Download Left ventricular performance during prolonged

Clinical Science (2001) 100, 529–537 (Printed in Great Britain)
Left ventricular performance during prolonged
exercise: absence of systolic dysfunction
Jack M. GOODMAN*, Peter R. McLAUGHLIN† and Peter P. LIU†
*Faculty of Physical Education and Health, University of Toronto, 55 Harbord Street, Toronto, Ontario, Canada M5S 2W6, and
†Heart & Stroke/Richard Lewar Centre of Excellence, Faculty of Medicine, University of Toronto, 150 College Street, rm 8,
Fitzgerald Building, Toronto, Ontario, Canada M5S 3E2
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We assessed left ventricular systolic and diastolic performance during and after prolonged
exercise under controlled conditions in a group of healthy, trained men. Previous studies have
examined the effects of prolonged effort on left ventricular function, yet it remains unclear
whether or not left ventricular dysfunction (e.g. cardiac fatigue) can be produced under such
conditions. We studied 15 healthy men, aged 27p1 years (meanpS.E.M.). Subjects exercised on
bicycles at a constant work rate (60 % of maximum oxygen uptake per min) for 150 min.
Measurements of gas exchange, blood pressure and haematocrit were obtained, concurrent with
the assessment of left ventricular function using equilibrium radionuclide angiography, at rest,
during exercise (every 30 min) and after 30 min of recovery. Fluid replacement was provided and
monitored during the exercise period. The baseline resting and exercise ejection fractions were
66p2 % and 78p2 % respectively. During exercise, subjects consumed 1816p136 ml of fluid, and
the haematocrit had increased at 120 min of exercise (from 47.2 %p0.6 to 49.9p0.8 % ; P 0.05).
There was no change in either systolic or diastolic blood pressure throughout the exercise
period, but heart rate drifted upwards from 141p2 beats/min after 30 min to 154p3 beats/min
after 150 min (P 0.05). There was a small decline (8 % ; P 0.05) in end-diastolic volume at
150 min. No changes were observed in left ventricular ejection fraction, the pressure/volume
ratio or end-systolic volume. After 30 min of sitting in recovery, heart rate was still higher than
the pre-exercise value (84p3 compared with 69p2 beats/min ; P 0.05), as were measures of
peak filling rate and time to peak filling (P 0.05). The ejection fraction in the post-exercise
recovery period was similar to the pre-exercise value. The results indicate that prolonged
exercise of moderate duration may not induce abnormal left ventricular systolic function or
cardiac fatigue during exercise.
INTRODUCTION
The normal left ventricular (LV) response to brief
submaximal exercise in the upright position has been well
characterized [1,2], and includes increases in both heart
rate (HR) and cardiac output, the latter increasing during
low to moderate intensities of exercise due to augmented
HR and stroke volume. Increases in stroke volume are
brought about largely by increased LV filling [1,3],
particularly during exercise performed at a low to
moderate intensity. Beyond this point, further increases
in cardiac output are brought about by continued
increases in HR, and a decrease in end-systolic volume
(ESV) secondary to increased contractility [1,3].
During prolonged exercise, an upward ‘ drift ’ in HR
and a decline in stroke volume characterize the car-
Key words : exercise, heart, left ventricle.
Abbreviations : EF, ejection fraction ; EDV, end-diastolic volume ; ESV, end-systolic volume ; HR, heart rate ; LV, left ventricular ;
RER, respiratory exchange ratio ; Vc O , oxygen uptake.
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Correspondence : Dr Jack M. Goodman (e-mail jack.goodman!utoronto.ca).
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2001 The Biochemical Society and the Medical Research Society
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J. M. Goodman, P. R. McLaughlin and P. P. Liu
Table 1
Studies examining LV systolic and/or diastolic function during prolonged exercise
DFR, diastolic filling rate ; E/A ratio, early/late diastolic flow velocity ; EDD, end-diastolic dimension ; ESD, end-systolic dimension ; FS, fractional shortening ; PVR,
pressure/volume ratio ; Q, cardiac output ; SV, stroke volume ; SBP, systolic blood pressure ; mVCF, mean velocity of circumferential shortening ; 2D, two-dimensional.
