Departments of Kinesiology and Anatomy and Physiology, Kansas State University, Manhattan, KS, USA.
Rehabilitation Clinical Trials Center, Division of Respiratory and Critical Care Physiology and Medicine, and The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
J Physiol. 2021 Feb;599(3):737-767. doi: 10.1113/JP279963. Epub 2020 Nov 19.
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 ( ). Its principal tenets were: limiting oxygen (O ) delivery to exercising muscle→increased glycolysis, La and H production→decreased muscle and blood pH→with increased H buffered by blood [HCO ]→increased CO release from blood→increased 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 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 ( ) 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 versus ) remains important in exercise training and in the clinic, but its conceptual basis should now be understood in light of lactate shuttle biology.
无氧阈 (AT) 在运动生理学和医学中仍然是一个广泛认可但存在争议的概念。正如卡尔曼·瓦瑟曼 (Karlman Wasserman) 所构想的那样,AT 将递增运动测试中血液乳酸浓度 ([La]) 的增加与过量的肺二氧化碳排出量 ( ) 结合在一起。其主要原理是:限制向运动肌肉输送氧气 (O)→增加糖酵解、乳酸和 H 的产生→降低肌肉和血液 pH 值→通过血液 [HCO ] 缓冲增加的 H→增加 CO 从血液中释放→增加 和肺通气。该方案激发了科学审查,挑战了肌肉缺氧是增加肌肉和血液 [La] 的基本前提。现在人们认识到,氧气不足不是乳酸性血症的主要基础。乳酸的增加产生和利用代表了对增加的工作率引起的糖酵解通量增加的反应,并决定了在动脉血中乳酸积累的氧气摄取量(乳酸阈;LT)。然而,持续的非氧化贡献运动能量的阈值是关键力量,它发生在代谢率通常远高于 LT 的情况下,并将重体力和极重/剧烈强度运动分开。现在人们认识到乳酸是一种至关重要的能量来源、主要的糖异生前体和信号分子,但没有事实证据表明肌肉缺氧或缺氧。使用气体交换阈值(与 呈非线性增加的 )非侵入性估计 LT 在运动训练和临床中仍然很重要,但现在应该根据乳酸穿梭生物学来理解其概念基础。