V˙o 2 kinetics in the horse during moderate and 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.

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.


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.


2000 ◽  
Vol 89 (3) ◽  
pp. 899-907 ◽  
Author(s):  
Helen Carter ◽  
Andrew M. Jones ◽  
Thomas J. Barstow ◽  
Mark Burnley ◽  
Craig A. Williams ◽  
...  

The purpose of the present study was to comprehensively examine oxygen consumption (V˙o 2) kinetics during running and cycling through mathematical modeling of the breath-by-breath gas exchange responses to moderate and heavy exercise. After determination of the lactate threshold (LT) and maximal oxygen consumption (V˙o 2 max) in both cycling and running exercise, seven subjects (age 26.6 ± 5.1 yr) completed a series of “square-wave” rest-to-exercise transitions at running speeds and cycling power outputs that corresponded to 80% LT and 25, 50, and 75%Δ (Δ being the difference between LT andV˙o 2 max).V˙o 2 responses were fit with either a two- (<LT) or three-phase ( >LT) exponential model. The parameters of theV˙o 2 kinetic response were similar between exercise modes, except for the V˙o 2 slow component, which was significantly ( P < 0.05) greater for cycling than for running at 50 and 75%Δ (334 ± 183 and 430 ± 159 ml/min vs. 205 ± 84 and 302 ± 154 ml/min, respectively). We speculate that the differences between the modes are related to the higher intramuscular tension development in heavy cycle exercise and the higher eccentric exercise component in running. This may cause a relatively greater recruitment of the less efficient type II muscle fibers in cycling.


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.


2003 ◽  
Vol 28 (2) ◽  
pp. 283-298 ◽  
Author(s):  
Stéphane Perrey ◽  
Jodie Scott ◽  
Laurent Mourot ◽  
Jean-Denis Rouillon

The purpose of the present study was to assess the relationship between the rapidity of increased oxygen uptake [Formula: see text] and increased cardiac output (CO) during heavy exercise. Six subjects performed repeated bouts on a cycle ergometer above the ventilatory threshold (∼80% of peak [Formula: see text]) separated by 10-min recovery cycling at 35% peak [Formula: see text]. [Formula: see text] was determined breath-by-breath and CO was determined continuously by impedance cardiography. CO and [Formula: see text] values were significantly higher during the 2-min period preceding the second bout. The overall responses for [Formula: see text] and CO were significantly related and were faster during the second bout. Prior heavy exercise resulted in a significant increase in the amplitude of the fast component of [Formula: see text] with no change in the time constant and a decrease in the slow component. Under these circumstances, the amplitude of the fast component was more sensitive to prior heavy exercise than was the associated time constant. Key words: impedance cardiography, exercise transitions, cardiac output, prior exercise


2002 ◽  
Vol 92 (6) ◽  
pp. 2467-2474 ◽  
Author(s):  
Yoshiyuki Fukuba ◽  
Naoyuki Hayashi ◽  
Shunsaku Koga ◽  
Takayoshi Yoshida

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O2 uptake (V˙o 2) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal V˙o 2) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 ± 0.3, 5.6 ± 0.9, and 6.7 ± 1.4 meq/l, respectively. An “effective” time constant (τ) of V˙o 2 with the use of the monoexponential model in L2-ex (τ: 36.8 ± 4.3 s) was significantly faster than that in L1-ex (τ: 52.3 ± 8.2 s). Warm-up arm cranking did not facilitate theV˙o 2 kinetics for the following A2-ex [τ: 51.7 ± 9.7 s]. The double-exponential model revealed no significant change of primary τ (phase II)V˙o 2 kinetics. Instead, the speeding seen in the effective τ during L2-ex was mainly due to a reduction of theV˙o 2 slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of V˙o 2 kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.


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.


2001 ◽  
Vol 90 (2) ◽  
pp. 461-468 ◽  
Author(s):  
Shunsaku Koga ◽  
Thomas J. Barstow ◽  
Tomoyuki Shiojiri ◽  
Tetsuo Takaishi ◽  
Yoshiyuki Fukuba ◽  
...  

The dependence of O2 uptake (V˙o 2) kinetics on the muscle mass recruited under conditions when fiber and muscle recruitment patterns are similar following the onset of exercise has not been determined. We developed a motorized cycle ergometer that facilitated one-leg (1L) cycling in which the electromyographic (EMG) profile of the active muscles was not discernibly altered from that during two-leg (2L) cycling. Six subjects performed 1L and 2L exercise transitions from unloaded cycling to moderate [<ventilatory threshold (VT)] and heavy (>VT) exercise. The 1L condition yielded kinetics that was unchanged from the 2L condition [the phase 2 time constants (τ1, in s) for <VT were as follows: 1L = 16.8±8.4 (SD), 2L = 18.4 ± 8.1, P > 0.05; for >VT: 1L = 26.8 ± 12.0; 2L = 27.8 ± 16.1, P > 0.05]. The overall V˙o 2 kinetics (mean response time) was not significantly different for the two exercise conditions. However, the gain of the fast component (the amplitude/work rate) during the 1L exercise was significantly higher than that for the 2L exercise for both moderate and heavy work rates. The slow-component responses evident for heavy exercise were temporally and quantitatively unaffected by the 1L condition. These data demonstrate that, when leg muscle recruitment patterns are unchanged as assessed by EMG analysis, on-transient V˙o 2 kinetics for both moderate and heavy exercise are not dependent on the muscle mass recruited.


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.


2006 ◽  
Vol 101 (5) ◽  
pp. 1432-1441 ◽  
Author(s):  
Andrew M. Jones ◽  
Nicolas J. A. Berger ◽  
Daryl P. Wilkerson ◽  
Claire L. Roberts

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (V̇o2) 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 (τ) of the V̇o2 response in phase 2 ( bout 1: 29 ± 10 vs. bout 2: 28 ± 4 s; P = 0.91) but reduced the amplitude of the V̇o2 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 τ ( bout 1: 38 ± 18 vs. bout 2: 24 ± 9 s; P = 0.03) but did not alter the amplitude of the V̇o2 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 V̇o2 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.


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