Study
Distance/duration
Measurement
technique
Douglas et al. [11]
Douglas et al. [12]
Douglas et al. [10]
Ketelhut et al. [13,17]
Ironman Triathlon
Ironman Triathlon
Ironman Triathlon
60 min cycling
2D echo
Doppler echo
Doppler echo
M-mode echo
Lucı! a et al. [21]
Marathon (42 km)
M-mode and Doppler
echo
Niemela$ et al. [8]
24 h run
M-mode echo
Niemela$ et al. [9]
Palatini et al. [20]
24 h run
50 min cycling
M-mode echo
M-mode echo
Perrault et al. [19]
42 km run
M-mode echo
Seals et al. [14]
Upton et al. [18]
Treadmill walking
120 min cycling
M-mode echo
First-pass RNA
Vanoverschelde et al. [15] 20 km run
Whyte et al. [16]
Half and full
Ironman Triathlon
M-mode and Doppler
echo, carotid
pulse tracings
M-mode and Doppler
echo
Position/recovery
or exercise data
Observations
3–19 min post-exercise
20 min post-exercise
3–23 min post-exercise
Immediately after 5 min and
60 min of exercise
Immediately before and after
exercise, and after 24–36 h
of recovery
Supine/recovery
Supine/recovery
Supine/recovery
Supine/exercise
EF, FS (segmental)
EDD
EDD, FS,
SV, Q, EF, FS ; ESD
Supine/recovery
Immediately to 25 min postexercise
Immediately post-exercise
During exercise at 10 min
intervals
Immediately to 40 min postexercise
10 min post-exercise
During exercise at 60 min
(submaximal) and 120 min
(maximal)
5 min after brief
and prolonged exercise
Supine/recovery
EF, mVCF during
recovery (vs. preexercise) ; E/A
ratio
EDD, ESD, FS, mVCF
Supine/recovery
Semi-supine/recovery
FS, DFR, EDD,
- EF, SV, PVR ; EDV
Supine/recovery
SBP, EF, VCF, ESD, EDD
Supine/recovery
Upright/exercise
FS, mVCF, EDD
- EDV or EF at 60 min
Supine/exercise and rest
ESD, EDD, SBP, FS,
EF (vs. rest), SV
Supine/recovery
EDD, SV, FS, EF for
full Ironman only ; E/A
ratio in both ; normal
48 h ratio
Timing of measurement
2 weeks pre-race ;
immediately after
race and 24 h recovery
diovascular response [4–6]. These responses are thought
to be largely the result of gradual reductions in ventricular
filling pressures and systemic blood pressure. The responses reflect a gradual decline in central blood volume,
probably occurring secondary to a redistribution of
blood volume to the venous capacitance vessels of the
cutaneous circulation through peripheral vasodilatation
[4,6,7]. This circulatory adjustment has been termed
‘ cardiovascular drift ’ [7]. It remains unclear if LV
dysfunction during such activity contributes to the
decrease in stroke volume. Some investigations have
described an impairment of LV function following
exercise of a prolonged nature [8–15]. It is possible that a
decline in ventricular output involves a depression in the
contractile state ; however, despite reports of a transient
decline in systolic function [8–14,16,17] and diastolic
filling characteristics [9,13,16], several studies have failed
to report a decline in LV performance [18–21]. The
disparate findings (Table 1) reflect a wide range of study
designs and physiological conditions. For example, the
studies reporting diminished LV function during pro#
2001 The Biochemical Society and the Medical Research Society
longed exercise failed to control or monitor fluid intake,
which is known to be important during prolonged effort
and may contribute indirectly to the decline in LV filling
pressures and stroke volume [22–25]. In addition, most
were conducted under field conditions that failed to
control for either the intensity of effort or the exercise
time. Moreover, in the majority of cases, LV function was
assessed at varying times during supine recovery. In those
studies reporting an impairment of systolic function, the
finding is typically transient, with normal values reported
after 12–24 h of recovery ; hence the term cardiac
‘ fatigue ’. Despite a low prevalence of cardiac events
during long-distance events such as the marathon (one
event per 50 000 participants) [26], certain individuals
remain predisposed to cardiac dysfunction and cardiac
sudden death during exercise [27]. Thus a more thorough
understanding of the LV response to prolonged exercise
is warranted.
To date, there is very little information describing
serial changes in LV function during prolonged exercise
under controlled conditions, and it remains unclear if a
Left ventricular function during prolonged exercise
true decline in LV systolic performance actually contributes to a reduction in stroke volume and\or a
reduction in cardiovascular performance. Therefore the
purpose of the present study was to examine, using
radionuclide techniques, LV function during constantload exercise and after recovery under controlled laboratory conditions.
