Download Telemetric Monitoring of Cardiovascular Parameters after Exercise

Telemetric Cardiovascular Monitoring in Exercise Trained Rats
31
Journal of Exercise Physiologyonline
(JEPonline)
Volume 13 Number 2 April 2010
Managing Editor
Tommy Boone, PhD, MPH
Editor-in-Chief
Jon K. Linderman, PhD
Review Board
Todd Astorino, PhD
Julien Baker, PhD
Tommy Boone, PhD
Eric Goulet, PhD
Robert Gotshall, PhD
Alexander Hutchison, PhD
M. Knight-Maloney, PhD
Len Kravitz, PhD
James Laskin, PhD
Derek Marks, PhD
Cristine Mermier, PhD
Chantal Vella, PhD
Ben Zhou, PhD
Official
Research Journal of
the American Society of
Exercise Physiologists
(ASEP)
ISSN 1097-975
Systems Physiology – Cardiopulmonary
Telemetric Monitoring of Cardiovascular Parameters after Exercise
Training in Normotensive Rats
LENICE BECKER1, JOSÉ SILVA1, ROBSON SANTOS1, MARIA
CAMPAGNOLE-SANTOS1
1Department
of Physiology and Biophysics, ICB, Federal University of
Minas Gerais, Belo Horizonte, MG, Brazil
ABSTRACT
Becker LK, Silva JR, Santos RAS, Campagnole-Santos MJ.
Telemetric Monitoring Of Cardiovascular Parameters After Exercise
Training In Normotensive Rats. JEPonline 2010;13(2):31-41. In the
present study we have evaluated, through telemetric recordings, the
circadian alterations in mean arterial pressure (MAP) and heart rate
(HR) and the variability of MAP and HR induced by exercise training
(ET) in normotensive rats. Sprague-Dawley (SD) rats were submitted
to 20 sessions of swimming, 1 h duration, 5 days a week for 4 weeks.
MAP and HR were continuously recorded every 10 min for 24 h by a
telemetric implant. In order to evaluate the effect of an entire week of
exercise training, data collected on the 3 last days of each week
were used for the analyses. ET did not change the circadian rhythm
or acrophase of the MAP and HR or the resting values of MAP during
the day or during the night. As expected, ET induced a fall in
baseline HR while resting bradycardia was only significant during the
night period (wakefulness). The resting bradycardia started at the
2nd week of training. Trained animals did not present alteration in
the HR variability. However, there was a significant increase in MAP
variability during the day (sleep period) of trained rats in comparison
to the night values or to the sedentary period. In addition, the motor
activity was significantly smaller after ET during the night in
comparison to SE. The data suggest that ET differentially interferes
with the mechanism of control of arterial pressure during the day
(sleep) and night (wakefulness) periods.
Key words: Telemetry, Exercise Training, Blood Pressure, Heart
Rate, Blood Pressure Variability.
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
32
INTRODUCTION
The cardiovascular parameters such as blood pressure (BP), heart rate (HR), stroke volume and
cardiac output change rhythmically according to the 24h cycle, being higher in the active phase in
relation to the resting phase (4,16). The internal body clock, which is responsible for generating 24h
rhythms, is located in the hypothalamic suprachiasmatic nucleus (SCN) that receives light information
from the retina and several others peripheral stimuli (sleep/ awake, hormones, body temperature). It
has been shown that the rhythm of BP and HR may be controlled by an endogenous circadian
oscillating system (34) in which the SCN plays an important role in rats (24). It is not completely
understood how the circadian information from the SCN is modulated/ processed to regulate the 24h
rhythm of BP and HR.
The neuronal activity originating in the SCN translates in circadian rhythms by inducing the release of
hormones from hyphothalamus and modifying the autonomic outflow through hypothalamic or brain
stem efferent pathways (8,16). Thus, it is well accepted that the autonomic nervous system, which
also follows a circadian pattern, is importantly involved in mediating the circadian variation of BP (8).
Exercise is recognized to affect circadian rhythmicity in a variety of ways. However, how exercise or
arousal provides a feedback to the biological clock is not well understood. Studies have observed
that exercise can affect circadian rhythm of different biological functions and it has been proposed
that exercise may alter the functioning of the circadian system in order to facilitate the emergence of
circadian rhythms in previously arrhythmic animals (4,15).
