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Impact of cholinergically‐mediated vasodilation on blood pressure at the onset of exercise in humans
Author(s) -
Vianna Lauro C,
Fadel Paul J,
Secher Niels H,
Fisher James P
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1138.39
Subject(s) - medicine , vasodilation , glycopyrrolate , cholinergic , blood pressure , atropine , brachial artery , blockade , metoprolol , forearm , endocrinology , vascular resistance , adrenergic , cardiology , surgery , receptor
Handgrip exercise evokes an initial decrease in the vascular resistance of the non‐exercising forearm which is antagonized by atropine, indicative of cholinergic‐mediated vasodilation in human skeletal muscle. However, the role of cholinergic‐mediated vasodilation in modulating the blood pressure (BP) response to exercise in humans remains unknown. To examine this, beat‐to‐beat BP (brachial artery), cardiac output (CO; Modelflow) and total vascular resistance (TVR; mean BP/CO) were continuously monitored in 9 men (23±5 yrs) while performing static handgrip at 40% MVC under control (no drug), cholinergic (glycopyrrolate) and β‐adrenergic (metoprolol or propranalol) blockade conditions. Exercise under control conditions produced a biphasic BP response at exercise onset, consisting of an initial rise (0–3s, +6±2 mmHg, P<0.05) and a subsequent fall to a nadir at 7–10s (+2±2 mmHg). TVR dropped progressively between 3–10s of exercise (−24±2% at 10s; P<0.05). β‐adrenergic blockade did not affect the magnitude or temporal pattern of the BP and TVR responses. However, cholinergic blockade abolished the exercise‐induced fall in TVR, and augmented the pressor response to exercise (+13±3 mmHg at 10s; P<0.05 vs. control). Changes in CO were similar between trials. These findings highlight for the first time the important role of cholinergic vasodilation on BP responses at exercise onset in humans.