METHODS
Subjects
A total of 15 male subjects between the ages of 20 and 30
years were recruited for the study, and each gave
informed consent. The protocol was approved by the
University of Toronto Committee on Human Research.
All subjects had been involved with competitive cycling
for a period of at least 1 year, and were studied after the
competitive cycling season. All subjects were free of any
medication during the course of the study.
Experimental design
All subjects performed two exercise sessions, separated
by a period not exceeding 7 days. Exercise was performed
in a 2-h fasted state, in a laboratory maintained at a
temperature between 21 and 22 mC and a relative humidity between 40 % and 50 %. Baseline data were
obtained during a preliminary graded exercise test before
the prolonged exercise study.
Control data and preliminary exercise test
Prior to exercise, gated equilibrium radionuclide angiography was performed at rest to determine resting LV
function, as described below. Subjects then performed a
graded exercise test to maximum on a cycle ergometer
(Monarch 850), with maximum oxygen uptake (Vc O max)
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determined by the open-circuit method, with expired
gases collected and analysed on a 15 s average basis using
a calibrated metabolic cart (Sensormedics 4400). Following a 45 min rest period, subjects performed an
additional 4 min of exercise at an intensity equivalent to
approx. 60–70 % of Vc O max (as determined earlier) for
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determination of LV function during submaximal exercise. This assessment was used as a ‘ baseline ’ (e.g.
short-term exercise) measurement of LV ejection fraction
(EF) during exercise. Each 1 min during exercise, a 12lead ECG was obtained (Hewlett Packard 4700A), as
were measurements of arterial systolic blood pressure
using an automated blood pressure cuff (Infrasound
D4000), verified by manual auscultation.
Prolonged exercise study
On the second visit, subjects performed prolonged
exercise of 150 min in duration, with the work rate held
constant at 70–74 % of the maximal HR determined
during the initial graded exercise test. A venous catheter
was first positioned in the right antecubital vein, with line
patency maintained with a saline drip during the course
of exercise. Subjects performed prolonged exercise on
‘ turbo-trainers ’, which are stationary training devices
upon which a bicycle is fixed, allowing a rear wheel to
rotate a friction-driven wind turbine which generates
pedalling resistance. The pedalling rate was fixed to a
given subject’s preference (70–80 rev.\min), with the
pedalling resistance adjusted by altering the bicycle gear.
This was fixed for the entire exercise session once a
plateau in target HR equal to 70–74 % of maximum HR
was obtained within the first 10 min of exercise. Once the
pedalling rate and resistance were set, they were monitored every 10 min throughout the exercise session and
kept constant. HRs were monitored continuously
throughout exercise using a portable HR monitor (Sport
Tester PE 3000).
Cardiorespiratory function
After every 30 min of exercise, subjects were transferred
immediately to a cycle ergometer (within 30 s) and
resumed their exercise for 5 min before assessment of
cardiorespiratory function. Each subject’s work rate (in
W) was adjusted to elicit the exercise HR measured
immediately before switching from the turbo trainers,
and this work rate was used for each subsequent
assessment. Both systolic and diastolic blood pressures
were monitored during this sequence of exercise, using an
automated cuff monitor (Infrasound D4000). Expired
gases were collected for a period of 2 min and reported as
an average during this time period. From these data,
minute ventilation, oxygen consumption (Vc O ) and the
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respiratory exchange ratio [RER ; CO production
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(Vc CO )\Vc O ] were determined. All measurements were
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made in the 3rd and 4th min of steady-state exercise.
Blood samples for determination of the haematocrit were
obtained at rest and immediately before cardiorespiratory
measurements, and were analysed in triplicate immediately after sampling using a microhaematocrit scale. In
addition, a general rating of perceived exertion was
obtained every 30 min using the 20-point Borg scale.
