac Rehabil 2: 402-408.
Jones, B. H. and J. J. Knapik (1999). "Physical training and exercise-related injuries.
Surveillance, research and injury prevention in military populations." Sports Med 27(2): 111-25.
Athletes and soldiers must both develop and maintain high levels of physical fitness for
the physically demanding tasks they perform; however, the routine physical activity
31
necessary to achieve and sustain fitness can result in training-related injuries. This article
reviews data from a systematic injury control programme developed by the US Army.
Injury control requires 5 major steps: (i) surveillance to determine the size of the injury
problem; (ii) studies to determine causes and risk factors for these injuries; (iii) studies to
ascertain whether proposed interventions actually reduce injuries; (iv) implementation of
effective interventions; and (v) monitoring to see whether interventions retain their
effectiveness. Medical surveillance data from the US Army indicate that unintentional
(accidental) injuries cause about 50% of deaths, 50% of disabilities, 30% of
hospitalisations and 40 to 60% of outpatient visits. Epidemiological surveys show that the
cumulative incidence of injuries (requiring an outpatient visit) in the 8 weeks of US
Army basic training is about 25% for men and 55% for women; incidence rates for
operational infantry, special forces and ranger units are about 10 to 12 injuries/100
soldier-months. Of the limited-duty days accrued by trainees and infantry soldiers who
were treated in outpatient clinics, 80 to 90% were the result of training-related injuries.
US Army studies document a number of potentially modifiable risk factors for these
injuries, which include high amounts of running, low levels of physical fitness, high and
low levels of flexibility, sedentary lifestyle and tobacco use, amongst others. Studies
directed at interventions showed that limiting running distance can reduce the risk for
stress fractures, that the use of ankle braces can reduce the likelihood of ankle sprains
during airborne operations and that the use of shock-absorbing insoles does not reduce
stress fractures during training. The US Army continues to develop a comprehensive
injury prevention programme encompassing surveillance, research, programme
implementation and monitoring. The findings from this programme, and the general
principles of injury control therein, have a wide application in civilian sports and exercise
programmes.
Kestin, A. S., P. A. Ellis, et al. (1993). "Effect of strenuous exercise on platelet activation state
and reactivity." Circulation 88(4 Pt 1): 1502-11.
BACKGROUND. It has been hypothesized that platelets are activated, or made more
activatible, by strenuous exercise and that these changes may play a role in the genesis of
exercise-induced coronary ischemia. Previous studies have yielded conflicting results but
have used assays (eg, platelet aggregation, plasma platelet factor 4, and plasma betathromboglobulin) that are subject to methodological problems. METHODS AND
RESULTS. In the present study, a whole blood flow cytometric method was used to
study the platelet activation state and reactivity of 12 physically active and 12 sedentary
individuals before and after standardized treadmill exercise testing. The peptide gly-proarg-pro (GPRP) was included in this assay to prevent fibrin polymerization and platelet
aggregation, thus allowing the measurement of the reactivity to thrombin of individual
platelets in the physiological milieu of whole blood. A panel of fluorescent-labeled
monoclonal antibodies was used to monitor activation-dependent platelet surface
changes: downregulation of glycoprotein (GP) Ib (6D1) and upregulation of GMP-140
(S12), the GPIIb-IIIa complex (PAC1), and GPIV (OKM5). In samples obtained before
exercise, platelets not exposed to thrombin showed no evidence of in vitro activation. In
the sedentary subjects, exercise caused a consistent and significant augmentation of the
platelet activation state and reactivity as judged by the binding of 6D1 in the presence of
thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P = .001), and 0 U/mL (P = .004) and by
32
the binding of OKM5 in the presence of thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P
= .029), and 0 U/mL (P = .035). Exercise increased the binding of PAC1 at only a single
thrombin concentration (0.005 U/mL, P = .027) and did not alter the binding of S12 at
any thrombin concentration. In contrast, in the physically active subjects, exercise failed
to cause a consistent alteration in either platelet activation state or platelet reactivity. No
significant differences were found between the 12 male and 12 female volunteers.
CONCLUSIONS. Strenuous exercise in sedentary subjects but not physically active
subjects resulted in both platelet activation and platelet hyperreactivity. These changes
were more readily detected with monoclonal antibodies directed against GPIb (6D1) and,
to a lesser extent, GPIV (OKM5) rather than those directed against the GPIIb-IIIa
complex (PAC1) and GMP-140 (S12). Platelet activation by thrombin, generally
regarded as the most physiologically important agonist, can be studied in whole blood in
a clinical setting through the use of the peptide GPRP.
Mann, G. V., H. L. Garrett, et al. (1969). "Exercise to prevent coronary heart disease. An
experimental study of the effects of training on risk factors for coronary disease in men." Am J
Med 46(1): 12-27.
