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 ( V̇O2 ), leg muscle microvascular oxygenation ( StO2 ; near-infrared spectroscopy) and time to exhaustion. Leg muscle StO2 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 V̇O2 or leg muscle StO2 from rest to moderate or severe exercise between conditions (P > 0.05 for all). Moreover, there was no significant difference in StO2 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.