scholarly journals O2 uptake kinetics during exercise at peak O2 uptake

2003 ◽  
Vol 95 (5) ◽  
pp. 2014-2022 ◽  
Author(s):  
Barry W. Scheuermann ◽  
Thomas J. Barstow

Compared with moderate- and heavy-intensity exercise, the adjustment of O2 uptake (V̇o2) to exercise intensities that elicit peak V̇o2 has received relatively little attention. This study examined the V̇o2 response of 21 young, healthy subjects (25 ± 6 yr; mean ± SD) during cycle ergometer exercise to step transitions in work rate (WR) corresponding to 90, 100, and 110% of the peak WR achieved during a preliminary ramp protocol (15-30 W/min). Gas exchange was measured breath by breath and interpolated to 1-s values. V̇o2 kinetics were determined by use of a two- or three-component exponential model to isolate the time constant (τ2) as representative of V̇o2 kinetics and the amplitude (Amp) of the primary fast component independent of the appearance of any V̇o2 slow component. No difference in V̇o2 kinetics was observed between WRs (τ90 = 24.7 ± 9.0; τ100 = 22.8 ± 6.7; τ110 = 21.5 ± 9.2 s, where subscripts denote percent of peak WR; P > 0.05); nor in a subgroup of eight subjects was τ2 different from the value for moderate-intensity (<lactate threshold) exercise (τ2 = 25 ± 12 s, P > 0.05). As expected, the Amp increased with increasing WRs (Amp90 = 2,089 ± 548; Amp100 = 2,165 ± 517; Amp110 = 2,225 ± 559 ml/min; Amp90 vs. Amp110, P < 0.05). However, the gain (G) of the V̇o2 response (ΔV̇o2/ΔWR) decreased with increasing WRs (G90 = 8.5 ± 0.6; G100 = 7.9 ± 0.6; G110 = 7.3 ± 0.6 ml·min-1·W-1; P < 0.05). The Amp of the primary component approximated 85, 88, and 89% of peak V̇o2 during 90, 100, and 110% WR transitions, respectively. The results of the present study demonstrate that, compared with moderate- and heavy-intensity exercise, the gain of the V̇o2 response (as ΔV̇o2/ΔWR) is reduced for exercise transitions in the severe-intensity domain, but the approach to this gain is well described by a common time constant that is invariant across work intensities. The lower ΔV̇o2/ΔWR may be due to an insufficient adjustment of the cardiovascular and/or pulmonary systems that determine O2 delivery to the exercising muscles or due to recruitment of motor units with lower oxidative capacity, after the onset of exercise in the severe-intensity domain.

Author(s):  
Ana Catarina Sousa ◽  
Gregoire P. Millet ◽  
João Viana ◽  
Jaime Milheiro ◽  
Vítor Reis

AbstractWe investigated the effects of hypoxia on matched-severe intensity exercise and on the parameters of the power-duration relationship. Fifteen trained subjects performed in both normoxia and normobaric hypoxia (FiO2=0.13, ~3000 m) a maximal incremental test, a 3 min all-out test (3AOT) and a transition from rest to an exercise performed to exhaustion (Tlim) at the same relative intensity (80%∆). Respiratory and pulmonary gas-exchange variables were continuously measured (K5, Cosmed, Italy). Tlim test’s V̇O2 kinetics was calculated using a two-component exponential model. V̇O2max (44.1±5.1 vs. 58.7±6.4 ml.kg-1.min-1, p<0.001) was decreased in hypoxia. In Tlim, time-to-exhaustion sustained was similar (454±130 vs. 484±169 s) despite that V̇O2 kinetics was slower (τ1: 31.1±5.8 vs. 21.6±4.7 s, p<0.001) and the amplitude of the V̇O2 slow component lower (12.4±5.4 vs. 20.2±5.7 ml.kg-1.min-1, p<0.05) in hypoxia. CP was reduced (225±35 vs. 270±49 W, p<0.001) but W’ was unchanged (11.3±2.9 vs. 11.4±2.7 kJ) in hypoxia. The changes in CP/V̇O2max were positively correlated with changes in W’ (r = 0.58, p<0.05). The lower oxygen availability had an impact on aerobic related physiological parameters, but exercise tolerance is similar between hypoxia and normoxia when the relative intensity is matched despite a slower V̇O2 kinetics in hypoxia.


