Abstract

Pre-menopausal women express a reduced arterial blood pressure and risk of cardiovascular disease relative to age-matched men. The mechanism for these outcomes purportedly relate to elevated estrogen levels increasing endothelial nitric oxide (NO) synthase activity and NO-mediated vasorelaxation. PURPOSE: Based on the role that NO plays in the relationship between O2 delivery and utilization, we tested the hypothesis that females would show a fundamentally higher O2 delivery/utilization ratio; especially during muscle contractions, compared to males. METHODS: To test this hypothesis, the spinotrapezius muscle of Sprague Dawley rats (14 total; female = 7, male = 7) was surgically exposed and electrically stimulated at 1 Hz. Oxyphor G4 was injected into the muscle and phosphorescence quenching employed to determine the temporal profile of muscle interstitial space O2 partial pressure (PintO2, determined by O2 delivery/utilization ratio). This was performed under three conditions: control (CON), 300 μM sodium nitroprusside (SNP; NO donor) superfusion, and 1.5 mM L-arginine methyl ester (L-NAME; NOS blockade) superfusion. RESULTS: No differences were found for baseline PintO2 (CON: 21 ± 1 vs 17 ± 2; SNP: 40 ± 3 vs 36 ± 3; L-NAME: 16 ± 2 vs 14 ± 2 mmHg (all p > 0.05)); nor ΔPintO2 during contractions (CON: 13 ± 1 vs 12 ± 2; SNP 20 ± 2 vs 18 ± 2; L-NAME: 11 ± 1 vs 9 ± 1 mmHg (all p > 0.05)) between males and females, respectively. The kinetics response (mean response time) to contractions did not differ in any condition (CON: 17 ± 2 vs 16 ± 3; SNP: 21 ± 2 vs 28 ± 5; L-NAME: 15 ± 2 vs 14 ± 1 seconds (all p > 0.05)) between males and females, respectively. DISCUSSION: In direct contrast to our hypothesis, no sex differences were evident at rest or during contractions under any condition. Therefore, at rest and during muscle contractions, the effect of estrogen on NO bioavailability and vascular control are either insignificant or redundant to other vasodilatory pathways.

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