Tn. Jacobsen et al., SKELETAL-MUSCLE VASCULAR-RESPONSES IN HUMAN LIMBS TO ISOMETRIC HANDGRIP, European journal of applied physiology and occupational physiology, 69(2), 1994, pp. 147-153
Studies of whole limb blood flow have shown that static handgrip elici
ts a vasodilatation in the resting forearm and vasoconstriction in the
resting leg. We asked if these responses occur in the skeletal muscle
vascular bed, and if so, what is the relative contribution of local m
etabolic versus other mechanisms to these vascular responses. Blood fl
ow recordings were made simultaneously in the skeletal muscle of the r
esting arm and leg using the Xenon-washout method in ten subjects duri
ng 3 min of isometric handgrip at 30% of maximal voluntary contraction
. In the arm, skeletal muscle vascular resistance (SMVR) decreased tra
nsiently at the onset of exercise followed by a return to baseline lev
els at the end of exercise. In the leg SMVR remained unchanged during
the 1st min of handgrip, but had increased to exceed baseline levels b
y the end of exercise. During exercise electromyography (EMG) recordin
gs from nonexercising limbs demonstrated a progressive 20-fold increas
e in activity in the arm, but remained at baseline in the leg. During
EMG-signal modelled exercise performed to mimic the inadvertent muscle
activity, decreases in forearm SMVR amounted to 57% of the decrease s
een with controlateral handgrip. The present study would seem to indic
ate that vascular tone in nonexercising skeletal muscle in the arm and
leg are controlled differently during the early stages of static hand
grip. Metabolic vasodilatation due to involuntary contraction could si
gnificantly modulate forearm skeletal muscle vascular responses, but o
ther factors, most likely neural vasodilator mechanisms, must make maj
or contributions. During the later stages of contralateral sustained h
andgrip, vascular adjustments in resting forearm skeletal muscle would
seem to be the final result of reflex sympathetic vasoconstricter dri
ve, local metabolic vasodilator forces and possibly neurogenic vasodil
ator mechanisms.