Radionuclide angiography and LV function
Concurrent with measurements of expired gases (described above), gated equilibrium radionuclide images
were obtained during exercise, as described previously
[1]. Briefly, each subject received an intravenous injection
of 2 mg of stannous pyrophosphate 15 min before modified in vitro labelling of the red blood cells with 925 MBq
of **mTc pertechnetate. Images for determination of LV
EF during exercise counts were acquired by a highsensitivity γ-radiation camera (Elscint Apex 409 AG\
ECT), with subjects positioned in the left anterior oblique
35–45 m position, with 15 m caudal angulation to optimize
right ventricle and LV separation. The LV EF was
determined by semi-automated edge detection of the
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2001 The Biochemical Society and the Medical Research Society
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J. M. Goodman, P. R. McLaughlin and P. P. Liu
averaged time–activity curve (using 300 cardiac cycles)
corrected for background activity, with a correlation
coefficient of 0.98 and
2 % standard error of the
estimate. LV end-diastolic volume (EDV) and ESV were
determined by a count-based technique [28], which has a
correlation coefficient of 0.96 and a standard error of the
scintigraphic estimate equal to 15.8 ml [29] in our
laboratory. An index of contractility was determined by
using the systolic blood pressure\ESV ratio [30]. Stroke
volume and cardiac output data were derived from the
ventricular volume data. All data for EDV and ESV (for
serial comparison purposes) were corrected for the
physical decay of **mTc and for changes in peripheral
haematocrit obtained at each sampling time period.
Resting diastolic filling rates were determined using
standard techniques [31] at rest and after a 30 min recovery period following prolonged exercise. A 4 min
acquisition of a minimum of 200 cardiac cycles was
performed, which allowed determination of the rapid
filling phase, time to peak filling, peak filling rate, and
atrial kick phase ( %).
Fluid intake
Subjects were provided with fluids ad libitum, and were
encouraged to consume water during exercise (200–
300 ml every 30 min) in an attempt to maintain isovolaemic status. Subjects received intravenous saline
[with 5 % (w\v) dextrose] throughout exercise, at a rate
sufficient to maintain catheter patency during the
150 min period. Total fluid consumption (saline and oral
consumption) was recorded over the 150 min exercise
period for each subject. Body mass (kg) was measured
without clothing and free of perspiration before and after
the exercise session.
Statistical analysis
Differences for each variable between baseline and
exercise measures were analysed using ANOVA for
repeated measures [Statistical Analysis System (SAS),
Carey, NC, U.S.A.]. A post hoc analysis was performed
to determine specific differences between each sample
time period using a Student–Newman–Keuls test. Baseline and recovery measurements of diastolic filling rates
were compared using the Student’s t-test for paired
samples. A probability level of P 0.05 was required for
significance.
Baseline maximal exercise data
The mean Vc O max of the group was 55.9p2.0
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ml:min–":kg–", or 4.06p0.17 litres\min. Subjects
achieved a maximal work rate of 338p11 W, reaching a
maximal HR of 191p3 beats\min. The maximal RER
was 1.20p0.19, and the maximal venous blood lactate
(obtained 3 min post-exercise) was 14.5p0.65 mmol\l.
The baseline LV EF at rest and at 70 % Vc O max was
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66p2 % and 78p2 % respectively.
Prolonged exercise study : cardiorespiratory
and metabolic data
Mean data describing all ventilatory and metabolic
measures are summarized in Table 2. Vc O remained
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constant throughout the exercise session, with only
minor variations evident. A significant decrease in the
RER was observed by 150 min (P 0.05). Venous blood
lactate was unchanged throughout the exercise session.
Ratings of perceived exertion increased by 38 % by the
end of exercise (P 0.01), despite a constant work rate
throughout exercise. Systolic and diastolic blood
pressures remained constant during exercise. However,
there was small and insignificant downward trend in
diastolic pressure.
LV function
Data describing LV function during exercise are presented in Figures 1–3. By the completion of the exercise
period at 150 min, a significant reduction in EDV (P
0.05), without any change in ESV, was observed (Figure
1). Consequently the drop in stroke volume after 90 min
of exercise (P 0.05) was largely due to a decrease in LV
EDV (Figure 1). HR demonstrated a progressive and
significant increase throughout exercise, increasing by
12 % during the course of the exercise period (Figure 2)
(P 0.01). Indices of systolic performance were unchanged during exercise (Figure 3), as EF remained
stable, within 2 % (range 76–78 %) of the 30 min value at
all time points and almost identical to the EF measured at
75 % Vc O max during the initial exercise test (78.6p2.1 %).
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The systolic pressure\volume ratio was also unchanged
throughout exercise (Figure 3). There was no significant
difference between measures of LV function after 30 min
compared with the control values obtained during the
baseline test.