McInnis, K., W. Herbert, et al. (2001). "Low compliance with national standards for
cardiovascular emergency preparedness at health clubs." Chest 120(1): 283-8.
There is heightened concern that older adults and individuals with occult or known heart
disease are exercising at fitness facilities that do not provide adequate cardiovascular
screening and emergency procedures, as outlined in contemporary recommendations. To
evaluate adherence to these standards, we surveyed 122 randomly chosen fitness clubs in
Ohio (53% response rate; n = 65) that included > 110,000 total members. Special
programs for older adults, cardiac patients, or both, were offered at 52% of these clubs.
More than one fourth of the clubs (28%) failed to employ pre-entry screening to identify
members with signs, symptoms, or history of cardiovascular disease, even though 17%
reported one or more cardiovascular emergencies (ie, acute myocardial infarction, sudden
cardiac death, or both) in their facility during the past 5 years. Moreover, a majority of
the clubs (53%) had no written emergency response plan and 92% failed to conduct
emergency response drills as described in published national standards. Only 3% of the
centers reported having automated external defibrillators. These findings indicate that
staff at public fitness facilities must work to identify members with signs, symptoms, or
history of cardiovascular disease and prepare for prompt and appropriate responses to
cardiovascular emergencies as described in contemporary national recommendations.
Such risk management procedures may reduce exercise-related cardiovascular events
among the escalating number of moderate-to-high-risk adults who are being
mainstreamed into health and fitness facilities.
Medicine, A. C. o. S. (2005). Guidelines for Exercise Testing and Prescription. Baltimore, MD,
Lippincott, Williams, and Wilkins.
Meyer, K., L. Samek, et al. (1995). "Relationship between ventilatory threshold and onset of
ischaemia in ECG during stress testing." Eur Heart J 16(5): 623-30.
33
The study was carried out to determine the relationship between ventilatory threshold and
the onset of ischaemia, as shown on the ECG (horizontal and/or descending ST
depression of 0.05 mV, on average). Twenty-seven male patients (aged 58 +/- 7 years)
with angiographically documented coronary artery disease (CAD) were assessed by
cardiopulmonary exercise testing without medication. Oxygen uptake (VO2), heart rate
(HR), rate-pressure-product (RPP) and blood lactate were measured and/or calculated
every 30 s during exercise. In addition, 10 patients, comparable with the above group,
were examined to find out the acute effects of isosorbide dinitrate (ISDN) at ventilatory
threshold in relation to ischaemic threshold. The first cardiopulmonary exercise test was
carried out without medication, the second 1 h later with 5 mg ISDN, taken sublingually
30 min before the test. RESULTS: (means, SD): (1) The mean ventilatory threshold
preceded the ischaemic threshold in relation to exercise capacity (48 +/- 14 vs 55 +/- 20
watts; P < 0.05), VO2.kg-1 (10.0 +/- 2.2 vs 12.0 +/- 2.9 ml.kg-1.min; P < 0.05), HR (93
+/- 15 vs 100 +/- 16.min-1; P < 0.01), RPP (15095 +/- 4424 vs 17166 +/- 5245; P < 0.01)
and blood lactate (1.28 +/- 0.53 vs 1.44 +/- 0.60 mmol.l-1; P < 0.05). (2) This relationship
was observed more often in the subgroup of patients with angina during cardiopulmonary
exercise testing or with myocardial infarction or with three-vessel disease than in patients
without angina or infarction or with one- and two-vessel disease.(ABSTRACT
TRUNCATED AT 250 WORDS)
Mittleman, M. A. (2002). "Triggers of acute cardiac events: new insights." Am J Med Sports 4:
99-102.
Mittleman, M. A., M. Maclure, et al. (1993). "Triggering of acute myocardial infarction by
heavy physical exertion. Protection against triggering by regular exertion. Determinants of
Myocardial Infarction Onset Study Investigators." N Engl J Med 329(23): 1677-83.
BACKGROUND. Despite anecdotal evidence suggesting that heavy physical exertion
can trigger the onset of acute myocardial infarction, there have been no controlled studies
of the risk of myocardial infarction during and after heavy exertion, the length of time
between heavy exertion and the onset of symptoms (induction time), and whether the risk
can be modified by regular physical exertion. To address these questions, we collected
data from patients with confirmed myocardial infarction on their activities one hour
before the onset of myocardial infarction and during control periods. METHODS.
