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.

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.

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.

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.

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.

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.

Dissociating external power from intramuscular exercise intensity during intermittent bilateral knee-extension in humans.

KEY POINTS: 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 O2 cost of exercise and increases tolerance. The extent to which this dissociation is reflected in the intramuscular bioenergetics is unknown. We used pulmonary gas exchange and 31 P magnetic resonance spectroscopy to measure whole-body V̇O2, quadriceps phosphate metabolism and pH during continuous and intermittent exercise of different work:recovery durations. Shortening the work:recovery durations (16:32 s vs. 32:64 s vs. 64:128 s vs. continuous) at a work rate estimated to require 110% peak aerobic power reduced V̇O2, muscle phosphocreatine breakdown and muscle acidification, eliminated the glycolytic-associated contribution to ATP synthesis, and increased exercise tolerance. Exercise intensity (i.e. magnitude of intramuscular metabolic perturbations) can be dissociated from the external power using intermittent exercise with short work:recovery durations. ABSTRACT: Compared 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 O2 storage fluctuations and/or contributions from oxidative and substrate-level bioenergetics is unknown. Using pulmonary gas-exchange and intramuscular 31 P magnetic resonance spectroscopy, we tested the hypotheses that, at the same power: ATP synthesis rates are similar, whereas peak V̇O2 amplitude is lower in intermittent vs. continuous exercise. Thus, we expected that: intermittent exercise relies less upon anaerobic glycolysis for ATP provision than continuous exercise; shorter intervals would require relatively greater fluctuations in intramuscular bioenergetics than in V̇O2 compared to longer intervals. Six men performed bilateral knee-extensor exercise (estimated to require 110% peak aerobic power) continuously and with three different intermittent work:recovery durations (16:32, 32:64 and 64:128 s). Target work duration (576 s) was achieved in all intermittent protocols; greater than continuous (252 ± 174 s; P < 0.05). Mean ATP turnover rate was not different between protocols (∼43 mm min-1 on average). However, the intramuscular phosphocreatine (PCr) component of ATP generation was greatest (∼30 mm min-1 ), and oxidative (∼10 mm min-1 ) and anaerobic glycolytic (∼1 mm min-1 ) components were lowest for 16:32 and 32:64 s intermittent protocols, compared to 64:128 s (18 ± 6, 21 ± 10 and 10 ± 4 mm min-1 , respectively) and continuous protocols (8 ± 6, 20 ± 9 and 16 ± 14 mm min-1 , respectively). As intermittent work duration increased towards continuous exercise, ATP production relied proportionally more upon anaerobic glycolysis and oxidative phosphorylation, and less upon PCr breakdown. However, performing the same high-intensity power intermittently vs. continuously reduced the amplitude of fluctuations in V̇O2 and intramuscular metabolism, dissociating exercise intensity from the power output and work done.

Prior exercise speeds pulmonary oxygen uptake kinetics and increases critical power during supine but not upright cycling.

NEW FINDINGS: 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[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 τV̇O2 (control 54 ± 18 s versus primed 39 ± 11 s; P < 0.001), increased τ[HHb] (control 8 ± 4 s versus primed 12 ± 4 s; P = 0.003) and increased CP (control 177 ± 31 W versus primed 185 ± 30 W, P = 0.006) compared with control conditions. However, priming exercise had no effect on τV̇O2 (control 37 ± 12 s versus primed 35 ± 8 s; P = 0.82), τ[HHb] (control 10 ± 5 s versus primed 14 ± 10 s; P = 0.10) or CP (control 235 ± 42 W versus primed 232 ± 35 W; P = 0.57) during upright exercise. The concomitant reduction of τV̇O2 and increased CP following priming in the supine group, effects that were absent in the upright group, provide the first experimental evidence that τV̇O2 is mechanistically related to critical power. The increased τ[HHb+Mb] suggests that this effect was mediated, at least in part, by improved oxygen availability.

Influence of oxygen uptake kinetics on physical performance in youth soccer.

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. METHODS: Seventeen highly trained youth soccer players (age: 13.3 ± 0.4 year, 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, and from moderate- to 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, three 2 × 20 min, 11 v 11 matches, to gain measures of physical performance during soccer match play. 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 and high-speed running efforts (HSReff): r = -0.66, P = 0.005]. 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.

Oxygen uptake kinetics in trained adolescent females.

UNLABELLED: Little evidence exists with regard to the effect that exercise training has upon oxygen uptake kinetics in adolescent females. PURPOSE: The aim of the study was to compare [Formula: see text] and muscle deoxygenation kinetics in a group of trained (Tr) and untrained (Utr) female adolescents. METHOD: 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. RESULT: Peak [Formula: see text] was significantly (p < 0.05) greater in the Tr compared to the Utr (Tr: 43.2 ± 3.2 mL kg(-1 )min(-1) vs. Utr: 34.6 ± 4.0 mL kg(-1 )min(-1)). The [Formula: see text] time constant was significantly (p < 0.05) faster in the Tr compared to the Utr (Tr: 26.3 ± 6.9 s vs. Utr: 35.1 ± 11.5 s). There was no inter-group difference in the time constant for muscle deoxygenation kinetics (Tr: 8.5 ± 3.0 s vs. Utr: 12.4 ± 8.3 s); a large effect size, however, was demonstrated (-0.804). CONCLUSION: Exercise training and/or genetic self-selection results in faster kinetics in trained adolescent females. The faster [Formula: see text] kinetics seen in the trained group may result from enhanced muscle oxygen utilisation.

Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee extension.

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).

Beetroot juice supplementation speeds O2 uptake kinetics and improves exercise tolerance during severe-intensity exercise initiated from an elevated metabolic rate.

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 VO2 kinetics (τ(p)) 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 VO2 τ(p) in 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 VO2 kinetics 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 VO2 kinetics and enhances exercise tolerance during severe-intensity exercise when initiated from an elevated metabolic rate.

Effects of magnitude and frequency of variations in external power output on simulated cycling time-trial performance.

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.

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.

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.