Article

Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training.

Dept. of Physiology, The Ohio State University, Columbus, OH 43210-1218, USA.
AJP Heart and Circulatory Physiology (Impact Factor: 4.01). 05/2006; 290(4):H1680-5. DOI: 10.1152/ajpheart.01034.2005
Source: PubMed

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.

Full-text

Available from: George Billman, Oct 27, 2014
0 Followers
 · 
61 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The effects of a 12-week low-intensity exercise conditioning program (walking) on blood pressure (BP), heart rate (HR), rate- pressure product (RPP), and cardiac autonomic function were measured in 40 sedentary women with hypertension. Women were assigned to either an exercise group (n = 20) or a control group (n = 20), matched for β-blockade treatment. They underwent testing at the beginning and at the end of the 12-week study period in three conditions: supine rest, standing, and low-intensity steady state exercise. The exercise group participated in a 12-week, low-intensity walking program, while the control group continued with usual sedentary activity. Compared with the control group, women in the exercise group showed reductions in systolic and diastolic BP and RPP (i.e., the estimated cardiac workload). β-Blockers increased baroreflex sensitivity and lowered BP and HR in all participants; however, those in the exercise group showed the effects of both treatments: a greater reduction in HR and RPP. The combination of exercise training and β-blockade produces cardiac and autonomic adaptations that are not observed with either treatment alone, suggesting that β-blockade enhances the conditioning effects of low-intensity exercise in women with hypertension.
    Biological Research for Nursing 10/2012; 15(4). DOI:10.1177/1099800412461562 · 1.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autonomic nervous system adjustments to the heart and blood vessels are necessary for mediating the cardiovascular responses required to meet the metabolic demands of working skeletal muscle during exercise. These demands are met by precise exercise intensity-dependent alterations in sympathetic and parasympathetic nerve activity. The purpose of this review is to examine the contributions of the sympathetic and parasympathetic nervous systems in mediating specific cardiovascular and hemodynamic responses to exercise. These changes in autonomic outflow are regulated by several neural mechanisms working in concert, including central command (a feed forward mechanism originating from higher brain centers), the exercise pressor reflex (a feed-back mechanism originating from skeletal muscle), the arterial baroreflex (a negative feed-back mechanism originating from the carotid sinus and aortic arch), and cardiopulmonary baroreceptors (a feed-back mechanism from stretch receptors located in the heart and lungs). In addition, arterial chemoreceptors and phrenic afferents from respiratory muscles (i.e., respiratory metaboreflex) are also capable of modulating the autonomic responses to exercise. Our goal is to provide a detailed review of the parasympathetic and sympathetic changes that occur with exercise distinguishing between the onset of exercise and steady-state conditions, when appropriate. In addition, studies demonstrating the contributions of each of the aforementioned neural mechanisms to the autonomic changes and ensuing cardiac and/or vascular responses will be covered. © 2015 American Physiological Society. Compr Physiol 5: 475-512, 2015.
    03/2015; 5(2):475-512. DOI:10.1002/cphy.c140022
  • Source
    [Show abstract] [Hide abstract]
    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. DOI:10.3389/fphys.2014.00073