O2 Uptake Kinetics Research Articles

Sodium Bicarbonate Ingestion Alters the Slow but Not the Fast Phase of V˙O2 Kinetics

The influence of metabolic alkalosis (ALK) on pulmonary O2 uptake (pVO2) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO2 kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. Seven healthy males completed step tests to a work rate requiring 80% pVO2max on six separate occasions: three times after ingestion of 0.3 g x kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO2 was measured breath-by-breath. NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO2 response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO2 slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 +/- 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO2 (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L x min(-1); P < 0.05). Metabolic alkalosis has no effect on phase II pVO2 kinetics but alters the pVO2 slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

The Adaptation of Oxygen Uptake, Limb Blood Flow, and Muscle Deoxygentation at the Onset of Moderate-Intensity Knee-Extension Exercise in Young and Old Adults

The slowed pulmonary O2 uptake (VO2p) kinetics (and muscle O2 consumption) of older adults may be limited by convective O2 delivery to the exercising limb. However, the effects of age on the kinetics of femoral artery blood flow (LBF) remain unknown. PURPOSE: To determine the effect of age on VO2p, LBF and muscle deoxygenation kinetics during moderate-intensity exercise. METHODS: 5 young (Y; 25 ± 2 yrs) and 5 old (O; 70 ± 6 yrs) male subjects performed repeated (n = 4) step-transitions (6 min) from an active baseline (3 W) to moderate-intensity (80% θL), alternate-leg, knee-extension (KE) exercise. VO2p was measured breath-by-breath by mass spectrometer and volume turbine. LBF was measured via Doppler ultrasound at the femoral artery. Deoxygenated hemoglobin/myoglobin (ΔHHb) of the vastus lateralis muscle was measured continuously by near-infrared spectroscopy. The VO2p, LBF and HHb data were filtered, time-aligned and ensemble-averaged to provide a single response for each subject, and then further averaged into 10 s (VO2p, LBF) or 5 s (ΔHHb) bins. VO2p data were fit with a monoexponential function from the phase 1- phase 2 interface to the end of exercise and LBF was fit from the onset to the end of exercise. Following a delay (HHbTD), HHb data were fit with a monoexponential function to 180 s to assess the adaptation of muscle deoxygenation during the adaptation period of VO2p. RESULTS: Phase 2 τVO2p was greater in O (45 ± 12 s) compared to Y (30 ± 5 s) during the on-transient of KE exercise. The magnitude of the steady-state increase in LBF (ΔLBF/Δ VO2p; O: 5.5 ± 1.3; Y: 5.3 ± 0.3) and the rate of increase of LBF (τLBF; O: 39 ± 19 s; Y: 29 ± 12 s) were not different between O and Y. HHbTD (O: 17 ± 4 s; Y: 17 ± 3 s), τHHb (O: 15 ± 8 s; Y: 10 ± 6 s) and the effective τHHb (HHbTD + τHHb; O: 32 ± 9 s; Y: 27 ± 5 s) were not different between groups. CONCLUSIONS: These results demonstrate a slower adaptation of VO2p in older subjects during moderate-intensity KE exercise but no significant age-related differences in the adaptation of bulk limb blood flow or muscle deoxygenation. The slower adaptation of muscle O2 consumption in O compared to Y and a similar adaptation of HHb (representing a faster contribution of HHb relative to the rise in VO2p in O compared to Y) would suggest that an impairment in microvascular flow/O2 delivery but not bulk limb blood flow contributes to the slower VO2p kinetics in O compared to Y.(Supported by NSERC)