Exercise training (ET) has been associated to improvement of cardiovascular function and reduction
of cardiovascular risk factors and mortality (1,31) Exercise training performed at moderate intensity
produces resting bradycardia and a significant reduction in mean arterial pressure (MAP) in
hypertensive patients and animals (1,14,30). Studies by Krieger, Negrão and colleagues have shown
that in hypertensive animals (SHR), ET improves baroreflex function, reduces resting HR and reduces
the sympathetic drive to the heart (28,29,32). However, in normotensive animals, results are
controversial. Studies showed no change or attenuation of the baroreflex bradycardia or a decrease
in the overall sensitivity of the baroreflex control of HR (7,21). On the other hand, after ET
normotensive rats present an increased gain of the aortic baroreceptor function (3), suggesting that
the attenuation in baroreflex may take place in other sites of the reflex arch. Accordingly, it was
shown that normotensive rats submitted to ET present in addition to a reduction in sympathetic tone,
a decreased vagal tone, a decreased bradicardic response to efferent vagal nerve stimulation and a
decrease in the pacemaker rate (20). Thus, decrease in the sensitivity of pacemaker cells may
overcome the increased gain of the aortic baroreceptor function.
Studies in humans, using spectral analysis of 24h ECG, have shown that the resting bradycardia is
more proeminent during the day (wakefulness) (5,27). In addition, there are an increase in HR
variability (5,17) accompanied by a decrease in the ratio LF/HF of the power spectrum, which is an
index of sympathetic activity (22,27), or an increase in HF component, which reflects parasympathetic
tone (12), mostly in the night period (sleep).
The contribution and the understanding of the mechanisms triggered by ET on circadian rhythm of BP
may help to improve our knowledge on the mechanisms involved in the control of BP. However, very
few studies have addressed this issue. Thus, the purpose of the present study was to investigate the
circadian rhythm of BP and HR in trained rats through telemetric monitoring, which allows a more
efficient assessment of cardiovascular parameters without the stress produced by the investigator
manipulation of the animals.
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
33
METHODS
Animals
Male Sprague-Dawley rats (300-350 g) were obtained from the animal facilities of the Hypertension
laboratory ICB, UFMG. Before the experiments were started, the animals underwent a 12-day
acclimatization period in an isolated telemetry room. The rats were housed in separated cages under
controlled conditions of temperature (25°C) and a 12:12-h light/dark cycle (light: 6:00 AM to 6:00 PM;
dark: 6:00 AM to 6:00 PM).
Radiotelemetry Monitoring of Blood Pressure (BP), Heart Rate (HR) and Motor Activity (MA)
A telemetry system (Data Sciences International, MN) was used for measuring systolic, diastolic, and
MAP, HR and locomotor activity. Arterial pressure was monitored by a radiofrequency transducer
model TA11-PA C40, a receiver, a matrix, and a personal computer with the software (Dataquest
A.R.T., Gold 2.0) to store and analyze the data. Under tribromoethanol anesthesia 2.5% (1 ml/100 g
body weight), the catheter-transducer was implanted into the abdominal aorta just above the
bifurcation of the iliac arteries, and the sensor was fixed to the abdominal wall. The animals were
returned to their individual cages for 7-10 days for the reestablishment of 24-hours oscillations of BP
and HR.
Exercise Training (ET)
ET was performed by 20 sessions of 1 hour swimming daily (Monday through Friday, between 1 to 2
pm), 5 days a week. At the first day the rats swam for 20 minutes, at the second day for 40 minutes,
and from the third day for 1 hour. Swimming was performed in individual pools at a water
temperature of 30oC, controlled by a thermostat. The blood pressure receiver was positioned beside
of the pools to record the cardiovascular parameters during the training session.
Data Analysis
The MAP and HR were calculated simultaneously from the pulsatile arterial pressure values with
software Dataquest ART. Data were sampled for 10s, every 10min, during 24h. The parameters
collected in the three days before the first week of training were considered resting values
(sedentary). To evaluate time course of blood pressure changes induced by exercise training, the
three last days of each training week were used (Friday, Saturday, and Sunday), because in these
days the data collected show the effect of the entire week of training. MAP and HR of night period
(wakefulness) were the data collected from 6:00 PM to 5:55 AM (72 values) and the MAP and HR for
the day period (sleep) were the data collected from 6:00 AM to 5:55 PM (72 values), except Friday
when day values refers to 6:00 AM to 01:00 PM ( 42 values). Data from 01:00PM to 05:55PM on
Friday were not used to eliminate the alterations caused by the exercise session and to assure that
the values were back to baseline. For statistical analysis, all values collected in these periods (1
value at each 10 min) for each rat were computed. Comparisons between day and night values within
the same rat were assessed by paired Student’s t-test (Prism 4.0, Graphpad Software). Comparisons
between the control period and the training period were analyzed by repeated measures one-way
ANOVA, followed by the Newman-Keuls test.