2004 ◽  
Vol 97 (2) ◽  
pp. 460-466 ◽  
Author(s):  
Samantha G. Fawkner ◽  
Neil Armstrong

The purpose of this study was to investigate longitudinal changes with age in the kinetic response to cycling at heavy-intensity exercise in boys and girls. Twenty-two prepubertal children (13 male, 9 female) carried out a series of exercise tests on two test occasions with a 2-yr interval. On each test occasion, the subject completed multiple transitions from baseline to 40% of the difference between their previously determined V-slope and peak O2 uptake (V̇o2) for 9 min on an electronically braked cycle ergometer. Each subject's breath-by-breath responses were interpolated to 1-s intervals, time aligned, and averaged. The data after phase 1 were fit with 1) a double exponential model and 2) a single exponential model within a fitting window that was previously identified to exclude the slow component. There were no significant differences in the parameters of the primary component between each model. Subsequent analysis was carried out using model 2. The V̇o2 slow component was computed as the difference between the amplitude of the primary component and the end-exercise V̇o2 and was expressed as the percent contribution to the total change in V̇o2. Over the 2-yr period, the primary time constant (boys 16.8 ± 5.3 and 21.7 ± 5.3 s, girls 21.1 ± 8.1 and 26.4 ± 8.4 s, first and second occasion, respectively) and the relative amplitude of the slow component (boys 9.4 ± 4.6 and 13.8 ± 5.3%, girls 10.3 ± 2.4 and 15.5 ± 2.8%, first and second occasion, respectively) significantly increased with no sex differences. The data demonstrate that children do display a slow-component response to exercise and are consistent with an age-dependent change in the muscles' potential for O2 utilization.


2005 ◽  
Vol 288 (1) ◽  
pp. R212-R220 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Tomoyuki Shiojiri ◽  
Narihiko Kondo ◽  
Yoshiyuki Fukuba ◽  
...  

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 O2 uptake (pV̇o2) kinetics and 2) to characterize the muscle blood flow, muscle V̇o2 (mV̇o2), and pV̇o2 kinetics during KE to investigate the rate-limiting factor(s) of pV̇o2 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 pV̇o2 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 mV̇o2 at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pV̇o2 for both moderate and heavy exercise was higher during KE (∼12 ml·W−1·min−1) compared with CE (∼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 mV̇o2 during heavy KE [25.8 ± 9.0 s (SD)] was not significantly different from that of the phase II pV̇o2. Moreover, the slow component of pV̇o2 evident for the heavy KE reflected the gradual increase in mV̇o2. The initial LBF kinetics after onset of KE were significantly faster than the phase II pV̇o2 kinetics (moderate: time constant LBF = 8.0 ± 3.5 s, pV̇o2 = 32.7 ± 5.6 s, P < 0.05; heavy: LBF = 9.7 ± 2.0 s, pV̇o2 = 29.9 ± 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pV̇o2. 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 pV̇o2, consistent with an intramuscular limitation to V̇o2 kinetics, i.e., a microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia.


2006 ◽  
Vol 1 (4) ◽  
pp. 361-374 ◽  
Author(s):  
Stephen B. Draper ◽  
Dan M. Wood ◽  
Jo Corbett ◽  
David V.B. James ◽  
Christopher R. Potter

We tested the hypothesis that prior heavy-intensity exercise reduces the difference between asymptotic oxygen uptake (VO2) and maximum oxygen uptake (VO2max) during exhaustive severe-intensity running lasting ≍2 minutes. Ten trained runners each performed 2 ramp tests to determine peak VO2 (VO2peak) and speed at venti-latory threshold. They performed exhaustive square-wave runs lasting ≍2 minutes, preceded by either 6 minutes of moderate-intensity running and 6 minutes rest (SEVMOD) or 6 minutes of heavy-intensity running and 6 minutes rest (SEVHEAVY). Two transitions were completed in each condition. VO2 was determined breath by breath and averaged across the 2 repeats of each test; for the square-wave test, the averaged VO2 response was then modeled using a monoexponential function. The amplitude of the VO2 response to severe-intensity running was not different in the 2 conditions (SEVMOD vs SEVHEAVY; 3925 ± 442 vs 3997 ± 430 mL/min, P = .237), nor was the speed of the response (τ; 9.2 ± 2.1 vs 10.0 ± 2.1 seconds, P = .177). VO2peak from the square-wave tests was below that achieved in the ramp tests (91.0% ± 3.2% and 92.0% ± 3.9% VO2peak, P < .001). There was no difference in time to exhaustion between conditions (110.2 ± 9.7 vs 111.0 ± 15.2 seconds, P = .813). The results show that the primary VO2 response is unaffected by prior heavy exercise in running performed at intensities at which exhaustion will occur before a slow component emerges.


