Heavy-intensity Cycling Exercise Research Articles

The fourth dimension: physiological resilience as an independent determinant of endurance exercise performance.

Endurance exercise performance is known to be closely associated with the three physiological pillars of maximal O2 uptake ( ), economy or efficiency during submaximal exercise, and the fractional utilisation of (linked to metabolic/lactate threshold phenomena). However, while 'start line' values of these variables are collectively useful in predicting performance in endurance events such as the marathon, it is not widely appreciated that these variables are not static but are prone to significant deterioration as fatiguing endurance exercise proceeds. For example, the 'critical power' (CP), which is a composite of the highest achievable steady-state oxidative metabolic rate and efficiency (O2 cost per watt), may fall by an average of 10% following 2h of heavy intensity cycle exercise. Even more striking is that the extent of this deterioration displays appreciable inter-individual variability, with changes in CP ranging from <1% to ∼32%. The mechanistic basis for such differences in fatigue resistance or 'physiological resilience' are not resolved. However, resilience may be important in explaining superlative endurance performance and it has implications for the physiological evaluation of athletes and the design of interventions to enhance performance. This article presents new information concerning the dynamic plasticity of the three 'traditional' physiological variables and argues that physiological resilience should be considered as an additional component, or fourth dimension, in models of endurance exercise performance.

Prediction of oxygen uptake kinetics during heavy-intensity cycling exercise by machine-learning analysis.

Non-intrusive estimation of oxygen uptake (V̇O2) is possible with wearable sensor technology and artificial intelligence. V̇O2 kinetics have been accurately predicted during moderate exercise using easy-to-obtain sensor inputs. However, V̇O2 prediction algorithms for higher intensity exercise with inherent nonlinearities are still being refined. The purpose of this investigation was to test if a machine learning model can accurately predict dynamic V̇O2 across exercise intensities, including slower V̇O2 kinetics normally observed during heavy- compared to moderate-intensity exercise. Fifteen young healthy adults (7 females; peak V̇O2: 42±5 mL·min-1·kg-1) performed three different pseudorandom binary sequence (PRBS) exercise tests ranging in intensity from low-to-moderate, low-to-heavy, and ventilatory threshold-to-heavy work rates. A temporal convolutional network was trained to predict instantaneous V̇O2, with model inputs including heart rate, percent heart rate reserve, estimated minute ventilation, breathing frequency, and work rate. Frequency domain analyses between V̇O2 and work rate were used to evaluate measured and predicted V̇O2 kinetics. Predicted V̇O2 had low bias (-0.017 L·min-1, 95% limits of agreement: [-0.289, 0.254]), and was very strongly correlated (rrm=0.974, p<0.001) with the measured V̇O2. The extracted indicator of kinetics, mean normalized gain (MNG), was not different between predicted and measured V̇O2 responses (main effect: p=0.374, ηp2=0.01), and decreased with increasing exercise intensity (main effect: p<0.001, ηp2=0.64). Predicted and measured V̇O2 kinetics indicators were moderately correlated across repeated measurements (MNG: rrm=0.680, p<0.001). Therefore, the temporal convolutional network accurately predicted slower V̇O2 kinetics with increasing exercise intensity, enabling non-intrusive monitoring of cardiorespiratory dynamics across moderate- and heavy-exercise intensities.

Physiological and performance effects of dietary nitrate and N-acetylcysteine supplementation during prolonged heavy-intensity cycling