Interviews with 1228 patients conducted an average of four days after myocardial
infarction provided data on their usual annual frequency of physical activity and the time,
type, and intensity of physical exertion in the 26 hours before the onset of myocardial
infarction. We compared the observed frequency of heavy exertion (6 or more metabolic
equivalents) with the expected values using two types of self-matched analyses based on
a new case-crossover study design. The low frequency of heavy exertion during the
control periods was validated by data from a population-based control group of 218
subjects. RESULTS. Of the patients, 4.4 percent reported heavy exertion within one hour
before the onset of myocardial infarction. The estimated relative risk of myocardial
infarction in the hour after heavy physical exertion, as compared with less strenuous
physical exertion or none, was 5.9 (95 percent confidence interval, 4.6 to 7.7), Among
people who usually exercised less than one, one to two, three to four, or five or more
times per week, the respective relative risks were 107 (95 percent confidence interval, 67
34
to 171), 19.4 (9.9 to 38.1), 8.6 (3.6 to 20.5), and 2.4 (1.5 to 3.7). Thus, increasing levels
of habitual physical activity were associated with progressively lower relative risks. The
induction time from heavy exertion to the onset of myocardial infarction was less than
one hour, and symptoms usually began during the activity. CONCLUSIONS. Heavy
physical exertion can trigger the onset of acute myocardial infarction, particularly in
people who are habitually sedentary. Improved understanding of the mechanisms by
which heavy physical exertion triggers the onset of myocardial infarction and the manner
in which regular exertion protects against it would facilitate the design of new preventive
approaches.
Mora, S., N. Cook, et al. (2007). "Physical activity and reduced risk of cardiovascular events:
potential mediating mechanisms." Circulation 116(19): 2110-8.
BACKGROUND: Higher levels of physical activity are associated with fewer
cardiovascular disease (CVD) events. Although the precise mechanisms underlying this
inverse association are unclear, differences in several cardiovascular risk factors may
mediate this effect. METHODS AND RESULTS: In a prospective study of 27,055
apparently healthy women, we measured baseline levels of hemoglobin A1c, traditional
lipids (total, low-density lipoprotein, and high-density lipoprotein cholesterol), novel
lipids [lipoprotein(a) and apolipoprotein A1 and B-100], creatinine, homocysteine, and
inflammatory/hemostatic biomarkers (high-sensitivity C-reactive protein, fibrinogen,
soluble intracellular adhesion molecule-1) and used women's self-reported physical
activity, weight, height, hypertension, and diabetes. Mean follow-up was 10.9+/-1.6
years, and 979 incident CVD events occurred. The risk of CVD decreased linearly with
higher levels of activity (P for linear trend < 0.001). Using the reference group of < 200
kcal/wk of activity yielded age- and treatment-adjusted relative risk reductions associated
with 200 to 599, 600 to 1499, and > or = 1500 kcal/wk of 27%, 32%, and 41%,
respectively. Differences in known risk factors explained a large proportion (59.0%) of
the observed inverse association. When sets of risk factors were examined,
inflammatory/hemostatic biomarkers made the largest contribution to lower risk (32.6%),
followed by blood pressure (27.1%). Novel lipids contributed less to CVD risk reduction
compared with traditional lipids (15.5% and 19.1%, respectively). Smaller contributions
were attributed to body mass index (10.1%) and hemoglobin A1c/diabetes (8.9%),
whereas homocysteine and creatinine had negligible effects (< 1%). CONCLUSIONS:
The inverse association between physical activity and CVD risk is mediated in substantial
part by known risk factors, particularly inflammatory/hemostatic factors and blood
pressure.
Muller, J. E. (1989). "Morning increase of onset of myocardial infarction. Implications
concerning triggering events." Cardiology 76(2): 96-104.
During the past 5 years it has been clearly established that there is a prominent morning
increase in the frequency of onset of acute myocardial infarction. Similar increases have
also been observed for the related conditions of sudden cardiac death, stroke and episodes
of transient myocardial ischemia. The period from 6 a.m. to noon is also a time when a
number of physiologic processes that could contribute to the onset of coronary
thrombosis are intensified. Arterial pressure, which could lead to plaque rupture, rises;
coronary tone increases; and platelet aggregability, which could contribute to a
35
hypercoagulable state, increases. The immediate significance of these observations is the
emphasis that should be placed on pharmacologic protection of patients during the
morning hours. The primary longer-term significance of the recognition of the morning
increase of onset of acute cardiovascular disease is the contribution it makes to the
concept that onset of coronary thrombosis at any time of the day is frequently triggered
by the activities of the patient. Investigation of this possibility may yield more
information about the mechanism of disease onset and facilitate design of more effective
preventive therapy.
Murray, P. M., D. M. Herrington, et al. (1993). "Should patients with heart disease exercise in
the morning or afternoon?" Arch Intern Med 153(7): 833-6.
OBJECTIVE: To compare the cardiovascular risk of exercise in the morning and
afternoon in patients with established heart disease. DESIGN: Retrospective cohort study.