Resting and recovery diastolic filling
measurements
RESULTS
Subject characteristics
All 15 subjects completed the study. The mean age of the
group was 27p1 years (pS.E.M.). The mean height and
body mass for the group were 1.78p0.2 m and
71.9p2.0 kg respectively.
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2001 The Biochemical Society and the Medical Research Society
Resting diastolic filling rates obtained before and after a
30 min recovery period demonstrated a significant
increase in the time to peak filling (0.174p0.01 and
0.201p0.013 ms respectively ; P l 0.02), with no significant change in the peak filling rate (2.72p0.14 and
3.28p0.19 EDV\s respectively ; P l 0.34). The atrial
contribution to stroke volume was unchanged (22.4 %
Left ventricular function during prolonged exercise
Table 2
Cardiorespiratory and metabolic response during 150 min of exercise
V0 E, minute ventilation ; RPE, rating of perceived exertion. Values are meanspS.E.M. Significance of differences : *P
Parameter
Duration of
exercise (min) …
V0 O2 (ml)
V0 E (l/min)
RER
Lactate (mmol/l)
Systolic pressure (mmHg)
Diastolic pressure (mmHg)
Mean arterial pressure (mmHg)
RPE
Figure 1
0n05 compared with 30 min value.
30
60
90
120
150
2458p120
60p3
1n04p0n01
2n8p0n3
158p4
79p2
105p2
10n6p0n6
2408p103
59p3
1n00p0n01
2n7p0n4
164p4
77p2
106p3
11n6p0n5
2461p115
62p3
0n98p0n01
2n6p0n4
163p3
75p3
104p3
12n2p0n4
2451p108
60p3
0n95p0n01*
2n5p0n3
168p3
73p3
104p3
13n4p0n3*
2476p109
61p4
0n93p0.01*
2n7p0n3
165p3
76p3
105p3
14n7p0n5*
LV EDV and ESV during prolonged exercise
Asterisks indicate values significantly different from the 30 min value (P
0.05).
Figure 3 LV EF and the pressure/volume ratio during prolonged exercise
SBP, systolic blood pressure.
Figure 2
HR and stroke volume during prolonged exercise
Asterisks indicate values significantly different from the 30 min value (P
intravenous saline was 443p11 ml, amounting to a mean
total fluid intake of 1816 ml. Haematocrit increased from
47.2p0.6 % at rest to 48.0p1.0 % after 30 min of
exercise. Thereafter a slow rise in haematocrit was
observed to 150 min of exercise, increasing to 49.9
p0.8 % after 60 min, 49.2p0.8 % after 90 min and
49.0p0.8 % at 120 min. The value at 150 min (49.7
p0.9 %) was significantly higher than that observed at
30 min (P 0.05). Body mass decreased slightly from
70.9p2 kg to 70.2p2 kg immediately after exercise, but
the decrease was not significant.
0.05).
p1.6 and 21.2p3.1 % respectively). HR during recovery
was significantly higher than pre-exercise values (84p3
compared with 69p2 beats\min ; P 0.01).
Hydration status : body mass, fluid intake
and haematocrit
The mean oral fluid intake was 1373p116 ml during the
course of exercise. In addition, the mean intake of
DISCUSSION
The decrease in stroke volume and EDV associated with
prolonged exercise is a well established observation [4–7].
We observed a classic upward drift in HR and a decrease
in EDV during 150 min of constant-load exercise. The
decline in EDV led to a non-significant decline in stroke
volume, with no decrease in systolic performance during
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2001 The Biochemical Society and the Medical Research Society
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J. M. Goodman, P. R. McLaughlin and P. P. Liu
exercise. In addition, although we observed a delay in the
time to peak filling, no other abnormality in LV filling
characteristics (peak filling rate or atrial kick) was
observed, nor was there evidence of depressed systolic
performance during the recovery period.
Metabolic and respiratory data
All subjects performed exercise under controlled conditions, yielding an intensity equivalent to 60–70 % of
Vc O max. There was very little variation in intensity
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according to measures of Vc O (Table 2), although the
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ratings of perceived exertion rose steadily with time.
Respiratory data (RER) suggest a shift towards fat
metabolism during the latter stages of exercise, with the
blood lactate concentration remaining steady throughout
the exercise challenge.