The degree of oscillation moment to moment, MAP and HR variability, was evaluated by the averaged
standard deviation (SD) of the MAP and HR values collected during the day or night in each rat. The
acrophase of the MAP and HR, which corresponds to the time of the 24h of the highest value (peak of
the circadian rhythm) expressed in hours, were obtained by rhythmic analysis (DQFIT software;
35,36) of the data collected in each of the last 3 days of each period (sedentary and 4th week of
training). Individual acrophases, derived from the DQ-FIT analysis, were averaged and compared
using circular statistics software (Software Oriana, version 1.06, Kovoch Computing Services, 1994).
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
34
The comparisons between the circular mean of the acrophases were performed using the Watson
f-test (33). Data are presented as mean ± SE and p< 0.05 was considered statistically significant.
RESULTS
MA
Counts/ min
HR
beats/ min
BP
mmHg
MA
counts/ min
HR
beats/ min
Figure 1 shows the typical recording of arterial pressure, HR and motor activity of one rat, during
sedentary period
and trained period.
A
Sedentary
Training Weeks
As
expected,
resting values of
500 15/02 06:00:00
MAP, HR and
400
motor activity were
300
smaller during the
200
day (sleep) in
100
comparison to the
30
values during the
20
night
10
(wakefulness)
0
period, illustrating
the
circadian
oscillatory pattern
200
of
the
160
cardiovascular
120
parameters, which
80
was kept during
40
the
weeks
of
0
24.0
4.0
8.0
12.0
16.0
20.0
28.0
32.0
36.0
days
training.
In
SAP
DAP
MAP
addition, in Figure
1C
between
TRAINED
SEDENTARY
B
C
arrows, it can be
seen the MAP, HR
22/03 06:00:00
500
22/02 06:00:00
and MA changes
300
during a session of
100
exercise.
30
20
10
MAP
mmHg
Figure 2 shows
that after 4 weeks
200
of ET there was
no
change
in
120
circadian
rhythm
40
6
12
18 24
30 36
42 48 54
60 66 72
0
0
6
12 18 24
30 36 42 48 54
60 66
72
of MAP, HR or
hours
hours
MA. Accordingly,
Figure 1. A- Heart rate (HR, beats/ min- top panel), motor activity (MA, counts/ min- middle
the acrophase of
panel) and blood pressure (BP mmHg, bottom panel) data collected by telemetry system in
all
parameters
the sedentary (green bar) and training weeks (red bar) of one animal. Systolic (SAP, black
line), mean (MAP, red line) and diastolic (DAP, blue line) arterial pressure are also shown. In
evaluated
were
detail are HR, MA and MAP values collected in three consecutives days of the sedentary
not changed after
period (B) and in the 4th week of training (C). Yellow bars on top represent day and the blue
ET: acrophase of
bars, night periods. Arrows in C set the limits of the duration of one exercise session (1h) and
HR
(sedentary
its recovery (2h).
period:
10:4201:04 PM vs trained period: 11:4800:22 PM); acrophase of the MAP (sedentary period:
0
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
35
09:110:34 PM vs trained period 09:2902:21 PM), and acrophase of the motor activity (sedentary:
11:4104:07 PM vs trained: 11:5102:46 PM).
More interestingly, as shown in Fig 4A, exercise did
not significantly alter HR variability, during the night
(5.2±1.0 beats/ min vs 6.0±1.1beats/ min, sedentary
period) or day period (8.8±1.1 beats/ min vs 5.6±2.2
beats/ min, sedentary period). However, after ET
there was a significant increase in the MAP
variability during the day (sleep period; 4.31.04
mmHg; Fig. 4B) in comparison to sedentary period
(2.1±0.4mmHg) p<0.05.
