Abstract
We tested the hypothesis that the vasodilatation responses to exercise were attenuated in homozygous individuals for the allele Asp298.Methods: from 287 volunteers genotyped, we studied 24 individuals: Glu/Glu (n=15, age 43±3 yr, BMI 22.9±0.3 kg/m2) and Asp/Asp (n=9, age 40±4 yr, BMI 23.5±0.9 kg/m2). Heart rate (HR), mean blood pressure (MBP) and forearm blood flow (FBF) were recorded during handgrip exercise (30% MVC).Results: FVC responses to exercise were lower in Asp/Asp, compared with Glu/Glu (Δ=0.07±0.14 vs. 0.57±0.09 units, P=.002). To investigate the mechanisms underlying the lowered vasodilatation in Asp/Asp, we studied FBF during L‐NMMA and L‐NMMA + phentolamine in a subset of 8 Glu/Glu and 7 Asp/Asp. We measured muscle sympathetic nerve activity (MSNA). L‐NMMA did not change FVC responses to exercise in Asp/Asp, compared with saline (Δ=−0.05±0.20 vs. −0.09±0.18 units, P=.52). In contrast, L‐NMMA reduced FVC in Glu/Glu (Δ0.79±0.14 vs. 0.14±0.09 units) and the difference between genotypes were no longer observed (P=.62). L‐NMMA + phento increased similarly FVC responses to exercise in Glu/Glu and Asp/Asp (Δ=1.16±0.26 vs. 0.56±0.24 units, P=.43). MBP and MSNA were similar among genotypes.Conclusion:Asp/Asp individuals have attenuated muscle vasodilatation responsiveness to exercise, which seems to be primarily mediated by a reduced nitric oxide bioavailability.
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