Hyper-Oxygenation Attenuates the Rapid Vasodilatory Response to Muscle Contraction and Compression
Abstract
A single muscle compression (MC) with accompanying hyperemia and hyper-oxygenation results in attenuation of a subsequent MC hyperemia, as long as the subsequent MC takes place when muscle oxygenation is still elevated. Whether this is due to the hyper-oxygenation, or compression-induced de-activation of mechano-sensitive structures is unclear. We hypothesized that increased oxygenation and not de-activation of mechano-sensitive structures was responsible for this attenuation and that both compression and contraction-induced hyperemia attenuate the hyperemic response to a subsequent muscle contraction, and vice-versa. Protocol-1) In eight subjects two MCs separated by a 25 s interval were delivered to the forearm without or with partial occlusion of the axillary artery, aimed at preventing hyperemia and increased oxygenation in response to the first MC. Tissue oxygenation [oxygenated (hemoglobin + myoglobin)/total (hemoglobin + myoglobin)] from forearm muscles and brachial artery blood flow were continuously monitored by means of spatially-resolved near-infrared spectroscopy (NIRS) and Doppler ultrasound, respectively. With unrestrained blood flow, the hyperemic response to the second MC was attenuated, compared to the first (5...Continue Reading
References
ATP synthesis and proton handling in muscle during short periods of exercise and subsequent recovery
Contribution of nitric oxide in the contraction-induced rapid vasodilation in young and older adults
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