These data suggest that the key indices of aerobic function may be accurately and reliably estimated during a single exercise test. This test may provide a basis for simplifying assessment and prescription of exercise training and experimental interventions.

During whole body exercise in health, maximal oxygen uptake (V̇o2max) is typically attained at or immediately before the limit of tolerance (LoT). At the V̇o2max and LoT of incremental exercise, a fundamental, but unresolved, question is whether maximal evocable power can be increased above the task requirement, i.e., whether there is a "power reserve" at the LoT. Using an instantaneous switch from cadence-independent (hyperbolic) to isokinetic cycle ergometry, we determined maximal evocable power at the limit of ramp-incremental exercise. We hypothesized that in endurance-trained men at LoT, maximal (4 s) isokinetic power would not differ from the power required by the task. Baseline isokinetic power at 80 rpm (Piso; measured at the pedals) and summed integrated EMG from five leg muscles (ΣiEMG) were measured in 12 endurance-trained men (V̇o2max = 4.2 ± 1.0 l/min). Participants then completed a ramp incremental exercise test (20-25 W/min), with instantaneous measurement of Piso and ΣiEMG at the LoT. Piso decreased from 788 ± 103 W at baseline to 391 ± 72 W at LoT, which was not different from the required ramp-incremental flywheel power (352 ± 58 W; P > 0.05). At LoT, the relative reduction in Piso was greater than the relative reduction in the isokinetic ΣiEMG (50 ± 9 vs. 63 ± 10% of baseline; P < 0.05). During maximal ramp incremental exercise in endurance-trained men, maximum voluntary power is not different from the power required by the task and is consequent to both central and peripheral limitations in evocable power. The absence of a power reserve suggests both the perceptual and physiological limits of maximum voluntary power production are not widely dissociated at LoT in this population.

The power-duration relationshipThe origins of intolerance during exercise have perplexed scientists for well over a century. A better understanding of the processes that contribute to limiting high-intensity exercise have far-reaching implications, not only for elite exercise performance, but also for the wide spectrum of health, quality of life and mortality. It is intriguing, therefore, that there has existed for about 50 years a mathematical model that has the capacity to predict intolerance during high-intensity constant-work rate exercise. This hyperbolic power-duration (P-d) relationship was first described by Monod and Scherrer for a single muscle group in 1965, and has since been extended to whole-body exercise (e.g. Poole et al. 1988). This model characterises a 'critical' power output (CP) or speed (CS) that, once exceeded, will lead to exhaustion in a duration predicted by the completion of a constant amount of work (W ) (Morton, 2006). CP, which lies between the lactate threshold and maximum oxygen uptake (V O2 max ), reflects an intrinsic threshold of aerobic energy provision -defining the highest constant-work rate for which steady states in ventilation, gas exchange (e.g.V O2 ) and metabolic (e.g. muscle and blood acid-base status) variables can be achieved (Poole et al. 1988). That CP reflects a parameter of aerobic function is supported by the fact that it is sensitive to interventions affecting oxygen transport and utilisation, such as breathing hypoxic gas mixtures or endurance exercise training. While W has been likened to a (predominantly) anaerobic energy source (Monod & Scherrer, 1965; potentially comprising stores of intramuscular glycogen, high-energy phosphates and oxygen), relatively less is known about the physiological underpinnings of this parameter.Importantly, the robust nature of the P-d relationship is demonstrated in its ability to characterise exercise tolerance for a wide range of exercise modalities (including cycling, running, swimming, kayaking, rowing and knee-extension over durations of ∼2-30 min; Morton, 2006), for different subject populations (ranging from adolescents to the elderly, and from elite athletes to patients with chronic heart or lung diseases), and for different species (humans, lungless salamanders, ghost crabs, mice, horses and now also rats; Copp et al. 2010). It is our belief, therefore, that a better understanding of the basis of the P-d relationship will elucidate the factor (or factors) that contribute to limiting exercise performance -the secrets of which are defined within the parameters that shape its curve. Surprisingly, however, there is relatively little evidence supporting the physiological origins of the P-d relationship. As such, the underlying physiological equivalents of the defining mathematical P-d parameters, CP and W , remain conjectural. Assessing skeletal muscle blood flow distributionThe recent characterisation of the P-d curve in the running rat published in The Journal of Physiology by Copp et al. (2010) has opened a new avenue...

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