Influence of exercise intensity on pulmonary oxygen uptake kinetics in young and late middle-aged adults

2012 ◽  
Vol 303 (8) ◽  
pp. R791-R798 ◽  
Author(s):  
Melitta A. McNarry ◽  
Michael I. C. Kingsley ◽  
Michael J. Lewis

It is unclear whether pulmonary oxygen uptake (V̇o2) kinetics demonstrate linear, first-order behavior during supra gas exchange threshold exercise. Resolution of this issue is pertinent to the elucidation of the factors regulating oxygen uptake (V̇o2) kinetics, with oxygen availability and utilization proposed as putative mediators. To reexamine this issue with the advantage of a relatively large sample size, 50 young (24 ± 4 yr) and 15 late middle-aged (54 ± 3 yr) participants completed repeated bouts of moderate and heavy exercise. Pulmonary gas exchange, heart rate (HR), and cardiac output (Q̇) variables were measured throughout. The phase II τ was slower during heavy exercise in both young (moderate: 22 ± 9; heavy: 29 ± 9 s; P ≤ 0.001) and middle-aged (moderate: 22 ± 9; heavy: 30 ± 8 s; P ≤ 0.001) individuals. The HR τ was slower during heavy exercise in young (moderate: 33 ± 10; heavy: 44 ± 15 s; P ≤ 0.05) and middle-aged (moderate: 30 ± 12; heavy: 50 ± 20 s; P ≤ 0.05) participants, and the Q̇ τ showed a similar trend (young moderate: 21 ± 13; heavy: 28 ± 16 s; middle-aged moderate: 32 ± 13; heavy: 40 ± 15 s; P ≥ 0.05). There were no differences in primary component V̇o2 kinetics between age groups, but the middle-aged group had a significantly reduced V̇o2 slow component amplitude in both absolute (young: 0.25 ± 0.09; middle-aged: 0.11 ± 0.06 l/min; P ≤ 0.05) and relative terms (young: 15 ± 10; middle-aged: 9 ± 4%; P ≤ 0.05). Thus V̇o2 kinetics do not demonstrate dynamic linearity during heavy intensity exercise. Speculatively, the slower phase II τ during heavy exercise might be attributable to reduced oxygen availability. Finally, the primary and slow components of V̇o2 kinetics appear to be differentially influenced by middle age.

Author(s):  
Alan R Barker ◽  
Neil Armstrong

The pulmonary oxygen uptake (pV̇O2) kinetic response to exercise provides valuable non-invasive insight into the control of oxidative phosphorylation and determinants of exercise tolerance in children and adolescents. Few methodologically robust studies have investigated pV̇O2 kinetics in children and adolescents, but age- and sex-related differences have been identified. There is a clear age-related slowing of phase II pV̇O2 kinetics during heavy and very heavy exercise, with a trend showing during moderate intensity exercise. During heavy and very heavy exercise the oxygen cost is higher for phase II and the pV̇O2 component is truncated in children. Sex-related differences occur during heavy, but not moderate, intensity exercise, with boys having faster phase II pV̇O2 kinetics and a smaller pV̇O2 slow component compared to girls. The mechanisms underlying these differences are likely related to changes in phosphate feedback controllers of oxidative phosphorylation, muscle oxygen delivery, and/or muscle fibre recruitment strategies.


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.


2008 ◽  
Vol 33 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Nicola Lai ◽  
Melita M. Nasca ◽  
Marco A. Silva ◽  
Fatima T. Silva ◽  
Brian J. Whipp ◽  
...  

The dynamics of the pulmonary oxygen uptake (VO2) responses to square-wave changes in work rate can provide insight into bioenergetic processes sustaining and limiting exercise performance. The dynamic responses at the onset of exercise and during recovery have been investigated systematically and are well characterized at all intensities in adults; however, they have not been investigated completely in adolescents. We investigated whether adolescents display a slow component in their VO2 on- and off-kinetic responses to heavy- and very heavy-intensity exercise, as demonstrated in adults. Healthy African American male adolescents (n = 9, 14–17 years old) performed square-wave transitions on a cycle ergometer (from and to a baseline work rate of 20 W) to work rates of moderate (M), heavy (H), and very heavy (VH) intensity. In all subjects, the VO2 on-kinetics were best described with a single exponential at moderate intensity (τ1, on = 36 ± 11 s) and a double exponential at heavy (τ1, on = 29 ± 9 s; τ2, on = 197 ± 92 s) and very heavy (τ1, on = 36 ± 9 s; τ2, on = 302 ± 14 s) intensities. In contrast, the VO2 off-kinetics were best described with a single exponential at moderate (τ1, off = 48 ± 9 s) and heavy (τ1, off = 53 ± 7 s) intensities and a double exponential at very heavy (τ1, off = 51 ± 3 s; τ2, off = 471 ± 54 s) intensity. In summary, adolescents consistently displayed a slow component during heavy exercise (on- but not off- transition) and very heavy exercise (on- and off-transitions). Although the overall response dynamics in adolescents were similar to those previously observed in adults, their specific characterizations were different, particularly the lack of symmetry between the on- and off-responses.


2000 ◽  
Vol 89 (4) ◽  
pp. 1387-1396 ◽  
Author(s):  
Mark Burnley ◽  
Andrew M. Jones ◽  
Helen Carter ◽  
Jonathan H. Doust

We tested the hypothesis that heavy-exercise phase II oxygen uptake (V˙o 2) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The V˙o 2 responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the V˙o 2 kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 ± 4.1 to 47.0 ± 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 ± 1.9 to 25.3 ± 2.9 s) of theV˙o 2 response in phase II. Instead, this “speeding” was due to a significant reduction in the amplitude of the V˙o 2 slow component. These results suggest phase II V˙o 2 kinetics are not speeded by prior heavy exercise.


