Hypertension is associated with blunted NO-mediated leg vasodilator responsiveness that is reversed by high-intensity training in postmenopausal women

The menopausal transition is associated with increased prevalence of hypertension, and in time postmenopausal women (PMW) will exhibit a cardiovascular disease risk-score similar to male counterparts. Hypertension is associated with vascular dysfunction, but whether hypertensive PMW have blunted nitric-oxide (NO)-mediated leg vasodilator responsiveness, and whether this is reversible by high-intensity training (HIT) is unknown. To address these questions, we examined the leg vascular conductance (LVC) in response to femoral-infusion of acetylcholine (ACh) and sodium nitroprusside (SNP), and skeletal muscle markers of oxidative stress and NO bioavailability before and after HIT in PMW (12.9±6.0 (mean±SD) years since last menstrual cycle). We hypothesized that ACh- and SNP-induced LVC responsiveness was reduced in hypertensive compared to normotensive PMW and that 10 weeks of HIT would reverse the blunted LVC response and decrease blood pressure (BP). 

Nine hypertensive (HYP; clinical systolic/diastolic BP 149±11/91±83 mmHg) and 8 normotensive (NORM; 122±13/75±8 mmHg) PMW completed 10 weeks of bi-weekly small-sided floorball training (4-5x3-5 min interspersed by 1-3 min rest periods). Before training, the SNP-induced change in LVC was lower (P<0.05) in HYP compared with NORM. With training, the ACh- and SNP-induced change in LVC at maximal infusion rates i.e. 100 and 6 μg∙min^-1∙kg leg mass^-1, respectively, improved (P<0.05) in HYP only. Further, training decreased (P<0.05) clinical systolic/diastolic BP (-15±11/-9±7 mmHg) in HYP, and systolic BP (-10±9 mmHg) in NORM. Thus, the SNP-mediated LVC responsiveness was blunted in hypertensive PMW, and reversed by a period of HIT that was associated with a marked decrease in clinical BP.