ABSTRACT The purpose of this study was to investigate effects of concurrent and independent administration of dietary nitrate (NO3 −), administered as NO3 –-rich beetroot juice (BR; ~12.4 mmol of NO3 −), and N-acetylcysteine (NAC; 70 mg·kg−1) on physiological responses during prolonged exercise and subsequent high-intensity exercise tolerance. Sixteen recreationally active males supplemented with NO3 –-depleted beetroot juice (PL) or BR for 6 days and ingested an acute dose of NAC or maltodextrin (MAL) 1 h prior to performing 1 h of heavy-intensity cycling exercise immediately followed by a severe-intensity time-to-exhaustion (TTE) test in four conditions: 1) PL+MAL, 2) PL+NAC, 3) BR+MAL and 4) BR+NAC. Pre-exercise plasma [NO3 −] and nitrite ([NO2 −]) were elevated following BR+NAC and BR+MAL (both P < 0.01) compared with PL+NAC and PL+MAL; plasma [cysteine] was increased in PL+NAC and BR+NAC (both P < 0.01) compared to PL+MAL. Muscle excitability declined over time during the prolonged cycling bout in all conditions but was better preserved in PL+NAC compared to BR+NAC (P < 0.01) and PL+MAL (P < 0.05). There was no effect of supplementation on subsequent TTE . These findings indicate that co-ingestion of BR and NAC does not appreciably alter physiological responses during prolonged heavy-intensity cycling or enhance subsequent exercise tolerance.

Heavy-intensity cycling and running work-rate associated to VO2max affects isokinetic strength, the dynamic control ratio but not the conventional H:Q ratio

BACKGROUND: Bilateral strength asymmetry and fatigue predispose athletes to various injuries and conventional methods appear to be poor predictors of lower extremity muscular performance under NF conditions. OBJECTIVE: The purpose of the study was to compare the conventional Hcon/Qcon (HQR) ratio and the dynamic control ratio (DCR: Hecc/Qcon) under non-fatiguing (NF) and fatiguing (F) conditions and verify the effects of heavy-intensity constant running and cycling exercise on the isokinetic performance. METHODS: Twenty healthy male participants performed running and cycling VO2max at work-rate associated with the achievement of VO2max (TTE). Isokinetic muscle strength performance was tested at 60 and 180∘/s before and after these sessions with 48-hour intervals. Quadriceps (QFR) and hamstring (HFR) muscle fatigue rates were also calculated during these sessions. Blood lactate concentration was measured before and two-minutes after running and cycling TTE. RESULTS: No between-condition differences were found for the HQR while the DCR decreased significantly at 180∘/s following cycling and running sessions (p&lt; 0.05). Cycling TTE was positively correlated with in dominant (r= 0.535, p= 0.015) and non-dominant (r= 0.446, p= 0.048) QFR. Positive correlations were also found between running TTE and dominant (r= 0.500, p= 0.25) and non-dominant (r= 0.465, p= 0.039) HFR. CONCLUSIONS: The DCR obtained at fast angular velocities following a strenuous exercise seems to be the best indicator of muscle performance while its assessment under F conditions reveals higher ratios compared to NF conditions and conventional methods.

Strategies to Ensure Accurate Calculation of Parameters of the VO2 Response Profile During Heavy Intensity Cycle Ergometer Exercise

BackgroundThe parameters of the VO2 response profile are obtained by fitting breath-by-breath VO2 data from an exercise test to an appropriate mathematical model. Several strategies have been recommended to ensure, or at least improve, the accuracy of the values.ObjectivesThe purpose of this study was to evaluate two strategies to enhance the accuracy of parameter estimates that describe the two-component VO2 response during heavy intensity exercise. The first was to use data from a number of tests rather than just one. The second was to ‘smooth’ the data, using three-breath, five-breath, or seven-breath rolling averages of the breath-by-breath VO2 data prior to fitting the data to the two-component model.MethodsTwenty participants (eight women and twelve men) performed six 6-min heavy-intensity (midway between the ventilatory threshold and VO2max) cycle ergometer tests. Breath-by-breath data and smoothed data from each test were fit to a two-component model. The parameter estimates from the first test, and the average of the values from the first two, first three, first four, first five, and all six tests were compared against the criterion value, which was the average of all six values obtained using five-breath averages.ResultsModeling five-breath averages of data from the first test generated values for the parameters that were closely related to the criterion values. Modeling data from two or three tests improved the accuracy slightly, but improvements were small, and negligible when more than three tests were included.ConclusionsDepending upon the accuracy required, that is depending upon how close each and every participant’s value must be to his or her ‘true’ value, smoothed data from one or two tests is sufficient to calculate the values that describe the two-parameter VO2 response profile in heavy intensity cycling exercise.

