Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training.
ABSTRACT The present study investigated the effects of long-duration exercise on heart rate variability [as a marker of cardiac vagal tone (VT)]. Heart rate variability (time series analysis) was measured in mongrel dogs (n = 24) with healed myocardial infarctions during 1 h of submaximal exercise (treadmill running at 6.4 km/h at 10% grade). Long-duration exercise provoked a significant (ANOVA, all P < 0.01, means +/- SD) increase in heart rate (1st min, 165.3 +/- 15.6 vs. last min, 197.5 +/- 21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power (VT: 1st min, 3.7 +/- 1.5 vs. last min, 1.0 +/- 0.9 ln ms(2)), R-R interval range (1st min, 107.9 +/- 38.3 vs. last min, 28.8 +/- 13.2 ms), and R-R interval SD (1st min, 24.3 +/- 7.7 vs. last min 6.3 +/- 1.7 ms). Because endurance exercise training can increase cardiac vagal regulation, the studies were repeated after either a 10-wk exercise training (n = 9) or a 10-wk sedentary period (n = 7). After training was completed, long-duration exercise elicited smaller increases in heart rate (pretraining: 1st min, 156.0 +/- 13.8 vs. last min, 189.6 +/- 21.9 beats/min; and posttraining: 1st min, 149.8 +/- 14.6 vs. last min, 172.7 +/- 8.8 beats/min) and smaller reductions in heart rate variability (e.g., VT, pretraining: 1st min, 4.2 +/- 1.7 vs. last min, 0.9 +/- 1.1 ln ms(2); and posttraining: 1st min, 4.8 +/- 1.1 vs. last min, 2.0 +/- 0.6 ln ms(2)). The response to long-duration exercise did not change in the sedentary animals. Thus the heart rate increase that accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the trained state.
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ABSTRACT: Aim: Increased sodium/calcium exchanger activity (NCX1, an important regulator of cardiomyocyte cystolic calcium) may provoke arrhythmias. Exercise training can decrease NCX1 expression in animals with heart failure improving cytosolic calcium regulation, and could thereby reduce the risk for ventricular fibrillation (VF). Methods: To test this hypothesis, a 2-min coronary occlusion was made during the last minute of exercise in dogs with healed myocardial infarctions; 23 had VF (S, susceptible) and 13 did not (R, resistant). The animals were randomly assigned to either 10-week exercise training (progressively increasing treadmill running; S n = 9; R n = 8) or 10-week sedentary (S n = 14; R n = 5) groups. At the end of the 10-week period, the exercise + ischemia test provoked VF in sedentary but not trained susceptible dogs. On a subsequent day, cardiac tissue was harvested and NCX1 protein expression was determined by Western blot. RESULTS: In the sedentary group, NCX1 expression was significantly (ANOVA, P < 0.05) higher in susceptible compared to resistant dogs. In contrast, NCX1 levels were similar in the exercise trained resistant and susceptible animals. Conclusion: These data suggest that exercise training can restore a more normal NCX1 level in dogs susceptible to VF, improving cystolic calcium regulation and could thereby reduce the risk for sudden death following myocardial infarction.Frontiers in Physiology 01/2011; 2:3.
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ABSTRACT: Measures of resting, exercise, and recovery heart rate are receiving increasing interest for monitoring fatigue, fitness and endurance performance responses, which has direct implications for adjusting training load (1) daily during specific training blocks and (2) throughout the competitive season. However, these measures are still not widely implemented to monitor athletes' responses to training load, probably because of apparent contradictory findings in the literature. In this review I contend that most of the contradictory findings are related to methodological inconsistencies and/or misinterpretation of the data rather than to limitations of heart rate measures to accurately inform on training status. I also provide evidence that measures derived from 5-min (almost daily) recordings of resting (indices capturing beat-to-beat changes in heart rate, reflecting cardiac parasympathetic activity) and submaximal exercise (30- to 60-s average) heart rate are likely the most useful monitoring tools. For appropriate interpretation at the individual level, changes in a given measure should be interpreted by taking into account the error of measurement and the smallest important change of the measure, as well as the training context (training phase, load, and intensity distribution). The decision to use a given measure should be based upon the level of information that is required by the athlete, the marker's sensitivity to changes in training status and the practical constrains required for the measurements. However, measures of heart rate cannot inform on all aspects of wellness, fatigue, and performance, so their use in combination with daily training logs, psychometric questionnaires and non-invasive, cost-effective performance tests such as a countermovement jump may offer a complete solution to monitor training status in athletes participating in aerobic-oriented sports.Frontiers in Physiology 01/2014; 5:73.
