Effects of acute selective cyclooxygenase-2 inhibition on skeletal muscle microvascular oxygenation and exercise tolerance
Abstract
The cyclooxygenase (COX) pathway regulates vascular tone and, therefore, local O2 delivery-utilization matching. The two main isoforms, COX-1 and COX-2, may promote opposing effects on contracting muscle O2 transport in health by inducing vasoconstriction and vasodilatation, respectively. Whether COX-2 and its main vasodilatory product (prostacyclin, PGI2) modulate microvascular O2 transport to skeletal muscle and thus exercise tolerance is unknown. We tested the hypothesis that acute selective COX-2 inhibition (SC2I) would impair cardiorespiratory and skeletal muscle microvascular responses from rest to exercise, thereby reducing exercise tolerance in healthy adults. Twelve individuals participated in a randomized, double-blind, crossover study to receive SC2I (200 mg celecoxib) or placebo (control, CON). Moderate and severe intensity cycling were performed with measurements of heart rate, arterial blood pressure, pulmonary oxygen uptake ( V̇O2${\dot V_{{{\mathrm{O}}_2}}}$ ), leg muscle microvascular oxygenation ( StO2${S_{{\mathrm{t}}{{\mathrm{O}}_2}}}$ ; near-infrared spectroscopy) and time to exhaustion. Leg muscle StO2${S_{{\mathrm{t}}{{\mathrm{O}}_2}}}$ was also assessed during cuff occlusion protocols. SC2I decreased the plasma concentration of the stable PGI2 metabolite 6-keto prostaglandin F1α (CON: 203 (54) pg/mL; SC2I: 108 (54) pg/mL; P = 0.002). There was no difference in exercise tolerance (CON: 278 (55) s; SC2I: 298 (75) s), arterial blood pressure, heart rate,…
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Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design.
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