2004 ◽  
Vol 96 (3) ◽  
pp. 1033-1038 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Sally Wilmshurst ◽  
Iain T. Campbell

We hypothesized that inhibition of nitric oxide synthase (NOS) by NG-nitro-l-arginine methyl ester (l-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (V̇o2) by nitric oxide and result in a speeding of phase II pulmonary V̇o2 kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak V̇o2 with and without prior intravenous infusion of l-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and V̇o2 kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and l-NAME conditions (L) for baseline V̇o2, the duration of phase I, or the amplitude of the primary V̇o2 response. However, the time constant of the V̇o2 response in phase II was significantly smaller (mean ± SE: C: 25.1 ± 3.0 s; L: 21.8 ± 3.3 s; P < 0.05), and the amplitude of the V̇o2 slow component was significantly greater (C: 240 ± 47 ml/min; L: 363 ± 24 ml/min; P < 0.05) after l-NAME infusion. These data indicate that inhibition of NOS by l-NAME results in a significant (13%) speeding of V̇o2 kinetics and a significant increase in the amplitude of the V̇o2 slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component V̇o2 kinetics after l-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial V̇o2 by nitric oxide. The cause of the larger V̇o2 slow-component amplitude with l-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.


2010 ◽  
Vol 22 (2) ◽  
pp. 314-325 ◽  
Author(s):  
Brynmor C. Breese ◽  
Craig A. Williams ◽  
Alan R. Barker ◽  
Joanne R. Welsman ◽  
Samantha G. Fawkner ◽  
...  

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


Author(s):  
Damir Zubac ◽  
Vladimir Ivančev ◽  
Zoran Valić ◽  
Boštjan Šimunič

We studied the effects of age on different physiological parameters, including those derived from (i) maximal cardiopulmonary exercise testing (CPET), (ii) moderate-intensity step transitions, and (iii) tensiomyography (TMG)-derived variables in moderately active women. Twenty-eight women (age, 19 to 53 years), completed 3 laboratory visits, including baseline data collection, TMG assessment, maximal oxygen uptake test via CPET, and a step-transition test from 20 W to a moderate-intensity cycling power output (PO), corresponding to oxygen uptake at 90% gas exchange threshold. During the step transitions, breath-by-breath pulmonary oxygen uptake, near infrared spectroscopy derived muscle deoxygenation (ΔHHb), and beat-by-beat cardiovascular response were continuously monitored. There were no differences observed between the young and middle-aged women in their maximal oxygen uptake and peak PO, while the maximal heart rate (HR) was 12 bpm lower in middle-aged compared with young (p = 0.016) women. Also, no differences were observed between the age groups in τ pulmonary oxygen uptake, ΔHHb, and τHR during on-transients. The first regression model showed that age did not attenuate the maximal CPET capacity in the studied population (p = 0.638), while in the second model a faster τ pulmonary oxygen uptake, combined with shorter TMG-derived contraction time (Tc) of the vastus lateralis (VL), were associated with a higher maximal oxygen uptake (∼30% of explained variance, p = 0.039). In conclusion, long lasting exercise involvement protects against a maximal oxygen uptake and τpulmonary oxygen uptake deterioration in moderately active women. Novelty: Faster τ pulmonary oxygen uptake and shorter Tc of the VL explain 33% of the variance in superior maximal oxygen uptake attainment. No differences between age groups were found in τ pulmonary oxygen uptake, τΔHHb, and τHR during on-transients.


2009 ◽  
Vol 106 (5) ◽  
pp. 1553-1563 ◽  
Author(s):  
Azmy Faisal ◽  
Keith R. Beavers ◽  
Andrew D. Robertson ◽  
Richard L. Hughson

Cardiorespiratory interactions at the onset of dynamic cycling exercise are modified by warm-up exercises. We tested the hypotheses that oxygen uptake (V̇o2) and cardiac output (Q̇) kinetics would be accelerated at the onset of heavy and moderate cycling exercise by warm-up. Nine male endurance athletes (peak V̇o2: 60.5 ± 3.2 ml·min−1·kg−1) performed multiple rides of two different 36-min cycling protocols, involving 6-min bouts at moderate and heavy intensities. Breath-by-breath V̇o2 and beat-by-beat stroke volume (SV) and Q̇, estimated by Modelflow from the finger pulse, were measured simultaneously with kinetics quantified from the phase II time constant (τ2). One novel finding was that both moderate (M) and heavy (H) warm-up bouts accelerated phase II V̇o2 kinetics during a subsequent bout of heavy exercise (τ2: after M = 22.5 ± 2.7 s, after H = 22.1 ± 2.9 vs. 26.2 ± 3.2 s; P < 0.01). Q̇ kinetics in heavy exercise were accelerated by both warm-up intensities (τ2: M = 22.0 ± 4.1 s, H = 23.8 ± 5.6 s vs. 27.4 ± 7.2 s; P < 0.05). During moderate exercise, prior heavy-intensity warm-up (one or two bouts) accelerated V̇o2 kinetics and elevated Q̇ at exercise onset, with no changes in Q̇ kinetics. A second novel finding was a significant overshoot in the estimate of SV from Modelflow in the first minutes of each moderate and heavy exercise bout. These findings suggest that the acceleration of V̇o2 kinetics during heavy exercise was enabled by the acceleration of Q̇ kinetics, and that rapid increases in Q̇ at the onset of moderate and heavy exercise might result, in part, from an overshoot of SV.


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.


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