Medium chain triglycerides with a C8:C10 ratio of 30:70 enhances cognitive performance and mitigates the cognitive decline associated with prolonged exercise in young and healthy adults.

INTRODUCTION: Prolonged exercise has been linked to a decline in cognitive function due to a variety of factors, such as a drop in oxygen in the prefrontal cortex and an increase in stress hormones and neurotransmitters. Medium chain triglycerides (MCTs) may possibly offset this decline as they provide energy for the brain via both direct and indirect pathways, alongside promoting chronic physiological adaptations within the brain. METHODS: Participants were divided into two groups; MCT (n = 9) and Placebo (n = 10). The MCT gels contained 6 g of MCT with a C8:C10 ratio of 30:70, whereas the placebo gels contained carbohydrates of similar calorific value to the MCT gels. Participants visited the laboratory on three occasions (familiarisation/fitness test, pre-supplementation, post-supplementation), during which they performed a battery of cognitive tasks assessing domains such as processing speed, working memory, selective attention, decision making and coordination, before and after a prolonged bout of exercise (60 mins at 90% gas exchange threshold (GET). A 2-week supplementation period between visits 2 and 3 involved the ingestion of 2 gels per day. RESULTS: Exercise resulted in detriments in most cognitive tasks pre-supplementation for both groups, and post-supplementation for the Placebo group (main effect ps< 0.05). Post-supplementation, the effect of exercise was mediated in the MCT group for all cognitive tasks (main effect ps< 0.05), except for the Digit and Spatial Span Backwards test phases (main effect ps> 0.05). Furthermore, MCT supplementation enhanced before-exercise cognitive performance and in some measures, such as working memory, this was maintained after-exercise (interaction effect ps> 0.05). CONCLUSIONS: Chronic MCT supplementation enhanced before-exercise cognitive performance and offset the cognitive decline caused by a prolonged bout of exercise. In some cases, improvements in before-exercise cognitive performance were maintained after-exercise.

A dynamic model of the bi-exponential reconstitution and expenditure of W' in trained cyclists.

ABSTRACTThe aim of this study was to investigate the effects of different recovery power outputs on the reconstitution of W' and to develop a dynamic bi-exponential model of W' during depletion and reconstitution. Ten trained cyclists (mass 71.7 ± 8.4 kg; V̇O2max 60.0 ± 6.3 ml·kg-1·min-1) completed three incremental ramps (20 W·min-1) to the limit of tolerance on each of six occasions with recovery durations of 30 and 240 s. Recovery power outputs varied between 50 W (LOW); 60% of critical power (CP) (MOD) and 85% of CP (HVY). W' reconstitution was measured following each recovery and fitted to a bi-exponential model. Amplitude and time constant (τ) parameters were then determined via regression analysis accounting for relative intensity and duration to produce a dynamic model of W'. W' reconstitution slowed disproportionately as recovery power output increased (p < 0.001) and increased with recovery duration (p < 0.001). The amplitudes of each recovery component were strongly correlated to W' reconstitution after 240 s at HVY (r = 0.95), whilst τ parameters were found to be related to the fractional difference between recovery power and CP. The predictive capacity of the resultant model was assessed against experimental data with no differences found between predicted and experimental values of W' reconstitution (p > 0.05). The dynamic bi-exponential model of W' accounting for varying recovery intensities closely described W' kinetics in trained cyclists facilitating real-time decisions about pacing and tactics during competition. The model can be customised for individuals from known CP and W' and a single additional test session.HighlightsA dynamic bi-exponential model of W' accounting for both varying power output and duration.Individual customisation of the model can be achieved with a single specific test session.W' reconstitution slows disproportionally with increasing intensity after repeated bouts.

Interaction of Factors Determining Critical Power.

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.

Bi-exponential modelling of [Formula: see text] reconstitution kinetics in trained cyclists.

PURPOSE: 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. METHODS: Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; [Formula: see text] 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. [Formula: see text] 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 [Formula: see text] 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.

Bioenergetic Mechanisms Linking V˙O2 Kinetics and Exercise Tolerance.

We hypothesize that the V˙O2 time constant (τV˙O2) 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 V˙O2 "slow component" and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits.

Dissociation between exercise intensity thresholds: mechanistic insights from supine exercise.

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.

The ramp and all-out exercise test to determine critical power: validity and robustness to manipulations in body position.

