Indication for cholinergically mediated cerebral vasodilatation during static exercise in humans

Abstract

Cholinergically mediated vasodilatation is reported in humans, but its importance for cerebral perfusion during exercise is unknown. The increase in middle cerebral artery blood flow velocity (MCA Vmean) during static handgrip exercise was evaluated by blockade of acetylcholine receptors as well as with beta‐adrenergic blockade, in nine males in separate, randomized and counterbalanced trials over two minutes. Mean arterial pressure (MAP) increased during both 25 % and 40 % maximal voluntary contraction (MVC) handgrip (P < 0.01) with no effect of treatment. Resting cardiac output was reduced by ~20% with beta‐adrenergic blockade (P < 0.05) and increased by ~40% with vagal‐blockade (P < 0.05). Compared to control, exercise‐induced increases in cardiac output were attenuated with beta‐adrenergic blockade (P < 0.01) and abolished with cholinergic blockade. MCA Vmean increased ~16% during control exercise (independent of intensity; P < 0.01). During 25% MVC handgrip, both cholinergic and beta‐adrenergic blockade abolished the exercise‐induced increase in MCA Vmean (~3 % and ~7 %, respectively), whereas at 40 % MVC only cholinergic blockade abolished the increase. These findings suggest that the increase in cerebral perfusion during exercise is dependent upon cardiac output, but that a cholinergically mediated vasodilatatory mechanism may also be important.