Muscle pump and central command during recovery from exercise in humans

Abstract

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.

Heart rate recovery after exercise: relations to heart rate variability and complexity

“…At the onset of exercise heart rate (and cardiac output) elevation is mediated mostly by central command signals via vagal withdrawal. As work intensity increases and heart rate approaches 100 beats/ min, sympathetic activity begins to rise, further increasing heart rate and plasma norepinephrine concentration and vasoconstricting vessels in visceral organs (2,(13)(14)(15).…”

“…Heart rate rapidly decreases during the first 1-2 min after the cessation of exercise, and gradually thereafter. During recovery from moderate and heavy exercise heart rate remains elevated above the pre-exercise level for a relatively long period of time (up to 60 min) (2,18,(26)(27)(28). Because of the presumed parasympathetic origin of both HRV and the rate of heart rate decrease after exercise we hypothesized that the HRV indices before and after exercise could be associated with the rate of heart rate recovery.…”

“…Autonomic contribution to cardiodeceleration after exercise (heart rate recovery) is less understood. Inactive recovery from dynamic exercise is associated with the cessation of the primary exer-^ cise stimulus from the brain (cerebral cortex -central command) which is responsible for the initial rapid drop of heart rate (2). Slower changes in the stimuli to metaboreceptors and baroreceptors accompanying clearance of metabolites and delayed elimination of body heat and catecholamines are thought to be other factors contributing to heart rate recovery after physical activity.…”

“…Slower changes in the stimuli to metaboreceptors and baroreceptors accompanying clearance of metabolites and delayed elimination of body heat and catecholamines are thought to be other factors contributing to heart rate recovery after physical activity. Nevertheless, parasympathetic activation is considered to be the main mechanism underlying exponential cardiodeceleration after exercise (1)(2)(3)(4).…”

The Effect of Cardiovascular Responses after Aerobic Exercise in Menstrual Cycle

“…In particular, recovery responses of HR and blood pressure are identified as important predictors, and the longer the recovery time after exercise, the higher the cardiovascular disease risk [9]. Post-exercise cardiovascular responses in recovery are a decrease in CO and BP following a reduction in HR and SV to restore our body to the pre-exercise resting level [10]. This is resulted from reduction in venous return as the termination of muscle contraction is followed by no action of muscle pump after completing exercise [11].…”