Lactic acid accumulation is an advantage/disadvantage during muscle activity

POINT-COUNTERPOINT COMMENTSLactic acid accumulation is an advantage/disadvantage during muscle activityMark Burnley, Daryl P. Wilkerson, and Andrew M. JonesMark Burnley, Daryl P. Wilkerson, and Andrew M. JonesPublished Online:01 Aug 2006https://doi.org/10.1152/japplphysiol.00504.2006This is the final version - click for previous versionMoreSectionsPDF (29 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The following letter is in response to the Point:Counterpoint: “Lactic acid accumulation is an advantage/disadvantage during muscle activity” that appeared in the April issue ( http://jap.physiology.org/content/vol100/).To the Editor: Although the “received wisdom” is that an exercise-induced lactacidosis should impair subsequent exercise performance, such is not consistently the case. In recent work, we used exercise-induced elevations in blood [lactate] to alter the pulmonary oxygen uptake (V̇o2) response to high-intensity exercise, following from the work of Gerbino et al. (3). In doing so, we also addressed the influence of such protocols on exercise performance. Our findings demonstrate that prior heavy exercise [performed above the “lactate threshold” (LT)] followed by 10 min of passive recovery, resulting in a mild increase in blood [lactate] at exercise onset (“baseline” blood [lactate] ∼3.0 mM), substantially improves time to exhaustion during a subsequent bout of exhaustive exercise (by 30–60%; Ref. 4). Moreover, follow-up work measuring changes in mean power output during a 7 min “performance trial” demonstrated that both prior moderate exercise (below LT, baseline blood [lactate] ∼1.0 mM) and prior heavy exercise (baseline blood [lactate] ∼3.0 mM) increased performance by 2–3% in well-trained cyclists (2). In contrast, prior sprint exercise (baseline blood [lactate] ∼6.0 mM) led to a nonsignificant 1.8% reduction in performance. In agreement with the work of Bangsbo et al. (1) repeated bouts of sprint exercise (baseline blood lactate ∼7.7 mM) reduces time to exhaustion during subsequent exercise (5). It would seem, therefore, that the performance of prior heavy exercise improves exercise performance despite (because of?) mild elevations in blood [lactate], but that more intense prior activity is disadvantageous.REFERENCES1 Bangsbo J, Madsen K, Kiens B, and Richter EA. Effect of muscle acidity on muscle metabolism and fatigue during intense exercise in man. J Physiol 495: 587–596, 1996.Crossref | PubMed | ISI | Google Scholar2 Burnley M, Doust JH, and Jones AM. Effects of prior warm-up regime on severe-intensity cycling performance. Med Sci Sports Exerc 37: 838–845, 2005.Crossref | ISI | Google Scholar3 Gerbino A, Ward SA, and Whipp BJ. Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans. J Appl Physiol 80: 99–107, 1996.Link | ISI | Google Scholar4 Jones AM, Wilkerson DP, Burnley M, and Koppo K. Prior heavy exercise enhances performance during subsequent perimaximal exercise. Med Sci Sports Exerc 35: 2085–2092, 2003.Crossref | ISI | Google Scholar5 Wilkerson DP, Koppo K, Barstow TJ, and Jones AM. Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise. J Appl Physiol 97: 1227–1236, 2004.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 101Issue 2August 2006Pages 683-683 Copyright & PermissionsCopyright © 2006 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00504.2006PubMed16690787History Published online 1 August 2006 Published in print 1 August 2006 Metrics

Kinetics of Pulmonary O2 Uptake and Muscle Deoxygenation During Active and Passive Recovery

Kinetics of Pulmonary O2 Uptake and Muscle Deoxygenation During Active and Passive Recovery

Effects of Acute Creatine Kinase Inhibition on Skeletal Muscle O2 Uptake Kinetics

Effects of Acute Creatine Kinase Inhibition on Skeletal Muscle O2 Uptake Kinetics

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.

Influence of blood donation on O2 uptake on‐kinetics, peak O2 uptake and time to exhaustion during severe‐intensity cycle exercise in humans

We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed 'step' exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, - 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.

