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 (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

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

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. 17 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 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 τV̇O2 (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 τV̇O2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τV̇O2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability

LIMITATIONS TO EXERCISE TOLERANCE IN TYPE 1 DIABETES: THE ROLE OF PULMONARY OXYGEN UPTAKE KINETICS AND PRIMING EXERCISE

We compared the time constant (τ_V ̇ O2) of the fundamental phase of pulmonary oxygen uptake (V ̇O2) kinetics between young adult males with type 1 diabetes and healthy controls. We also assessed the impact of priming exercise on τ_V ̇ O2, critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. 17 males with type 1 diabetes and 17 healthy male controls performed moderate-intensity exercise to determine τ_V ̇ O2. A subset of 7 participants with type 1 diabetes performed an additional eight visits, whereby critical power, τ_V ̇ O2 and muscle deoxyhaemoglobin + 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-minute bout of heavy exercise. τ_V ̇ O2 was greater in participants with type 1 diabetes compared to controls (type 1 diabetes: 50±13 vs. control: 32±12 s; P<0.001). Critical power was greater in PRI compared to CON (PRI: 161±25 W vs. CON: 149±22 W; P<0.001), whereas τ_V ̇ O2 (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 to CON. Type 1 diabetes patients showed slower pulmonary V ̇O2 kinetics when compared to controls; priming exercise speeded V ̇O2 and [HHb + Mb] kinetics, and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterisation of the power-duration relationship in type 1 diabetes, and the first experimental evidence that τ_V ̇ O2 is an independent determinant of critical power in this population

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

The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics (τ_V ̇ O2) and critical power (CP) during supine cycle exercise. 8 healthy males completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold (GET). Eight separate visits followed, whereby CP, τ_V ̇ O2 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 (FiO2 = 0.5). A 6-minute bout of moderate intensity exercise (70% GET) was also undertaken prior to each severe intensity bout, in both conditions. CP was greater (hyperoxia = 148 ± 29 W vs. normoxia = 134 ± 27 W, P = 0.006) and the τ_V ̇ O2 was reduced (hyperoxia = 33 ± 12 s vs. normoxia = 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared to normoxia. Furthermore, [HbO2] was enhanced in hyperoxia compared to normoxia (hyperoxia: 67 ± 10 versus normoxia: 63 ± 11 μM; P = 0.020). τ_V ̇ O2 was significantly related to CP in hyperoxia (r = 0.89, P < 0.001), however no relationship was observed in normoxia (r = 0.03, P = 0.68). Muscle oxygenation was increased, τ_V ̇ O2 was reduced and CP was increased in hyperoxia compared to normoxia, suggesting that τ_V ̇ O2 is an independent determinant of CP. That τ_V ̇ O2 was related to CP in hyperoxia but not normoxia further supports this notion

Effects of Dietary Nitrate Supplementation on Performance and Muscle Oxygenation during Resistance Exercise in Men

The purpose of the current study was to assess the effects of acute and short-term nitrate (NO3−)-rich beetroot juice (BR) supplementation on performance outcomes and muscle oxygenation during bench press and back squat exercise. Fourteen recreationally active males were assigned in a randomized, double-blind, crossover design to supplement for 4 days in two conditions: (1) NO3−-depleted beetroot juice (PL; 0.10 mmol NO3− per day) and (2) BR (11.8 mmol NO3− per day). On days 1 and 4 of the supplementation periods, participants completed 2 sets of 2 × 70%1RM interspersed by 2 min of recovery, followed by one set of repetitions-to-failure (RTF) at 60%1RM for the determination of muscular power, velocity, and endurance. Quadriceps and pectoralis major tissue saturation index (TSI) were measured throughout exercise. Plasma [NO3−] and nitrite ([NO2−]) were higher after 1 and 4 days of supplementation with BR compared to PL (p \u3c 0.05). Quadriceps and pectoralis major TSI were not different between conditions (p \u3e 0.05). The number of RTF in bench press was 5% greater after acute BR ingestion compared to PL (PL: 23 ± 4 vs. BR: 24 ± 5, p \u3c 0.05). There were no differences between BR and PL for RTF for back squat or power and velocity for back squat or bench press (p \u3e 0.05). These data improve understanding on the ergogenic potential of BR supplementation during resistance exercise

Over 55 years of critical power: Fact

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)

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

REPLY TO FRANCESCATO ET AL.: ON CORRECT COMPUTATION OF CONFIDENCE INTERVALS FOR KINETIC PARAMETERS

No abstract availabl