PATIENTS: Patients with established heart disease referred for participation in a
comprehensive cardiac rehabilitation program. INTERVENTION: Supervised,
submaximal exercise (1 hour three times per week) performed either in the morning (7:30
AM) or the afternoon (3 PM). MAIN OUTCOME: Documented cardiac events that
occurred while patients were exercising in the rehabilitation programs. RESULTS: There
were five cardiac events in 168,111 patient-hours of exercise in the morning, with an
incidence of 3.0 +/- 1.3 events per 100,000 patient-hours. There were two events during
the 84,491 patient-hours of exercise in the afternoon, for an incidence of 2.4 +/- 1.5
events per 100,000 patient-hours (not significant). The risk ratio of cardiac events during
exercise in the morning compared with the afternoon was 1.27 (95% confidence interval,
0.25 to 6.55). CONCLUSION: In patients with coronary artery disease, the incidence of
cardiac events is low during regular, submaximal exercise whether performed in the
morning or the afternoon.
Nishi, I., T. Noguchi, et al. (2007). "Are cardiac events during exercise therapy for heart failure
predictable from the baseline variables?" Circ J 71(7): 1035-9.
BACKGROUND: Exercise training (ET) is an emerging therapy for chronic heart failure,
but the baseline patient characteristics for predicting cardiac events (CEs) during the
course of ET remain unknown. METHODS AND RESULTS: Of the 111 stable heart
failure patients who participated in a 3-month ET program, 6 withdrew from the program
for cardiac reasons and 9 had transient interruptions in the program because of CEs. The
baseline clinical characteristics of these 15 patients (CE group) and the remaining 96
patients (No-CE group) were compared. Compared with the No-CE group, the CE group
had a significantly higher prevalence of pacemaker/implantable cardioverterdefibrillators, larger left ventricular end-diastolic diameter (LVEDDs), lower peak
oxygen uptake, greater ventilation drive, and higher plasma brain natriuretic peptide
concentration at baseline. Multivariate logistic regression analysis showed that a larger
LVEDD was a significant predictor of the occurrence of a transient interruption to or
permanent withdrawal from the ET program because of CEs. Receiver operating
characteristic curve analysis demonstrated that an LVEDD > or = 65 mm had a
sensitivity of 93% and specificity of 48% in predicting CEs. CONCLUSIONS: Patients
with a large LVEDD (> or = 65 mm) at baseline should be monitored carefully during the
course of an ET program.
36
Northcote, R. J., C. Flannigan, et al. (1986). "Sudden death and vigorous exercise--a study of 60
deaths associated with squash." Br Heart J 55(2): 198-203.
The circumstances surrounding 60 sudden deaths (59 men, one woman) associated with
squash playing are described. The mean age (SD) of those who died was 46 (10.3) years
(range 22-66 years). Necropsy reports were available in 51. The certified cause of death
was coronary artery disease in 51 cases, valvar heart disease in four, cardiac arrhythmia
in two cases, and hypertrophic cardiomyopathy in one case. There were only two deaths
from non-cardiac causes. Forty five of those who died had reported prodromal symptoms,
the most common of which was chest pain, and 22 were known to have had at least one
medical condition related to the cardiovascular system during life, the most common of
which was systemic hypertension (14 subjects). Those dying from coronary artery disease
had a high frequency of risk factors. Some of these deaths might have been prevented by
appropriate counselling of players after prospective medical screening, which would have
detected most of the patients with overt cardiovascular disease and some of those with
subclinical coronary artery disease.
Pavy, B., M. C. Iliou, et al. (2006). "Safety of exercise training for cardiac patients: results of the
French registry of complications during cardiac rehabilitation." Arch Intern Med 166(21): 232934.
BACKGROUND: Cardiac rehabilitation is widely recognized as a medical management
procedure that reduces mortality, but the cardiovascular safety of exercise training has
not been clearly established. Published data are retrospective or outdated, as patient
management has substantially progressed in recent years. The aim of this prospective
registry was to determine the current complication rate during exercise performed in the
course of cardiac rehabilitation. METHODS: This study was conducted by the Functional
Evaluation and Cardiac Rehabilitation Working Group of the French Society of
Cardiology. During a 1-year period, 65 cardiac rehabilitation centers reported that serious
events had occurred during or 1 hour after an exercise stress test or a training session.
Severe cardiovascular events were validated by a scientific committee. RESULTS: A
total of 25,420 patients (78% men; mean age, 61.3 years) were included in the study.
Initial indications for cardiac rehabilitation were post-cardiac surgery (coronary bypass,
34.3%; valvular surgery, 18.4%); recent percutaneous coronary intervention (21.6%); and
other coronary (13.2%) and noncoronary (12.5%) conditions. The study population
underwent 42,419 exercise stress tests and 743,471 patient-hours of exercise training.
Twenty severe cardiac events were reported: 5 were related to exercise testing and 15
were related to exercise training. The event rate was 1 per 8484 exercise stress tests and 1
per 49,565 patient-hours of exercise training; the cardiac arrest rate was 1.3 per million
patient-hours of exercise. Neither fatal complications nor emergency defibrillations were
reported. CONCLUSION: The frequency of major cardiovascular complications during
supervised exercise training in France is quite low.