1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)


1997 ◽  
Vol 83 (4) ◽  
pp. 1235-1241 ◽  
Author(s):  
I. Langsetmo ◽  
G. E. Weigle ◽  
M. R. Fedde ◽  
H. H. Erickson ◽  
T. J. Barstow ◽  
...  

Langsetmo, I., G. E. Weigle, M. R. Fedde, H. H. Erickson, T. J. Barstow, and D. C. Poole.V˙o 2 kinetics in the horse during moderate and heavy exercise. J. Appl. Physiol. 83(4): 1235–1241, 1997.—The horse is a superb athlete, achieving a maximal O2 uptake (∼160 ml ⋅ min−1 ⋅ kg−1) approaching twice that of the fittest humans. Although equine O2 uptake (V˙o 2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peakV˙o 2(V˙o 2 peak), and kinetic features of theirV˙o 2 response to “square-wave” work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 ± 0.7 m/s (i.e., between Tlac andV˙o 2 peak) sustained for 6 min. V˙o 2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate.V˙o 2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (τ1 = 10.0 ± 0.9 s) that followed a time delay (TD1 = 18.9 ± 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 ± 1.2 s); however, the phase 2 time constant was significantly slower (τ1 = 20.7 ± 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase inV˙o 2 became evident 135.7 ± 28.5 s after the exercise transition. This “slow component” accounted for ∼12% (5.8 ± 2.7 l/min) of the net increase in exercise V˙o 2. We conclude that, at exercise intensities below and above Tlac, qualitative features ofV˙o 2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2utilization within equine muscle fibers.


Author(s):  
Alan Chorley ◽  
Richard P. Bott ◽  
Simon Marwood ◽  
Kevin L. Lamb

Abstract Purpose The aim of this study was to investigate the individual $$W^{^{\prime}}$$ W ′ reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal mathematical model to describe $$W^{^{\prime}}$$ W ′ reconstitution. Methods Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; $$\dot{V}{\text{O}}_{2\max }$$ V ˙ O 2 max 58.6 ± 7.1 mL kg min−1) completed three incremental ramps (20 W min−1) to the limit of tolerance with varying recovery durations (15–360 s) on 5–9 occasions. $$W^{^{\prime}}$$ W ′ reconstitution was measured following the first and second recovery periods against which mono-exponential and bi-exponential models were compared with adjusted R2 and bias-corrected Akaike information criterion (AICc). Results A bi-exponential model outperformed the mono-exponential model of $$W^{^{\prime}}$$ W ′ reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adjR2 = 0.999) for the first recovery when optimised with parameters of fast component (FC) amplitude = 50.67%; slow component (SC) amplitude = 49.33%; time constant (τ)FC = 21.5 s; τSC = 388 s. Following the second recovery, W′ reconstitution reduced by 9.1 ± 7.3%, at 180 s and 8.2 ± 9.8% at 240 s resulting in an increase in the modelled τSC to 716 s with τFC unchanged. Individual bi-exponential models also fit well (adjR2 = 0.978 ± 0.017) with large individual parameter variations (FC amplitude 47.7 ± 17.8%; first recovery: (τ)FC = 22.0 ± 11.8 s; (τ)SC = 377 ± 100 s; second recovery: (τ)FC = 16.3.0 ± 6.6 s; (τ)SC = 549 ± 226 s). Conclusions W′ reconstitution kinetics were best described by a bi-exponential model consisting of distinct fast and slow phases. The amplitudes of the FC and SC remained unchanged with repeated bouts, with a slowing of W′ reconstitution confined to an increase in the time constant of the slow component.


2009 ◽  
Vol 106 (6) ◽  
pp. 1875-1887 ◽  
Author(s):  
Stephen J. Bailey ◽  
Daryl P. Wilkerson ◽  
Fred J. DiMenna ◽  
Andrew M. Jones

