Lactic acid is produced constantly, not just during hard exercise. The constancy of the blood lactic acid level, during rest or exercise, means that the entry into and removal of lactate from the blood are in balance. Recent studies have demonstrated that the turnover of lactic acid during exercise to be several times greater for a given blood lactate level during exercise than during rest (Brooks et al, 1996). Blood lactate concentration during incremental exercise does not necessarily reflect muscle lactate production; rather it reflects the difference between release of lactate from the muscle into the blood (muscle efflux) and uptake of blood lactate by muscle and other tissues. Thus, the accumulation of blood lactate per se does not play an underlying role in the alteration of metabolic processes during exercise. Causes of muscle and whole-body lactic acid production are several. At the level of isolated muscle tissue, factors such as contraction pattern, duration of contraction, substrate availability, hypoxia, and adrenergic stimulation play pivotal roles. Recent findings suggest that metabolic control systems in the cells produce significant modulator effects, and that ischaemia is a unique issue. At the whole-body level, circulation lactate levels depend on the balance of release and uptake of lactate from diverse tissues, which can, depending on the conditions, change from net producers to consumers or vice versa. An O2 limitation to metabolism can increase muscle lactate production and raise circulation levels, but hypoxia is only one of the causes of elevated lactate production and accumulation. Usually, O2 limited metabolism is not a cause of lactate production. A major effector of blood lactate is the adrenergic receptor system. Throughout the literature it suggests that it is a mistake to interpret lactate accumulation solely on the basis of increased production. Rather, lactate is a metabolic intermediate that can be formed, shared, and utilised within and among cells and tissues (Stainsby & Brooks, 1990). The cause of excess post-exercise O2 consumption (EPOC) is the general disturbance to homeostasis brought on by exercise. Exercise causes a rise in tissue temperatures, changes in intra- and extracellular ion concentrations, and changes in metabolite and hormone levels. Because these physiological changes persist into recovery, their effects serve to elevate O2 consumption immediately after exercise (Brooks et al, 1996). Immediately post-exercise, lactic acid provides a readily metabolisable reservoir of substrate. Depending on the conditions of recovery, this lactate reservoir may be mostly oxidised, or it may also contribute to the reestablishment of normal blood glucose levels. Lactic acid oxidation does not in itself result in elevated O2 consumption because the lactate substitutes for other substrates. Rather it is the energy necessary to return the organism to the pre-exercise condition that results in EPOC, with lactate merely supplying the fuel (Brooks et al, 1996).
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