Wat is Critical Power, en waardoor wordt het bepaald?

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. (Abstract, p. 595)

Critical power separates the heavy and severe exercise-intensity domains wherein qualitatively divergent physiological responses are observed, such that CP represents the threshold intensity above which a metabolic steady state cannot be attained during exercise. (Conclusies, p. 608)

Critical power defines the boundary between the heavy- and severe-intensity exercise domains and represents the highest power output for which a metabolic steady state may be attained. The W′ comprises a fixed and finite volume of work that is expendable above CP. During severe-intensity exercise, task failure occurs when W′ = 0. (Bijschrift fig. 1, p. 596)

When time to task failure is plotted against power output, the relationship is curvilinear, with the ability to sustain exercise falling away more rapidly at higher power outputs (Fig. 1). This power-time relationship is well described by a hyperbolic function, with an asymptote known as critical power (CP) and the curvature constant termed W′ (i.e. W prime). This relationship is described by the following equation: T = W′ / (P − CP), where T is the tolerable duration and P is the power output of a given exercise task.

Since the seminal work by Prof. David Poole and colleagues in the late 1980s, it has been repeatedly demonstrated that CP reflects the upper limit at which a metabolic steady state can be sustained. (p. 596)

For example, V̇O₂ rises to V̇O₂max during exercise above, but not at or below, CP, accompanied by similarly inexorable trajectories of blood [lactate], [HCO₃⁻] and pH. […] More recently, non-invasive (³¹P-magnetic resonance spectroscopy, near-infrared spectroscopy) and invasive (i.e. muscle biopsy) studies have demonstrated the achievement of a steady state in the exercising muscle below, but not above, CP in muscle V̇O₂, [phosphocreatine] ([PCr]), [inorganic phosphate] [Pi], pH and muscle [lactate]. (p. 597)

This threshold intensity can be determined by undertaking three to five high-intensity, constant-power output cycle ergometer tests to the point of task failure on separate days. The tests should be selected to last no less than 2 and no more than 15 min in duration, with the precise time to task failure and power output at which each test is conducted recorded. These durations are recommended for a valid determination of this intensity, as it is essential that V̇O₂max is attained at the end of trial in order to meet the requirement for all prediction trials to be performed within the severe-intensity domain.

The current study demonstrates that after 2 familiarization sessions, reliable CP and W′ parameters can be obtained from trained cyclists using only 2 maximal-exercise trials. These results offer practitioners a practical, time-efficient solution for incorporating power-duration testing into applied athlete support. (conclusie abstract)

That CP represents the threshold intensity above which exercise cannot be sustained in a steady state indicates that it is a parameter of aerobic function. Consequently, it follows that CP may be affected by any step in the O₂ transport and utilisation cascade, from atmospheric air down to the muscle mitochondria themselves. Specifically, these steps include: (1) transport of atmospheric O₂ into the blood via pulmonary diffusion; (2) bulk transport of O₂ to the muscle via convection (i.e. convective O₂ delivery); (3) diffusion of O₂ from capillary to muscle mitochondria (i.e. diffusive O₂ delivery); and (4) the utilisation of O₂ by the muscle mitochondria (Fig. 2).

Schematic illustrating each of the factors that has been demonstrated to impact upon critical power. Convective and diffusive O₂ delivery act in concert with muscle O₂ utilisation to determine the degree of intracellular metabolic perturbation and fatigue induction incurred during the rest-to-exercise transition. The extent of such metabolic perturbations, in turn, determines whether an exercise bout can be met in a metabolic steady state within a given myocyte. Within a given individual, whether an extant power output is met in a whole-body steady state will depend on the muscle fibre-type composition of the individual, the muscle recruitment patterns employed during the task, and the extent of metabolic derangement and fatigue induction incurred in the recruited fibres during the rest-to-exercise transition.

Hence, studies have consistently shown that CP is sensitive to both increased and decreased FiO₂.