During the night
(wakefulness period) the MAP variability was not
changed (1.10.2 mmHg vs 1.7±0.5 mmHg,
sedentary period; Fig. 4B).
HR, bpm
Day
400
350
*
Night
*†
300
250
200
B
MA counts/ min
In addition, ET induced a significant fall in MA from
the first week of training (Figure 2B and Table 1
p<0.05). ET did not alter MAP values during the
day or night (Fig 2C, Table 1). The smaller HR
value during the night with no change in day HR,
resulted in a small difference between the day and
night HR values (34±4 beats/ min vs 43±2 beats/
min in the sedentary period; Fig 3A). No change
was observed in the day and night difference of
MAP (Fig. 3B).
A
C
Sedentary
Trained
3
*
2
*†
1
0
Sedentary
Trained
110
*
MAP, mmHg
ET induced a significant decrease in HR, however,
only during the night period (wakefulness; Table 1
and Fig. 2 A p<0.05). The HR resting values during
the day were not significantly different from the
sedentary period, except for the third week of
training p<0.05 (Table 1). In contrast, resting HR
values during the night period were significantly
smaller from the second week of training in
comparison to the sedentary period (Table 1).
*
100
90
During the training session, as expected, swimming
80
Sedentary
Trained
induced an increase in MAP (130 ± 4 mmHg vs 99 ±
st
2 mmHg, resting values; in the 1 week of training) Figure 2. Heart rate (HR, beats/ min; A), motor
accompanied by an increase in HR (406±5 activity (MA, counts/ min; B) and mean arterial
beats/min vs 300±2 beats/min, resting values; in the pressure (MAP, mmHg; C) during the period of day
night (wakefulness) in sedentary or
1st week of training). The pressor and tachycardic (sleep) and
trained (4th week) rats (n=5). *p< 0.05 in comparison
response to exercise did not change over the 4 to day (paired Student t test); +p<0.01 in comparison
weeks of training (data not shown). After 2 hours of to respective sedentary (repeated measures one-way
the end of the exercise session, both BP and HR ANOVA followed by Newman-Keuls).
were back to baseline values (data not shown). The
time of recovery of the cardiovascular parameters did not alter in the 4 weeks of training (data not
shown).
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
36
DISCUSSION
Telemetric Monitoring Advantages
The present study evaluated for the first time the cardiovascular parameters during 24h in rats
submitted
to
Table 1. Mean arterial pressure (MAP, mmHg), heart rate (HR, beats/ min)
exercise
and motor activity (MA, counts/ min) values during the day and night in each
training. The BP
week of training.
recording
by
Sedentary
Training weeks
telemetry
allowed
an
1
2
3
4
evaluation of the
Day
99  0.6
99  0.5
100  0.6
98  0.5
101  0.7
cardiovascular
MAP
parameters
Night
1050.4*
1030.2*
1060.3*
1030.5*
104  0.3*
without
the
stress produced
Day
3023.3
300 1.8
2962.0
2881.2*
297  2.0
by investigator
HR
manipulation of
Night
3462.4*
341 2.2*
334  2.1*†
329  2.4*†
332  2.4*†
the
animals.
Day
0.7  0.09
1.0  0.07
0.6  0.05
0.8  0.08
0.7  0.1
The rats were
MA
submitted to 1h
Night
2.5  0.11*†
1.9  0.07*† 1.7  0.08*† 1.7  0.07*†
1.5  0.06*†
swimming,
5
days a week,
Values are mean  SD. *; p< 0.05 compared to day, †; p< 0.05 compared to sedentary, n=5.
during 4 weeks
without extra-workload, such as, the addition of tail weights. This protocol of swimming training is
considered to induce low exercise intensity (11). It has been shown that sedentary rats are able to
keep a stable lactate blood entry/ removal ratio in workload up to 6% of the body weight (11).
Therefore ET carried out below 6% of the body weight can be considered sub-threshold.
mmHg
beats/min
Exercise Training Effects on Circadian BP and HR
It is well accepted, both in humans and animals, that low intensity exercise produces beneficial effects
in
reference
to
the
HR Difference
MAP Difference
cardiovascular
system,
(night - day)
(night - day)
especially in lowering MAP
50
15
and HR of hypertensive
*
subjects (30,1). The results
10
obtained in the present work
30
showing that the ET did not
5
change resting values of the
10
MAP or HR or the circadian
rhythm of MAP and HR in
0
0
normotensive rats, is in
Sedentary
Trained
Sedentary
Trained
agreement with data obtained Figure 3. Difference between day and night values of heart rate (HR, beats/
in normotensive individuals min; A) and mean arterial pressure (MAP, mmHg; B) during the sedentary
(14,6). The fall in BP that is period and after 4 weeks of ET (n=5). *p< 0.05 in comparison to sedentary
observed in hypertensive rats (paired Student t test).
is believed to be related to the
higher prevailing sympathetic tone of these animals.
