Effects of acute selective cyclooxygenase‐2 inhibition on skeletal muscle microvascular oxygenation and exercise tolerance

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Abstract The cyclooxygenase (COX) pathway regulates vascular tone and, therefore, local O 2 delivery‐utilization matching. The two main isoforms, COX‐1 and COX‐2, may promote opposing effects on contracting muscle O 2 transport in health by inducing vasoconstriction and vasodilatation, respectively. Whether COX‐2 and its main vasodilatory product (prostacyclin, PGI 2 ) modulate microvascular O 2 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 (), leg muscle microvascular oxygenation (; near‐infrared spectroscopy) and time to exhaustion. Leg muscle was also assessed during cuff occlusion protocols. SC2I decreased the plasma concentration of the stable PGI 2 metabolite 6‐keto prostaglandin F 1α (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, pulmonary or leg muscle from rest to moderate or severe exercise between conditions ( P > 0.05 for all). Moreover, there was no significant difference in during cuff occlusion protocols between conditions. Contrary to our hypothesis, these data indicate that COX‐2 is not obligatory for the regulation of skeletal muscle microvascular oxygenation at rest or during moderate or severe intensity exercise, and therefore does not modulate exercise tolerance in healthy adults.

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