Mitchell et al. recently demonstrated a striking relationship between CP and skeletal muscle capillary density (r = 0.50), capillary-to-fibre ratio (r = 0.88) and capillary contacts per type 1 fibre (r = 0.94) in a homogenous group of endurance-trained individuals (63.2 ± 4.1 mL kg⁻¹ min⁻¹, range: 58.7–72.2 mL kg⁻¹ min⁻¹). These findings indicate that enhancements in diffusive O₂ flux enable a metabolic steady state to be attained for a greater range of power outputs (i.e. extending the range upwards), thus increasing CP.

A sentinel parameter defining the skeletal muscle bioenergetics system is the time constant of the fundamental phase of muscle V̇O₂ kinetics (i.e. τV̇O₂), which is reflective of the time taken to attain 63% of the V̇O₂ amplitude in response to a change in metabolic demand. […] The delayed response of pulmonary and muscle V̇O₂ kinetics that is encapsulated in the parameter τV̇O₂ necessitates an energy deficit that must be met via a reduction in O₂ stores and an increased rate of substrate-level phosphorylation. (p. 603)

They demonstrated a strong inverse correlation between τV̇O₂ and CP (r = 0.95) […] All else being equal, therefore, faster V̇O₂ kinetics will result in a higher CP. (p. 603)

That each of τV̇O₂, convective and diffusive O₂ delivery has an independent role in determining CP is evinced by the fact that each can alter CP without a concomitant change in the other. (p. 604)

To summarise, CP is sensitive to muscle fibre type composition because it is a parameter of aerobic function. Hence, the oxidative characteristics inherent within type I fibres, such as rapid V̇O₂ kinetics, greater rates of blood flow, and higher capillary and interstitial PO₂ values, allow the attainment of high rates of ATP utilisation with minimal derangement of the intracellular metabolic milieu. Therefore, all else being equal, individuals with a relatively greater proportion of type I skeletal muscle fibres will tend to possess greater CP values when compared with individuals of equivalent training status with a greater proportion of type II fibres.

Interventions that increase motor unit recruitment are also conducive to high CP values, as a greater number of motor units/muscle fibres performing a given task will lessen the metabolic strain on each individual fibre. Hence, when muscular recruitment is increased, each fibre is able to maintain intramuscular metabolite accumulation below its critical threshold for a wider range of ATP utilisation rates, thus enabling a greater CP.

It has been demonstrated that alterations in delivery of O₂ to the exercising muscles, via both convection and diffusion, impact upon CP. The rates of O₂ utilisation during exercise, particularly during the transition from rest to work, also play a key role in determining CP by governing the degree of matching between the rates of ATP utilisation and production. These factors each interact with one another, and via this interaction determine the degree of intracellular metabolic disturbance required to sustain a given power output. How each of these factors interacts to determine CP at the whole-body level will be dependent upon the muscle fibre-type composition and their recruitment patterns during exercise.

[CP is] the ideal candidate upon which to prescribe training and assess training load, for both amateur and professional cyclists, especially when compared to the standard FTP measurement which is designated as an arbitrary 60-min point on the power-duration relationship sitting well away from any physiological measurement. Severe intensity training is a mainstay of endurance training programmes, with the duration and intensity of tolerable work being dictated by W′ in addition to CP. Prescription of such training as a proportion of FTP or CP alone simply does not work owing to the lack of proportionality between such measurements and W′. Instead, basing severe intensity work on the fractional usage of W′ allows training to be planned and executed with much greater precision in order to meet desired training outcomes. High-intensity interval training cannot be optimized or prescribed individually using current techniques; however, modelling of W′ reconstitution would allow both the work and recovery phases of such sessions to be built into specific plans by athletes and coaches. The Skiba models demonstrate how this can be achieved with the addition of a single Tau parameter; however, it appears that W′ reconstitution is a complex matter, involving considerable individual variability and a slowing effect following repeated efforts, necessitating the validation of models against different protocols and with heterogeneous groups of cyclists. Nonetheless, while additional research is needed to improve the W′ reconstitution models, it is possible that training prescription could be better defined, and race plans based on knowledge of the reconstitution and expenditure of W′.