Changes in the power-duration relationship following prolonged exercise: estimation using conventional and all-out protocols and relationship with muscle glycogen.

It is not clear how the parameters of the power-duration relationship [critical power (CP) and W'] are influenced by the performance of prolonged endurance exercise. We used severe-intensity prediction trials (conventional protocol) and the 3-min all-out test (3MT) to measure CP and W' following 2 h of heavy-intensity cycling exercise and took muscle biopsies to investigate possible relationships to changes in muscle glycogen concentration ([glycogen]). Fourteen participants completed a rested 3MT to establish end-test power (Control-EP) and work done above EP (Control-WEP). Subsequently, on separate days, immediately following 2 h of heavy-intensity exercise, participants completed a 3MT to establish Fatigued-EP and Fatigued-WEP and three severe-intensity prediction trials to the limit of tolerance (Tlim) to establish Fatigued-CP and Fatigued-W'. A muscle biopsy was collected immediately before and after one of the 2-h exercise bouts. Fatigued-CP (256 ± 41 W) and Fatigued-EP (256 ± 52 W), and Fatigued-W' (15.3 ± 5.0 kJ) and Fatigued-WEP (14.6 ± 5.3 kJ), were not different (P > 0.05) but were ~11% and ~20% lower than Control-EP (287 ± 46 W) and Control-WEP (18.7 ± 4.7 kJ), respectively (P < 0.05). The change in muscle [glycogen] was not significantly correlated with the changes in either EP (r = 0.19) or WEP (r = 0.07). The power-duration relationship is adversely impacted by prolonged endurance exercise. The 3MT provides valid estimates of CP and W' following 2 h of heavy-intensity exercise, but the changes in these parameters are not primarily determined by changes in muscle [glycogen].

Strategies to Ensure Accurate Calculation of Parameters of the VO2 Response Profile During Heavy Intensity Cycle Ergometer Exercise

Background: The parameters of the VO2 response profile are obtained by fitting breath-by-breath VO2 data from an exercise test to an appropriate mathematical model. Several strategies have been recommended to ensure, or at least improve, the accuracy of the values. Objectives: The purpose of this study was to evaluate two strategies to enhance the accuracy of parameter estimates that describe the two-component VO2 response during heavy intensity exercise. The first was to use data from a number of tests rather than just one. The second was to ‘smooth’ the data, using three-breath, five-breath, or seven-breath rolling averages of the breath-by-breath VO2 data prior to fitting the data to the two-component model. Methods: Twenty participants (eight women and twelve men) performed six 6-min heavy-intensity (midway between the ventilatory threshold and VO2max) cycle ergometer tests. Breath-by-breath data and smoothed data from each test were fit to a two-component model. The parameter estimates from the first test, and the average of the values from the first two, first three, first four, first five, and all six tests were compared against the criterion value, which was the average of all six values obtained using five-breath averages. Results: Modeling five-breath averages of data from the first test generated values for the parameters that were closely related to the criterion values. Modeling data from two or three tests improved the accuracy slightly, but improvements were small, and negligible when more than three tests were included. Conclusions: Depending upon the accuracy required, that is depending upon how close each and every participant’s value must be to his or her ‘true’ value, smoothed data from one or two tests is sufficient to calculate the values that describe the two-parameter VO2 response profile in heavy intensity cycling exercise.

