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Neural and non‐neural control of skin blood flow during isometric handgrip exercise in the heat stressed human
Author(s) -
Shibasaki Manabu,
Rasmussen Peter,
Secher Niels H.,
Crandall Craig G.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.169201
Subject(s) - microdialysis , forearm , isometric exercise , medicine , vasoconstriction , anesthesia , blood flow , vasodilation , cardiology , anatomy , central nervous system
During heat stress, isometric handgrip (IHG) exercise causes cutaneous vasoconstriction, but it remains controversial whether neural mechanisms are responsible for this observation. The objective of this study was to test the hypothesis that cutaneous vasoconstriction during IHG exercise in heat stressed individuals occurs via a neural mechanism. An axillary nerve blockade was performed to block efferent nerve traffic to the left forearm in seven healthy subjects. Two intradermal microdialysis probes were placed within forearm skin of the blocked area. Forearm skin blood flow was measured by laser‐Doppler flowmetry over the microdialysis probes as well as from skin of the contralateral (unblocked) forearm. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure. Effectiveness of nerve blockade was verified by the absence of tactile sensation, as well as an absence of sweating and cutaneous vasodilatation during a whole‐body heat stress. Upon this confirmation, adenosine was perfused through one of the microdialysis probes to increase skin blood flow similar to that of the unblocked site. After internal temperature increased ∼0.7°C, subjects performed 2 min of IHG exercise at 35% of maximal voluntary contraction using the non‐blocked arm. IHG exercise significantly decreased CVC at the unblocked site (82.3 ± 5.7 to 70.9 ± 5.4%max, P = 0.005, means ± s.e.m. ) and the adenosine treated site of the blocked arm (75.2 ± 7.2 to 68.3 ± 6.6%max, P = 0.005), whereas CVC was unchanged at the blocked site that did not receive adenosine (15.7 ± 2.8 to 13.7 ± 2.0%max, P = 0.10). Importantly, the reduction in CVC was greater at the unblocked site than at the adenosine treated site (11.4 ± 2.6 vs. 6.9 ± 1.6%max, respectively, P = 0.01). These findings suggest that neural and non‐neural mechanisms contribute to the reduction in forearm CVC during IHG exercise in heat stressed humans.