Muscle metaboreflex contribution to sinus node regulation during static exercise - Insights from spectral analysis of heart rate variability

Background-It is currently assumed that during static exercise, central com mand increases heart rate (HR) through a decrease in parasympathetic activi ty, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the meta boreflex activation is maintained during postexercise muscle ischemia, BP r emains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympa thetic activation and that the arterial baroreflex is involved in the HR re covery of postexercise muscle ischemia. Methods and Results-Eleven healthy male volunteers performed 4-minute stati c leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was inv estigated by spectral analysis of HR variability (HRV), and baroreflex cont rol of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV th at remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baro reflex sensitivity was significantly reduced during SLE and returned to con trol levels during ALC when BP was kept elevated above the resting level wh ile HR recovered. Conclusions-The muscle metaboreflex contributes to KR regulation during sta tic exercise via a sympathetic activation. The bradycardia that occurs duri ng postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outf low to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.