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
37
mmHg
beats/min
From the second week of training, it was observed a significant decrease in resting HR during the
night, and the bradycardia was maintained until the end of the training period. A significant reduction
in HR during the day was only observed after the third week of training. Resting bradycardia is
observed in several studies after a low intensity exercise by treadmill and swimming (10,13,
14,26,28,32), which serves as a marker for exercise training adaptation (13,2). In addition, our study
shows that the effect of exercise in producing resting bradycardia was more effective during the
wakefulness
MAP variability
HR variability
A
B
Day
15
6
period (night) of
†
Night
the rat.
This
5
result
is
in
4
10
agreement with
previous studies
3
in men (5, 25,
2
5
27,29). It is not
1
clear which are
the mechanisms
0
0
Sedentary
Sedentary
Trained
Trained
involved in the
HR
reduction
Figure 4. Heart rate (HR, beats/ min; A) and mean arterial pressure (MAP, mmHg; B) variability
th
after ET.
In
during the day (sleep) and night (wakefulness) period in sedentary and trained (4 week) rats
(n=5). †; p< 0.05 in comparison to respective sedentary period (repeated measures one-way
normotensive
ANOVA followed by Newman–Keuls).
rats
it
was
shown a decrease in both the sympathetic and parasympathetic components of the HR control after
exercise training (20). In addition, the alterations in autonomic control were accompanied by a
decrease in the intrinsic HR, which suggest alteration in the sinus node cells (20). Other studies
however, suggest that resting bradycardia induced by exercise may result from an increase in vagal
tone (31). In hypertensive rats, ET induces a fall in sympathetic activity to a similar level found in the
normotensive rats, however, without changes in vagal tone (10). Our data suggested that ET induces
alteration preferentially in the sympathetic system, since during the wakefulness period this system
predominates in the control of the HR. During the sleep period, the autonomic control of arterial
pressure is mainly regulated by the parasympathetic system, since the decrease in sympathetic
activity is higher, especially during the REM phase (18).
Our data suggest that the fall in HR can also be related to the decrease in motor activity during the
night (awake period) that was shown by the animals after ET. The decrease in motor activity after ET
can be attributed to an increase in the release of endorphins and/or another opioid peptides, which
are well known to be released after ET and are involved, among others, with the activity behavior of
the animal (9).
In parallel to the HR changes, ET produced no consistent changes in resting MAP values, which is in
agreement with studies (3,21) that showed that low or moderate exercise intensities does not change
the resting MAP of normotensive rats. However, MAP variability was significantly higher, after 4
weeks of exercise training, only during the sleep period (day). The increase in MAP variability
suggests a decrease in baroreflex sensitivity during the day (sleep period). Negrão et al.(21) have
shown that ET performed on a motor treadmill for 13 weeks in normotensive rats induce a significant
lower renal sympathetic nerve activity (RSNA) accompanied by an impairment of baroreflex control of
RSNA (in response to MAP fall) and baroreflex control of HR (bradycardia). Reduced sensitivity of
the baroreflex control of HR was observed after exercise training in both humans (19,23) and animals
(7,20). Our study adds new data showing that the possible impairment of baroreflex sensitivity
induced by ET is only attained to the day period, where sympathetic influence to the control of BP is
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
38
lower. Thus, this result is in keeping with the hypothesis that the main effect of the ET in
normotensive rats is on the modulation of the sympathetic tonus.
CONCLUSION
This is the first study to show the cardiovascular effects induced by ET using a continuous (24 hours)
BP monitoring by telemetry. Our data, showing an increased MAP variability during the day and a
decreased baseline HR (resting bradycardia) during the night, reinforces the hypothesis that ET
induces an important alteration in autonomic balance towards a significant decrease in sympathetic
tonus to the cardiovascular system, which is a key modulator of physiological functions during
wakefulness. The contribution and the understanding of the mechanisms triggered by ET on
circadian rhythm of BP may help to improve the treatment and knowledge of the pathophysiological
mechanisms of the cardiovascular diseases.
