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.

Evaluating the progressive cardiovascular health benefits of short-term high-intensity interval training.

PURPOSE: High-intensity training is recognised as a time-efficient way of improving aerobic fitness. However, there is a lack of consensus regarding the temporal nature of adaptation response and which peripheral and cardiac changes occur using the same exercise stimulus and protocol. Therefore, this study aimed to evaluate the progression of vascular and cardiac changes over a 6-week training period. METHODS: Twelve healthy males (age 21 ± 2 years; 42.5 ± 8.3 ml min-1 kg-1) participated in a high-intensity training programme consisting of 1-min sprints, interspersed with 2 min active recovery, 3 days/week for 6 weeks on a cycle ergometer. Cardiac, vascular, blood lipids and VO2max measurements were taken at 0, 3 and 6 weeks and compared against a participant-matched control group (age 21 ± 2 years; 37.7 ± 8.3 ml min-1 kg-1). RESULTS: There was a significant improvement in VO2max (42.5 ± 8.3-47.4 ± 8.5 ml min-1 kg-1; p = 0.009) in the training group and a significant decrease in systolic blood pressure (8%) from 0 to 6 weeks (p = 0.025). There was a small yet significant decrease in ejection fraction and increased end-systolic volume in both groups over time (p = 0.01) with no significant interaction effect (p > 0.05). A between-group difference in peak velocity of early diastolic mitral annular motion was also observed (p = 0.01). No improvements were seen in blood lipid profiles, central arterial stiffness and cardiometabolic risk score. CONCLUSIONS: Six weeks of high-intensity training increases aerobic fitness and is enough to stimulate initial reductions in peripheral pressure, but not sufficient to elicit structural and functional cardiac changes, reduce arterial stiffness or lower CV risk.

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.

Changing incidence of bovine babesiosis in Ireland.

BACKGROUND: In Ireland bovine babesiosis is caused by the tick-borne blood parasite, Babesia divergens. A survey of veterinary practitioners and farmers in the 1980's revealed an annual incidence of 1.7% associated with considerable economic losses. However, two subsequent surveys in the 1990's indicated a decline in clinical babesiosis. Recent evidence from continental Europe suggests that, probably due to climate change, the distribution of the tick vector of B. divergens, Ixodes ricinus is extending to more northerly regions and higher altitudes. In addition, milder winters are thought to widen the window of tick activity. In order to determine whether any such changes have affected the incidence of bovine babesiosis in Ireland, a questionnaire survey of farmers and veterinarians was carried out and compared with data from previous surveys. RESULTS: Our survey indicates that while the incidence of clinical disease has continued to decline, cases can occur at any time of year. In contrast to previous surveys, affected farms were the same size as unaffected ones. There was no correlation between disease risk and the presence of deer on the land. Disease severity and mortality rates were increased because many infections were advanced by the time they were detected and treated. CONCLUSION: While the precise reasons for the decline in the incidence of redwater are unknown, changes in agricultural practice are likely to be of importance. A reversal of the trend could be devastating, as vigilance among farmers and veterinarians is flagging and the national herd is losing its protective immunity to disease.

Orthostatic effects on echocardiographic measures of ventricular function.

Orthostatic-induced alterations in Doppler echocardiographic measures of ventricular function have not been well-defined. Identifying such changes may provide useful insights regarding the responses of these measures to variations in ventricular loading conditions. Standard assessment of mitral inflow velocity and tissue Doppler imaging (TDI) of left ventricular longitudinal myocardial velocities was performed on 14 young males (mean age 17.9 ± 0.7 years) in the supine position and then 5 minutes after assuming a sitting position with legs dependent. Upon sitting, average values of stroke volume and cardiac output fell by 28% and 18%, respectively, while heart rate increased from 64 ± 10 to 73 ± 12 beats/min (+14%) and calculated systemic vascular resistance rose from 12.9 ± 2.2 to 16.4 ± 3.1 units (+27%). Mitral E peak velocity declined from 87 ± 16 to 64 ± 16 cm/sec, and average TDI-E' and TDI-S both decreased (by -44% and -20%, respectively). When adjusted for orthostatic decreases in left ventricular end-diastolic volume, the mean decrease in TDI-E' was reduced to -29 (P < 0.01), but no significant decline was observed in adjusted TDI-S. Average E/E' rose with sitting by 40% (P = 0.02). These findings suggest that (a) decreases in TDI measures when assuming the upright position reflect the reduction of left ventricular size; (b) orthostatic fall in TDI-E' is also related to smaller ventricular size but, in addition, to a nonspecified reduction in ventricular relaxation; and (c) values of E/E' do not reflect alterations in ventricular preload, which occur during an orthostatic challenge.

Time-of-day effect on cardiac responses to progressive exercise.

This study was designed to examine time-of-day effects on markers of cardiac functional capacity during a standard progressive cycle exercise test. Fourteen healthy, untrained young males (mean ± SD: 17.9 ± 0.7 yrs of age) performed identical maximal cycle tests in the morning (08:00-11:00 h) and late afternoon (16:00-19:00 h) in random order. Cardiac variables were measured at rest, submaximal exercise, and maximal exercise by standard echocardiographic techniques. No differences in morning and afternoon testing values at rest or during exercise were observed for oxygen uptake, heart rate, cardiac output, or markers of systolic and diastolic myocardial function. Values at peak exercise for Vo(2) at morning and afternoon testing were 3.20 ± 0.49 and 3.24 ± 0.55 L min(-1), respectively, for heart rate 190 ± 11 and 188 ± 15 bpm, and for cardiac output 19.5 ± 2.8 and 19.8 ± 3.5 L min(-1). Coefficients of variation for morning and afternoon values for these variables were similar to those previously published for test-retest reproducibility. This study failed to demonstrate evidence for significant time-of-day variation in Vo(2)max or cardiac function during standard progressive exercise testing in adolescent males.

Pulmonary oxygen uptake and muscle deoxygenation kinetics during recovery in trained and untrained male adolescents.

Previous studies have demonstrated faster pulmonary oxygen uptake (VO2) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine VO2 kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, VO2max 54.9 ± 6.4 mL kg(-1) min(-1)) and 8 untrained (15 ± 0.5 years, VO2max 44.0 ± 4.6 mL kg(-1) min(-1)) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding "baseline" of exercise at a workload equivalent to 80% lactate threshold; VO2 (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of VO2 off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P < 0.01) and mean response time (trained 24.2 ± 9.2 s vs. untrained 34 ± 13 s, P = 0.05) of muscle deoxyhaemoglobin off-kinetics was faster in the trained subjects compared to the untrained subjects. VO2 kinetics was unaffected by training status; the faster muscle deoxyhaemoglobin kinetics in the trained subjects thus indicates slower blood flow kinetics during recovery from exercise compared to the untrained subjects.

Myocardial function and aerobic fitness in adolescent females.

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO(2)) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO(2) 43.5 ± 3.4 ml kg(-1) min(-1)) and nine untrained girls (peak VO(2) 36.0 ± 5.1 ml kg(-1) min(-1)) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m(-2)), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S') and diastolic (tissue Doppler E', mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.