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.

Clustered cardiometabolic risk and arterial stiffness of recreational adult tennis players.

BACKGROUND: Recent evidence highlights racquet sports as being associated with a substantially reduced risk of CVD mortality. The purpose of this investigation was to evaluate clustered cardiometabolic risk (CMR) and arterial stiffness in recreational adult tennis players. METHODS: Forty-three recreational tennis players (T) and a matched group of 45 healthy, active non-tennis (NT) players, mean age (±SEM) 41.6±1.8 years participated in this cross-sectional comparative study. Measurements included emerging and traditional CMR factors with pulse wave analysis/velocity utilised to assess indexes of arterial stiffness. Clustered cardiometabolic risk was calculated using two composites: CMR1 (central aortic systolic blood pressure, carotid-femoral pulse wave velocity, percentage body fat, HDL-C and maximal oxygen uptake) and CMR2 (brachial systolic blood pressure, triglycerides, TC:HDL-C, percentage body fat, HbA1c and maximal oxygen uptake). RESULTS: Analysis of covariance, controlling for age, revealed T had significantly lower (healthier) CMR1 scores than NT (EMM±SEM, T: -0.48±0.3 vs. NT: 0.50±0.3, P=0.03). Similarly, T also demonstrated lower clustered CMR2 scores (EMM, T: -0.66±0.4 vs. NT: 0.59±0.4, P=0.04). Augmentation index of the pulse pressure wave, normalised to heart rate 75 bpm (AIx75), was lower in T vs NT (EMM, T: 10.7±1.7% vs. NT: 12.7±1.6%; P=0.03), when controlling for age and gender. CONCLUSIONS: Tennis appears to be a suitable and effective physical activity modality for targeting cardiometabolic and vascular health and should be more frequently advocated in physical activity promotion strategies.

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.

The Musculoskeletal Health Benefits of Tennis.

BACKGROUND: The prevalence of musculoskeletal (MSK) conditions is increasing, and although current guidelines for physical activity attempt to combat this, many fail to achieve the recommended targets. The present study sought to investigate whether regular tennis participation is more effective at enhancing MSK function than meeting the current international physical activity guidelines. HYPOTHESIS: Tennis players will display significantly enhanced MSK function when compared with age-matched healthy active nonplayers. STUDY DESIGN: Cross-sectional study. LEVEL OF EVIDENCE: Level 3. METHODS: Ninety participants (age range, 18-65 years) took part in this study; there were 43 tennis players (18 men, 25 women) and 47 nonplayers (26 men, 21 women). MSK function was assessed by cluster analysis of 3 factors: (1) electromyographic fatigability of prime movers during handgrip, knee extension, and knee flexion; (2) isometric strength in the aforementioned movements; and (3) body composition measured by bioelectrical impedance analysis. Maximal oxygen uptake was also assessed to characterize cardiorespiratory fitness. RESULTS: Tennis players displayed significantly greater upper body MSK function than nonplayers when cluster scores of body fat percentage, handgrip strength, and flexor carpi radialis fatigue were compared by analysis of covariance, using age as a covariate (tennis players, 0.33 ± 1.93 vs nonplayers, -0.26 ± 1.66; P < 0.05). Similarly, tennis players also demonstrated greater lower extremity function in a cluster of body fat percentage, knee extension strength, and rectus femoris fatigue (tennis players, 0.17 ± 1.76 vs nonplayers, -0.16 ± 1.70; P < 0.05). CONCLUSION: The present study offers support for improved MSK functionality in tennis players when compared with age-matched healthy active nonplayers. This may be due to the hybrid high-intensity interval training nature of tennis. CLINICAL RELEVANCE: The findings suggest tennis is an excellent activity mode to promote MSK health and should therefore be more frequently recommended as a viable alternative to existing physical activity guidelines.

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.

"Work-to-Work" exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W' during supine cycling.

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.

Elevated baseline work rate slows pulmonary oxygen uptake kinetics and decreases critical power during upright cycle exercise.

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.

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.

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.

Cardiac strain during upright cycle ergometry in adolescent males.

Little evidence exists with regard to changes in cardiac strain that occur during submaximal exercise in young males. The aims of the study were to evaluate the changes that occur in longitudinal (L), radial (R), and endocardial circumferential (EC) strain during submaximal upright cycle ergometry and to examine the test-retest reproducibility of these measurements. Fourteen recreationally active, adolescent (age: 17.9 ± 0.7 years) males volunteered for the study. All subjects underwent an incremental (40 W) submaximal cycle ergometer test. L, R, and EC strain values were obtained using speckle tracking, from two-dimensional B-mode images of the left ventricle (LV) during rest and the initial stages of submaximal exercise (40 and 80 W). The average of 6 LV segments was used to determine both peak wall deformation (%) and the time to peak deformation (ms). There was a statistically (P < 0.05) significant increase from rest to submaximal exercise for peak deformation for L, R, and EC strain. There was a statistically significant (P < 0.05) decrease from rest to submaximal exercise for time to peak for L and R and EC strain and between submaximal workloads for time to peak for L strain and EC strain. Coefficients of variation demonstrated reproducibility for upright strain and strain rate measurements similar to published supine measurements. This study has demonstrated that changes in left ventricular wall deformation (L, R and EC strain) that occur during the transition from rest to submaximal exercise can be reliably measured and confirm that a healthy LV has a hyperdynamic response to exercise.

Skin microvascular reactivity in trained adolescents.

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.

Skin microvascular reactivity in children and adolescents with type 1 diabetes in relation to levels of physical activity and aerobic fitness.

No studies to date have evaluated the relationship between exercise and microvascular function in youth with type 1 diabetes mellitus (T1DM). Twenty-nine complication free children and adolescents with T1DM were assessed for skin microvascular reactivity, aerobic fitness (VO2peak) and physical activity. VO2peak but not physical activity was significantly and independently associated with maximal hyperemia of the skin microcirculation (p < .01). No significant associations were found between venoarteriolar reflex (VAR) vasoconstriction and VO2peak or physical activity. Aerobic fitness may be an important indicator or mediator of effective microvascular endothelial function in youth with T1DM.