Pelliccia, A., D. Corrado, et al. (2006). "Recommendations for participation in competitive sport
and leisure-time physical activity in individuals with cardiomyopathies, myocarditis and
pericarditis." Eur J Cardiovasc Prev Rehabil 13(6): 876-85.
37
Several relatively uncommon, but important cardiovascular diseases are associated with
increased risk for acute cardiac events during exercise (including sudden death), such as
hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), arrhythmogenic
right ventricular cardiomyopathy (ARVC) and myo-pericarditis. Practising cardiologists
are frequently asked to advise on exercise programmes and sport participation in young
individuals with these cardiovascular diseases. Indeed, many asymptomatic (or mildly
symptomatic) patients with cardiomyopathies aspire to a physically active lifestyle to
take advantage of the many documented benefits of exercise. While recommendations
dictating the participation in competitive sport for athletes with cardiomyopathies and
myo-pericarditis have recently been published as a consensus document of the European
Society of Cardiology, no European guidelines have addressed the possible participation
of patients with cardiomyopathies in recreational and amateur sport activities. The
present document is intended to offer a comprehensive overview to practising
cardiologists and sport physicians of the recommendations governing safe participation in
different types of competitive sport, as well as the participation in a variety of
recreational physical activities and amateur sports in individuals with cardiomyopathies
and myo-pericarditis. These recommendations, based largely on the experience and
insights of the expert panel appointed by the European Society of Cardiology, include the
most up-to-date information concerning regular exercise and sports activity in patients
with cardiomyopathies and myo-pericarditis.
Physiology, C. S. f. E. (1994). PAR-Q and You.
Pollock, M. L., L. R. Gettman, et al. (1977). "Effects of frequency and duration of training on
attrition and incidence of injury." Med Sci Sports 9(1): 31-6.
Eighty-seven male inmates from a state prison and 70 inmates from a county jail
volunteered as subjects. The subjects, age 20 to 35 yrs, were assigned randomly into a
control or exercise group. Their Vo2max and treadmill performance values were
determined before and after a 20 week jogging program. Training intensity was between
85 and 90 percent of maximum heart rate and involved workouts 3 days/week for 15, 30,
or 45-min duration at the state prison and for 30-min 1, 3, or 5 days/week at the country
jail. Cardiorespiratory fitness improved in direct proportion to frequency and duration of
training. Injury, occurred in 22%, 24% and 54% of the 15, 30, and 45-min duration
groups and in 0%, 12%, and 39% of the 1, 3, and 5-day/week groups, respectively.
Attrition resulting from injury occurred in 0%, 0%, and 17% and in 0%, 4%, and 6% of
the same respective groups. Attrition due to lack of interest was similar for all training
groups (25%), but was significantly lower in the control groups (10%). Although the
results showed a greater increase in cardiorespiratory fitness for the 45-min duration and
5-day/week groups, these programs are not recommened for beginning joggers because of
the significantly greater percent of injuries.
Powell, K. E., P. D. Thompson, et al. (1987). "Physical activity and the incidence of coronary
heart disease." Annu Rev Public Health 8: 253-87.
Our review focuses on all articles in the English language that provide sufficient data to
calculate a relative risk or odds ratio for CHD at different levels of physical activity. The
inverse association between physical activity and incidence of CHD is consistently
38
observed, especially in the better designed studies; this association is appropriately
sequenced, biologically graded, plausible, and coherent with existing knowledge.
Therefore, the observations reported in the literature support the inference that physical
activity is inversely and causally related to the incidence of CHD. The two most
important observations in this review are, first, better studies have been more likely than
poorer studies to report an inverse association between physical activity and the incidence
of CHD and, second, the relative risk of inactivity appears to be similar in magnitude to
that of hypertension, hypercholesterolemia, and smoking. These observations suggest that
in CHD prevention programs, regular physical activity should be promoted as vigorously
as blood pressure control, dietary modification to lower serum cholesterol, and smoking
cessation. Given the large proportion of sedentary persons in the United States (91), the
incidence of CHD attributable to insufficient physical activity is likely to be surprisingly
large. Therefore, public policy that encourages regular physical activity should be
pursued.
Ragosta, M., J. Crabtree, et al. (1984). "Death during recreational exercise in the State of Rhode
Island." Med Sci Sports Exerc 16(4): 339-42.
From January 1, 1975 to May 1, 1982, 81 individuals died during or immediately after
recreational exercise in the State of Rhode Island. Deaths occurred during a variety of
activities, but the majority of deaths occurred during golf (23%), jogging (20%), and
swimming (11%). Atherosclerotic coronary heart disease (ASHD) was the presumed
cause of 88% of the deaths, primarily in subjects over age 29 with known cardiac
abnormalities. Only 7% of ASHD victims had no relevant medical history or ASHD risk
factors and were considered healthy by their families and physicians. In contrast, deaths
in young subjects were rarely associated with ASHD or prior knowledge of
cardiovascular disease. Only six deaths in individuals aged 29 or younger occurred
during the study period. These deaths were associated with congenital cardiovascular
disease (N = 2), valvular heart disease (N = 1), hemorrhagic gastritis (N = 1), idiopathic
myocardial hypertrophy (N = 1), and hypertrophic cardiomyopathy with ASHD (N = 1).