ACKNOWLEDGEMENTS
This study was supported by grants “Programa de Grupos de Excelência - PRONEX" from the CNPq/
FAPEMIG, “Edital Universal” to M.J.C-S from CNPq and from CAPES.
Address for correspondence: Maria José Campagnole-Santos, PhD, Departamento de Fisiologia e
Biofísica, Av. Antonio Carlos, 6627 – ICB – UFMG, 31270-901 – Belo Horizonte, MG, Brasil, FAX:
(55-31) 3409-2924; Phone: (55-31) 3409-2951, E-mail: [email protected].
REFERENCES
1.
Arakawa K. Antihypertensive mechanism of exercise. J Hypertens 1993;11:223-229.
2.
Aresgog, N. Effects and adverse effects of autonomic blockade in physical exercise. Am J
Cardiol 1985;55:132-134.
3.
Brum P, Silva G, Moreira E, Ida F, Negrão C, Krieger EM. Exercise training increases
baroreceptor gain sensitivity in normal and hypertension rats. Hypertens 2000;36:1018-1022.
4.
Cambras T, Vilaplana J, Campuzano A, Canal-Corretger, MM, Carulla, M, Diez-Noguerra, A.
Entrainment of the rat motor activity rhythm: effects of the light-dark cycle and physical
exercise. Physiol Behav 2000;70(3-4):227-232.
5.
Catai AM, Chacon-Mikahil MPT, Martinelli FS, Forti VAM, Silva E, Golfetti R, Martins LEB,
Szrajer JS, Wanderley JS, Lima-filho EC, Milan LA, Marin-Neto JA, Maciel BC, Gallo-Junior L.
Effects of aerobic exercise training on heart rate variability during wakefulness and sleep and
cardiorespiratory responses of young and middle-aged healthy men. Braz J Med Biol Res
2002;35:741-752.
6.
Derk P, Veerman Bem, Imholz M, Wouter W, Wesseling K, Montfrans G. Circadian profile of
systemic hemodynamics. Hypertens 1995;26:55-59.
7.
Di Carlo SE, Bishop VS Exercise training attenuated baroreflex regulation of nerve activity in
conscious rabbits. Am J Physiol 1988;255:H974-H979.
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
39
8.
Diedrich A, Jordan J, Tank J, Shannon JR, Robertson RM, Luft FC, Robertson D, Biaggioni I.
The sympathetic nervous system in hypertension. Assessment by blood pressure variability
and ganglionic blockade. J Hypertens 2003;21:1677-1686.
9.
Dishman RK. Brain monoamines, exercise, and behavioral stress: animal models. Meds Sci
Sports 1997;29(1):63-74.
10.
Gava S, Véras-Silva A, Negrão CE, Krieger EM. Low-intensity exercise training attenuates
cardiac b- adrenergic tone during exercise in sponstaneously hypertensive rats. Hypertens
1995;26:1129-1133.
11.
Gobbato, AC, Mello M, Subuya C, Azevedo J, Santos L, Kokubun E. Maximal lactate steady
state in rats submitted to swimming exercise. Comp Biochem Physiol 2001;Part A 130:2127.
12.
Goldsmith RL, Bigger JT Jr, Steinman RC, Fleiss JL. Comparison of 24-hour parasympathetic
activity in endurance-trained and untrained young men. J Am Coll Cardiol 1992;20(3):552558.
13.
Katona PG, McLean M, Dighton DH, Guz A. A sympathetic and parasympathetic cardiac
control in athletes and nonathletes at rest. J Appl Physiol 1992;72:1749-1753.
14.
Krieger M. E, Brum CP, Negrão CE. Influence of exercise training on neurogenic control of
blood pressure in spontaneously hypertensive rats. Hypertens 1999;34(2):720-723.
15.
Lax, P, Zamora, S, Madrid, JA. Coupling effect of locomotor activity on the rat’s circadian
system. Am J Physiol 1998; 275(2Pt 2):580-587.
16.
Lemmer B. Cardiovascular chronobiology and chronopharmacology. In: Biologic Rhythms in
Clinical and Laboratory Medicine edited by Touitou Y and Haus E. Heidelberg, Germany:
Springer-Verlag, 1992:418–427.
