Possible mechanisms of the anaerobic threshold. A review

The anaerobic threshold consists of a lactate threshold and a ventilatory threshold. In some conditions there may actually be 2 ventilatory thresholds. Much of the work detailing the lactate threshold is strongly based on blood lactate concentration. Since, in most cases, blood lactate concentration does not reflect production in active skeletal muscle, inferences about the metabolic state of contracting muscle will not be valid based only on blood lactate concentration measurements. Numerous possible mechanisms may be postulated as generating a lactate threshold. However, it is very difficult to design a study to influence only one variable. One may ask, does reducing F1O2 cause an earlier occurrence of a lactate threshold during progressive exercise by reducing oxygen availability at the mitochondria? By stimulating catecholamine production? By shifting more blood flow away from tissues which remove lactate from the blood? Or by some other mechanism? Processes considered essential to the generation of a lactate threshold include: (a) substrate utilisation in which the ability of contracting muscle cells to oxidise fats reaches maximal power at lactate threshold; and (b) catecholaminergic stimulation, for without the presence of catecholamines it appears a lactate threshold cannot be generated. Other mechanisms discussed which probably enhance the lactate threshold, but are not considered essential initiators are: (a) oxygen limitation; (b) motor unit recruitment order; (c) lactate removal; (d) muscle temperature receptors; (e) metabolic stimulation; and (f) a threshold of lactate efflux. Some mechanisms reviewed which may induce or contribute to a ventilatory threshold are the effects of: (a) the carotid bodies; (b) respiratory mechanics; (c) temperature; and (d) skeletal muscle receptors. It is not yet possible to determine the hierarchy of effects essential for generating a ventilatory threshold. This may indicate that the central nervous system integrates a broad range of input signals in order to generate a non-linear increase in ventilation. Evidence indicates that the occurrence of the lactate threshold and the ventilatory threshold may be dissociated; sometimes the occurrence of the lactate threshold significantly precedes the ventilatory threshold and at other times the ventilatory threshold significantly precedes the lactate threshold. It is concluded that the 2 thresholds are not subserved by the same mechanism.