(Circulation. 1999;100:27-32.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise
Insights From Spectral Analysis of Heart Rate Variability
From the Dipartimento di Medicina Interna (F.I., M.M., G.R., G.P., J.M.L.), Università di Roma "Tor Vergata," Rome, Italy, and Ospedale S. Gerardo (P.P.), Monza, Italy.
Correspondence to Dr Ferdinando Iellamo, Dipartimento Medicina Interna, Università di Roma "Tor Vergata," Via O. Raimondo, 8, 00173 Roma, Italy. E-mail iellamo{at}med.uniroma2.it
Background—It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia.
Methods and Results—Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered.
Conclusions—The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.
Key Words: exercise • muscles • heart rate • nervous system, autonomic • baroreceptors
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