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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.

Purpose The aim of this study was to investigate the individual $$W^{^{\prime}}$$ W ′ reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal mathematical model to describe $$W^{^{\prime}}$$ W ′ reconstitution. Methods Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; $$\dot{V}{\text{O}}_{2\max }$$ V ˙ O 2 max 58.6 ± 7.1 mL kg min−1) completed three incremental ramps (20 W min−1) to the limit of tolerance with varying recovery durations (15–360 s) on 5–9 occasions. $$W^{^{\prime}}$$ W ′ reconstitution was measured following the first and second recovery periods against which mono-exponential and bi-exponential models were compared with adjusted R2 and bias-corrected Akaike information criterion (AICc). Results A bi-exponential model outperformed the mono-exponential model of $$W^{^{\prime}}$$ W ′ reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adjR2 = 0.999) for the first recovery when optimised with parameters of fast component (FC) amplitude = 50.67%; slow component (SC) amplitude = 49.33%; time constant (τ)FC = 21.5 s; τSC = 388 s. Following the second recovery, W′ reconstitution reduced by 9.1 ± 7.3%, at 180 s and 8.2 ± 9.8% at 240 s resulting in an increase in the modelled τSC to 716 s with τFC unchanged. Individual bi-exponential models also fit well (adjR2 = 0.978 ± 0.017) with large individual parameter variations (FC amplitude 47.7 ± 17.8%; first recovery: (τ)FC = 22.0 ± 11.8 s; (τ)SC = 377 ± 100 s; second recovery: (τ)FC = 16.3.0 ± 6.6 s; (τ)SC = 549 ± 226 s). Conclusions W′ reconstitution kinetics were best described by a bi-exponential model consisting of distinct fast and slow phases. The amplitudes of the FC and SC remained unchanged with repeated bouts, with a slowing of W′ reconstitution confined to an increase in the time constant of the slow component.

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.

We hypothesize that the V̇O(2) time constant (τ(V̇O2)) determines exercise tolerance by defining the power output associated with a “critical threshold” of intramuscular metabolite accumulation (e.g. inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V̇O(2) “slow component”, and its consequences (increased pulmonary, circulatory and neuromuscular demands) determine performance limits.

We read with interest the paper by Gorostiaga et al.1 entitled “Over 55 years of critical power: Fact or artifact?”. It is our opinion, however, that the conclusions drawn by the authors (chiefly that critical power should be considered a mathematical artifact) stem from a grave misunderstanding of the critical power concept and its underlying physiology. The authors’ position is based upon a number of erroneous arguments (i) that critical power fails its own “definition” of being sustainable for “a long time without fatigue” (Monod & Scherrer, p.3292), (ii) use of arbitrary exercise durations to establish the power-duration curve (iii), that critical power approaches a high fraction of the speed or power providing the longest exercise duration, and (iv) critical power not residing at a fixed fraction of maximal oxygen uptake (V̇O2max) or maximal voluntary contraction (MVC).

Introduction/Purpose: Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance, however its physiological determinants are incompletely understood. The present study determined the impact of hyperoxia on CP, the time constant of phase II pulmonary oxygen uptake kinetics (τ_V O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in 9 healthy men performing upright cycle ergometry. Methods: CP was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via 4 severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, τ_V O2 and the time constant of muscle deoxyhaemoglobin kinetics (τ[HHb]), alongside absolute concentrations of muscle oxyhaemoglobin ([HbO2]), were determined. Results: CP was greater (hyperoxia: 216 ± 30 vs. normoxia: 197 ± 29W; P < 0.001) whereas W’ was reduced (hyperoxia: 15.4 ± 5.2 kJ, normoxia: 17.5 ± 4.3 W; P = 0.037) in hyperoxia compared to normoxia. τ_V O2 (hyperoxia: 35 ± 12 vs normoxia: 33 ± 10 s; P = 0.33) and τ[HHb] (hyperoxia: 11 ± 5 vs. normoxia: 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO2] during exercise was greater in hyperoxia compared to normoxia (hyperoxia: 73 ± 20 vs. normoxia: 66 ± 15 μM; P = 0.001). Conclusion: This study provides novel insights into the physiological determinants of CP and by extension, exercise tolerance. Microvascular oxygenation and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter τ_V O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, i.e. CP.