LV volumes
Our results are in agreement with previous data describing a decrease in LV EDV during prolonged exercise
[8–16]. We have described a small, non-significant reduction in stroke volume (6 %) during prolonged effort,
secondary to a decrease in EDV late in the exercise
session ; this decrease is markedly less than in some
studies, but comparable with that in one echocardiography study [19]. However, previous studies have
examined subjects after endurance events ranging from
60 min in duration [13] to 42 km in length (e.g. marathon)
[19] to the Ironman Triathlon [10–12,16] to a 24 h run
[8,9]. Comparison between previous studies and the
present data remains problematical, because most of
the former assessed LV function in the supine position,
and none monitored fluid consumption. A redistribution
of central blood volume to the skin vasculature due to
thermoregulatory adjustment would theoretically contribute to reduced ventricular filling according to the
Frank–Starling relationship [6,7]. In fact, it has been the
generally accepted view that cardiovascular drift is indeed
secondary to a rise in cutaneous blood flow, with a
decrease in stroke volume as core temperature rises [7].
As a compensatory measure to mitigate this response,
HR increases progressively in order to maintain cardiac
output. It is possible that we attenuated the declines in
EDV and stroke volume by minimizing plasma volume
loss with fluid replacement. Hamilton et al. [32] showed
that fluid replacement during prolonged exercise arrests
the decline in stroke volume and attenuates the rise in HR
during 120 min of cycling at 70 % of Vc O max. Despite our
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efforts to maintain regular fluid intake (approx. 250 ml\
20 min), we observed a modest decrease in body mass and
a haemoconcentration, suggestive of fluid loss. While
some of this response may be due to compartmental
shifts observed during exercise, such changes are nor#
2001 The Biochemical Society and the Medical Research Society
mally restricted to the initial 10–15 min of exercise [33],
and changes in plasma volume of this magnitude would
not contribute to altered haemodynamics [34].
The direct role of cutaneous blood flow in causing
cardiovascular drift has recently been challenged [35].
Fritzche and colleagues used a selective β-blocker during
60 min of exercise (57 % peak effort), and found that the
reduction in stroke volume was related to HR, but not to
cutaneous blood flow [35]. Thus ventricular filling time
or other factors affecting ventricular diastolic function
may play a dominant role in the diminished stroke
volume response.
Abnormal diastolic filling has been observed during
recovery from prolonged exercise [9,10,14,16,21], suggesting impairment of LV relaxation and\or changes in
compliance. We observed an increase in the time to peak
filling after 30 min of recovery. However, these changes
were concomitant with an increase in HR, which is
related directly to the peak filling rate and inversely to the
time to peak filling [36]. It is therefore difficult to make
meaningful conclusions about diastolic filling owing to
the complexity of its nature and the interactive effects of
HR. These limitations can also be applied to previous
studies reporting impaired diastolic function in recovery.
Although EF can also influence diastolic filling rates
[31,36], there was no change in EF during recovery
compared with pre-exercise values. Afterload reduction
can also enhance diastolic filling, making it difficult to
draw conclusions about ventricular compliance. Our
subjects demonstrated a decrease in systolic blood
pressure during recovery (compared with pre-exercise
resting values), which may in part account for the increase
in the peak filling rate. While others have reported
diminished filling characteristics after exercise [9,11,13],
these data were derived from subjects in the supine
position, and obtained while HRs remained elevated.
LV systolic performance
A rise in EF of at least 5 % is considered a normal LV
response to exercise, with EF increasing throughout
incremental exercise [1–3]. While EF has been used
widely as a global measure of systolic performance, few
studies have measured it during prolonged exercise in the
upright position. We observed no change in EF throughout 150 min of exercise, in agreement with a previous
study [18] that reported no change in EF after 60 min of
exercise, or after 120 min at maximal effort. It is highly
unlikely that prolonged exercise in itself induces myocardial damage. Abnormal myocardial enzyme levels
after marathon running have been reported previously
[37]. However, increases in the creatine kinase MB
fraction may accompany skeletal muscle damage, as small
quantities of this isoenzyme have been detected in skeletal
muscle [38]. In fact, elevated creatine kinase enzyme
levels were reported in subjects after an ultramarathon
Left ventricular function during prolonged exercise
event [39]. However, a later report by the same authors
using a more sensitive cardiac-specific troponin T
immunoassay failed to duplicate these findings, and could
not detect myocardial damage [40]. Similar results were
observed in subjects after completion of a marathon : the
authors failed to demonstrate evidence of myocardial
damage using specific markers for troponin T and
troponin I [21]. In contrast with these studies, a recent
study did observe a small increase in troponin T levels in
subjects after a half-Ironman and a full Ironman competition [16]. However, pre-race values were obtained 2
weeks before the race, and the authors reported that
troponin T levels had returned to normal after 48 h,
which is much earlier than the expected 5–14-day time
course normally expected if myocyte damage were
present. Furthermore, the value for early measurements
of troponin T ( 6 h after suspected myocardial damage)
may be unreliable [41] ; this aspect requires further study,
particularly as it relates to endurance exercise.