Pulmonary oxygen uptake and muscle deoxygenation kinetics during heavy intensity cycling exercise in patients with emphysema and idiopathic pulmonary fibrosis

BackgroundLittle is known about the mechanistic basis for the exercise intolerance characteristic of patients with respiratory disease; a lack of clearly defined, distinct patient groups limits interpretation of many studies. The purpose of this pilot study was to investigate the pulmonary oxygen uptake ( overset{.}{V} O2) response, and its potential determinants, in patients with emphysema and idiopathic pulmonary fibrosis (IPF).MethodsFollowing a ramp incremental test for the determination of peak overset{.}{V} O2 and the gas exchange threshold, six emphysema (66 ± 7 years; FEV1, 36 ± 16%), five IPF (65 ± 12 years; FEV1, 82 ± 11%) and ten healthy control participants (63 ± 6 years) completed three repeat, heavy-intensity exercise transitions on a cycle ergometer. Throughout each transition, pulmonary gas exchange, heart rate and muscle deoxygenation ([HHb], patients only) were assessed continuously and subsequently modelled using a mono-exponential with ( overset{.}{V} O2, [HHb]) or without (HR) a time delay.ResultsThe overset{.}{V} O2 phase II time-constant (τ) did not differ between IPF and emphysema, with both groups significantly slower than healthy controls (Emphysema, 65 ± 11; IPF, 69 ± 7; Control, 31 ± 7 s; P < 0.05). The HR τ was slower in emphysema relative to IPF, with both groups significantly slower than controls (Emphysema, 87 ± 19; IPF, 119 ± 20; Control, 58 ± 11 s; P < 0.05). In contrast, neither the [HHb] τ nor [HHb]:O2 ratio differed between patient groups.ConclusionsThe slower overset{.}{V} O2 kinetics in emphysema and IPF may reflect poorer matching of O2 delivery-to-utilisation. Our findings extend our understanding of the exercise dysfunction in patients with respiratory disease and may help to inform the development of appropriately targeted rehabilitation strategies.

The effect of priming exercise on O2 uptake kinetics, muscle O2 delivery and utilization, muscle activity, and exercise tolerance in boys

This study used priming exercise in young boys to investigate (i) how muscle oxygen delivery and oxygen utilization, and muscle activity modulate oxygen uptake kinetics during exercise; and (ii) whether the accelerated oxygen uptake kinetics following priming exercise can improve exercise tolerance. Seven boys that were aged 11.3 ± 1.6 years completed either a single bout (bout 1) or repeated bouts with 6 min of recovery (bout 2) of very heavy-intensity cycling exercise. During the tests oxygen uptake, muscle oxygenation, muscle electrical activity and exercise tolerance were measured. Priming exercise most likely shortened the oxygen uptake mean response time (change, ±90% confidence limits; -8.0 s, ±3.0), possibly increased the phase II oxygen uptake amplitude (0.11 L·min(-1), ±0.09) and very likely reduced the oxygen uptake slow component amplitude (-0.08 L·min(-1), ±0.07). Priming resulted in a likely reduction in integrated electromyography (-24% baseline, ±21% and -25% baseline, ±19) and a very likely reduction in Δ deoxyhaemoglobin/Δoxygen uptake (-0.16, ±0.11 and -0.09, ±0.05) over the phase II and slow component portions of the oxygen uptake response, respectively. A correlation was present between the change in tissue oxygenation index during bout 2 and the change in the phase II (r = -0.72, likely negative) and slow component (r = 0.72, likely positive) oxygen uptake amplitudes following priming exercise, but not for muscle activity. Exercise tolerance was likely reduced (change -177 s, ±180) following priming exercise. The altered phase II and slow component oxygen uptake amplitudes in boys following priming exercise are linked to an improved localised matching of muscle oxygen delivery to oxygen uptake and not muscle electrical activity. Despite more rapid oxygen uptake kinetics following priming exercise, exercise tolerance was not enhanced.