Introduction Cocoa flavanols (CF) may exert health benefits through their potent vasodilatory effects, which are perpetuated by elevations in nitric oxide (NO) bioavailability. These vasodilatory effects may contribute to improved delivery of blood and oxygen (O2) to exercising muscle. Purpose Therefore, the objective of this study was to examine how CF supplementation impacts pulmonary O2 uptake ($$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 ) kinetics and exercise tolerance in sedentary middle-aged adults. Methods We employed a double-blind cross-over, placebo-controlled design whereby 17 participants (11 male, 6 female; mean ± SD, 45 ± 6 years) randomly received either 7 days of daily CF (400 mg) or placebo (PL) supplementation. On day 7, participants completed a series of ‘step’ moderate- and severe-intensity exercise tests for the determination of $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 kinetics. Results During moderate-intensity exercise, the time constant of the phase II $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 kinetics ($$\tau \dot{V}{\text{O}}_{2}$$ τ V ˙ O 2 ) was decreased by 15% in CF as compared to PL (mean ± SD; PL 40 ± 12 s vs. CF 34 ± 9 s, P = 0.019), with no differences in the amplitude of $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 (A$$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 ; PL 0.77 ± 0.32 l min−1 vs. CF 0.79 ± 0.34 l min−1, P = 0.263). However, during severe-intensity exercise, $$\tau \dot{V}{\text{O}}_{2}$$ τ V ˙ O 2 , the amplitude of the slow component ($${\text{SC}}\dot{V}{\text{O}}_{2}$$ SC V ˙ O 2 ) and exercise tolerance (PL 435 ± 58 s vs. CF 424 ± 47 s, P = 0.480) were unchanged between conditions. Conclusion Our data show that acute CF supplementation enhanced $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 kinetics during moderate-, but not severe-intensity exercise in middle-aged participants. These novel effects of CFs, in this demographic, may contribute to improved tolerance of moderate-activity physical activities, which appear commonly present in daily life. Trial registration Registered under ClinicalTrials.gov Identifier no. NCT04370353, 30/04/20 retrospectively registered

Purpose We tested the hypothesis that incremental ramp cycling exercise performed in the supine position (S) would be associated with an increased reliance on muscle deoxygenation (deoxy[heme]) in the deep and superficial vastus lateralis (VLd and VLs, respectively) and the superficial rectus femoris (RFs) when compared to the upright position (U). Methods 11 healthy men completed ramp incremental exercise tests in S and U. Pulmonary $$\dot{V}$$ V ˙ O2 was measured breath-by-breath; deoxy[heme] was determined via time-resolved near-infrared spectroscopy in the VLd, VLs and RFs. Results Supine exercise increased the overall change in deoxy[heme] from baseline to maximal exercise in the VLs (S: 38 ± 23 vs. U: 26 ± 15 μM, P S: 36 ± 21 vs. U: 25 ± 15 μM, P S: 32 ± 23 vs. U: 29 ± 26 μM, P > 0.05). Conclusions The present study supports that the impaired balance between O2 delivery and O2 utilization observed during supine exercise is a regional phenomenon within superficial muscles. Thus, deep muscle defended its O2 delivery/utilization balance against the supine-induced reductions in perfusion pressure. The differential responses of these muscle regions may be explained by a regional heterogeneity of vascular and metabolic control properties, perhaps related to fiber type composition.

Purpose The purpose of the present study was to determine whether a contiguous ramp and all-out exercise test could accurately determine critical power (CP) in a single laboratory visit during both upright and supine cycle exercise. Methods Healthy males completed maximal ramp-incremental exercise on a cycle ergometer in the upright (n = 15) and supine positions (n = 8), with task failure immediately followed by a 3-min all-out phase for determination of end-test power (EP). On separate days, participants undertook four constant-power tests in either the upright or supine positions with the limit of tolerance ranging from ~ 2 to 15 min for determination of CP. Results During upright exercise, EP was highly correlated with (R2 = 0.93, P P = 0.085, 95% limits of agreement − 30, 19 W). During supine exercise, EP was also highly correlated with (R2 = 0.94, P P = 0.293, 95% limits of agreement − 16, 24 W). Conclusion The present data suggest that EP derived from a contiguous ramp all-out exercise test is not different from the gold-standard method of CP determination during both upright and supine cycle exercise when assessed at the group level. However, the wide limits of agreement observed within the present study suggest that EP and CP should not be used interchangeably.