In pathological states, the inability to reduce ESV in
the presence of afterload reduction can indicate depression of LV systolic function [42]. Despite limited
data from animals that describe impaired myocardial
calcium uptake during prolonged exercise [43,44], studies
in humans remain limited to load-dependent measures of
contractility. For example, observations of a decrease in
fractional shortening [9,10,12–15] are confounded by the
observation of afterload reduction in long-distance
athletes after prolonged effort [17,34]. Since many of
these indices of myocardial contractility (e.g. fractional
shortening) are load-dependent [11], they have limited
value. The study of Seals et al. [14], which is most similar
to the present study in terms of exercise intensity (approx.
70 % of Vc O max), demonstrated a decrease in LV frac#
tional shortening, despite a reduction in wall stress, after
170 min of treadmill running in 12 athletes. However,
the limitations of load-dependent measures of contractility used in echocardiography are well recognized, and
are difficult to compare with the present investigation.
Unlike previous studies that based their conclusions on
post-exercise recovery data, Palatini et al. [20] observed
no change in systolic performance using exercise data.
Similar to our design, they provided some fluid replacement, and concluded that limited fluid consumption
and use of recovery data may account for the discrepant
results among these studies. We observed no change in
the pressure\volume ratio during exercise, and, although
this index of contractility has its limitations [30], particularly because peak systolic pressure is not measured,
it is not afterload-dependent. In addition, we avoided
using the recovery data to compare against the exercise
data, and obtained them much later (30 min) than in most
studies, when LV dimensions are less liable to undergo
rapid change [20]. Ketelhut et al. [17] reported that
abnormal ventricular function after 60 min of exercise
may be independent of decreases in arterial pressure.
However, in that particular study, data were obtained
from subjects in the supine position during recovery and
therefore are limited. In addition, the extent of postexercise hypotension can vary greatly and is strongly
linked to various factors, including hydration state, blood
volume shifts to the periphery, thermal stress and
sympathetic activation [34].
Limitations of the study
We chose to evaluate LV function under conditions that
would mimic typical steady-state exercise conditions ;
that is, exercise intensity was held constant and HR was
allowed to drift upwards. We are the first to report LV
volumes and systolic performance under controlled
conditions over 120 min using non-geometric-based
measurements to determine volumes. Nevertheless,
count-based measures of LV volume used with equilibrium radionuclide angiography are not without
limitations. Movement artifact may have contributed to
the large variability in the findings (e.g. EDV), leading to
an underestimation of the reported decline in stroke
volume. However, this technique still avoids potential
changes in cavity shape and allows for serial measurements without added exposure to radiation [29,31].
Furthermore, data from the present study were acquired
during upright exercise, allowing for more physiologically relevant conclusions than those acquired during
recovery in the supine position. A further limitation may
be the trained nature of the subjects. In light of the
evidence that training attenuates cardiovascular drift, the
application of our findings to less-trained individuals
may be limited [45] and could understate the risk of
participation in such events.
Conclusions
We could not detect diminished LV systolic function
during prolonged effort in conditioned young adults.
Despite fluid replacement, cardiovascular drift occurred
as exercise time increased, characterized by a progressive
increase in HR and a decrease in EDV. This response was
not accompanied by any evidence of LV systolic dysfunction during exercise or in the recovery period.
ACKNOWLEDGMENTS
Many thanks are owed to Andre Laprade and Yasmin
Allidina for their technical assistance and support in the
Nuclear Cardiology Laboratory. This work was supported by the Canadian Fitness and Lifestyle Research
Institute.
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2001 The Biochemical Society and the Medical Research Society
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536
J. M. Goodman, P. R. McLaughlin and P. P. Liu
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Received 13 June 2000/27 November 2000; accepted 1 February 2001
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