Differences in oxidative metabolism modulation induced by ischemia/reperfusion between trained and untrained individuals assessed by NIRS

Endurance training is associated with skeletal muscle adaptations that regulate the oxidative metabolism during ischemia/reperfusion. The aim of this study was to noninvasively assess in vivo differences in the oxidative metabolism activity during ischemia/reperfusion between trained and untrained individuals, using near infrared spectroscopy (NIRS) combined with a vascular occlusion test (VOT) technique (NIRS‐VOT). Sixteen untrained (26.3 ± 5.1 year) and seventeen trained (29.4 ± 4.9 year) healthy young adult men were submitted to a VOT (2 min baseline, 5 min occlusion, and 8 min reperfusion). Oxygen utilization was estimated from the area under the curve of the NIRS‐derived deoxyhemoglobin [HHb] signal during occlusion (AUCocc). Muscle reperfusion was derived from the area above the curve (AACrep) of the [HHb] signal after cuff release. The AUCocc of the untrained participants (21010 ± 9553 % · s) was significantly larger than the AUCocc of their trained counterparts (12320 ± 3283 % · s); P = 0.001). The AACrep of the untrained participants (5928 ± 3769 % · s) was significantly larger than the AACrep of the trained participants (3745 ± 1900 % · s; P = 0.042). There was a significant correlation between AUCocc and AACrep (r = 0.840; P = 0.001). NIRS assessment of oxidative metabolism showed that trained individuals are more efficient in shifting between oxidative and anaerobic metabolism in response to ischemia and reperfusion. Endurance training is associated with skeletal muscle adaptations that regulate the oxidative metabolism during ischemia/reperfusion. However, most of the studies assessing oxidative metabolism in trained and untrained individuals are in vitro or through invasive techniques. Then, this study demonstrated, through a noninvasive and in vivo technique (NIRS‐VOT) assessment of skeletal muscle oxidative metabolism, that trained individuals are more efficient in shifting between oxidative and anaerobic metabolism in response to ischemia and reperfusion.