Influence of hormone replacement therapy and aerobic exercise training on oxygen uptake kinetics in postmenopausal women

The purpose of this study was to determine the effects of aerobic exercise training on the adjustment of pulmonary oxygen (O2) uptake (VO2p) kinetics in postmenopausal women in 2 groups: those using hormone replacement therapy (HRT) (HRT group) (n = 7, aged 56 ± 4 years) and those not using HRT (nonHRT group) (n = 8, aged 60 ± 5 years). The influence of training (cycle-ergometer 3 times per week for 6 weeks) on step transitions to both moderate-intensity (80% of the gas exchange threshold) and heavy-intensity (Δ50) cycling exercise was studied. Breath-by-breath VO2p data were collected using a mass spectrometer. There were no differences in baseline characteristics between the HRT and nonHRT groups. Moderate-intensity exercise VO2p kinetics were significantly speeded (p < 0.05) with the τVO2p decreasing from 46 ± 8 s before training to 32 ± 4 s after training. Similarly, during the heavy-intensity exercise, on-transient phase 2 τVO2p was reduced from before training (48 ± 7 s) to after training (38 ± 6 s). The use of HRT did not influence the effect of the endurance exercise training on τVO2p during moderate or heavy exercise in healthy postmenopausal women. To provide insight into the mechanism of adjustment, knee extension exercise was studied, and the VO2p kinetics were significantly speeded (p < 0.05), with the τVO2p of the knee extension exercise decreasing from 62.2 ± 18.3 s before training to 48.0 ± 16.2 s after training. Thus, 6 weeks of exercise training resulted in appreciably faster cycling phase 2 VO2p kinetics during moderate and heavy exercise in older women, independent of HRT use.

Stretching and deep and superficial massage do not influence blood lactate levels after heavy-intensity cycle exercise

The study aimed to assess the role of deep and superficial massage and passive stretching recovery on blood lactate concentration ([La−]) kinetics after a fatiguing exercise compared to active and passive recovery. Nine participants (age 23 ± 1 years; stature 1.76 ± 0.02 m; body mass 74 ± 4 kg) performed on five occasions an 8-min fatiguing exercise at 90% of maximum oxygen uptake, followed by five different 10-min interventions in random order: passive and active recovery, deep and superficial massage and stretching. Interventions were followed by 1 hour of recovery. Throughout each session, maximum voluntary contraction (MVC) of the knee extensor muscles, [La−], cardiorespiratory and metabolic variables were determined. Electromyographic signal (EMG) from the quadriceps muscles was also recorded. At the end of the fatiguing exercise, [La−], MVC, EMG amplitude, and metabolic and cardiorespiratory parameters were similar among conditions. During intervention administration, [La−] was lower and metabolic and cardiorespiratory parameters were higher in active recovery compared to the other modalities (P < 0.05). Stretching and deep and superficial massage did not alter [La−] kinetics compared to passive recovery. These findings indicate that the pressure exerted during massage administration and stretching manoeuvres did not play a significant role on post-exercise blood La− levels.

Effects of prior heavy-intensity exercise on oxygen uptake and muscle deoxygenation kinetics of a subsequent heavy-intensity cycling and knee-extension exercise

This study examined the effects of prior heavy-intensity exercise on the adjustment of pulmonary oxygen uptake (VO(2p)) and muscle deoxygenation Δ[HHb] during the transition to subsequent heavy-intensity cycling (CE) or knee-extension (KE) exercise. Nine young adults (aged 24 ± 5 years) performed 4 repetitions of repeated bouts of heavy-intensity exercise separated by light-intensity CE and KE, which included 6 min of baseline exercise, a 6-min step of heavy-intensity exercise (H1), 6-min recovery, and a 6-min step of heavy-intensity exercise (H2). Exercise was performed at 50 r·min(-1) or contractions per minute per leg. Oxygen uptake (VO(2)) mean response time was ∼20% faster (p < 0.05) during H2 compared with H1 in both modalities. Phase 2 time constants (τ) were not different between heavy bouts of CE (H1, 29.6 ± 6.5 s; H2, 28.0 ± 4.6 s) or KE exercise (H1, 31.6 ± 6.7 s; H2, 29.8 ± 5.6 s). The VO(2) slow component amplitude was lower (p < 0.05) in H2 in both modalities (CE, 0.19 ± 0.06 L·min(-1); KE, 0.12 ± 0.07 L·min(-1)) compared with H1 (CE, 0.29 ± 0.09 L·min(-1); KE, 0.18 ± 0.07 L·min(-1)), with the contribution of the slow component to the total VO(2) response reduced (p < 0.05) in H2 during both exercise modes. The effective τHHb was similar between bouts for CE (H1, 18.2 ± 3.0 s; H2, 18.0 ± 3.6 s) and KE exercise (H1, 26.0 ± 7.0 s; H2, 24.0 ± 5.8 s). The ΔHHb slow component was reduced during H2 in both CE and KE (p < 0.05). In conclusion, phase 2 VO(2p) was unchanged with priming exercise; however, a faster mean response time of VO(2p) during the heavy-intensity exercise preceded by a priming heavy-intensity exercise was attributed to a smaller slow component and reduced muscle deoxygenation indicative of improved muscle O(2) delivery during the second bout of exercise.

