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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.

We show that supine exercise causes a greater degree of muscle deoxygenation in both deep and superficial muscle and increases the spatial heterogeneity of muscle deoxygenation. Therefore, this study suggests that any O2 delivery gradient toward deep versus superficial muscle is insufficient to mitigate impairments in oxidative function in response to reduced whole muscle O2 delivery. More heterogeneous muscle deoxygenation is associated with slower V̇o2 kinetics.

Purpose This study examined the relationship of physiological and anthropometric characteristics with parameters of the critical power (CP) model, and in particular the reconstitution of W′ following successive bouts of maximal exercise, amongst trained and untrained cyclists. Methods Twenty male adults (trained nine; untrained 11; age 39 ± 15 year; mass 74.7 ± 8.7 kg; V̇O2max 58.0 ± 8.7 mL kg−1 min−1) completed three incremental ramps (20 W min−1) to exhaustion interspersed with 2-min recoveries. Pearson’s correlation coefficients were used to assess relationships for W′ reconstitution after the first recovery (W′rec1), the delta in W′ reconstituted between recoveries (∆W′rec), CP and W′. Results CP was strongly related to V̇O2max for both trained (r = 0.82) and untrained participants (r = 0.71), whereas W′ was related to V̇O2max when both groups were considered together (r = 0.54). W′rec1 was strongly related to V̇O2max for the trained (r = 0.81) but not untrained (r = 0.18); similarly, ∆W′rec was strongly related to V̇O2max (r = − 0.85) and CP (r = − 0.71) in the trained group only. Conclusions Notable physiological relationships between parameters of aerobic fitness and the measurements of W′ reconstitution were observed, which differed among groups. The amount of W′ reconstitution and the maintenance of W′ reconstitution that occurred with repeated bouts of maximal exercise were found to be related to key measures of aerobic fitness such as CP and V̇O2max. This data demonstrates that trained cyclists wishing to improve their rate of W′ reconstitution following repeated efforts should focus training on improving key aspects of aerobic fitness such as V̇O2max and CP.

Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance and is related to the time constant of phase II pulmonary oxygen uptake kinetics (τVO2). To test the hypothesis that this relationship is causal we determined the impact of prior exercise (“priming”) on CP and τVO2 in the upright and supine positions. 17 healthy men were assigned to either upright or supine exercise groups, whereby CP, τVO2 and muscle deoxyhaemoglobin kinetics (τ[HHb]) were determined via constant-power tests to exhaustion at four work-rates with (primed) and without (control) priming exercise at ∼31%Δ. During supine exercise, priming reduced τVO2 (control: 54 ± 18 vs. primed: 39 ± 11 s; P < 0.001), increased τ[HHb] (control: 8 ± 4 vs. primed: 12 ± 4 s; P = 0.003) and increased CP (control: 177 ± 31 vs. primed: 185 ± 30 W, P = 0.006) compared to control. However, priming exercise had no effect on τVO2 (control: 37 ± 12 vs. primed: 35 ± 8 s; P = 0.82), τ[HHb] (CON: 10 ± 5 s vs. PRI: 14 ± 10; P = 0.10), or CP (control: 235 ± 42 vs. primed: 232 ± 35 W; P = 0.57) during upright exercise. The concomitant reduction of τVO2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τVO2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability.

It has previously been shown that cyclists are unable to maintain a constant power output during cycle time-trials on hilly courses. The purpose of the present study is therefore to quantify these effects of power variation using a mathematical model of cycling performance. A hypothetical cyclist (body mass: 70 kg, bicycle mass: 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance was modelled over three hypothetical 40-km courses, comprising repeated 2.5-km sections of uphill and downhill with gradients of 1%, 3%, and 6%, respectively. Amplitude (5-15%) and distance (0.31-20.00 km) of variation were modelled over a range of mean power outputs (200-600 W) and compared to sustaining a constant power. Power variation was typically detrimental to performance; these effects were augmented as the amplitude of variation and severity of gradient increased. Varying power every 1.25 km was most detrimental to performance; at a mean power of 200 W, performance was impaired by 43.90 s (±15% variation, 6% gradient). However at the steepest gradients, the effect of power variation was relatively independent of the distance of variation. In contrast, varying power in parallel with changes in gradient improved performance by 188.89 s (±15% variation, 6% gradient) at 200 W. The present data demonstrate that during hilly time-trials, power variation that does not occur in parallel with changes in gradient is detrimental to performance, especially at steeper gradients. These adverse effects are substantially larger than those previously observed during flat, windless time-trials.