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ABSTRACT: Cardiovascular disease (CVD) is the number one cause of death globally. There already exists a structured guideline to cardiac rehabilitation for CVD patients as a means of preventing recurrence(s) of any cardiac events and return to an active, healthy and satisfying lifestyle. Despite the availability of cardiac rehabilitation programs, utilisation among eligible patients has been less than 20%. The barriers to this underutilisation have been factors relating to patients, services, and professionals. An alternative approach is a home-based cardiac rehabilitation has shown some improvements in the patients’ uptake of these services. Recent developments in physiological monitoring, information processing, and communication technologies have shown potential to enable a home-based cardiac rehabilitation program for better uptake and adherence and coordination between a team of multidisciplinary carers. One approach has been to use communication technologies such as mobile phone platform to help improve the carers’ ability to give multimodal feedback to the patients regularly and enable the use of other multimedia formats.09/2009: pages 329-352;
“FINAL ACCEPTED VERSION”
Title: Cardiac Vagal Modulation of Heart Rate During Prolonged Submaximal Exercise in
Animals with Healed Myocardial Infarctions: Effects of Training
Authors: Monica Kukielka1, Douglas R. Seals2, and George E. Billman1
1Department of Physiology and Cell Biology, The Ohio State University,
Columbus, OH and 2Department of Integrative Physiology, University of Colorado at Boulder,
Address for Correspondence: George E. Billman, Ph.D., F.A.H.A.
Department of Physiology and Cell Biology
The Ohio State University
304 Hamilton Hall
1645 Neil Ave.
Columbus OH 43210-1218
Telephone: (614) 292-5189
Fax: (614) 292-4888
Running title: Heart rate variability is reduced during exercise
Articles in PresS. Am J Physiol Heart Circ Physiol (December 9, 2005). doi:10.1152/ajpheart.01034.2005
Copyright © 2005 by the American Physiological Society.
The present study investigated the effects of long-duration exercise on heart rate variability (as a
marker of cardiac vagal activity, VT). Heart rate variability (time series analysis) was measured
in mongrel dogs (n=24) with healed myocardial infarctions during 1 hour of submaximal
exercise (treadmill running at 6.4 kph/10% grade). Long-duration exercise provoked a
significant (ANOVA, all P<0.01, mean±SD) increase in heart rate (1st min 165.3±15.6 vs. last
min 197.5±21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power
(VT, 1st min 3.7±1.5 vs. last min, 1.0±0.9 ln ms2), R-R interval range (1st min 107.9±38.3 vs. last
min, 28.8±13.2 ms), and R-R interval SD (1st min 24.3±7.7 vs. last min 6.3±1.7 ms). As
endurance exercise training can increase cardiac vagal regulation, the studies were repeated after
either a 10-week exercise training (n=9) or a 10-week sedentary period (n=7). After training,
long-duration exercise elicited smaller increases in heart rate (pre-training, 1st min 156.0±13.8
vs. last min 189.6±21.9; post-training, 1st min 149.8±14.6 vs. last min 172.7±8.8 beats/min) and
smaller reductions in heart rate variability (e.g., VT, pre-training, 1st min 4.2±1.7 vs. last min
0.9±1.1; post-training, 1st min 4.8±1.1 vs. last min 2.0±0.6 ln ms2). The response to long-
duration exercise did not change in the sedentary animals. Thus, the heart rate increase that
accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal
regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart
rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the
Key Words: parasympathetic nervous system, exercise training, autonomic nervous system
Myocardial infarction elicits profound alterations in cardiac autonomic regulation (10).