We hypothesized that a short-term training program involving repeated all-out sprint training (RST) would be more effective than work-matched, low-intensity endurance training (ET) in enhancing the kinetics of oxygen uptake (V̇o2) and muscle deoxygenation {deoxyhemoglobin concentration ([HHb])} following the onset of exercise. Twenty-four recreationally active subjects (15 men, mean ± SD: age 21 ± 4 yr, height 173 ± 9 cm, body mass 71 ± 11 kg) were allocated to one of three groups: RST, which completed six sessions of four to seven 30-s RSTs; ET, which completed six sessions of work-matched, moderate-intensity cycling; and a control group (CON). All subjects completed moderate-intensity and severe-intensity “step” exercise transitions before (Pre) and after the 2-wk intervention period (Post). Following RST, [HHb] kinetics were speeded, and the amplitude of the [HHb] response was increased during both moderate and severe exercise ( P < 0.05); the phase II V̇o2 kinetics were accelerated for both moderate (Pre: 28 ± 8, Post: 21 ± 8 s; P < 0.01) and severe (Pre: 29 ± 5, Post: 23 ± 5 s; P < 0.05) exercise; the amplitude of the V̇o2 slow component was reduced (Pre: 0.52 ± 0.19, Post: 0.40 ± 0.17 l/min; P < 0.01); and exercise tolerance during severe exercise was improved by 53% (Pre: 700 ± 234, Post: 1,074 ± 431 s; P < 0.01). None of these parameters was significantly altered in the ET and CON groups. Six sessions of RST, but not ET, resulted in changes in [HHb] kinetics consistent with enhanced fractional muscle O2 extraction, faster V̇o2 kinetics, and an increased tolerance to high-intensity exercise.


1995 ◽  
Vol 79 (6) ◽  
pp. 1914-1920 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. J. MacDonald ◽  
R. L. Hughson

The rates of increase in O2 uptake (VO2) after step changes in work rate from 25 W to 60% of pretraining peak VO2 (VO2 peak) were measured at various times during an endurance training program (2 h/day at 60% pretraining VO2 peak). Seven untrained males [23 +/- 1 (SE) yr] performed a series of repeated step changes in work rate before training (PRE) and after 4 days (4D), 9 days (9D), and 30 days (30D) of training. VO2 kinetic responses were determined from breath-by-breath data averaged across four repetitions and analyzed using a two-component exponential model. Mean response time (time taken to reach 63% of steady-state VO2) was faster (P < 0.01) than PRE (38.1 +/- 2.6 s) at both 4D (34.9 +/- 2.4 s) and 9D (32.5 +/- 1.8 s) and was faster (P < 0.01) at 30D than at all other times (28.3 +/- 1.0 s). Blood lactate concentrations (after 6 min of cycling) were also lower at 4D and 9D than PRE (P < 0.01) and were lower at 30D than at all other times (P < 0.01). VO2 peak was unchanged from PRE (3.52 +/- 0.20 l/min) at 8D (3.55 +/- 0.20 l/min) but was increased (P < 0.01) at 30D (3.89 +/- 0.18 l/min). Muscle oxidative capacity (maximal citrate synthase activity) was not significantly increased until 30D (P < 0.01). It is concluded that at least part of the acceleration of whole body VO2 kinetics with endurance training is a rapid phenomenon, occurring before changes in VO2 peak and/or muscle oxidative potential.


2010 ◽  
Vol 109 (5) ◽  
pp. 1394-1403 ◽  
Author(s):  
Stephen J. Bailey ◽  
Paul G. Winyard ◽  
Anni Vanhatalo ◽  
Jamie R. Blackwell ◽  
Fred J. DiMenna ◽  
...  

It has recently been reported that dietary nitrate (NO3−) supplementation, which increases plasma nitrite (NO2−) concentration, a biomarker of nitric oxide (NO) availability, improves exercise efficiency and exercise tolerance in healthy humans. We hypothesized that dietary supplementation with l-arginine, the substrate for NO synthase (NOS), would elicit similar responses. In a double-blind, crossover study, nine healthy men (aged 19–38 yr) consumed 500 ml of a beverage containing 6 g of l-arginine (Arg) or a placebo beverage (PL) and completed a series of “step” moderate- and severe-intensity exercise bouts 1 h after ingestion of the beverage. Plasma NO2− concentration was significantly greater in the Arg than the PL group (331 ± 198 vs. 159 ± 102 nM, P < 0.05) and systolic blood pressure was significantly reduced (123 ± 3 vs. 131 ± 5 mmHg, P < 0.01). The steady-state O2 uptake (V̇o2) during moderate-intensity exercise was reduced by 7% in the Arg group (1.48 ± 0.12 vs. 1.59 ± 0.14 l/min, P < 0.05). During severe-intensity exercise, the V̇o2 slow component amplitude was reduced (0.58 ± 0.23 and 0.76 ± 0.29 l/min in Arg and PL, respectively, P < 0.05) and the time to exhaustion was extended (707 ± 232 and 562 ± 145 s in Arg and PL, respectively, P < 0.05) following consumption of Arg. In conclusion, similar to the effects of increased dietary NO3− intake, elevating NO bioavailability through dietary l-Arg supplementation reduced the O2 cost of moderate-intensity exercise and blunted the V̇o2 slow component and extended the time to exhaustion during severe-intensity exercise.


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