Purpose: To examine the relationship between oxygen uptake kinetics (VO2 kinetics) and physical measures associated with soccer match-play, within a group of highly trained youth soccer players.\ud Methods: Seventeen highly trained youth soccer players (age: 13.3 ± 0.4 yr, self-assessed Tanner Stage: 3 ± 1) volunteered for the study. Players initially completed an incremental treadmill protocol to exhaustion, to establish gaseous exchange threshold (GET) and VO2max (59.1 ± 5.4 mL.kg-1.min-1). On subsequent visits players completed a step transition protocol from, rest–moderate intensity exercise, followed by an immediate transition from moderate–severe intensity exercise (moderate: 95%GET, severe: 60%∆), during which VO2 kinetics were determined. Physical soccer-based performance was assessed using a maximal Yo-Yo Intermittent Recovery test level 1 (Yo-Yo IR1) and via GPS derived measures of physical soccer performance during soccer match-play, 3 2 x 20min, 11 v 11 matches, to gain measures of physical performance during soccer match-play. \ud Results: Partial correlations revealed significant inverse relationships between the unloaded to moderate transition time constant (tau) and: Yo-Yo IR1 performance (r = -0.58, P = 0.02) and GPS variables (Total distance (TD): r = - 0.64, P = 0.007, High speed running (HSR): r = - 0.64, P = 0.008, High speed running efforts (HSReff): r = - 0.66, P = 0.005). \ud Conclusion: Measures of VO2 kinetics are related to physical measures associated with soccer match-play and could potentially be used to distinguish between those of superior physical performance, within a group of highly-trained youth soccer players.

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.

Previous studies have demonstrated faster pulmonary oxygen uptake ( $$ \dot{V}{\text{O}}_{2} $$ ) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine $$ \dot{V}{\text{O}}_{2} $$ kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, $$ \dot{V}{\text{O}}_{2\max}$$ 54.9 ± 6.4 mL kg−1 min−1) and 8 untrained (15 ± 0.5 years, $$ \dot{V}{\text{O}}_{2\max }$$ 44.0 ± 4.6 mL kg−1 min−1) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding “baseline” of exercise at a workload equivalent to 80% lactate threshold; $$ \dot{V}{\text{O}}_{2} $$ (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of $$ \dot{V}{\text{O}}_{2} $$ off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO(2)) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO(2) 43.5 ± 3.4 ml kg(-1) min(-1)) and nine untrained girls (peak VO(2) 36.0 ± 5.1 ml kg(-1) min(-1)) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m(-2)), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S') and diastolic (tissue Doppler E', mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.

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.

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys (V(O)(2)(peak): 55 +/- 6 mL kg(-1) min(-1)) and nine age- and maturation-matched untrained controls (V(O)(2)(peak): 43 +/- 5 mL kg(-1) min(-1)) aged 13-15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 +/- 4 vs. 9 +/- 3 perfusion units (PU), p < 0.05; SkBF(max): 282 +/- 120 vs. 204 +/- 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC(max): 3 +/- 1 vs. 2 +/- 1 PU mmHg(-1), p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 +/- 21 vs. 35 +/- 15 PU, p < 0.05; area under curve: 1596 +/- 739 vs. 962 +/- 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.

The tricarboxylic acid (TCA) cycle is the major final common pathway for oxidation of carbohydrates, lipids and some amino acids, which produces reducing equivalents in the form of nicotinamide adenine dinucleotide and flavin adenine dinucleotide that result in production of large amounts of adenosine triphosphate (ATP) via oxidative phosphorylation. Although regulated primarily by the products of ATP hydrolysis, in particular adenosine diphosphate, the rate of delivery of reducing equivalents to the electron transport chain is also a potential regulatory step of oxidative phosphorylation. The TCA cycle is responsible for the generation of approximately 67% of all reducing equivalents per molecule of glucose, hence factors that influence TCA cycle flux will be of critical importance for oxidative phosphorylation. TCA cycle flux is dependent upon the supply of acetyl units, activation of the three non-equilibrium reactions within the TCA cycle, and it has been suggested that an increase in the total concentration of the TCA cycle intermediates (TCAi) is also necessary to augment and maintain TCA cycle flux during exercise. This article reviews the evidence of the functional importance of the TCAi pool size for oxidative metabolism in exercising human skeletal muscle. In parallel with increased oxidative metabolism and TCA cycle flux during exercise, there is an exercise intensity-dependent 4- to 5-fold increase in the concentration of the TCAi. TCAi concentration reaches a peak after 10-15 minutes of exercise, and thereafter tends to decline. This seems to support the suggestion that the concentration of TCAi may be of functional importance for oxidative phosphorylation. However, researchers have been able to induce dissociations between TCAi pool size and oxidative energy provision using a variety of nutritional, pharmacological and exercise interventions. Brief periods of endurance training (5 days or 7 weeks) have been found to result in reduced TCAi pool expansion at the start of exercise (same absolute work intensity) in parallel with either equivalent or increased oxidative energy provision. Cycloserine inhibits alanine aminotransferase, which catalyses the predominant anaplerotic reaction in exercising human muscle. When infused into contracting rat hindlimb muscle, TCAi pool expansion was reduced by 25% with no significant change in oxidative energy provision or power output. Glutamine supplementation has been shown to enhance TCAi pool expansion at the start of exercise with no increase in oxidative energy provision. In summary, there is a consistent dissociation between the extent of TCAi pool expansion at the onset of exercise and oxidative energy provision. At the other end of the spectrum, the parallel loss of TCAi, glycogen and adenine nucleotides and accumulation of inosine monophosphate during prolonged exercise has led to the suggestion that there is a link between muscle glycogen depletion, reduced TCA cycle flux and the development of fatigue. However, analysis of serial biopsies during prolonged exercise demonstrated dissociation between muscle TCAi content and both muscle glycogen content and muscle oxygen uptake. In addition, the delay in fatigue development achieved through increased carbohydrate availability does not attenuate TCAi reduction during prolonged exercise. Therefore, TCAi concentration in whole muscle homogenate does not seem to be of functional importance. However, TCAi content can currently only be measured in whole muscle homogenate rather than the mitochondrial subfraction where TCA cycle reactions occur. In addition, anaplerotic flux rather than TCAi content per se is likely to be of greater importance in determining TCA cycle flux, since TCAi content is probably merely reflective of anaplerotic substrate concentration. Methodological advances are required to allow researchers to address the questions of whether oxidative phosphorylation is limited by mitochondrial TCAi content and/or anaplerotic flux.

