Abstract
We tested whether: 1) the compensatory vasodilation in skeletal muscle during hypoxic exercise is attenuated in aging humans, and 2) local inhibition of NO synthesis in the forearm of aging humans will have less impact on the compensatory dilation during rhythmic exercise with hypoxia. Isocapnic hypoxia (arterial O2 saturation 80%) was generated with a rebreathing system in 11 older subjects (6F/5M; 61 ± 2). Subjects performed incremental forearm exercise (10% and 20% of maximum) during saline infusion (control) and NO synthase inhibition with L-NMMA under normoxic and hypoxic conditions. Forearm vascular conductance (FVC; ml/min/100mmHg) was calculated from blood flow (ml/min) and blood pressure (mmHg). Data were compared to previously published data in young subjects (n =12). During the control condition, the compensatory vasodilator response to hypoxia (% change in Ä FVC compared to respective normoxic exercise trial) was similar between the old and young groups at 10% exercise (28 ± 6% vs. 40 ± 8%, P = 0.22) but attenuated at 20% exercise (14 ± 4% vs. 31 ± 6%, P < 0.05). L-NMMA during hypoxic exercise only blunted the compensatory vasodilator response in the young group (P < 0.05). Our data indicate that aging reduces the compensatory vasodilator response to hypoxic exercise via blunted NO signaling. NIH HL-46493 (MJJ) and AR-55819 (DPC) and CTSA RR-024150
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