Role of oxygen in shaping the power-duration curve
Updated: Aug 21, 2020
POOLE, DAVID C.; BURNLEY, MARK; VANHATALO, ANNI; ROSSITER, HARRY B.; JONES, ANDREW M.
According to the traditional interpretation of the power–duration parameters (Fig. 1 left ), Critical Power (CP) represents the greatest rate of “wholly oxidative” energy provision, and the W′ is a finite work capacity above CP chiefly derived from anaerobic metabolism (61). This definition of the W′ as a fixed anaerobic energy store has been challenged by the findings that W′ is associated with the kinetic features of the V˙O2 response (e.g., 3,11,64,102). Burnley and Jones (17) proposed that W′ is a function of the V˙O2 slow component, V˙O2 max, and the depletion of limited intramuscular substrates (i.e., muscle PCr and glycogen) and the associated accumulation of fatigue-related metabolites, such as H+, adenosine diphosphate (ADP), and Pi; each of which is associated with impaired muscle contractile function. The V˙O2 slow component reflects a loss of efficiency of muscular work, stemming predominantly from active muscle (74). The power–duration relationship may, therefore, reflect the V˙O2 kinetics and the underlying respiratory control mechanism(s), which are ultimately constrained during severe-intensity exercise by the attainment of V˙O2 max. Here we summarize the current evidence in support of this interpretation.
Cellular bioenergetics entail an intricate signaling network that governs the flux of electrons from energy substrate to O2. In healthy, non sedentary individuals exercising under normal ambient conditions, the maximal mitochondrial oxidative rate is greater than what can be achieved in vivo during whole-body exercise due to an O2 delivery limitation (72,73,80). V˙O2 max is reached when the mitochondrial flux can increase no further despite continued elevation of metabolic stimulation (through accumulation of ADP and Cr) (44). O2 delivery is therefore one presiding mechanism that can limit cellular respiration during severe-intensity exercise.
A 3-min all-out cycling test against fixed resistance represents an ideal experimental model that results in the attainment of V˙O2 max and yields a large V˙O2 slow component amplitude and complete utilization of W′ (98,103). During a 3-min all-out exercise test the finite work capacity indicated by W′ is depleted, such that after ~2.5 min the W′ is reduced to zero and power output plateaus at CP (98,99). A maximal all-out sprint sends a maximal metabolic signal to the mitochondria to increase respiration such that as the power output approaches CP the V˙O2 approaches and then plateaus at V˙O2 max. Therefore, the high O2 cost (V˙O2 max) of generating an end-test power output of only ~50%Δ (where Δ is the difference between the power output at V˙O2 max and LT/GET) defines a significant loss of efficiency during a 3-min all-out test. A positive correlation between W′ and the amplitude of the V˙O2 slow components during both all-out (103) and constant work rate exercise (64) points toward a mechanistic link between W′, the development of fatigue, and the loss of muscular efficiency (17).
A useful intervention to explore the mechanistic bases of the power–duration parameters is the manipulation of the inspired O2. A hyperoxic inspirate elevates the O2 pressure gradient between the microvasculature and the mitochondria and reduces the slow components of pulmonary V˙O2 (106) and muscle PCr (40). Using single-leg knee extension exercise, Vanhatalo et al. (100) showed that the inspiration of 70% O2 compared with air significantly increased CP while decreasing W′. As a result, the power–duration curve predicted that exercise tolerance was improved at work rates less than ~150% of CP (Fig. 3). These data support the traditional notion that CP is a parameter of aerobic fitness but challenge the traditional definition of W′ as an anaerobic work capacity. The rate at which muscle PCr and pH fell during the prediction trials was attenuated in hyperoxia, indicating a slower progression of metabolic perturbation, allowing longer exercise duration before the same end-exercise PCr and pH values were reached (100). These results indicate that within the severe exercise intensity domain, consistently low levels of intramuscular PCr and pH are reached at intolerance irrespective of the work rate or inspired O2, as hypothesized by Poole et al. (76). Intolerance in severe exercise might occur when a particular intramuscular environment is achieved (of which the PCr and pH are two indices among others), and the hyperoxia intervention suggests that the extent of the disturbance to homeostasis during exercise is sensitive to the conditions of muscle O2 delivery (100).
A schematic illustration of the group mean power–duration curves redrawn on the basis of data from Vanhatalo et al. (100). The solid curve indicates power–duration relationship for knee extension exercise in normoxia and the dashed curve in hyperoxia (70% O2). The solid horizontal line indicates CP in normoxia and the dashed line indicates CP in hyperoxia. The arrows denote the crossover point for the two curves at approximately 150% of CP and 4 min of exercise tolerance.
Hypoxia has detrimental effects on muscle metabolism and exercise tolerance (2,26). During high-intensity exercise, there is an accelerated depletion of PCr and glycogen and a more rapid accumulation of fatigue-related metabolites (e.g., 40,44). Hypoxia also causes a reduction in the maximal oxidative metabolic rate, and this is reflected in a slowing of muscle PCr recovery kinetics after exercise. In addition, the inspiration of hypoxic gas mixtures decreases peripheral O2 diffusion, which may contribute to the slowing of V˙O2 kinetics at the onset of exercise (93). CP is reduced by the acute inspiration of hypoxic gas (13%–15% O2), which is associated with an arterial O2 saturation of ~76%–82% at the end of exhaustive exercise (26,85). In these studies, W′ was not significantly affected by acute hypoxia, but both noted great interindividual variability in responses, which ranged from large decreases (~44%–36%) to considerable increases in W′ (~38%–66%), and an inverse relationship between changes in W′ and changes in CP (26,85). Parker Simpson et al. (85) also reported that the change in W′ was positively correlated with the change in the “distance” between V˙O2 max and CP between normoxia and hypoxia. That is, those subjects in whom W′ increased most in hypoxia also showed the greatest increase in the range of the severe domain (i.e., CP-V˙O2 max). These data illustrate that W′, or the ability to access W′, may be inherently linked to indices of aerobic fitness (i.e., CP and V˙O2 max; cf. van der Vaart et al.  for contrary data).
Complete blood flow occlusion imposes the most extreme O2 delivery limitation for skeletal muscle and challenges the applicable range of the power–duration relationship. Using brachial occlusion in a hand-grip exercise model, Broxterman et al. (12) reduced CP to less than zero, whereas W′ significantly increased. Putative explanations for this elevated W′ include (a) some of the oxidative adenosine 5′ triphosphate (ATP) turnover normally quantified within CP appeared as W′, (b) the muscle somehow accessed more substrate-level phosphorylation, and/or (c) the efficiency of muscle contraction and/or ATP resynthesis increased. From a theoretical perspective, the negative CP indicates that under cuff occlusion there is no metabolic rate that is sustainable, including the resting metabolic rate, which makes intuitive sense. It is noteworthy that the hyperbolic nature of the power–duration relationship was conserved under blood flow occlusion. However, the precise physiological underpinnings of the shifts in the asymptote and curvature of the power–duration relationship under occlusive conditions warrant further investigation.