Influence of post-exercise tissue-reoxygenation on phosphocreatine recovery after static and dynamic calf muscle exercise in human

Kurzfassung

During recovery from muscle contraction orthostasis simulated by LBNP in comparison with horizontal body position reduces the time constant of phosphocreatine resynthesis (tau_PCr). This time constant reflects the rate of mitochondrial ATP formation. Recovery from exercise is accompanied by a reactive hyperemia. During recovery LBNP further increases blood volume but not flow. It is a common assumption, that after muscle contraction the increased blood flow alone results in a non-limiting oxygen supply for ATP formation during recovery. How can the increased blood volume by orthostasis enhance the rate of mitochondrial ATP formation? The following study tested the dogma about oxygen supply during recovery from exercise. ³¹Phosphorus magnetic resonance spectroscopy (³¹P MRS) and near infrared spectroscopy (NIRS) were simultaneously applied to study oxidative phosphorylation during contraction and recovery. Seven healthy subjects performed with their right calf muscles dynamic and static plantar flexions during arterial occlusion until PCr concentrations were reduced to 40 % of their resting values. Oxygen consumption measured by NIRS immediately increased with the onset of contraction and was about 4 times higher during dynamic exercise than during static contraction. After a linear initial phase the rate of oxygen consumption slowly decreased, but significant rates were still observed after 2 min of ischemic exercise. This time course was found to be incompatible with the frequently used model supposing a Michaelis-Menten type control by free cytosolic ADP and inorganic phosphate. Moreover, the time constants of PCr recovery (tau_PCr) after dynamic and static exercise were not different. So we failed to observe different recovery kinetics for different sub-populations of motor units with different mitochondrial densities. After both modes of exercise, tau_PCr was positively correlated with the time constant of hemoglobin and myoglobin reoxygenation (tau_Hb/MbO2). For slower PCr resynthesis (tau_PCr > 40s) both time constants approached the identity line which suggests limiting influence of the rate of tissue reoxygenation on the rate of mitochondrial ATP formation. Therefore, mitochondrial oxygen supply cannot be neglected as a rate controlling factor in mitochondrial ATP formation during recovery from contraction in healthy muscle.