Continuous high-intensity constant-power exercise is unsustainable, with maximal oxygen uptake (V̇O2 max ) and the limit of tolerance attained after only a few minutes. Performing the same power intermittently reduces the OCompared with work-matched high-intensity continuous exercise, intermittent exercise dissociates pulmonary oxygen uptake (V̇O2) from the accumulated work. The extent to which this reflects differences in O

Recent research has suggested that dietary nitrate (NO3−) supplementation might alter the physiological responses to exercise via specific effects on type II muscle. Severe-intensity exercise initiated from an elevated metabolic rate would be expected to enhance the proportional activation of higher-order (type II) muscle fibers. The purpose of this study was, therefore, to test the hypothesis that, compared with placebo (PL), NO3−-rich beetroot juice (BR) supplementation would speed the phase II V̇o2kinetics (τp) and enhance exercise tolerance during severe-intensity exercise initiated from a baseline of moderate-intensity exercise. Nine healthy, physically active subjects were assigned in a randomized, double-blind, crossover design to receive BR (140 ml/day, containing ∼8 mmol of NO3−) and PL (140 ml/day, containing ∼0.003 mmol of NO3−) for 6 days. On days 4, 5, and 6 of the supplementation periods, subjects completed a double-step exercise protocol that included transitions from unloaded to moderate-intensity exercise (U→M) followed immediately by moderate to severe-intensity exercise (M→S). Compared with PL, BR elevated resting plasma nitrite concentration (PL: 65 ± 32 vs. BR: 348 ± 170 nM, P < 0.01) and reduced the V̇o2τpin M→S (PL: 46 ± 13 vs. BR: 36 ± 10 s, P < 0.05) but not U→M (PL: 25 ± 4 vs. BR: 27 ± 6 s, P > 0.05). During M→S exercise, the faster V̇o2kinetics coincided with faster near-infrared spectroscopy-derived muscle [deoxyhemoglobin] kinetics (τ; PL: 20 ± 9 vs. BR: 10 ± 3 s, P < 0.05) and a 22% greater time-to-task failure (PL: 521 ± 158 vs. BR: 635 ± 258 s, P < 0.05). Dietary supplementation with NO3−-rich BR juice speeds V̇o2kinetics and enhances exercise tolerance during severe-intensity exercise when initiated from an elevated metabolic rate.

What is the central question of this study? Critical power (CP) represents the highest work rate for which a metabolic steady state is attainable. The physiological determinants of CP are unclear, but research suggests that CP might be related to the time constant of phase II oxygen uptake kinetics (τV̇O2). What is the main finding and its importance? We provide the first evidence that τV̇O2 is mechanistically related to CP. A reduction of τV̇O2 in the supine position was observed alongside a concomitant increase in CP. This effect may be contingent on measures of oxygen availability derived from near-infrared spectroscopy. Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance and is related to the time constant of phase II pulmonary oxygen uptake kinetics (τV̇O2). To test the hypothesis that this relationship is causal, we determined the impact of prior exercise ('priming') on CP and τV̇O2 in the upright and supine positions. Seventeen healthy men were assigned to either upright or supine exercise groups, whereby CP, τV̇O2 and muscle deoxyhaemoglobin kinetics (τ

COPD patients have reduced muscle glutamate which may contribute to an impaired response of oxidative metabolism to exercise. We hypothesised that prior glutamine supplementation would enhance View the MathML source peak, View the MathML source at lactate threshold and speed pulmonary oxygen uptake kinetics in COPD. 13 patients (9 males, age 66 ± 5 years, mean ± SD) with severe COPD (mean FEV1 0.88 ± 0.23 l, 33 ± 7% predicted) performed on separate days ramp cycle-ergometry (5–10 W min−1) to volitional exhaustion and subsequently square-wave transitions to 80% estimated lactate threshold (LT) following consumption of either placebo (CON) or 0.125 g kg bm−1 of glutamine (GLN) in 5 ml kg bm−1 placebo. Oral glutamine had no effect on peak or View the MathML source at LT, {View the MathML source peak: CON = 0.70 ± 0.1 l min−1 vs. GLN = 0.73 ± 0.2 l min−1; LT: CON = 0.57 ± 0.1 l min−1 vs. GLN = 0.54 ± 0.1 l min−1} or View the MathML source kinetics {tau: CON = 68 ± 22 s vs. GLN = 68 ± 16 s}. Ingestion of glutamine before exercise did not improve indices of oxidative metabolism in this patient group.

