Interaction of Factors Determining Critical Power

Abstract

The physiological determinants of high-intensity exercise tolerance are important for both elite human performance and morbidity, mortality and disease in clinical settings. The asymptote of the hyperbolic relation between external power and time to task failure, critical power, represents the threshold intensity above which systemic and intramuscular metabolic homeostasis can no longer be maintained. After ~ 60 years of research into the phenomenon of critical power, a clear understanding of its physiological determinants has emerged. The purpose of the present review is to critically examine this contemporary evidence in order to explain the physiological underpinnings of critical power. Evidence demonstrating that alterations in convective and diffusive oxygen delivery can impact upon critical power is first addressed. Subsequently, evidence is considered that shows that rates of muscle oxygen utilisation, inferred via the kinetics of pulmonary oxygen consumption, can influence critical power. The data reveal a clear picture that alterations in the rates of flux along every step of the oxygen transport and utilisation pathways influence critical power. It is also clear that critical power is influenced by motor unit recruitment patterns. On this basis, it is proposed that convective and diffusive oxygen delivery act in concert with muscle oxygen utilisation rates to determine the intracellular metabolic milieu and state of fatigue within the myocytes. This interacts with exercising muscle mass and motor unit recruitment patterns to ultimately determine critical power.

No sex differences in oxygen uptake or extraction kinetics in the moderate or heavy exercise intensity domains

“…For instance, Ansdell et al (2019) showed female knee-extensors had a greater relative critical torque than males during single-limb exercise. Whereas during cycling, where O 2 delivery is a determinant of critical power (Goulding & Marwood, 2023), this metabolic threshold was not different between sexes (Ansdell et al, 2020a). Whilst consensus on whether O 2 delivery does (Hughson et al, 2001) or does not (Grassi, 2001) limit τV O 2 has not been reached, it is conceivable that during tasks where O 2 delivery and utilisation are both determinants in the metabolic response to exercise, the superior female skeletal muscle oxidative capacity (Cardinale et al, 2018) and vasodilatory response to exercise (Parker et al, 2007) is counteracted by an inferior O 2 carrying capacity (Murphy, 2014).…”

“…Despite more aerobically-suited skeletal muscle, females have lower levels of haemoglobin (Murphy, 2014), which is thought to impair O 2 carrying capacity during exercise (Harms et al ., 1998; Diaz-Canestro et al ., 2022). During exercise where O 2 delivery and utilisation are both limiting factors (e.g., cycling, Goulding & Marwood, 2023), these factors are thought to counteract each other to enable comparable relative metabolic thresholds (i.e., critical power) between the sexes (Ansdell et al ., 2020b). To date, the only investigation to systematically investigate the oxidative adjustment at the onset of exercise between sexes did so during low intensity treadmill walking (Beltrame et al ., 2017).…”

“…Data from this study suggested faster O 2 extraction in females, quantified as the change in de-oxyhaemoglobin and myoglobin (HHb+Mb) signal in near-infrared spectroscopy (NIRS), fitting with the notion that phase II V□O 2 kinetics are influenced by intramuscular factors in healthy humans (Poole & Jones, 2012). However, the demands of treadmill walking differ to those of high-intensity cycling exercise, where it has recently been argued that all levels of the O 2 cascade are considered to be influential in determining metabolic responses to exercise (Goulding & Marwood, 2023). Thus, given the lack of evidence regarding physiological responses to exercise in females (James et al ., 2023), it remains to be determined how sex differences in convective and diffusive contributions to O 2 delivery mediate the rate of V□O 2 adjustment to exercise.…”

Critical power is a key threshold determining the magnitude of post‐exercise hypotension in non‐hypertensive young males

“…severe exercise), a steady‐state is unattainable for both $${\dot{V}}_{{{\mathrm{O}}}_{\mathrm{2}}}$$ and blood [lactate], with $${\dot{V}}_{{{\mathrm{O}}}_{\mathrm{2}}{\mathrm{max}}}$$ being attained shortly prior to task failure (Goulding & Marwood, 2023; Goulding et al., 2021; Jones et al., 2011; Poole et al., 2016). In practical terms, healthy individuals perform most activities of daily living below GET, whereas for those with chronic diseases, the elderly and very inactive individuals, activities of daily living may be carried out above GET and/or critical power (Goulding & Marwood, 2023; Poole et al., 2021). These thresholds therefore partition the full range of aerobic activities performed in daily life.…”

Effect of Ischemic Preconditioning (IPC) on Recovery of Exercise Performance Following a Bout of Exercise to Volitional Exhaustion

“…The physiological mechanisms that underpin the possible improvements in exercise performance seen as a result of IPC, have not been fully elucidated [9]. A number of mechanisms have however been postulated for any positive effects of IPC, including augmented oxygen uptake kinetics [10], which are an important determinant of aerobic exercise performance [11,12]. It is proposed that increases in blood flow through an upregulation of endothelial function following IPC allows for an improved (reduced) time constant () of the fundamental phase of oxygen uptake kinetics, in addition to an attenuation of the slow component [1].…”