Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake

2000 ◽  
Vol 88 (5) ◽  
pp. 1812-1819 ◽  
Author(s):  
R. L. Hughson ◽  
D. D. O'Leary ◽  
A. C. Betik ◽  
H. Hebestreit

We tested the hypothesis that kinetics of O2 uptake (V˙o 2) measured in the transition to exercise near or above peakV˙o 2(V˙o 2 peak) would be slower than those for subventilatory threshold exercise. Eight healthy young men exercised at ∼57, ∼96, and ∼125%V˙o 2 peak. Data were fit by a two- or three-component exponential model and with a semilogarithmic transformation that tested the difference between required V˙o 2 and measuredV˙o 2. With the exponential model, phase 2 kinetics appeared to be faster at 125% V˙o 2 peak[time constant (τ2) = 16.3 ± 8.8 (SE) s] than at 57%V˙o 2 peak(τ2 = 29.4 ± 4.0 s) but were not different from that at 96%V˙o 2 peakexercise (τ2 = 22.1 ± 2.1 s).V˙o 2 at the completion of phase 2 was 77 and 80%V˙o 2 peak in tests predicted to require 96 and 125%V˙o 2 peak. WhenV˙o 2 kinetics were calculated with the semilogarithmic model, the estimated τ2 at 96%V˙o 2 peak (49.7 ± 5.1 s) and 125%V˙o 2 peak (40.2 ± 5.1 s) were slower than with the exponential model. These results are consistent with our hypothesis and with a model in which the cardiovascular system is compromised during very heavy exercise.

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.


2001 ◽  
Vol 90 (5) ◽  
pp. 1700-1706 ◽  
Author(s):  
Craig A. Williams ◽  
Helen Carter ◽  
Andrew M. Jones ◽  
Jonathan H. Doust

The purpose of this study was to compare the kinetics of the oxygen uptake (V˙o 2) response of boys to men during treadmill running using a three-phase exponential modeling procedure. Eight boys (11–12 yr) and eight men (21–36 yr) completed an incremental treadmill test to determine lactate threshold (LT) and maximum V˙o 2. Subsequently, the subjects exercised for 6 min at two different running speeds corresponding to 80% of V˙o 2 at LT (moderate exercise) and 50% of the difference betweenV˙o 2 at LT and maximumV˙o 2 (heavy exercise). For moderate exercise, the time constant for the primary response was not significantly different between boys [10.2 ± 1.0 (SE) s] and men (14.7 ± 2.8 s). The gain of the primary response was significantly greater in boys than men (239.1 ± 7.5 vs. 167.7 ± 5.4 ml · kg−1 · km−1; P < 0.05). For heavy exercise, theV˙o 2 on-kinetics were significantly faster in boys than men (primary response time constant = 14.9 ± 1.1 vs. 19.0 ± 1.6 s; P < 0.05), and the primary gain was significantly greater in boys than men (209.8 ± 4.3 vs. 167.2 ± 4.6 ml · kg−1 · km−1; P < 0.05). The amplitude of theV˙o 2 slow component was significantly smaller in boys than men (19 ± 19 vs. 289 ± 40 ml/min; P < 0.05). The V˙o 2responses at the onset of moderate and heavy treadmill exercise are different between boys and men, with a tendency for boys to have faster on-kinetics and a greater initial increase inV˙o 2 for a given increase in running speed.


1999 ◽  
Vol 87 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Shunsaku Koga ◽  
Tomoyuki Shiojiri ◽  
Manabu Shibasaki ◽  
Narihiko Kondo ◽  
Yoshiyuki Fukuba ◽  
...  

It is presently unclear how the fast and slow components of pulmonary oxygen uptake (V˙o 2) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (V˙o 2 equal to 50% of the difference between LT and peakV˙o 2) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in V˙o 2was similar in the two positions, butV˙o 2 kinetics were slower in the supine position. During heavy exercise, the rate of adjustment ofV˙o 2 to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component ofV˙o 2, without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exerciseV˙o 2 was the same in the two positions. The changes inV˙o 2 kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component forV˙o 2 but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.


1998 ◽  
Vol 85 (5) ◽  
pp. 1833-1841 ◽  
Author(s):  
H. Hebestreit ◽  
S. Kriemler ◽  
R. L. Hughson ◽  
O. Bar-Or

The objective of this study was to compare the O2 uptake (V˙o 2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9–12 yr, and 8 men, aged 19–27 yr, performed a continuous incremental cycling task to determine peak V˙o 2(V˙o 2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50%V˙o 2 peak for 3.5 min, once by cycling at 100%V˙o 2 peak for 2 min, and once by cycling at 130%V˙o 2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50%V˙o 2 peak task: 6.6 ± 11.1 vs. 5.5 ± 7.3 ml ⋅ min−1 ⋅ kg−1; 100% V˙o 2 peak task: 28.5 ± 8.1 vs. 31.8 ± 6.3 ml ⋅ min−1 ⋅ kg−1; and 130%V˙o 2 peaktask: 30.1 ± 5.7 vs. 35.8 ± 5.3 ml ⋅ min−1 ⋅ kg−1). To assess the kinetics, phase I was excluded from analysis. Phase IIV˙o 2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50%V˙o 2 peaktask: 22.8 ± 5.1 vs. 26.4 ± 4.1 s; 100%V˙o 2 peak task: 28.0 ± 6.0 vs. 28.1 ± 4.4 s; and 130%V˙o 2 peak task: 19.8 ± 4.1 vs. 20.7 ± 5.7 s). In conclusion, O2 deficit and fast-componentV˙o 2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.


