Have we missed that neural vasodilator mechanisms may contribute to exercise hyperemia at onset of voluntary exercise?

Abstract

Whether neurally-mediated vasodilatation may contribute to exercise hyperemia has not been completely understood. Bülbring and Burn (1935) found for the first time the existence of sympathetic cholinergic nerve to skeletal muscle contributing to vasodilatation in animals. Blair et al. (1959) reported that atropine-sensitive vasodilatation in skeletal muscle appeared during arousal behavior or mental stress in humans. However, such sympathetic vasodilator mechanism for muscle vascular bed in humans is generally denied at present, because surgical sympathectomy, autonomic blockade, and local anesthesia of sympathetic nerves cause no substantial influence on vasodilatation in muscle not only during mental stress but also during exercise. On the other hand, neural mechanisms may play an important role in regulating blood flow to non-contracting muscle. Careful consideration of the neural mechanisms may lead us to an insight about a possible neural mechanism responsible for exercise hyperemia in contracting muscle. Referring to our recent study measuring muscle tissue blood flow with higher time resolution, this review has focused on whether or not central command may transmit vasodilator signal to skeletal muscle especially at the onset of voluntary exercise.

Keywords: central command; exercise; near infrared spectroscopy; skeletal muscle; vasodilatation.

Figure 1

(A) The effect of atropine on the responses in heart rate (HR), arterial blood pressure (AP), and brachial blood flow during voluntary static exercise in a conscious cat. In the presence of atropine, the increase in brachial blood flow was blunted, although the baseline blood flow was not altered. (B) The effect of atropine on the average responses in HR, mean arterial blood pressure (MAP), brachial blood flow, and brachial vascular conductance during static exercise. All cardiovascular responses at the onset of exercise were blunted by atropine. Especially, the peak increases in brachial blood flow and vascular conductance were decreased by atropine to 54–55% of the control responses. ^†Significant difference (P < 0.05) before and after atropine. ^*Significant difference (P < 0.05) at a given time from the preexercise level. Adopted from Komine et al. (2008) with permission.

Figure 2

(A) The time courses of the relative changes in oxygenated-hemoglobin (Oxy-Hb) and deoxygenated-hemoglobin (Deoxy-Hb) of the contracting (•) and non-contracting (◦) vastus lateralis (VL) muscles during voluntary one-legged cycling exercise in humans. Vertical dashed lines indicate the start and end of one-legged cycling. A vertical dotted line is placed at 15 s from the exercise onset. At the start of voluntary one-legged exercise, Oxy-Hb in the contracting and non-contracting VL muscles increased with the same time course and magnitude. There was no significant difference (P > 0.05) in the Oxy-Hb response between the two muscles at the initial 15 s period of exercise. Subsequently, Oxy-Hb decreased and Deoxy-Hb increased in the contracting VL as long as exercise was continued. Adopted from Ishii et al. (2012) with permission. (B) A hypothesis that centrally-induced vasodilator signal is equally transmitted to bilateral VL muscles at the start of voluntary one-legged exercise in humans.