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 O 2 ). However, whether the change in P mb O 2 during muscle contraction modulates m 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 O 2 peak significantly increased by 32%. Although the P mb O 2 during muscle contraction did not affect the increased m 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 O 2 kinetics in endurance-trained muscle.