A diagnosis was made before death only in the individual with valvular disease. We
conclude that death during recreational exercise is predominantly due to ASHD and
occurs in men with recognized ASHD risk factors, relevant medical histories, or known
disease. Death during exercise in asymptomatic subjects is rare and relatively more
frequent in younger age groups.
Raum, E., D. Rothenbacher, et al. (2007). "Heavy physical activity: risk or protective factor for
cardiovascular disease? A life course perspective." Ann Epidemiol 17(6): 417-24.
PURPOSE: The objective of this analysis was to examine the impact of lifetime physical
activity (PA) on major cardiovascular disease. METHODS: At the baseline examination
of the ESTHER study, a cohort study with 9953 participants, ages 50-74 years, with a
lifetime history of PA and a physician-diagnosed myocardial infarction or stroke (major
cardiovascular events, MCVE) were documented. The average number of hours per week
of light and heavy PA (occupational and leisure time) between 20 and 50 years of age
were calculated, and their association with the occurrence of MCVE after the age of 50
years was assessed by multiple logistic regression controlling for age, sex, smoking, body
mass index, and education. RESULTS: A total of 569 study participants (6.1%)
39
experienced a MCVE. Participants with no heavy PA at all or >or=40 hours per week had
an increased risk for MCVE compared with study participants with PA up to 7 hours per
week (odds ratios, 95% confidence intervals: 1.65, 1.10-2.46, and 1.69, 1.17-2.45,
respectively). CONCLUSIONS: Both absence and (typically occupation related) excess
of heavy PA during adulthood seem to increase the risk of MCVE. Health effects of
heavy PA are likely to be a matter of type and of dose.
Siscovick, D. S. (1997). "Exercise and its role in sudden cardiac death." Cardiol Clin 15(3): 46772.
This article summarizes available population-based data related to the risk of sudden
cardiac death during exercise and the factors that influence the risk among apparently
healthy adults in the community. Recent evidence puts into perspective the cardiac risks
and benefits of exercise. The data suggest that although the occurrence of sudden cardiac
death during acute bouts of exercise is not a chance occurrence, the transient increase in
risk is outweighed by the cardiac benefits of habitual exercise. The implications of these
findings for both clinical practice and public health are reviewed.
Siscovick, D. S., N. S. Weiss, et al. (1984). "The incidence of primary cardiac arrest during
vigorous exercise." N Engl J Med 311(14): 874-7.
To examine the risk of primary cardiac arrest during vigorous exercise, we interviewed
the wives of 133 men without known prior heart disease who had had primary cardiac
arrest. Cases were classified according to their activity at the time of cardiac arrest and
the amount of their habitual vigorous activity. From interviews with wives of a random
sample of healthy men, we estimated the amount of time members of the community
spent in vigorous activity. Among men with low levels of habitual activity, the relative
risk of cardiac arrest during exercise compared with that at other times was 56 (95 per
cent confidence limits, 23 to 131). The risk during exercise among men at the highest
level of habitual activity was also elevated, but only by a factor of 5 (95 per cent
confidence limits, 2 to 14). However, among the habitually vigorous men, the overall risk
of cardiac arrest--i.e., during and not during vigorous activity--was only 40 per cent that
of the sedentary men (95 per cent confidence limits, 0.23 to 0.67). Although the risk of
primary cardiac arrest is transiently increased during vigorous exercise, habitual vigorous
exercise is associated with an overall decreased risk of primary cardiac arrest.
Thompson, P. D. (1996). "The cardiovascular complications of vigorous physical activity." Arch
Intern Med 156(20): 2297-302.
OBJECTIVE: To review the cardiovascular risks of exercise for practicing physicians.
DATA SOURCES: Relevant medical literature as well as the author's clinical and
research experience on the topic. RESULTS: The predominant causes of exercise-related
cardiovascular complications are congenital abnormalities in young subjects and
atherosclerotic coronary disease in adults. The absolute incidence of exercise deaths is
low. Only approximately 0.75 and 0.13 per 100,000 young male and female athletes and
6 per 100,000 middle-aged men die during exertion per year. Nevertheless, exercise does
acutely and transiently increase the risk of cardiac events. CONCLUSIONS: Routine
cardiovascular testing to prevent exercise events (echocardiography in the young and
exercise testing in adults) has limited usefulness because of the rarity of such events, the
40
cost of screening, and poor predictive accuracy of exercise testing for exercise events.