Oxygen Uptake and Muscle Desaturation Kinetics during Intermittent Cycling

To investigate the kinetics of O2 uptake (VO2) and m. vastus lateralis [deoxyhemoglobin] ([Hb]) (near-infrared spectroscopy) for supramaximal intermittent cycling. Six males performed a ramp test for determination of VO2peak and lactate threshold. On different days, they completed four intermittent "work:recovery" tests (10 s:20 s, 30 s:60 s, 60 s:120 s, 90 s:180 s) for 30 min or to the tolerable limit; "work" = 120% peak work rate (WRpeak) attained on the ramp, "recovery" = 20 W. Arterialized capillary [lactate] ([L]c) profiles were dependent on duty-cycle length and resembled those for constant-load exercise classically used to assign exercise intensity: 10 s:20 s-no increase (i.e., "moderate", with first-order VO2 kinetics); 30 s:60 s-increased but stable (i.e., "heavy," with first-order VO2 kinetics supplemented by a slow component (VO2 sc) that stabilizes); 60s:120s-progressive increase that was more marked for 90 s:180 s (i.e., "very heavy" or "severe," with first-order VO2 kinetics supplemented by a VO2 sc projecting to VO2peak). VO2 and Delta[Hb] oscillated with WR, the ensemble-averaged single-cycle oscillation amplitudes (peak-to-nadir) for each individual subject increasing with WR duty-cycle duration. In the 30-s:60-s test, with [L]c being elevated, there was also a tendency towards a modest VO2 sc, with an increase in individual VO2 peak values early in the test and VO2 not fully recovering back to baseline in recovery. This was more marked for the 60-s:120-s duty cycle: VO2 failed to recover completely back to baseline, and the peaks of the VO2 oscillations increased significantly with time (F = 30.7, P < 0.001); in some cases, VO2peak was attained and exhaustion rapidly ensued. VO2 kinetics in intermittent exercise over a range of duty-cycle durations tended to associate with blood [lactate] profiles, similarly to previous demonstrations for sustained constant-load exercise.

Linear relation between time constant of O2 uptake kinetics and total creatine in vitro

Linear relation between time constant of O2 uptake kinetics and total creatine in vitro

Muscle glycogen reduction in man: relationship between surface EMG activity and oxygen uptake kinetics during heavy exercise

The purpose of this study was to determine whether muscle glycogen reduction prior to exercise would alter muscle fibre recruitment pattern and change either on-transient O2 uptake (VO2) kinetics or the VO2 slow component. Eight recreational cyclists (VO2peak, 55.6 +/- 1.3 ml kg (-1) min(-1)) were studied during 8 min of heavy constant-load cycling performed under control conditions (CON) and under conditions of reduced type I muscle glycogen content (GR). VO2 was measured breath-by-breath for the determination of VO2 kinetics using a double-exponential model with independent time delays. VO2 was higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. The mean power frequency (MPF) of electromyography activity for the vastus medialis increased over time during both trials, with a greater rate of increase observed in the GR trial compared to the CON trial. The results suggest that the recruitment of additional type II motor units contributed to the slow component in both trials. An increase in fat metabolism and augmented type II motor unit recruitment contributed to the higher VO2 in the GR trial. However, the greater rate of increase in the recruitment of type II motor units in the GR trial may not have been of sufficient magnitude to further elevate the slow component when VO2 was already high and approaching VO2peak .

Influence of hyperoxia on pulmonary O2 uptake kinetics following the onset of exercise in humans

The purpose of this study was to examine the influence of hyperoxic gas (50% O2 in N2) inspiration on pulmonary oxygen uptake (V(O2)) kinetics during step transitions to moderate, severe and supra-maximal intensity cycle exercise. Seven healthy male subjects completed repeat transitions to moderate (90% of the gas exchange threshold, GET), severe (70% of the difference between the GET and V(O2) peak) and supra-maximal (105% V(O2) peak) intensity work rates while breathing either normoxic (N) or hyperoxic (H) gas before and during exercise. Hyperoxia had no significant effect on the Phase II V(O2) time constant during moderate (N: 28+/-3s versus H: 31+/-7s), severe (N: 32+/-9s versus H: 33+/-6s) or supra-maximal (N: 37+/-9s versus H: 37+/-9s) exercise. Hyperoxia resulted in a 45% reduction in the amplitude of the V(O2) slow component during severe exercise (N: 0.60+/-0.21 L min(-1) versus H: 0.33+/-0.17 L min(-1); P < 0.05) and a 15% extension of time to exhaustion during supra-maximal exercise (N: 173+/-28 s versus H: 198+/-41 s; P < 0.05). These results indicate that the Phase II V(O2) kinetics are not normally constrained by (diffusional) O2 transport limitations during moderate, severe or supra-maximal intensity exercise in young healthy subjects performing upright cycle exercise.

