Blood lactate levels can also rise during submaximal exercise at intensities less than 100% V02max. Exercises 3.13 shows that blood lactate levels measured during the same progressive treadmill test used to determine the V02max remain low at low running speeds. Ultimately, a running speed is reached above which blood lactate levels appear to rise more precipitously. This point has by convention
After training become known as the lactate tumpoint or the anaerobic threshold. It seems that both terms are incorrect.
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The original explanation for the rise in blood lactate concentrations at the lactate tumpoint was that at the tumpoint, the oxygen supply to the muscles was inadequate to cover their oxygen demands. The muscles therefore became “anaerobic” and, as a result, released lactate in increasing amounts. The origin of this belief can probably be traced to the influence of A.V. Hill who proposed that lactate was the signal that initiated muscle contraction and that the “function of oxygen is to remove the (lactic) acid, once it has been formed” (1927, p. 66). It is now clear that lactate is a product of, not the cause of, muscle contraction. More importantly, there is little evidence that lactate is released only by muscles that are anaerobic or that muscles become anaerobic during exercise.
First, muscles can release lactate even when their oxygen supply is more than adequate (Connett et al, 1984, 1986). Thus muscle lactate production is not synonymous with anaerobic conditions in the muscles.
Second, there is no conclusive evidence that muscles become anaerobic during exercise at intensities approximating the lactate threshold (Connett et al, 1985; Gayeski et al, 1985) or even during maximal exercise (Graham & Saltin, 1989). For these reasons the term anaerobic threshold is clearly inappropriate.