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.
figure legend As originally posited and defended most ardently by Karlman Wasserman and Brian J. Whipp, the anaerobic threshold (AT) concept represents the epitome of integrative physiological control. The graph at the upper right portrays blood La−, arterial CO2 partial pressure (PCO2) and ventilation (V̇E) as a function of V̇O2 increasing from rest to maximum (V̇O2max). The AT is identified (black arrow) by the departure of V̇E from linearity without PCO2 decreasing. As shown rightwards from the ‘Original theory’ box, the AT held that lack of (or very low) muscle O2, via the Pasteur effect, increased muscle and blood lactic acid, then H+ dissociated from the lactic acid and was buffered by bicarbonate thus increasing CO2 evolution from the blood; this stimulated the ‘extra’ V̇E at AT simultaneous with the increase in La−. Currently we understand that neither anoxia nor dysoxia underpins increased muscle La− production and efflux, but rather its increase in the blood is attributed to the rate of La− appearance being greater than disappearance. Also, as long appreciated, the variability in, and complexities of, the control of breathing dictate that the V̇CO2 versus V̇O2 relation (gas exchange threshold) more reliably approximates the lactate threshold than does the ventilatory profile. At the bottom, the modern understanding of metabolism is that La− is a central element linking glycolysis (Gly) and oxidative phosphorylation (OxPhos) energetics. Via cell signalling, La− also plays roles in short‐ and long‐term adaptations in both health and disease.
Keywords: arterioles; blood flow dynamics; capillary function; exercise physiology; muscle microcirculation; oxygen delivery; oxygen uptake kinetics; venules Article Note: Edited by: Michael Hogan & ...Russell Hepple Linked articles: This Perspectives article highlights an article by Mendelson et al. To read this paper, visit Byline: David C. Poole
: The hyperbolic form of the power-duration relationship is rigorous and highly conserved across species, forms of exercise, and individual muscles/muscle groups. For modalities such as cycling, the ...relationship resolves to two parameters, the asymptote for power (critical power CP) and the so-called W' (work doable above CP), which together predict the tolerable duration of exercise above CP. Crucially, the CP concept integrates sentinel physiological profiles-respiratory, metabolic, and contractile-within a coherent framework that has great scientific and practical utility. Rather than calibrating equivalent exercise intensities relative to metabolically distant parameters such as the lactate threshold or V˙O2max, setting the exercise intensity relative to CP unifies the profile of systemic and intramuscular responses and, if greater than CP, predicts the tolerable duration of exercise until W' is expended, V˙O2max is attained, and intolerance is manifested. CP may be regarded as a "fatigue threshold" in the sense that it separates exercise intensity domains within which the physiological responses to exercise can (<CP) or cannot (>CP) be stabilized. The CP concept therefore enables important insights into 1) the principal loci of fatigue development (central vs. peripheral) at different intensities of exercise and 2) mechanisms of cardiovascular and metabolic control and their modulation by factors such as O2 delivery. Practically, the CP concept has great potential application in optimizing athletic training programs and performance as well as improving the life quality for individuals enduring chronic disease.
The maximal lactate steady state (MLSS) and the critical power (CP) are two widely used indices of the highest oxidative metabolic rate that can be sustained during continuous exercise and are often ...considered to be synonymous. However, while perhaps having similarities in principle, methodological differences in the assessment of these parameters typically result in MLSS occurring at a somewhat lower power output or running speed and exercise at CP being sustainable for no more than approximately 20–30 min. This has led to the view that CP overestimates the ‘actual’ maximal metabolic steady state and that MLSS should be considered the ‘gold standard’ metric for the evaluation of endurance exercise capacity. In this article we will present evidence consistent with the contrary conclusion: i.e., that (1) as presently defined, MLSS naturally underestimates the actual maximal metabolic steady state; and (2) CP alone represents the boundary between discrete exercise intensity domains within which the dynamic cardiorespiratory and muscle metabolic responses to exercise differ profoundly. While both MLSS and CP may have relevance for athletic training and performance, we urge that the distinction between the two concepts/metrics be better appreciated and that comparisons between MLSS and CP, undertaken in the mistaken belief that they are theoretically synonymous, is discontinued. CP represents the genuine boundary separating exercise in which physiological homeostasis can be maintained from exercise in which it cannot, and should be considered the gold standard when the goal is to determine the maximal metabolic steady state.
The maximal lactate steady state (MLSS) and the critical power (CP) are two indices of the highest oxidative metabolic rate that can be sustained during continuous exercise and are often considered to be synonymous. We discuss evidence consistent with the interpretation that CP provides a more robust representation of the boundary separating exercise domains wherein a metabolic steady‐state can or cannot be achieved.
Crucially, T2D ablates the cardiovascular disease risk advantage of pre-menopausal females over males and a more severe crippling of cardiorespiratory fitness and exercise tolerance have been ...associated, though not unequivocally,3 with greater morbidity and mortality in females than males with T2D.2,5,16 With respect to its vascular and energetic capacities in health, skeletal muscle represents a ‘sleeping giant’ with maximal blood flow capacities in excess of 4 L/kg/min and a prodigious total capillary length and surface area.10,17 Exercise training-induced improvements in skeletal muscle structure and function therefore have the demonstrated ability to reduce the plethora of pernicious metabolic and physiological sequelae of T2D. ...it is pertinent that sexual dimorphism in the NO pathway for vasodilation has been reported recently with intact female rats decreasing microvascular oxygen pressures far more than males in response to L-NAME (L-NG-Nitro arginine methyl ester) induced NO oxide synthase inhibition.19 Furthermore, female rats in heart failure with reduced ejection fraction (HFrEF) appear to be more responsive to nitrate supplementation than their male counterparts.20 If Green et al.'s current findings18 are reproducible across larger and more diverse cohorts of female T2D patients and are truly representative of a sexual dimorphism in vascular plasticity to exercise training, rather than simply an effect of greater training-induced maximal voluntary contraction(s), this is tremendously exciting. Specifically, it may help instigate development of sex-specific exercise and possibly pharmacological interventions directed more precisely to the burgeoning female T2D population: A demographic that has been historically underserved in preclinical and clinical trials. ...that a common endurance/resistance training paradigm promoted a substantial increase in plantar flexor muscle strength (MVC) in females but not males in the face of equivalent improvements in peak oxygen uptake and oxygen uptake kinetics3,18 is intriguing and highly relevant clinically.
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