The anaerobic threshold: 50+years of controversy

The anaerobic threshold (AT) remains a widely recognized, and contentious, concept in exercise physiology and medicine. As conceived by Karlman Wasserman, the AT coalesced the increase of blood lactate concentration ([La-]), during a progressive exercise test, with an excess pulmonary carbon dioxide output (V?CO2). Its principal tenets were: limiting oxygen (O-2) delivery to exercising muscle -> increased glycolysis, La- and H+ production -> decreased muscle and blood pH -> with increased H+ buffered by blood [HCO3-]-> increased CO2 release from blood -> increased V?CO2 and pulmonary ventilation. This schema stimulated scientific scrutiny which challenged the fundamental premise that muscle anoxia was requisite for increased muscle and blood [La-]. It is now recognized that insufficient O-2 is not the primary basis for lactataemia. Increased production and utilization of La- represent the response to increased glycolytic flux elicited by increasing work rate, and determine the oxygen uptake (V?O2) at which La- accumulates in the arterial blood (the lactate threshold; LT). However, the threshold for a sustained non-oxidative contribution to exercise energetics is the critical power, which occurs at a metabolic rate often far above the LT and separates heavy from very heavy/severe-intensity exercise. Lactate is now appreciated as a crucial energy source, major gluconeogenic precursor and signalling molecule but there is no ipso facto evidence for muscle dysoxia or anoxia. Non-invasive estimation of LT using the gas exchange threshold (non-linear increase of V?CO2 versus V?O2) remains important in exercise training and in the clinic, but its conceptual basis should now be understood in light of lactate shuttle biology.