Muscle pH regulation: role of training

In most cell types, including resting skeletal muscle fibers, internal pH (pHi) is kept constant at a relatively alkaline level. The high pHi is obtained in spite of a chronic acid load resulting from cellular metabolism and passive influx of protons driven by electrochemical forces. Regulation of pHi depends on continuous activity of membrane transport systems that mediate an outflux of H+ (or bicarbonate influx), whereby the acid load is counterbalanced. The transporters involved in muscle pH regulation at rest are the Na+/H+ exchange system as well as the Na+-dependent and Na+-independent Cl- bicarbonate transport systems. The Na+/H+ exchanger seems to be active at resting pHi levels in skeletal muscle. Therefore, pH homeostasis in skeletal muscle most likely involves an equilibrium between counter-directed H+ fluxes. A minor fraction of H+ release during intense exercise is mediated by the Na+/H+ exchanger. The capacity of this system is increased with training and hypoxia in rat skeletal muscle. The dominant acid extruding system associated with intense exercise is the lactate/H+ co-transporter. It has been demonstrated that the capacity of the lactate/H+ co-transporter of rat skeletal muscle is upregulated with training and chronic electrical stimulation, and that it is reduced upon denervation and hindlimb unweighting. Moreover, athletes can have an elevated lactate/H+ co-transport capacity, whereas the thigh muscle of spinal cord-injured individuals has a lower transport capacity than the one of healthy untrained subjects. Thus, it appears that the capacity of the lactate/H+ transporter is affected by the level of muscle activity in both rats and humans. In addition, the rate of H+ release from muscle may also be influenced by capillarization and local blood flow. Finally the resulting pH displacement during acid accumulation is determined by the cellular buffer capacity, which may also undergo adaptive changes.