The influence of priming exercise on oxygen uptake, cardiac output, and muscle oxygenation kinetics during very heavy-intensity exercise in 9- to 13-yr-old boys

The present study examined the effect of priming exercise on O(2) uptake (Vo(2)) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O(2) delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II Vo(2) tau, 3) elevate the phase II Vo(2) total amplitude, and 4) reduce the magnitude of the Vo(2) slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests Vo(2), muscle oxygenation (near infrared spectroscopy), and cardiac output (Q) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q at baseline and throughout the second exercise bout. The phase II Vo(2) tau was not altered by priming exercise (bout 1: 22 + or - 7 s vs. bout 2: 20 + or - 4 s; P = 0.30). However, the time constant describing the entire Vo(2) response from start to end of exercise was accelerated (bout 1: 43 + or - 8 s vs. bout 2: 36 + or - 5 s; P = 0.002) due to an increased total phase II Vo(2) amplitude (bout 1: 1.73 + or - 0.33 l/min vs. bout 2: 1.80 + or - 0.59 l/min; P = 0.002) and a reduced Vo(2) slow component amplitude (bout 1: 0.18 + or - 0.08 l/min vs. bout 2: 0.12 + or - 0.09 l/min; P = 0.048). These results suggest that phase II Vo(2) kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the Vo(2) total phase II and slow component amplitudes may be O(2) delivery sensitive.

Longitudinal Changes in the Oxygen Uptake Kinetic Response to Heavy-Intensity Exercise in 14- to 16-Year-Old Boys

This study examined longitudinal changes in the pulmonary oxygen uptake (pV̇O2) kinetic response to heavy-intensity exercise in 14–16 yr old boys. Fourteen healthy boys (age 14.1 ± 0.2 yr) completed exercise testing on two occasions with a 2-yr interval. Each participant completed a minimum of three ‘step’ exercise transitions, from unloaded pedalling to a constant work rate corresponding to 40% of the difference between the pV̇O2 at the gas exchange threshold and peak pV̇O2 (40% Δ). Over the 2-yr period a significant increase in the phase II time constant (25 ± 5 vs. 30 ± 5 s; p = .002, ω2 = 0.34), the relative amplitude of the pV̇O2 slow component (9 ± 5 vs. 13 ± 4%; p = .036, ω2 = 0.14) and the pV̇O2 gain at end-exercise (11.6 ± 0.6 vs. 12.4 ± 0.7 mL·min−1·W−1; p &lt; .001, ω2 = 0.42) were observed. These data indicate that the control of oxidative phosphorylation in response to heavy-intensity cycling exercise is age-dependent in teenage boys.

