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 ( V̇CO2 ). Its principal tenets were: limiting oxygen (O₂ ) 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 V̇CO2 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 O₂ 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 ( V̇O2 ) 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 V̇CO2 versus V̇O2 ) remains important in exercise training and in the clinic, but its conceptual basis should now be understood in light of lactate shuttle biology.

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