In particular, cardiac vagal regulation is depressed in both animals and patients following
myocardial infarction (3, 7, 20, 39). In fact, animals or patients with the greatest reductions in
heart rate variability, an accepted non-invasive marker of cardiac vagal regulation (13, 40),
exhibit the greatest risk for sudden death due to malignant changes in cardiac rhythm (i.e.,
ventricular fibrillation) (7, 17, 22, 24, 36). It is therefore likely that interventions that enhance
cardiac vagal function could also reduce mortality in these high-risk patients.
It is well established that regular exercise can improve cardiac autonomic balance
(increasing parasympathetic while decreasing sympathetic regulation of the heart) (35, 41). In
both man and animals, heart rate at submaximal-workloads is reduced in trained individuals
compared to sedentary controls (35, 41), while the presence of a resting bradycardia is frequently
used to confirm that training has been effective (9, 16, 27, 37, 44). Exercise training programs
have also been reported to increase heart rate variability in patients recovering from myocardial
infarction (25, 28, 31) and may reduce the incidence of sudden death and arrhythmias in both
man and animal models (5, 8, 29, 33). As such, aerobic exercise conditioning has become an
essential component of most cardiac rehabilitation programs (14, 26). In order to achieve the
maximum benefit (i.e., reductions in secondary cardiovascular events), an individual should
exercise continuously for at least 20-60 minutes several days a week (14, 26).
Acute exercise, however, could pose a risk in some patients (1). Exercise provokes
increases in heart rate by both increasing cardiac sympathetic and reducing cardiac
parasympathetic activity. These autonomic changes have been linked to an enhanced risk for
sudden death in post-myocardial infarction patients (10). Furthermore, during long-duration
exercise, heart rate continues to rise throughout the exercise period, a phenomenon known as
cardiovascular (or heart rate) drift (11). The mechanisms responsible for this heart rate increase
are presently unknown. A gradual withdrawal or inhibition of cardiac parasympathetic activity
could contribute to this heart rate increase, which potentially could increase the risk for adverse
events in the patients with cardiovascular disease.
It was therefore the purpose of this study to investigate the effects of long-duration
exercise on heart rate variability in mongrel dogs with healed myocardial infractions. In
particular, the hypothesis that exercise-induced increases in heart rate were accompanied by
progressively increasing reductions in heart rate variability was tested. The effects of exercise
training on the heart rate and heart rate variability response to long-duration exercise were also
examined. As such, the hypothesis that exercise training would attenuate the progressive
reductions in heart rate variability induced by long-duration exercise was also tested.
The principles governing the care and use of animals as expressed by the Declaration of
Helsinki, and as adopted by the American Physiological Society, were followed at all times
during this study. In addition, the Ohio State University Institutional Animal Care and Use
Committee approved all the procedures used in this study.
Thirty-six heartworm free mongrel dogs (age 1-3 years) weighing 16.4 – 24.5 kg (19.2 ±
1.8 kg) were used in this study. The animals were anesthetized and instrumented as previously
described (7, 8, 17, 36). Briefly, using strict aseptic procedures, a left thoracotomy was made in
the fourth intercostal space. The heart was exposed and supported by a pericardial cradle. The
left circumflex coronary artery was dissected free of the surrounding tissue. Both a 20 MHz
pulsed Doppler flow transducer and a hydraulic occluder were then placed around this vessel.
Two pairs of silver coated copper wires were also sutured on the epicardial surface of the left and
right ventricles and were used to obtain a ventricular electrogram. A two-stage occlusion of the
left anterior descending artery was then performed approximately one-third the distance from its
origin in order to produce an anterior wall myocardial infarction. This vessel was partially
occluded for 20 minutes and then tied off. Twelve dogs died within the first 72-hrs of the
myocardial infarction. Thus, studies were completed on 24 dogs.
Long-duration Exercise Protocol
The studies began 3-4 weeks after the production of the myocardial infarction. During
this recovery period, the dogs were trained to run on a motor driven treadmill. The cardiac
response to long-duration exercise was then determined. Pre-exercise values for heart rate and