The existence of an acetyl group deficit at or above 90% of maximal oxygen uptake (VO(2max)) has proved controversial, with contradictory results likely relating to limitations in previous research. The purpose of the present study was to determine whether the "acetyl group deficit" occurs at the start of exercise at 90%VO(2max) in a well-controlled study. Eight male participants (age: 33.6 +/- 2.0 years; VO(2max): 3.60 +/- 0.21 litres . min(-1)) completed two exercise bouts at 90%VO(2max) for 3 min following either 30 min of saline (control) or dichloroacetate (50 mg . kg(-1) body mass) infusion, ending 15 min before exercise. Muscle biopsies were obtained immediately before and after exercise while continuous non-invasive measures of pulmonary oxygen uptake and muscle deoxygenation were made. Muscle pyruvate dehydrogenase activity was significantly higher before exercise following dichloroacetate infusion (control: 2.67 +/- 0.98 vs. dichloroacetate: 17.9 +/- 1.1 mmol acetyl-CoA . min(-1) . mg(-1) protein, P = 0.01) and resulted in higher pre- and post-exercise muscle acetylcarnitine (pre-exercise control: 3.3 +/- 0.95 vs. pre-exercise dichloroacetate: 8.0 +/- 0.88 vs. post-exercise control: 11.9 +/- 1.1 vs. post-exercise dichloroacetate: 17.2 +/- 1.1 mmol . kg(-1) dry muscle, P < 0.05). However, substrate-level phosphorylation (control: 125 +/- 20 vs. dichloroacetate: 113 +/- 13 mmol adenosine triphosphate . kg(-1) dry muscle) and VO(2) kinetics (control: 19.2 +/- 2.2 vs. dichloroacetate: 22.8 +/- 2.5 s), were unaltered. Furthermore, dichloroacetate infusion blunted the slow component of VO(2) and muscle deoxygenation and slowed muscle deoxygenation kinetics, possibly by enhancing oxygen delivery during exercise. These data support the hypothesis that the "acetyl group deficit" does not occur at or above 90%VO(2max).

Exercise training results in a speeding of pulmonary oxygen uptake (V˙ O2) kinetics at the onset of exercise in adults; however, only limited research has been conducted with children and adolescents. Purpose: The aim of the present study was to examine V˙ O2 and muscle deoxygenation kinetics in trained and untrained male adolescents. Methods: Sixteen trained (15 T 0.8 yr, V˙ O2peak = 54.7 T 6.2 mLIkgj1Iminj1, selfassessed Tanner stage range 2–4) and nine untrained (15 T 0.6 yr, V˙ O2peak = 43.1 T 5.2 mLIkgj1Iminj1, Tanner stage range 2–4) male adolescents performed two 6-min exercise transitions from a 3-min baseline of 10 W to a workload equivalent to 80% lactate threshold separated by a minimum of 1 h of passive rest. Oxygen uptake (breath-by-breath) and muscle deoxygenation (deoxyhemoglobin signal from near-infrared spectroscopy) were measured continuously throughout baseline and exercise transition. Results: The time constant of the fundamental phase of V˙ O2 kinetics was significantly faster in trained versus untrained subjects (trained: 22.3 T 7.2 s vs untrained:29.8 T 8.4 s, P = 0.03). In contrast, neither the time constant (trained: 9.7 T 2.9 s vs untrained: 10.1 T 3.4 s, P = 0.78) nor the mean response time (trained: 17.4 T 2.5 s vs untrained: 18.3 T 2.3 s, P = 0.39) of muscle deoxygenation kinetics differed with training status. Conclusions: The present data suggest that exercise training results in faster V˙ O2 kinetics in male adolescents, although inherent capabilities cannot be ruled out. Because muscle deoxygenation kinetics were unchanged, it is likely that faster V˙ O2 kinetics were due to adaptations to both the cardiovascular system and the peripheral musculature.