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 < 0.001) and not different from CP (CP = 221 ± 40 W vs. EP = 226 ± 46 W, P = 0.085, 95% limits of agreement - 30, 19 W). During supine exercise, EP was also highly correlated with (R2 = 0.94, P < 0.001) and not different from CP (CP = 140 ± 42 W vs. EP = 136 ± 40 W, 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.

Cocoa-flavanols enhance moderate-intensity pulmonary [Formula: see text] kinetics but not exercise tolerance in sedentary middle-aged adults.

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 ([Formula: see text]) 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 [Formula: see text] kinetics. RESULTS: During moderate-intensity exercise, the time constant of the phase II [Formula: see text] kinetics ([Formula: see text]) 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 [Formula: see text] (A[Formula: see text]; 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, [Formula: see text], the amplitude of the slow component ([Formula: see text]) 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 [Formula: see text] 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.

Impact of supine versus upright exercise on muscle deoxygenation heterogeneity during ramp incremental cycling is site specific.

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 [Formula: see text]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 < 0.001) and RFs (S: 36 ± 21 vs. U: 25 ± 15 µM, P < 0.001), but not in the VLd (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.

The effects of medium chain triglyceride (MCT) supplementation using a C8:C10 ratio of 30:70 on cognitive performance in healthy young adults.

PURPOSE: 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. METHODS: 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 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 (ps<0.001) 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 (ps<0.05). There was minimal difference between the two MCT intervention groups in most measures (ps>0.05). 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 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.

Physiological and anthropometric determinants of critical power, W' and the reconstitution of W' in trained and untrained male cyclists.

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.

Effect of priming exercise and body position on pulmonary oxygen uptake and muscle deoxygenation kinetics during cycle exercise.

We hypothesized that the performance of prior heavy exercise would speed pulmonary oxygen uptake (V̇o2) kinetics (i.e., as described by the time constant, [Formula: see text]) and reduce the amplitude of muscle deoxygenation (deoxy[heme]) kinetics in the supine (S) but not upright (U) body position. Seventeen healthy men completed heavy-intensity constant-work rate exercise tests in S and U consisting of two bouts of 6-min cycling separated by 6-min cycling at 20 W. Pulmonary V̇o2 was measured breath by breath; total and deoxy[heme] were determined via time-resolved near-infrared spectroscopy (NIRS) at three muscle sites. Priming exercise reduced [Formula: see text] in S (bout 1: 36 ± 10 vs. bout 2: 28 ± 10 s, P < 0.05) but not U (bout 1: 27 ± 8 s vs. bout 2: 25 ± 7 s, P > 0.05). Deoxy[heme] amplitude was increased after priming in S (bout 1: 25-28 µM vs. bout 2: 30-35 µM, P < 0.05) and U (bout 1: 13-18 µM vs. bout 2: 17-25 µM, P > 0.05), whereas baseline total[heme] was enhanced in S (bout 1: 110-179 µM vs. bout 2: 121-193 µM, P < 0.05) and U (bout 1: 123-186 µM vs. bout 2: 137-197 µM, P < 0.05). Priming exercise increased total[heme] in both S and U, likely indicating enhanced diffusive O2 delivery. However, the observation that after priming the amplitude of the deoxy[heme] response was increased in S suggests that the reduction in [Formula: see text] subsequent to priming was related to a combination of both enhanced intracellular O2 utilization and increased O2 delivery.NEW & NOTEWORTHY Here we show that oxygen uptake (V̇o2) kinetics are slower in the supine compared with upright body position, an effect that is associated with an increased amplitude of skeletal muscle deoxygenation in the supine position. After priming in the supine position, the amplitude of muscle deoxygenation remained markedly elevated above that observed during upright exercise. Hence, the priming effect cannot be solely attributed to enhanced O2 delivery, and enhancements to intracellular O2 utilization must also be contributory.

Impact of supine exercise on muscle deoxygenation kinetics heterogeneity: mechanistic insights into slow pulmonary oxygen uptake dynamics.