1998 ◽  
Vol 111 (1) ◽  
pp. 7-37 ◽  
Author(s):  
S. Nikonov ◽  
N. Engheta ◽  
E.N. Pugh

The kinetics of the dark-adapted salamander rod photocurrent response to flashes producing from 10 to 105 photoisomerizations (Φ) were investigated in normal Ringer's solution, and in a choline solution that clamps calcium near its resting level. For saturating intensities ranging from ∼102 to 104 Φ, the recovery phases of the responses in choline were nearly invariant in form. Responses in Ringer's were similarly invariant for saturating intensities from ∼103 to 104 Φ. In both solutions, recoveries to flashes in these intensity ranges translated on the time axis a constant amount (τc) per e-fold increment in flash intensity, and exhibited exponentially decaying “tail phases” with time constant τc. The difference in recovery half-times for responses in choline and Ringer's to the same saturating flash was 5–7 s. Above ∼104 Φ, recoveries in both solutions were systematically slower, and translation invariance broke down. Theoretical analysis of the translation-invariant responses established that τc must represent the time constant of inactivation of the disc-associated cascade intermediate (R*, G*, or PDE*) having the longest lifetime, and that the cGMP hydrolysis and cGMP-channel activation reactions are such as to conserve this time constant. Theoretical analysis also demonstrated that the 5–7-s shift in recovery half-times between responses in Ringer's and in choline is largely (4–6 s) accounted for by the calcium-dependent activation of guanylyl cyclase, with the residual (1–2 s) likely caused by an effect of calcium on an intermediate with a nondominant time constant. Analytical expressions for the dim-flash response in calcium clamp and Ringer's are derived, and it is shown that the difference in the responses under the two conditions can be accounted for quantitatively by cyclase activation. Application of these expressions yields an estimate of the calcium buffering capacity of the rod at rest of ∼20, much lower than previous estimates.


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.


1982 ◽  
Vol 80 (1) ◽  
pp. 83-102 ◽  
Author(s):  
L Goldman ◽  
J L Kenyon

Na inactivation was studied in Myxicola (two-pulse procedure, 6-ms gap between conditioning and test pulses). Inactivation developed with an initial delay (range 130-817 microseconds) followed by a simple exponential decline (time constant tau c). Delays (deviations from a simple exponential) are seen only for brief conditioning pulses were gNa is slightly activated. Hodgkin-Huxley kinetics with series resistance, Rs, predict deviations from a simple exponential only for conditioning pulses that substantially activate gNa. Reducing INa fivefold (Tris substitution) had no effect on either tau c or delay. Delay in not generated by Rs or by contamination from activation development. The slowest time constant in Na tails is approximately 1 ms (Goldman and Hahin, 1978) and the gap was 6 ms. Shortening the gap to 2 ms had no effect on either tau c or delay. Delay is a true property of the channel. Delay decreased with more positive conditioning potentials, and also decreased approximately proportionally with time to peak gNa during the conditioning pulse, as expected for sequentially coupled activation and inactivation. In a few cases the difference between Na current values for brief conditioning pulses and the tau c exponential could be measured. Difference values decayed exponentially with time constant tau m. The inactivation time course is described by a model that assumes a process with the kinetics of gNa activation as a precursor to inactivation.


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 18 (2) ◽  
pp. 197-206 ◽  
Author(s):  
F. Lothian ◽  
M. R. Farrally ◽  
C. Mahoney

The validity and reliability of the Cosmed K2 was tested in comparison with a Quinton on-line oxygen analysing system. A female subject was monitored on a treadmill using a progressive protocol and was measured on three occasions with each system. It was found at low workloads that the Cosmed K2 and the Quinton gave the same measure of oxygen uptake; at higher workloads the Cosmed K2 gave lower values, and at peak oxygen uptake the Cosmed K2 measured 22.2% less than the Quinton. The difference in the measurement of [Formula: see text] at peak oxygen uptake was 13%. The Cosmed K2's measurement of [Formula: see text] showed a greater variability between trials (variation coefficient 3.0-11.4%) than the Quinton (variation coefficient 1.1-3.9%). Key words: Cosmed K2, validity, telemetry


2012 ◽  
Vol 37 (1) ◽  
pp. 138-148 ◽  
Author(s):  
Sarah Margaret Cleland ◽  
Juan Manuel Murias ◽  
John Michael Kowalchuk ◽  
Donald Hugh Paterson

This study examined the effects of prior heavy-intensity exercise on the adjustment of pulmonary oxygen uptake (VO2p) 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 (VO2) 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 VO2 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 VO2 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 VO2p was unchanged with priming exercise; however, a faster mean response time of VO2p 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 O2 delivery during the second bout of exercise.


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