Abstract
Despite the anecdotal claims that exercise is effective in alleviating stress, the scientific community has been much more reluctant to make such claims due to issues regarding the nature of the relationship between exercise and stress, including the time course of stress-induced cardiovascular changes following exercise as well as plausible mechanisms underlying the effects. PURPOSE To determine the time course of cardiovascular reactivity and recovery from mental arithmetic following acute aerobic exercise. A related purpose was to examine the role of the autonomic nervous system (ANS), using low and high frequency components of heart rate (HR) variability, as a contributing mechanism underlying cardiovascular responses to stress following exercise. METHODS Ninety (48 male; 42 female) participants initially completed a maximal treadmill test for the determination of maximal oxygen consumption. The effects of 30 min of high- and low-intensity (i.e., 75–80% & 50–55% VO2 max, respectively) aerobic exercise were compared to the effects of a 30 min sedentary control condition on cardiovascular responses to a 6 min mental arithmetic challenge administered at 5, 30, or 60 min post exercise. Measures of HR, HR variability, systolic blood pressure, and diastolic blood pressure were assessed during baseline, stress, and recovery periods. Participants also completed measures of state anxiety, affect, and perceived difficulty before and following the stressor. RESULTS Both low- and high-intensity exercise resulted in significantly reduced stress reactivity and recovery following exercise. Furthermore, high-intensity exercise was more effective at reducing cardiovascular reactivity and enhancing recovery when the stressor was administered at 5, 30, and 60 min post-exercise. CONCLUSION The results indicated that attenuated stress responses following acute exercise depend both on exercise intensity and time of exposure to psychological stress. The results also demonstrated greater cardiac vagal tone following exercise that persisted during exposure to the laboratory stressor, suggesting that parasympathetic rebound may be a viable mechanism underlying exercise-induced reductions in cardiovascular responses to stress.
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