Physicians should (1) perform routine screening and cardiac auscultation in young
athletes; (2) carefully evaluate exercise-induced symptoms; and (3) ensure that adults
know the symptoms of cardiac ischemia.
Thompson, P. D., B. A. Franklin, et al. (2007). "Exercise and acute cardiovascular events placing
the risks into perspective: a scientific statement from the American Heart Association Council on
Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology."
Circulation 115(17): 2358-68.
Habitual physical activity reduces coronary heart disease events, but vigorous activity can
also acutely and transiently increase the risk of sudden cardiac death and acute
myocardial infarction in susceptible persons. This scientific statement discusses the
potential cardiovascular complications of exercise, their pathological substrate, and their
incidence and suggests strategies to reduce these complications. Exercise-associated
acute cardiac events generally occur in individuals with structural cardiac disease.
Hereditary or congenital cardiovascular abnormalities are predominantly responsible for
cardiac events among young individuals, whereas atherosclerotic disease is primarily
responsible for these events in adults. The absolute rate of exercise-related sudden
cardiac death varies with the prevalence of disease in the study population. The incidence
of both acute myocardial infarction and sudden death is greatest in the habitually least
physically active individuals. No strategies have been adequately studied to evaluate their
ability to reduce exercise-related acute cardiovascular events. Maintaining physical
fitness through regular physical activity may help to reduce events because a
disproportionate number of events occur in least physically active subjects performing
unaccustomed physical activity. Other strategies, such as screening patients before
participation in exercise, excluding high-risk patients from certain activities, promptly
evaluating possible prodromal symptoms, training fitness personnel for emergencies, and
encouraging patients to avoid high-risk activities, appear prudent but have not been
systematically evaluated.
Thompson, P. D., M. P. Stern, et al. (1979). "Death during jogging or running. A study of 18
cases." JAMA 242(12): 1265-7.
We investigated the circumstances of death and the medical and activity histories of 18
individuals who died during or immediately after jogging. Thirteen men died of coronary
heart disease (CHD) and four men and one woman died of other causes. Six CHD
subjects had medical histories relevant to the cardiovascular system, but only one had
diagnosed CHD. Six CHD subjects experienced prodromal symptoms but continued
vigorous exercise programs. Two subjects had exercised less than a month, but most had
trained regularly for years. The CHD risk factors for the CHD cases did not differ
significantly from those for other age-matched, physically active men. Superior physical
fitness does not guarantee protection against exercise deaths. Physicians and exercising
adults should be aware of this fact and give appropriate attention to possible prodromal
symptoms.
Van Camp, S. P. and R. A. Peterson (1986). "Cardiovascular complications of outpatient cardiac
rehabilitation programs." JAMA 256(9): 1160-3.
41
To determine the incidence of major cardiovascular complications in outpatient cardiac
rehabilitation programs, we obtained data from 167 randomly selected cardiac
rehabilitation programs via mailed questionnaires and follow-up telephone calls. These
167 programs reported that 51 303 patients exercised 2 351 916 hours from January 1980
through December 1984. Twenty-one cardiac arrests (18 in which the patient was
successfully resuscitated and three fatal) and eight nonfatal myocardial infarctions were
reported. The incidence rates per million patient hours of exercise were 8.9 for cardiac
arrests (one per 111 996 patient-hours), 3.4 for myocardial infarctions (one per 293 990
patient-hours), and 1.3 for fatalities (one per 783 972 patient-hours). There was no
statistically significant difference in frequency of these events among programs of
varying size or extent of electrocardiographic monitoring. These data indicate that current
cardiac rehabilitation practice allows for prescribed supervised exercise by patients with
cardiovascular disease to be performed at a low risk of major cardiovascular
complications.
Vongvanich, P., M. J. Paul-Labrador, et al. (1996). "Safety of medically supervised exercise in a
cardiac rehabilitation center." Am J Cardiol 77(15): 1383-5.
Medically supervised exercise continues to have a low major cardiovascular complication
rate. Direct gym supervision by a physician does not appear necessary for safety. The
currently proposed cardiac rehabilitation risk stratification criteria do not appear to
identify patients at risk for these major complications. The safety of exercise programs
with less supervision and electrocardiographic telemetry monitoring is unknown.
Vuori, I. (1986). "The cardiovascular risks of physical activity." Acta Med Scand Suppl 711:
205-14.
The incidence of sudden death, serious arrhythmias, and myocardial infarction in
connection with both recreational and rehabilitative physical activity is small. However,
the incidence of e.g. sudden death is several times higher in exercise than at other times.
