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Submitted on February 12, 2003
From the Department of Medicine, Division of Cardiology (U.A.L., S.M.-M., M.H., K.G., L.I.S.), and Department of Health Evaluation Sciences (A.K.), Pennsylvania State College of Medicine, Milton S. Hershey Medical Center, Hershey, and Lebanon Veterans Affairs Medical Center, Lebanon, Pa (K.G., L.I.S.). * To whom correspondence should be addressed. E-mail: uleuenberger{at}psu.edu.
Background--Exercise activates the sympathetic nervous system as a function of the type and intensity of exercise and of the target organ studied. Although central command and activity of metabolically sensitive afferents from exercising muscle are the principal determinants of sympathetic outflow directed to skeletal muscle, the mechanisms that govern sympathetic outflow directed to skin are less clear. Methods and Results--We measured skin sympathetic nerve activity (SSNA) during intermittent static handgrip (SHG; at 45% of maximal voluntary contraction; four 5-second contractions per minute for 3 minutes), during unrestricted forearm perfusion (control), during stimulation of forearm mechanoreceptors with venous congestion, and during ischemia produced by forearm circulatory arrest. Under all 3 conditions, SSNA increased within 1 to 2 seconds of the onset of handgrip. During ischemia but not during venous congestion, SSNA increased more compared with control (P<0.05) and remained elevated when forearm ischemia was maintained after handgrip exercise (posthandgrip circulatory arrest). In addition, simulated handgrip and intermittent forearm compression produced by a pneumatic cuff also evoked brief increases of SSNA. Conclusions--In addition to central neural factors, afferent input from exercising muscle plays an important role in modulating sympathetic outflow directed to skin.
Revised on June 9, 2003
Accepted on July 9, 2003
Control of Skin Sympathetic Nerve Activity During Intermittent Static Handgrip Exercise
Urs A. Leuenberger MD*,
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