Autonomic nervous control of heart rate during blood-flow restricted exercise in man |
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Authors: | J. C. L. Sun O. Eiken I. B. Mekjavic |
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Affiliation: | (1) School of Kinesiology, Simon Fraser University, V5A 1S6 Burnaby, British Columbia, Canada;(2) Department of Clinical Physiology, Huddinge Hospital, 14186 Huddinge, Sweden |
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Abstract: | Summary Power spectra of instantaneous heart rate (fc) allows the estimation of the contribution of sympathetic and parasympathetic control of fc during steady-state conditions. The present study was designed to examine autonomic control of fc as influenced by normal dynamic leg exercise and by ischemic leg exercise. Eight subjects performed supine cycle ergometry at 30% of their control peak work rate, with and without blood-flow restriction. Blood-flow restriction was induced by exposing the exercising legs to a supra-atmospheric pressure of 6.7 kPa (leg positive pressure; LPP). The exercise responses of arterial pressure and fc increased (P<0.05) by LPP exposure. The exaggerated pressor response may be attributed to a chemoreflex drive originating in the ischemic muscles. Exposure to LPP during exercise also produced a significant decrease in parasympathetically mediated high frequency (HF; 0.15-1.00 Hz) fluctuation of fc, as indicated by a decrease (P<0.05) in percent HF power compared to the control exercise level. During LPP exercise, the sympathetically mediated very low frequency (VLF; 0–0.05 Hz) fluctuation of fc increased, as indicated by an increase (P<0.05) in percent VLF power above control exercise levels. Both LPP and control exercise conditions decreased (P<0.05) power in all frequency ranges of interest compared to their respective resting conditions. The results suggest that the increase in fc associated with normal dynamic exercise was mediated predominantly by parasympathetic withdrawal, whereas the exaggerated fc response during ischemic exercise resulted from a combination of cardiac sympathetic drive and parasympathetic withdrawal. The increase in sympathetic activity is attributable to a muscle chemoreflex drive, which also may have attenuated parasympathetic activity by reciprocal inhibition. Alternatively, augmented central command mediated parasympathetic withdrawal during ischemic exercise. |
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Keywords: | Power spectra of instantaneous heart rate Sympathetic nervous activity Parasympathetic nervous activity Ischemic muscle exercise |
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