This relative risk is highest in middle-aged men, and higher in strenuous than in
nonstrenuous exercise. In the vast majority of the cases the underlying cause is advanced
coronary heart disease, which in large proportion of the cases has been asymptomatic and
has allowed regular strenuous training. Attempts to prevent the complications by special
large scale screening programs would be ineffective and individual counselling limited
by lack of resources. These measures should, however, be used in selected groups and
individuals. Another approach is to inform the exercisers and their families at large by
systematic, well-planned and repeated messages of the risks of physical activity, of the
symptoms and findings indicating this risk, of the individual and environmental factors
increasing the risk, and of the necessary measures to be taken to minimize the risk. Even
if all available measures at present were used, the cardiovascular complications of
physical activity could not be totally prevented. Fortunately, preliminary evidence
suggests that at population level the cardiovascular hazards of physical activity are
outweighed by its cardiovascular benefits.
Whang, W., J. E. Manson, et al. (2006). "Physical exertion, exercise, and sudden cardiac death in
women." JAMA 295(12): 1399-403.
42
CONTEXT: Exercise is associated with a lower risk of cardiovascular events but may
transiently increase the risk of ventricular arrhythmias. Its short-term and long-term
associations with risk of sudden cardiac death among women are unclear. OBJECTIVES:
To compare the risk of sudden cardiac death in women during moderate to vigorous
exertion with the risk of sudden cardiac death during lighter or no exertion; and to assess
the long-term association between moderate to vigorous exercise and sudden cardiac
death. DESIGN, SETTING, AND PARTICIPANTS: Prospective, nested case-crossover
study of 288 cases of sudden cardiac death within the Nurses' Health Study (1980-2004);
and a prospective cohort analysis of 69,693 participants without prior cardiovascular
disease followed up from 1986-2004. MAIN OUTCOME MEASURE: Risk of sudden
cardiac death associated with moderate to vigorous exertion. RESULTS: The absolute
risk of sudden cardiac death associated with moderate to vigorous exertion was
exceedingly low at 1 per 36.5 million hours of exertion. In case-crossover analyses, the
risk of sudden cardiac death was transiently elevated during moderate to vigorous
exertion (relative risk [RR], 2.38; 95% confidence interval [CI], 1.23-4.60; P = .01)
compared with the risk during lesser or no exertion. Habitual moderate to vigorous
exertion modified this transient risk (P = .005 for interaction) and the risk was no longer
significantly elevated among those who exercised 2 or more hours per week. In the
cohort analyses, an increasing amount of moderate to vigorous exercise was associated
with a lower long-term risk of sudden cardiac death in age-adjusted and multivariable
models that excluded biological intermediates (P = .006 for trend). This relationship was
attenuated when biological intermediates were included (P = .06 for trend); however, the
reduction in risk remained significant among women who exercised 4 or more hours per
week (adjusted RR, 0.41; 95% CI, 0.20-0.83; P = .01) compared with women who did not
exercise. CONCLUSIONS: These prospective data suggest that sudden cardiac death
during exertion is an extremely rare event in women. Regular exercise may significantly
minimize this small transient risk and may lower the overall long-term risk of sudden
cardiac death.
Willich, S. N., M. Lewis, et al. (1993). "Physical exertion as a trigger of acute myocardial
infarction. Triggers and Mechanisms of Myocardial Infarction Study Group." N Engl J Med
329(23): 1684-90.
BACKGROUND. It is controversial whether the onset of myocardial infarction occurs
randomly or is precipitated by identifiable stimuli. Previous studies have suggested a
higher risk of cardiac events in association with exertion. METHODS. Consecutive
patients with acute myocardial infarction were identified by recording all admissions to
our hospital in Berlin and by monitoring a general population of 330,000 residents in
Augsburg, Germany. Information on the circumstances of each infarction was obtained
by means of standardized interviews. The data analysis included a comparison of patients
with matched controls and a case-crossover comparison (one in which each patient serves
as his or her own control) of the patient's usual frequency of exertion with the last
episode of exertion before the onset of myocardial infarction. RESULTS. From January
1989 through December 1991, 1194 patients (74 percent of whom were men; mean age
[+/- SD], 61 +/- 9 years) completed the interview 13 +/- 6 days after infarction. We found
that 7.1 percent of the case patients had engaged in physical exertion (> or = 6 metabolic
equivalents) at the onset of infarction, as compared with 3.9 percent of the controls at the
43
onset of the control event. For the patients as compared with the matched controls, the
adjusted relative risk of having engaged in strenuous physical activity at the onset of
infarction or the control event was 2.1 (95 percent confidence interval, 1.1 to 3.6). The
case-crossover comparison yielded a similar relative risk of 2.1 (95 percent confidence
interval, 1.6 to 3.1) for having engaged in strenuous physical activity within one hour
before myocardial infarction. Patients whose frequency of regular exercise was less than
four and four or more times per week had relative risks of 6.9 and 1.3, respectively (P <
0.01). CONCLUSIONS. A period of strenuous physical activity is associated with a
temporary increase in the risk of having a myocardial infarction, particularly among
patients who exercise infrequently. These findings should aid in the identification of the
triggering mechanisms for myocardial infarction and improve prevention of this common
and serious disorder.