The V̇O2 Slow Component: Relationship between Plasma Ammonia and EMG Activity

An increased recruitment of type II muscle fibers has been suggested as a major cause of the slow component of O(2) uptake (VO(2)) kinetics. Furthermore, the rise in plasma ammonia (NH(3)) during high-intensity exercise, where a slow component is observed, has been associated with the activation of type II muscle fibers. Therefore, the purpose of this study was to examine the relationship between the VO(2) slow component, plasma NH3 concentration, and electromyography (EMG) responses during constant-load cycling. Eight healthy adults (mean age +/- SEM: 21.4 +/- 1.0 yr) performed 7 min of heavy constant-load exercise. The breath-by-breath VO(2) response was characterized using a two-term exponential model. Plasma NH(3) concentration was measured at rest, following 3 min of unloaded cycling and at 3 and 7 min of constant-load exercise. Surface EMG activity of the right vastus lateralis muscle was measured during the final 10 s of every minute of exercise. The amplitude of the slow component was 561 +/- 52 mL.min(-1), and occurred 132 +/- 11 s following the onset of constant-load exercise. Plasma NH(3) concentration increased significantly from 3 to 7 min of constant-load exercise by 32.2 +/- 2.9 micromol.L(-1). The rise in plasma NH(3) concentration correlated significantly with the amplitude of the slow component (r = 0.79, P < 0.05). The mean power frequency of the EMG increased significantly while the integrated EMG/VO(2) ratio remained constant over the duration of the slow component. The rise in NH(3) concentration and the amplitude and spectral components of the EMG are consistent with a progressive increase in the recruitment of type II muscle fibers during the slow component phase of exercise.

Effects of prior heavy-intensity exercise during single-leg knee extension on v̇o2 kinetics and limb blood flow

The effects of prior heavy-intensity exercise on O(2) uptake (Vo(2)) kinetics of a second heavy exercise may be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. This study examined the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with Vo(2) kinetics. Five young subjects completed five to eight repeats of two 6-min bouts of heavy-intensity one-legged, knee-extension exercise separated by 6 min of loadless exercise. Vo(2) was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. Vo(2) and blood flow velocity data were fit using a monoexponential model to identify phase II and phase III time periods and estimate the response amplitudes and time constants (tau). Phase II Vo(2) kinetics was speeded on the second heavy-intensity exercise [mean tau (SD), 29 (10) s to 24 (10) s, P < 0.05] with no change in the phase II (or phase III) amplitude. Qleg was elevated before the second exercise [1.55 (0.34) l/min to 1.90 (0.25) l/min, P < 0.05], but the amplitude and time course [tau, 25 (13) s to 35 (13) s] were not changed, such that throughout the transient the Qleg (and DeltaQleg/DeltaVo(2)) did not differ from the prior heavy exercise. Thus Vo(2) kinetics were accelerated on the second exercise, but the faster kinetics were not associated with changes in Qleg. Thus limb blood flow appears not to limit Vo(2) kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered Vo(2) response after heavy-intensity prior exercise.