The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max.

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.

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.

Purpose: The extent that enhanced ventricular function contributes to superior aerobic fitness of trained athletes is unclear. This study compared cardiovascular responses to progressive cycle exercise in 12 adolescent soccer players and 10 untrained boys with assessment of ventricular inotropic and relaxation properties by Doppler ultrasound techniques. Methods: Resting cardiac dimensions were measured by M-mode echocardiography. Stroke volume was estimated by the Doppler technique, and systolic function by peak aortic flow velocity and ejection flow rate. Diastolic transmitral pressure gradient was assessed by pulse wave peak E-wave velocity, ventricular relaxation properties by tissue Doppler imaging (E' velocity, adjusted for ventricular size), and ventricular filling pressure by E/E' ratio. Results: Size-adjusted cardiac dimensions were significantly greater in the athletes. Peak V[spacing dot above]O2 values for the athletes and nonathletes were 57.4 +/- 4.8 and 44.4 +/- 6.6 mL[middle dot]kg-1[middle dot]min-1, respectively. Maximal cardiac index and stroke index were greater in the athletes (11.10+/- 1.52 vs 9.02 +/- 2.05 L[middle dot]min-1[middle dot]m-2; 59 +/- 8 vs 46 +/- 10 mL[middle dot]m-2). Athletes and nonathletes demonstrated similar maximal peak aortic velocity (231 +/- 20 and 208 +/- 45 cm[middle dot]s-1, respectively) and ejection rate (13.3 +/- 1.0 and 12.5 +/- 2.8 mL[middle dot]s-1[middle dot]cm-2 x 10-2, respectively). No significant group differences were observed in Emax (155 +/- 17 and 149 +/- 23 cm[middle dot]s-1 for athletes and nonathletes, respectively), adjusted E'max (5.9 +/- 1.2 and 5.8 +/- 1.2 cm[middle dot]s-1[middle dot]mm-1 for athletes and nonathletes, respectively), and E/E'max (265 +/- 40 and 262 +/- 56 for athletes and nonathletes, respectively). Conclusions: This study revealed no differences between young trained athletes and nonathletes in myocardial functional responses to progressive exercise, implying that greater aerobic fitness in these athletes reflected volume expansion of the cardiovascular system without contribution of enhanced systolic or diastolic ventricular function. Such findings should be considered limited to the context of young athletes with limited duration of athletic training.

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.

Little evidence exists with regard to the effect that exercise training has upon oxygen uptake kinetics in adolescent females. The aim of the study was to compare $$\dot{V}{\text{O}}_{2}$$ and muscle deoxygenation kinetics in a group of trained (Tr) and untrained (Utr) female adolescents. Twelve trained (6.4 ± 0.9 years training, 10.3 ± 1.4 months per year training, 5.2 ± 2.0 h per week) adolescent female soccer players (age 14.6 ± 0.7 years) were compared to a group (n = 8) of recreationally active adolescent girls (age 15.1 ± 0.6 years) of similar maturity status. Subjects underwent two, 6-min exercise transitions at a workload equivalent to 80 % of lactate threshold from a 3-min baseline of 10 W. All subjects had a passive rest period of 1 h between each square-wave transition. Breath-by-breath oxygen uptake and muscle deoxygenation were measured throughout and were modelled via a mono-exponential decay with a delay relative to the start of exercise. Peak $$\dot{V}{\text{O}}_{2}$$ was significantly (p