17.
Levy WC, Cerqueira MD, Harp GD, Johannessen KA, Abrass IB, Schwartz RS, Stratton JR.
Effect of endurance exercise training on heart rate variability at rest in healthy young and older
men. Am J Cardiol 1998;82(10):1236-1241.
18.
Loewy A, Spyer. Central Regulation of Autonomic Functions. 1
Press New York 1991, 367-374.
19.
Mtinangi BL, Hainsworth R. Effects of moderate exercise training on plasma volume,
baroreceptor sensitivity and orthostatic tolerance in healthy subjects.
Exp Physiol
1999;84:121-130.
20.
Negrao CE, Moreira ED, Santos MCLM, Farah VMA, Krieger EM. Vagal function impairment
after exercise training. J Appl Physiol 1992;72:1749-1753.
21.
Negrão, EC, Irigoyen MC, Moreira ED, Brum PC, Freiere PM, Krieger EM. Effect of exercise
training on RSNA, baroreflex control, and blood pressure responsiveness. Am J Physiol 1993;
265 34:356-370.
st
Edition Oxford University
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
40
22.
Pigozzi F, Alabiso A, Parisi A, Di Salvo V, Di Luigi L, Spataro A, Iellamo F. Effects of aerobic
exercise training on 24 hr profile of heart rate variability in female athletes. J Sports Med
Phys Fitness 2001;41(1):101-107.
23.
Raven, PB, Stevens GH. Endurance exercise training reduces orthostatic tolerance in humans.
Physiologist 1990;56-58.
24.
Sano H, Hayashi H, Makino M, Takezawa H, Hirai M, Saito H, and Ebihara S. Effects of
suprachiasmatic lesions on circadian rhythms of blood pressure, heart rate and locomotor
activity in rat. Jpn Circ J 1995;59:565–573.
25.
Seals R, Reiling M. Effects of regular exercise on 24-hr arterial pressure in older hypertensive
humans. Hypertens 1991;18:583-592.
26.
Shaible T, Sheuer J. Effects of physical training by running or swimming on ventricular
performance of rat hearts. J Appl Physiol 1997;46 (4):854-860.
27.
Shiotani H Umegaki Y, Tanaka M, Kimura M, Ando H. Efffects of aerobic exercise on the
rhythm of heart rate and blood pressure. Chronobiol Int 2009;26(8):1636-1646.
28.
Silva GJ, Brum PC, Negrao CE, Krieger EM. Acute and chronic effects of exercise on
baroreflexes in spontaneously hypertensive rats. Hypertens 1997;30(3pt2):714-719.
29.
Somers K, Conway J, Johnston J, Sleight. Effects of endurance exercise training on baroreflex
sensitivity and blood pressure in borderline hypertension. Lancet 1991;337:1363-1368.
30.
Tipton CM. Exercise, training, and hypertension: an update. Exerc Sport Sci 1991;4:447-505.
31.
Tipton CM. The autonomic nervous system. In: Exercise Physiology: People and Ideas,
edited by Tipton CM. New York: Oxford University Press,p: 2003,188–254.
32.
Véras-Silva AS, Mattos KC, Gava NS, Brum PC, Negrão CE, Krieger EM. Low-intensity
exercise training decrease cardiac output and hypertesion in spontaneously hypertensive rats.
Am J Physiol Heart Circ Physiol 1997;(42):273:2627-2631.
33.
Watson GS. Another test for the uniformity of a circular distribution. Biometrika 1967;54:675–
677.
34.
Witte K and Lemmer B. Free-running rhythms in blood pressure and heart rate in normotensive
and transgenic hypertensive rats. Chronobiol Int 1995;12:237–247.
35.
Witte K, Zuther P, and Lemmer B. Analysis of telemetric time series data for periodic
components using DQ-FIT. Chronobiol Int 1997;14:561–574.
36.
Zuther P, Witte K, and Lemmer B. ABPM-FIT and CV-SORT: an easy-to-use software package
for detailed analysis of data from ambulatory blood pressure monitoring. Blood Press Monit
1996;1:347–354.
Telemetric Cardiovascular Monitoring in Exercise Trained Rats
41
Disclaimer
The opinions expressed in JEPonline are those of the authors and are not attributable to JEPonline,
the editorial staff or ASEP.