Pulmonary O2 Uptake Kinetics In Sprint And Endurance Trained Master Athletes

Pulmonary O2 uptake (VO2) kinetics following the onset of exercise are slowed with advancing age beyond ∼ 40 years. Short-term exercise training interventions result in a speeding of VO kinetics in older individuals such that the time constant for the Phase 11VO response (τ) can approach that observed in young sedentary subjects. However, it is not known whether the speed of the VO2 kinetic response in 'elite' older athletes is similar to that observed in younger athletes. PURPOSE To examine the VO2 kinetic response to moderate intensity cycle exercise in endurance-trained and sprint-trained master athletes. METHODS 86 master athletes (aged 35–85yrs) who were competing at either the British or European veteran athletics championships acted as subjects, and were classified as either endurance (END: 800m-Marathon; n=42), or sprint (SPR: 100m-400m; n=44) specialists. Subjects completed two 6 min 'step' transitions to a work rate predicted to be of moderate intensity (i.e. below the lactate threshold, LT) on a cycle ergometer. Pulmonary gas exchange was measured breath-by-breath and fingertip blood samples were analysed for blood [lactate] before and after exercise. RESULTS Blood [lactate] data confirmed that the selected work rates were <LT. Analysis of variance revealed that SPR athletes had slower VO2 kinetics (i.e. greater ?) compared to END athletes (P <0.05): 35–44yrs (END: 24.9 ± 1.8 vs. SPR: 30.5 ± 5.0 s), 45–54yrs(END: 28.7 ±2.8 vs. SPR: 35.6 ±9.1 s), 55–64yrs (END: 23.7 ±4.7 vs. SPR: 34.0 ± 8.5 s), 65–74yrs (END: 28.0 ± 9.5 vs. SPR: 40.1 ± 20.6 s) and 75–85yrs (END: 31.3 ± 10.4 vs. SPR: 48.6 ± 18.3 s). However, there was no significant slowing of VO2 kinetics with age. CONCLUSION Elite master END athletes have similar × values to their younger counterparts (∼ 25 s) suggesting that chronic END training and/or genetic factors limit the slowing of VO2 kinetics with age in this population. The slower VO kinetics in SPR compared to END master athletes is consistent both with differences in physiology (e.g. muscle fiber type, oxidative/glycolytic capacity) and training between these specialist athletes.

Pulmonary O2 Uptake Kinetics In Sprint And Endurance Trained Master Athletes

Pulmonary O2 uptake (VO2) kinetics following the onset of exercise are slowed with advancing age beyond ∼ 40 years. Short-term exercise training interventions result in a speeding of VO kinetics in older individuals such that the time constant for the Phase 11VO response (τ) can approach that observed in young sedentary subjects. However, it is not known whether the speed of the VO2 kinetic response in 'elite' older athletes is similar to that observed in younger athletes. PURPOSE To examine the VO2 kinetic response to moderate intensity cycle exercise in endurance-trained and sprint-trained master athletes. METHODS 86 master athletes (aged 35–85yrs) who were competing at either the British or European veteran athletics championships acted as subjects, and were classified as either endurance (END: 800m-Marathon; n=42), or sprint (SPR: 100m-400m; n=44) specialists. Subjects completed two 6 min 'step' transitions to a work rate predicted to be of moderate intensity (i.e. below the lactate threshold, LT) on a cycle ergometer. Pulmonary gas exchange was measured breath-by-breath and fingertip blood samples were analysed for blood [lactate] before and after exercise. RESULTS Blood [lactate] data confirmed that the selected work rates were <LT. Analysis of variance revealed that SPR athletes had slower VO2 kinetics (i.e. greater ?) compared to END athletes (P <0.05): 35–44yrs (END: 24.9 ± 1.8 vs. SPR: 30.5 ± 5.0 s), 45–54yrs(END: 28.7 ±2.8 vs. SPR: 35.6 ±9.1 s), 55–64yrs (END: 23.7 ±4.7 vs. SPR: 34.0 ± 8.5 s), 65–74yrs (END: 28.0 ± 9.5 vs. SPR: 40.1 ± 20.6 s) and 75–85yrs (END: 31.3 ± 10.4 vs. SPR: 48.6 ± 18.3 s). However, there was no significant slowing of VO2 kinetics with age. CONCLUSION Elite master END athletes have similar × values to their younger counterparts (∼ 25 s) suggesting that chronic END training and/or genetic factors limit the slowing of VO2 kinetics with age in this population. The slower VO kinetics in SPR compared to END master athletes is consistent both with differences in physiology (e.g. muscle fiber type, oxidative/glycolytic capacity) and training between these specialist athletes.