Purpose: This study was conducted to test whether a low-frequency vibration-like stimulus (rapid variable resistance) applied during a single session of knee extension exercise would alter muscle performance. Methods: Torque, knee joint angle, EMG activity of rectus femoris (RF) and vastus lateralis (VL) muscles, and VL muscle oxygenation status (near-infrared spectroscopy) were recorded during metronome-guided knee extension exercise. Nine healthy adults completed four trials exercising at contraction intensities of 35% (L) or 70% (H) of one-repetition maximum (1RM) in control (no vibration, Vb-) or vibrated condition (superimposed 10-Hz vibration-like stimulus, Vb+). Maximum voluntary contraction and 1RM were tested pre- and postexercise. Results: During 1RM tests, muscle dynamic strength (P = 0.02) and power (P = 0.05) were significantly higher during vibrated rather than nonvibrated trials, and strength was significantly higher post- than preexercise (P = 0.002), except during LVb- trial. Median spectral frequency of VL and RF EMG activity was significantly higher during postexercise than preexercise 1RM test in the vibration trials but unchanged in the control trials (P < 0.02). The rate of muscle deoxygenation was 58% faster during H than L exercise (P = 0.001), and vibration superimposition tended to speed muscle deoxygenation rate (P = 0.065, 36% effect size) particularly during L trials. Conclusion: Vibration superimposition during knee extension exercise at low contraction intensity enhanced muscle performance. This effect appears to result from adaptation of neural factors such as motor unit excitability (recruitment and firing frequency, conduction velocity of excitation) in response to sensory receptor stimulation. Muscle vibration may increase the training effects derived from light-to-moderate exercise.

Objectives: Ventricular systolic functional response to exercise has been reported to be superior in adult men compared to women. This study explored myocardial responses to maximal upright progressive exercise in late pubertal males and females. Methods: Doppler echocardiographic techniques were utilized to estimate myocardial function response to a bout of progressive cycle exercise. Results: Systolic functional capacity, as indicated by ejection rate (12.5 ± 2.8 and 13.1 ± 1.0 [×10−2] ml s−1 cm−2 for boys and girls, respectively) and peak aortic velocity (208 ± 45 and 196 ± 12 cm s−1, respectively) at maximal exercise, did not differ between the two groups. Similarly, peak values as well as increases in transmitral pressure gradient (mitral E flow velocity), ventricular relaxation (tissue Doppler imaging E′), and left ventricular filling pressure (E/E′ ratio) as estimates of diastolic function were similar in males and females. Conclusions: This study failed to reveal qualitative or quantitative differences between adolescent boys and girls in ventricular systolic or diastolic functional responses to maximal cycle exercise. Am. J. Hum. Biol. 22:680–682, 2010. © 2010 Wiley-Liss, Inc.

Mechanical models of cycling time-trial performance have indicated adverse effects of variations in external power output on overall performance times. Nevertheless, the precise influences of the magnitude and number of these variations over different distances of time trial are unclear. A hypothetical cyclist (body mass 70 kg, bicycle mass 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance times were modelled over distances of 4-40 km, mean power outputs of 200-600 W, power variation amplitudes of 5-15% and variation frequencies of 2-32 per time-trial. Effects of a "fast-start" strategy were compared with those of a constant-power strategy. Varying power improved 4-km performance at all power outputs, with the greatest improvement being 0.90 s for ± 15% power variation. For distances of 16.1, 20 and 40 km, varying power by ± 15% increased times by 3.29, 4.46 and 10.43 s respectively, suggesting that in long-duration cycling in constant environmental conditions, cyclists should strive to reduce power variation to maximise performance. The novel finding of the present study is that these effects are augmented with increasing event distance, amplitude and period of variation. These two latter factors reflect a poor adherence to a constant speed.

Glutamine enhances the exercise-induced expansion of the tricarboxylic acid intermediate pool. The aim of the present study was to determine whether oral glutamine, alone or in combination with hyperoxia, influenced oxidative metabolism and cycle time-trial performance. Eight participants consumed either placebo or 0.125 g kg body mass(-1) of glutamine in 5 ml kg body mass(-1) placebo 1 h before exercise in normoxic (control and glutamine respectively) or hyperoxic (FiO(2) = 50%; hyperoxia and hyperoxia + glutamine respectively) conditions. Participants then cycled for 6 min at 70% maximal oxygen uptake (VO(2max)) immediately before completing a brief high-intensity time-trial (approximately 4 min) during which a pre-determined volume of work was completed as fast as possible. The increment in pulmonary oxygen uptake during the performance test (DeltaVO(2max), P = 0.02) and exercise performance (control: 243 s, s(x) = 7; glutamine: 242 s, s(x) = 3; hyperoxia: 231 s, s(x) = 3; hyperoxia + glutamine: 228 s, s(x) = 5; P0.01) were significantly improved in hyperoxic conditions. There was some evidence that glutamine ingestion increased DeltaVO(2max) in normoxia, but not hyperoxia (interaction drink/FiO(2), P = 0.04), but there was no main effect or impact on performance. Overall, the data show no effect of glutamine ingestion either alone or in combination with hyperoxia, and thus no limiting effect of the tricarboxylic acid intermediate pool size, on oxidative metabolism and performance during maximal exercise.