Heterogeneity of muscle deoxygenation kinetics during two bouts of repeated heavy exercises

This study examines the effect of prior heavy exercise on the spatial distribution of muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Young untrained male adults (n = 16) performed two consecutive bouts of 6 min of high intensity cycle exercise separated by 6 min at 35 W. Muscle deoxygenation (HHb) was monitored continuously by near-infrared spectroscopy at eight sites in the quadriceps. Prior heavy exercise reduced the delay before the increase in HHb (9 +/- 2 vs. 5 +/- 2 s; P < 0.001). The standard deviation of TD HHb of the eight sites was decreased by the performance of prior exercise (1.1 +/- 0.5 vs. 0.8 +/- 0.4 s; P < 0.05). The transient decrease in HHb during the first 10 s of exercise was less during the second bout than during the first bout (0.6 +/- 0.6 vs. 0.3 +/- 0.3 A.U.; P < 0.01). The standard deviation of this decrease was also reduced by prior exercise (0.5 +/- 0.3 vs. 0.3 +/- 0.2 A.U.; P < 0.01). Lastly, prior exercise decreased significantly the standard deviation of the HHb rise during the time period corresponding to the pulmonary VO(2) slow component. These results indicate that prior heavy exercise reduced the spatial heterogeneity of muscle deoxygenation kinetics at the early onset of heavy exercise and during the development of the pulmonary VO(2) slow component. It indicates that the distribution of the VO(2)/O(2) delivery ratio within muscle was improved by the performance of a prior exercise.

Influence of Blood Donation on Oxygen Uptake Kinetics During Moderate and Heavy Intensity Cycle Exercise

The purpose of this study was to determine the effects of a reduced whole body blood volume on the kinetic response of VO(2) during moderate and heavy intensity exercise. Six males and four females (age, 21+/-2 yrs; height, 175.2+/-5.1 cm; weight, 66.4+/-2.8 kg; VO(2)max, 53.0+/-4.1 ml x kg (-1) x min(-1)), completed a square-wave cycling ramp test to determine ventilatory threshold (VT) and VO(2max). Kinetics trials were completed 24 h pre and post donation of 450 cm (3) of blood. The kinetics trials were moderate intensity (80%VT) and heavy intensity (Delta50% VT - VO(2max)). Breath-by-breath gas exchange, heart rate, blood pressure, haemoglobin O(2) saturation, and blood [lactate] were measured throughout the trials. Post-donation haemoglobin, haematocrit and erythrocyte count were all significantly reduced (p<or= 0.05). Blood donation caused a significant increase in resting heart rate (P<or= 0.05). There were non-significant differences in the time constants or amplitude of phase II VO(2) kinetics in either moderate or heavy exercise (p>or= 0.05), or in the amplitude of the slow component. The capacity of the cardiovascular system to meet the metabolic demands of skeletal muscle at the onset of exercise does not limit the oxygen uptake.

Longitudinal Changes in the Oxygen Uptake Kinetic Response to Heavy-Intensity Exercise in 14- to 16-Year-Old Boys

This study examined longitudinal changes in the pulmonary oxygen uptake (pVO(2)) kinetic response to heavy-intensity exercise in 14-16 yr old boys. Fourteen healthy boys (age 14.1 +/- 0.2 yr) completed exercise testing on two occasions with a 2-yr interval. Each participant completed a minimum of three 'step' exercise transitions, from unloaded pedalling to a constant work rate corresponding to 40% of the difference between the pVO(2) at the gas exchange threshold and peak pVO(2) (40% Delta). Over the 2-yr period a significant increase in the phase II time constant (25 +/- 5 vs. 30 +/- 5 s; p = .002, omega(2) = 0.34), the relative amplitude of the pVO(2) slow component (9 +/- 5 vs. 13 +/- 4%; p = .036, omega(2) = 0.14) and the pVO(2) gain at end-exercise (11.6 +/- 0.6 vs. 12.4 +/- 0.7 mL x min(-1) x W(-1); p < .001, omega(2) = 0.42) were observed. These data indicate that the control of oxidative phosphorylation in response to heavy-intensity cycling exercise is age-dependent in teenage boys.

Thigh muscle activation distribution and pulmonary V̇o2kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise.

Effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of subsequent heavy exercise

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.

Effects of “priming” exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.