Endurance training facilitates myoglobin desaturation during muscle contraction in rat skeletal muscle

At onset of muscle contraction, myoglobin (Mb) immediately releases its bound O(2) to the mitochondria. Accordingly, intracellular O(2) tension (P(mb)O(2)) markedly declines in order to increase muscle O(2) uptake (m[Image: see text]O(2)). However, whether the change in P(mb)O(2) during muscle contraction modulates m[Image: see text]O(2) and whether the O(2) release rate from Mb increases in endurance-trained muscles remain unclear. The purpose of this study was, therefore, to determine the effect of endurance training on O(2) saturation of Mb (S(mb)O(2)) and P(mb)O(2) kinetics during muscle contraction. Male Wistar rats were subjected to a 4-week swimming training (Tr group; 6 days per week, 30 min × 4 sets per day) with a weight load of 2% body mass. After the training period, deoxygenated Mb kinetics during muscle contraction were measured using near-infrared spectroscopy under hemoglobin-free medium perfusion. In the Tr group, the m[Image: see text]O(2)peak significantly increased by 32%. Although the P(mb)O(2) during muscle contraction did not affect the increased m[Image: see text]O(2) in endurance-trained muscle, the O(2) release rate from Mb increased because of the increased Mb concentration and faster decremental rate in S(mb)O(2) at the maximal twitch tension. These results suggest that the Mb dynamics during muscle contraction are contributing factors to faster [Image: see text]O(2) kinetics in endurance-trained muscle.