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

Article · May 2006with22 Reads
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.

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  • ...Indeed, this elevated HR (representing elevated internal intensity, regardless of the external load) may be the cause for any change in HRV, rather than any direct effect of exercise duration. Conversely, prolonged exercise duration may be associated with progressive parasympathetic withdrawal (indicated by lower HRV), and this in turn might contribute to cardiovascular drift (Kukielka et al., 2006). Regardless of the direction of any cause-effect relationship, it is difficult to infer what affects HRV under conditions of different HR-values, as HR likely has a purely mathematical effect on HRV (Billman, 2013a;Sacha, 2013Sacha, , 2014), whereby a greater HR can reduced HRV despite no change in the actual variability of autonomic outflow. ...
  • ...In animal studies, myocardial ischaemia responses have been stratified into (i) susceptible vs. (ii) resistant states with respect to ventricular fibrillation induction in pre-training conditions (Billman, 2006). It was found that brief (2 min) periods of coronary artery occlusion can provoke significantly greater increases in heart rate (accompanied by reductions in heart rate variability – an index of cardiac vagal tone) in animals susceptible to sudden cardiac death compared to disease resistant animals (Billman, 2006; Billman & Kukielka, 2006). Exercise training significantly reduced the heart rate response to exercise onset and enhanced (accelerated) return of heart rate to baseline at exercise offset (Billman & Kukielka, 2007). ...
  • ...HRV measures during exercise have been used as a measure of fitness level (Tulppo et al., 1996Tulppo et al., , 1998b; Sandercock and Brodie, 2006; Lewis et al., 2007). However, limited data exists in humans on their ability to track training-induced changes in fatigue and/or fitness within the same individuals (Billman and Hoskins, 1989; Kukielka et al., 2006 ). Indeed, there are several limitations to their usefulness as a training monitoring tool. ...
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