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Critical Power represents a metabolic rate


In contrast to historical definitions, Critical Power (CP) is now considered to represent the greatest metabolic rate that results in wholly oxidative energy provision, where wholly oxidative considers the active organism in toto and means that energy supply through substrate-level phosphorylation reaches a steady state, and that there is no progressive accumulation of blood lactate or breakdown of intramuscular phosphocreatine (PCr), i.e., the rate of lactate production in active muscle is matched by its rate of clearance in muscle and other tissues. It is important to note here, however, that there will always be some error in the estimation of CP, and CP varies slightly from day to day in the same subject (91). Although it is possible to estimate CP to the nearest watt (e.g., 200 W), given a typical error of ~5%, the “actual” CP might lie between approximately 190 and 210 W in a given individual. Therefore, asking a subject to exercise exactly at his or her estimated CP runs the risk that he or she will be above their individual CP with associated implications for physiological responses and exercise tolerance. As CP is primarily a rate of oxidative metabolism (rather than the mechanical power output, by which it is typically measured), it might be more properly termed “critical V˙O2.” During cycling, the external power output corresponding to this critical V˙O2 can be altered as a consequence of the chosen pedal rate for example (6). Similarly, the actual CS equivalent to critical V˙O2 during other forms of exercise will depend on movement economy. However, it is because the critical V˙O2 is expressed “functionally” in units of power or speed that it is so powerful in the prediction of exercise tolerance or exercise performance (47).

The CP threshold lies approximately equidistant between the so-called lactate threshold (LT) or gas exchange threshold (GET) and the maximum power output attained during incremental exercise. However, both LT/GET and CP can vary widely among individuals depending on the state of health or training. Specifically, LT/GET and CP occur at 50%–65% and 70%–80%V˙O2 max, respectively, in healthy young subjects. In contrast, in well-trained individuals (where the maximal rates of oxidative metabolism are increased by endurance training) or in some patients with chronic disease (where maximal rates of O2 transport and utilization are selectively reduced), LT/GET and CP can reach approximately 70%–80% and 80%–90% V˙O2 max, respectively (96). Crucially, physiological behavior differs markedly according to whether constant-power exercise is performed below or above these thresholds. Poole et al. (76) measured the physiological responses of human volunteers exercising on a cycle ergometer at constant-power outputs set at or just above (+5% of ramp test peak power) the predetermined CP. During exercise at CP, the subjects attained a steady state in pulmonary gas exchange, ventilation, and blood lactate concentration, and all were able to complete the target of 24 min of exercise without difficulty. In contrast, during exercise above CP, steady-state behavior was not observed, with V˙O2 progressing to V˙O2 max and blood lactate increasing inexorably until exercise was terminated before the 24-min target. This study clearly indicates that CP is a “threshold” that separates exercise intensity domains within which V˙O2 and blood lactate do not continue to rise (termed “heavy” for the domain which is above LT/GET but below CP) from that within which they do (termed “severe”). Moreover, this study indicates that there is a range of power outputs, that are ostensibly “submaximal,” but for which the V˙O2 max will be reached if exercise is continued to intolerance. For both heavy and severe-intensity exercise, the presence of the V˙O2 slow component erodes the description of exercise intensity/work rate as a %V˙O2 max because, at a given work rate, V˙O2 increases as a function of time.

Using knee extension exercise during 31P-magnetic resonance spectroscopy, Jones et al. (48) confirmed that this threshold concept of CP also applied to intramuscular metabolism. During exercise 10% below CP, muscle PCr and inorganic phosphate (Pi) concentrations and pH each reached constant values within 1–2 min of the start of exercise and were maintained constant for 20 min, whereas during exercise 10% above CP, these variables changed progressively with time until the limit of tolerance was reached (in approximately 12 min). The progressive slow component increase in V˙O2 (76) and the decline in PCr concentration (48) observed during constant-power exercise above CP indicate a continuous loss of skeletal muscle efficiency with important implications for the fatigue process (17,38).

Vanhatalo et al. (100) studied the intramuscular responses to exercise at different power outputs (and correspondingly different times-to-intolerance, in the range of 2–15 min) above CP. Intriguingly, the values of PCr, Pi, and pH achieved at intolerance were the same in normoxia and hyperoxia. It is tempting to interpret this to indicate that exercise intolerance above CP is related to the attainment of a particular muscle metabolic milieu comprising “critically low” and/or “critically high” values of representative muscle substrates and metabolites, which act either directly to impair contractile function or indirectly to limit muscle activation. It is equally tempting to speculate that the mechanisms causing intolerance may be different for exercise performed above CP, wherein the W′ is drawn upon continuously and cardiorespiratory and muscle metabolic responses to exercise cannot be stabilized compared with exercise performed below CP (see next section). It is important to appreciate, however, that CP does not separate power outputs that are unsustainable from those that are sustainable. Rather, exercise tolerance above a known CP is predictable (from equation 1) from knowledge of the power output and W′.

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