Abstract

The vasodilatory response to passive leg movement (PLM) is predominantly nitric oxide (NO) mediated. Due to reduced NO bioavailability with advancing age, PLM-induced vasodilation is attenuated in older sedentary subjects. PURPOSE: We sought to determine the impact of varying levels of physical activity on PLM-induced vasodilation, and therefore NO bioavailability, in older subjects. METHODS: PLM was performed on four subject groups (young sedentary (YS), 23 ± 1 yrs, n = 12; old sedentary (OS), 73 ± 2 yrs, n = 12; old active (OA), 71 ± 2 yrs, n = 10; old endurance trained (OT), 72 ± 1 yrs, n = 10) in the upright-seated posture. Central and peripheral hemodynamic responses were determined second-by-second with finger photoplethysmography and Doppler ultrasound, respectively. RESULTS: Peak VO2 was significantly different between all subject groups (YS = 42 ± 3, OS = 26 ± 2, OA = 34 ± 2, OT = 52 ± 2 ml/kg/min; P < 0.05). PLM-induced peak change in leg vascular conductance (ΔLVCpeak) was significantly attenuated in OS compared to YS (OS: 4.4 ± 0.8, YS: 11.8 ± 1.3 ml/min/mmHg; P < 0.05). Both OA and OT groups demonstrated augmented ΔLVCpeak compared to OS (OA: 7.3 ± 0.8, OT: 7.6 ± 0.9 ml/min/mmHg; P < 0.05). However, OA and OT groups were not different (P = 0.82), and remained attenuated compared to YS (P < 0.05). The rapid vasodilatory response (slope of LVC over time; ml/min/mmHg/s), also thought to be partially NO-dependent, was not different between YS, OA, and OT (YS: 1.08 ± 0.14, OA: 0.75 ± 0.10, OT: 0.79 ± 0.14 ml/min/mmHg/s; P < 0.05), but was decreased in OS compared to the other three groups (0.42 ± 0.06 ml/min/mmHg/s; P < 0.05). CONCLUSIONS: These data suggest that remaining physically active during aging likely augments NO-mediated vascular function. However, physical activity, even at levels achieved by highly trained older individuals, failed to fully restore vasodilatory responses to that of the young.

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