Oxygen uptake (V̇o2) kinetics are slowed in the supine (S) position purportedly due to impaired muscle O2 delivery ([Formula: see text]); however, these conclusions are predicated on single-site measurements in superficial muscle using continuous-wave near-infrared spectroscopy (NIRS). This study aimed to determine the impact of body position [i.e., upright (U) versus S] on deep and superficial muscle deoxygenation (deoxy[heme]) using time-resolved (TR-) NIRS, and how these relate to slowed pulmonary V̇o2 kinetics. Seventeen healthy men completed constant power tests during 1) S heavy-intensity exercise and 2) U exercise at the same absolute work rate, with a subset of 10 completing additional tests at the same relative work rate as S. Pulmonary V̇o2 was measured breath-by-breath and, deoxy- and total[heme] were resolved via TR-NIRS in the superficial and deep vastus lateralis and superficial rectus femoris. The fundamental phase V̇o2 time constant was increased during S compared with U (S: 36 ± 10 vs. U: 27 ± 8 s; P < 0.001). The deoxy[heme] amplitude (S: 25-28 vs. U: 13-18 µM; P < 0.05) and total[heme] amplitude (S: 17-20 vs. U: 9-16 µM; P < 0.05) were greater in S compared with U and were consistent for the same absolute (above data) and relative work rates (n = 10, all P < 0.05). The greater deoxy- and total[heme] amplitudes in S vs. U supports that reduced perfusive [Formula: see text] in S, even within deep muscle, necessitated a greater reliance on fractional O2 extraction and diffusive [Formula: see text]. The slower V̇o2 kinetics in S versus U demonstrates that, ultimately, these adjustments were insufficient to prevent impairments in whole body oxidative metabolism.NEW & NOTEWORTHY 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.

Limitations to exercise tolerance in type 1 diabetes: the role of pulmonary oxygen uptake kinetics and priming exercise.

We compared the time constant (τV̇O2) of the fundamental phase of pulmonary oxygen uptake (V̇o2) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on τV̇O2, critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. Seventeen men with type 1 diabetes and 17 healthy male control subjects performed moderate-intensity exercise to determine τV̇O2. A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, τV̇O2, and muscle deoxyhemoglobin + myoglobin ([HHb+Mb], via near-infrared spectroscopy) kinetics (described by a time constant, τ[HHb+Mb]) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. τV̇O2 was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; P < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; P < 0.001), whereas τV̇O2 (PRI 36 ± 15 vs. CON 50 ± 21 s; P = 0.006) and τ[HHb+Mb] (PRI 10 ± 5 vs. CON 17 ± 11 s; P = 0.037) were reduced in PRI compared with CON. Type 1 diabetes patients showed slower pulmonary V̇o2 kinetics compared with control subjects; priming exercise speeded V̇o2 and [HHb + Mb] kinetics and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterization of the power-duration relationship in type 1 diabetes and the first experimental evidence that τV̇O2 is an independent determinant of critical power in this population.NEW & NOTEWORTHY 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.

Effect of Hyperoxia on Critical Power and V˙O2 Kinetics during Upright Cycling.

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 (τV˙O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in nine healthy men performing upright cycle ergometry. METHODS: Critical power was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via four severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, τV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τ[HHb]), alongside absolute concentrations of muscle oxyhemoglobin ([HbO2]), were determined. RESULTS: Critical power was greater (hyperoxia, 216 ± 30 W vs normoxia, 197 ± 29 W; 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 with normoxia. τV˙O2 (hyperoxia, 35 ± 12 s vs normoxia, 33 ± 10 s; P = 0.33) and τ[HHb] (hyperoxia, 11 ± 5 s vs normoxia, 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO2] during exercise was greater in hyperoxia compared with normoxia (hyperoxia, 73 ± 20 vs normoxia, 66 ± 15 µM; P < 0.001). CONCLUSIONS: 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 τV˙O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, that is, CP.

Hyperoxia speeds pulmonary oxygen uptake kinetics and increases critical power during supine cycling.

NEW FINDINGS: What is the central question of this study? 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 ( τV̇O2 ). To test whether this relationship is causal, we assessed the impact of hyperoxia on τV̇O2 and critical power during supine cycle exercise. What is the main finding and its importance? The results demonstrate that hyperoxia increased muscle oxygenation, reduced τV̇O2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τV̇O2 is a determinant of the upper limit for steady-state exercise, i.e. critical power. ABSTRACT: The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics ( τV̇O2 ) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, τV̇O2 and absolute concentrations of oxyhaemoglobin ([HbO2 ]; via near-infrared spectroscopy) were determined via four constant-power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O2  = 0.5). A 6 min bout of moderate-intensity exercise (70% of gas exchange threshold) was also undertaken before each severe-intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the τV̇O2 reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, [HbO2 ] was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 µm versus normoxia, 63 ± 11 µm; P = 0.020). The τV̇O2 was significantly related to CP in hyperoxia (R2  = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, τV̇O2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τV̇O2 is an independent determinant of CP. The finding that τV̇O2 was related to CP in hyperoxia but not normoxia also supports this notion.