Prior Arm Exercise Speeds the &amp;OV0312;O2 Kinetics during Arm Exercise above the Heart Level

To test the hypothesis that the initial O2 uptake kinetics during exercise where the rise in blood flow (and, by implication, O2 delivery) to the working muscles during an abrupt increase in exercise intensity is reduced (i.e., arm exercise performed above the level of the heart) would be faster when preceded by a bout of high-intensity exercise. Eleven physically active males completed two protocols, each consisting of two consecutive bouts of 6 min of high-intensity arm crank exercise separated by 6 min of recovery. In one protocol, the arm crank exercise was performed with the arms below the level of the heart (<HL); in the other, the arms were above the level of the heart (>HL). In the <HL protocol, the VO2 fast component time constant was not significantly affected by prior exercise (35.9+/-8.7 and 35.5+/-8.9 s in bouts 1 and 2, respectively). The amplitudes of the VO2 fast and slow component were respectively significantly higher and significantly lower in the second bout. In the >HL protocol, the amplitudes of the VO2 fast and slow component were unaffected by prior exercise, whereas the VO2 fast component time constant was significantly reduced in the second bout (49.8+/-22.1 vs 40.7+/-13.2 s; P<0.05). The results of this study demonstrate that prior high-intensity exercise caused a significant speeding of the VO2 fast component response during subsequent high-intensity arm crank exercise performed above, and not below, the level of the heart.

Effect of contractile duration on intracellular Po2kinetics inXenopussingle skeletal myocytes

It has been suggested that skeletal muscle O(2) uptake (Vo(2)) kinetics follow a first-order control model. Consistent with that, Vo(2) should show both 1) similar onset kinetics and 2) an on-off symmetry across submaximal work intensities regardless of the metabolic perturbation. To date, consensus on this issue has not been reached in whole body studies due to numerous confounding factors associated with O(2) availability and fiber-type recruitment. To test whether single myocytes demonstrate similar intracellular Po(2) (Pi(O(2))) on- and off-transient kinetics at varying work intensities, we studied Xenopus laevis single myocyte (n = 8) Pi(O(2)) via phosphorescence quenching during two bouts of electrically induced isometric muscle contractions of 200 (low)- and 400 (high)-ms contraction duration (1 contraction every 4 s, 15 min between trials, order randomized). The fall in Pi(O(2)), which is inversely proportional to the net increase in Vo(2), was significantly greater (P < 0.05) during the high (24.1 +/- 3.2 Torr) vs. low (17.4 +/- 1.6 Torr) contraction bout. However, the mean response time (MRT; time to 63% of the overall change) for the fall in Pi(O(2)) from resting baseline to end contractions was not different (high, 77.8 +/- 11.5 vs. low, 76.1 +/- 13.6 s; P > 0.05) between trials. The initial rate of change at contraction onset, defined as DeltaPi(O(2))/MRT, was significantly greater (P < 0.05) in high compared with low. Pi(O(2)) off-transient MRT from the end of the contraction bout to initial baseline was unchanged (high, 83.3 +/- 18.3 vs. low, 80.4 +/- 21.6 s; P > 0.05) between high and low trials. These data revealed that Pi(O(2)) dynamics in frog isolated skeletal myocytes were invariant despite differing contraction durations and, by inference, metabolic demands. Thus these findings demonstrate that mitochondria can respond more rapidly at the initial onset of contractions when challenged with an augmented metabolic stimulus in accordance with an apparent first-order rate law.

Prior heavy-intensity exercise speeds V̇o2 kinetics during moderate-intensity exercise in young adults

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.

Comparison of oxygen uptake kinetics during knee extension and cycle exercise

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.

Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.