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Updated: Jun 4, 2026

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Ageing reduces the compensatory vasodilatation during hypoxic exercise: the role of nitric oxide
Darren P Casey1, Branton G Walker, Timothy B Curry
1Department of Anesthesiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA. casey.darren@mayo.edu
Abstract:
We tested the hypotheses that (1) the compensatory vasodilatation in skeletal muscle during hypoxic exercise is attenuated in ageing humans and (2) local inhibition of nitric oxide (NO) synthesis in the forearm of ageing humans will have less impact on the compensatory dilatation during rhythmic exercise with hypoxia, due to a smaller compensatory dilator response. Eleven healthy older subjects (61 ± 2 years) performed forearm exercise (10% and 20% of maximum) during saline infusion (control) and NO synthase inhibition (NG-monomethyl-L-arginine; L-NMMA) under normoxic and normocapnic hypoxic (80% arterial O2 saturation) conditions. Forearm vascular conductance (FVC; ml min⁻¹ (100 mmHg)⁻¹) was calculated from forearm blood flow(ml min⁻¹) and blood pressure (mmHg). To further examine the effects of ageing on the compensatory vasodilator response to hypoxic exercise we compared the difference in ΔFVC (% change compared to respective normoxic exercise trial) between the older subjects (present study) and previously published data from an identical protocol in young subjects. During the control condition, the compensatory vasodilator response to hypoxia was similar between the old and young groups at 10% exercise (28 ± 6% vs. 40 ± 8%, P =0.11) 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 suggest that ageing reduces the compensatory vasodilator response to hypoxic exercise via blunted NO signalling.
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