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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.

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.

This study tested the hypothesis that the respiratory compensation point (RCP) and breakpoint in deoxygenated [heme] [deoxy[heme]BP, assessed via near-infrared spectroscopy (NIRS)] during ramp incremental exercise would occur at the same metabolic rate in the upright (U) and supine (S) body positions. Eleven healthy men completed ramp incremental exercise tests in U and S. Gas exchange was measured breath-by-breath and time-resolved-NIRS was used to measure deoxy[heme] in the vastus lateralis (VL) and rectus femoris (RF). RCP (S: 2.56 ± 0.39, U: 2.86 ± 0.40 L·min−1, P = 0.02) differed from deoxy[heme]BP in the VL in U (3.10 ± 0.44 L·min−1, P = 0.002), but was not different in S in the VL (2.70 ± 0.50 L·min−1, P = 0.15). RCP was not different from the deoxy[heme]BP in the RF for either position (S: 2.34 ± 0.48 L·min−1, U: 2.76 ± 0.53 L·min−1, P > 0.05). However, the deoxy[heme]BP differed between muscles in both positions ( P < 0.05), and changes in deoxy[heme]BP did not relate to ΔRCP between positions (VL: r = 0.55, P = 0.080, RF: r = 0.26, P = 0.44). The deoxy[heme]BP was consistently preceded by a breakpoint in total[heme], and was, in turn, itself preceded by a breakpoint in muscle surface electromyography (EMG). RCP and the deoxy[heme]BP can be dissociated across muscles and different body positions and, therefore, do not represent the same underlying physiological phenomenon. The deoxy[heme]BP may, however, be mechanistically related to breakpoints in total[heme] and muscle activity.

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).

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.

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.

The aim of this study was to investigate the individual [Formula: see text] reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal mathematical model to describe [Formula: see text] reconstitution.Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; [Formula: see text] 58.6 ± 7.1 mL kg minA bi-exponential model outperformed the mono-exponential model of [Formula: see text] reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adjRW' 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.

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.

The brain can utilise medium chain triglycerides (MCTs) as an alternative fuel to glucose, and research has shown that MCT ingestion improves cognitive function in diseased and/or elderly individuals. The aim of this study is to determine if these improvements can also be observed in young, healthy adults. Furthermore, we aim to establish the ideal dosage and timeframe necessary for an effect.Participants were divided equally into three groups of 10 (Placebo (0 g), 12 g and 18 g MCT/day) and were supplemented for 4 weeks. The supplement had a CAfter 2-3 weeks of supplementation, MCT ingestion enhanced performance in cognitive tasks, including: Trail Making A/B and Digit Span Forwards/Backwards (ps0.001) when compared to a placebo group taking a carbohydrate gel. In Spatial Span Backwards, there was a significant main effect of group (p = 0.002). Where significance was seen, there were main effects of time after 2-3 weeks (ps0.05). There was minimal difference between the two MCT intervention groups in most measures (ps0.05). There were also null results in tasks measuring attention and reaction time (ps0.05).MCT ingestion improved cognitive performance after 2-3 weeks, with minimal difference between taking 12 g and 18 g MCT/day groups, suggesting a possible dose-response threshold at 12 g MCT/day when supplementing over a short period.

Background: 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 to exercising muscle.Objective: Therefore, the objective of this study was to examine how CF supplementation impacts pulmonary oxygen uptake (V̇O2) 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 oxygen uptake kinetics.Results: During moderate-intensity exercise, the time constant of the fundamental phase of V̇O2 kinetics (τV̇O2) was decreased by 15% in CF as compared to PL (mean±SD; PL: 40±12 vs. CF: 34±9 s, P=0.019), with no differences in the amplitude of V̇O2 (AV̇O2; PL: 0.77±0.32 vs. CF: 0.79±0.34 l min−1, P=0.263). However, during severe-intensity exercise, τV̇O2,the amplitude of the slow component (SCV̇O2) and exercise tolerance (PL: 435±58 vs. CF: 424±47 s, P=0.480) were unchanged between conditions.Conclusions: Our data show that acute CF supplementation enhanced oxygen uptake 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.Registered under ClinicalTrials.gov Identifier no. NCT04370353

Patients with type 1 diabetes demonstrated slower oxygen uptake (V̇o2) kinetics compared with healthy control subjects. Furthermore, a prior bout of high-intensity exercise speeded V̇o2 kinetics and increased critical power in people with type 1 diabetes. Prior exercise speeded muscle deoxygenation kinetics, indicating that V̇o2 kinetics in type 1 diabetes are limited primarily by oxygen extraction and/or intracellular factors. These findings highlight the potential for interventions that decrease metabolic inertia for enhancing exercise tolerance in this condition.

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.

PURPOSE: The brain can utilise medium chain triglycerides (MCTs) as an alternative fuel than glucose, and research has shown that MCT ingestion improves cognitive function in diseased and/or elderly individuals. The aim of this study is to determine if these improvements can also be observed in young, healthy adults. Furthermore, we aim to establish the ideal dosage and timeframe necessary for an effect. METHODS: Participants were divided equally into three groups of 10 (Placebo (0g), 12g and 18g MCT/day) and were supplemented for 4 weeks. The supplement had a C8:C10 ratio of 30:70. Participants visited the laboratory once a week for 5 weeks (baseline, test weeks 1-4) to undergo a battery of cognitive tests; Trail Making, Digit Span, Spatial Span, Covert Shift of Attention, and Rapid Visual Information Processing. RESULTS: After 2-3 weeks of supplementation, MCT ingestion enhanced performance in cognitive tasks, including: Trail Making A/B and Digit Span Forwards/Backwards (ps0.05). There were also null results in tasks measuring attention and reaction time (ps>0.05). CONCLUSIONS: MCT ingestion improved cognitive performance after 2-3 weeks, with minimal difference between taking 12g and 18g MCT/day groups, suggesting a possible dose-response threshold at 12g MCT/day when supplementing over a short period.

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.

We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics (τv˙o2) is an independent determinant of critical power (CP) when O2 availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O2 availability is impaired remains unknown. During supine exercise, which causes an O2 availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on τv˙o2 and CP. CP, τv˙o2, and muscle oxygenation status (the latter via near‐infrared spectroscopy) were determined via four severe‐intensity constant‐power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate‐intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and τv˙o2 was greater (U→S = 45 ± 16 sec, vs. M→S = 69 ± 129 sec, P = 0.001) when compared to U→S. There was no difference in tissue oxyhemoglobin concentration ([HbO2 + MbO2]) at baseline or during exercise. The concomitant increase in τv˙o2 and reduction in CP during M→S compared to U→S shows for the first time that τv˙o2 is an independent determinant of CP in conditions where O2 availability is limiting.

Critical power is a fundamental parameter defining high‐intensity exercise tolerance, and is related to the phase II time constant of pulmonary oxygen uptake kinetics (τV˙O2). Whether this relationship is causative is presently unclear. This study determined the impact of raised baseline work rate, which increases τV˙O2, on critical power during upright cycle exercise. Critical power was determined via four constant‐power exercise tests to exhaustion in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a baseline work rate of 90% of the gas exchange threshold (M→S). During these exercise transitions, τV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τ [HHb + Mb]) (the latter via near‐infrared spectroscopy) were determined. In M→S, critical power was lower (M→S = 203 ± 44 W vs. U→S = 213 ± 45 W, P = 0.011) and τV˙O2 was greater (M→S = 51 ± 14 sec vs. U→S = 34 ± 16 sec, P = 0.002) when compared with U→S. Additionally, τ [HHb + Mb] was greater in M→S compared with U→S (M→S = 28 ± 7 sec vs. U→S = 14 ± 7 sec, P = 0.007). The increase in τV˙O2 and concomitant reduction in critical power in M→S compared with U→S suggests a causal relationship between these two parameters. However, that τ [HHb + Mb] was greater in M→S exculpates reduced oxygen availability as being a confounding factor. These data therefore provide the first experimental evidence that τV˙O2 is an independent determinant of critical power. Keywords critical power, exercise tolerance, oxygen uptake kinetics, power‐duration relationship, muscle deoxyhemoglobin kinetics, work‐to‐work exercise.

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

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

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.

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.

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 use of blended learning, face-to-face contact alongside e-based activities, provides academic staff with an opportunity to match their teaching strategies with the changing student cohort. This study report students’ perceptions of e-learning activities early in bioscience modules; students from all three levels of undergraduate study were included. Students in their first year were most receptive to e-learning, using the opportunity to access learning resources from an ‘off-campus’ location and welcomed more blended learning. Students in their third year engaged to the same level as first year students but valued the task less, preferring face to face contact with staff. Second year students seem to be the key; they valued the task more than third year students but their qualitative comments indicated that they too were placing value on campus based activities. E-learning provides first year students with an opportunity, at ‘high risk’ times, to draw on familial support and to ‘process’ knowl...

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.

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with (31)P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n = 14). Unlocalized (31)P spectra were collected from the quadriceps throughout using a dual-tuned ((1)H and (31)P) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min(-1)) or change in [PCr] (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min(-1); each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min(-1) (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min(-1), or 26 ± 30%; P 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r(2) = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O).

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.

Neoadjuvant chemotherapy (NAC) followed by surgery for resectable oesophageal or gastric cancer improves outcome when compared with surgery alone. However NAC has adverse effects. We assess here whether NAC adversely affects physical fitness and whether such an effect is associated with impaired survival following surgery.We prospectively studied 116 patients with oesophageal or gastric cancer to assess the effect of NAC on physical fitness, of whom 89 underwent cardiopulmonary exercise testing (CPET) before NAC and proceeded to surgery. 39 patients were tested after all cycles of NAC but prior to surgery. Physical fitness was assessed by measuring oxygen uptake (VO₂ in ml kg(-1) min(-1)) at the estimated lactate threshold (θL) and at peak exercise (VO₂ peak in ml kg(-1) min(-1)).VO₂ at θL and at peak were significantly lower after NAC compared to pre-NAC values: VO₂ at θL 14.5 ± 3.8 (baseline) vs. 12.3 ± 3.0 (post-NAC) ml kg(-1) min(-1); p ≤ 0.001; VO₂ peak 20.8 ± 6.0 vs. 18.3 ± 5.1 ml kg(-1) min(-1); p ≤ 0.001; absolute VO₂ (ml min(-1)) at θL and peak were also lower post-NAC; p ≤ 0.001. Decreased baseline VO₂ at θL and peak were associated with increased one year mortality in patients who completed a full course of NAC and had surgery; p = 0.014.NAC before cancer surgery significantly reduced physical fitness in the overall cohort. Lower baseline fitness was associated with reduced one-year-survival in patients completing NAC and surgery, but not in patients who did not complete NAC. It is possible that in some patients the harms of NAC may outweigh the benefits. Trials Registry Number: NCT01335555.

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.