Comparison of oxygen uptake kinetics during knee extension and cycle exercise

2005 ◽  
Vol 288 (1) ◽  
pp. R212-R220 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Tomoyuki Shiojiri ◽  
Narihiko Kondo ◽  
Yoshiyuki Fukuba ◽  
...  
Keyword(s):  
Blood Flow ◽  
Time Constant ◽  
Phase Ii ◽  
Slow Component ◽  
Muscle Blood Flow ◽  
Knee Extension ◽  
Primary Component ◽  
Heavy Exercise ◽  
Muscle Energetics ◽  
Kinetics Of

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.

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

2005 ◽  
Vol 99 (4) ◽  
pp. 1462-1470 ◽  
Author(s):  
Nicole D. Paterson ◽  
John M. Kowalchuk ◽  
Donald H. Paterson
Keyword(s):  
Blood Flow ◽  
Phase Ii ◽  
Time Course ◽  
Muscle Blood Flow ◽  
Knee Extension ◽  
Phase Iii ◽  
Limb Blood Flow ◽  
Heavy Exercise ◽  
Pulsed Wave Doppler ◽  
Young Subjects

The effects of prior heavy-intensity exercise on O2 uptake (V̇o2) 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 V̇o2 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. V̇o2 was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. V̇o2 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 (τ). Phase II V̇o2 kinetics was speeded on the second heavy-intensity exercise [mean τ (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 [τ, 25 ( 13 ) s to 35 ( 13 ) s] were not changed, such that throughout the transient the Qleg (and ΔQleg/ΔV̇o2) did not differ from the prior heavy exercise. Thus V̇o2 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 V̇o2 kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered V̇o2 response after heavy-intensity prior exercise.

Kinetics of V̇o2 and femoral artery blood flow during heavy-intensity, knee-extension exercise

2005 ◽  
Vol 99 (2) ◽  
pp. 683-690 ◽  
Author(s):  
Nicole D. Paterson ◽  
John M. Kowalchuk ◽  
Donald H. Paterson
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Time Course ◽  
Slow Component ◽  
Knee Extension ◽  
Artery Blood Flow ◽  
Phase 2 ◽  
Femoral Artery Blood Flow ◽  
Knee Extension Exercise ◽  
Kinetics Of

It has been suggested that, during heavy-intensity exercise, O2 delivery may limit oxygen uptake (V̇o2) kinetics; however, there are limited data regarding the relationship of blood flow and V̇o2 kinetics for heavy-intensity exercise. The purpose was to determine the exercise on-transient time course of femoral artery blood flow (Q̇leg) in relation to V̇o2 during heavy-intensity, single-leg, knee-extension exercise. Five young subjects performed five to eight repeats of heavy-intensity exercise with measures of breath-by-breath pulmonary V̇o2 and Doppler ultrasound femoral artery mean blood velocity and vessel diameter. The phase 2 time frame for V̇o2 and Q̇leg was isolated and fit with a monoexponent to characterize the amplitude and time course of the responses. Amplitude of the phase 3 response was also determined. The phase 2 time constant for V̇o2 of 29.0 s and time constant for Q̇leg of 24.5 s were not different. The change (Δ) in V̇o2 response to the end of phase 2 of 0.317 l/min was accompanied by a ΔQ̇leg of 2.35 l/min, giving a ΔQ̇leg-to-ΔV̇o2 ratio of 7.4. A slow-component V̇o2 of 0.098 l/min was accompanied by a further Q̇leg increase of 0.72 l/min (ΔQ̇leg-to-ΔV̇o2 ratio = 7.3). Thus the time course of Q̇leg was similar to that of muscle V̇o2 (as measured by the phase 2 V̇o2 kinetics), and throughout the on-transient the amplitude of the Q̇leg increase achieved (or exceeded) the Q̇leg-to-V̇o2 ratio steady-state relationship (ratio ∼4.9). Additionally, the V̇o2 slow component was accompanied by a relatively large rise in Q̇leg, with the increased O2 delivery meeting the increased V̇o2. Thus, in heavy-intensity, single-leg, knee-extension exercise, the amplitude and kinetics of blood flow to the exercising limb appear to be closely linked to the V̇o2 kinetics.

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
Keyword(s):  
Gas Exchange ◽  
Oxygen Uptake ◽  
Phase Ii ◽  
Slow Component ◽  
Primary Component ◽  
Oxygen Availability ◽  
Large Sample Size ◽  
Heavy Exercise ◽  
Middle Aged ◽  
Pulmonary Oxygen Uptake

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.

scholarly journals A prior bout of contractions speeds V̇o2 and blood flow on-kinetics and reduces the V̇o2 slow-component amplitude in canine skeletal muscle contracting in situ

2010 ◽  
Vol 108 (5) ◽  
pp. 1169-1176 ◽  
Author(s):  
Andrés Hernández ◽  
James R. McDonald ◽  
Nicola Lai ◽  
L. Bruce Gladden
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Time Constant ◽  
Potential Role ◽  
Near Infrared ◽  
Slow Component ◽  
Metabolic Activation ◽  
Component Amplitude ◽  
Kinetics Of

It was the purpose of this study to examine the effect of a priming contractile bout on oxygen uptake (V̇o2) on-kinetics in highly oxidative skeletal muscle. Canine gastrocnemii ( n = 12) were stimulated via their sciatic nerves (8 V, 0.2-ms duration, 50 Hz, 200-ms train) at a rate of 2 contractions/3 s (≈70% peak V̇o2) for two 2-min bouts, separated by 2 min of recovery. Blood flow was recorded with an ultrasonic flowmeter, and muscle oxygenation monitored via near-infrared spectroscopy. Compared with the first bout ( bout 2 vs. bout 1), the V̇o2 primary time constant (mean ± SD, 9.4 ± 2.3 vs. 12.0 ± 3.9 s) and slow-component amplitude (5.9 ± 6.3 vs. 12.1 ± 9.0 ml O2·kg wet wt−1·min−1) were significantly reduced ( P < 0.05) during the second bout. Blood flow on-kinetics were significantly speeded during the second bout (time constant = 7.7 ± 2.6 vs. 14.8 ± 5.8 s), and O2 extraction was greater at the onset of contractions (0.050 ± 0.030 vs. 0.020 ± 0.010 ml O2/ml blood). Kinetics of muscle deoxygenation were significantly slower at the onset of the second bout (7.2 ± 2.2 vs. 4.4 ± 1.2 s), while relative oxyhemoglobin concentration was elevated throughout the second bout. These results suggest that better matching of O2 delivery to V̇o2 speeds V̇o2 on-kinetics at this metabolic rate, but do not eliminate a potential role for enhanced metabolic activation. Additionally, altered motor unit recruitment at the onset of a second bout is not a prerequisite for reductions in the V̇o2 slow-component amplitude after a priming contractile bout in canine muscle in situ.

scholarly journals Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise

1996 ◽  
Vol 81 (6) ◽  
pp. 2500-2508 ◽  
Author(s):  
Marielle Engelen ◽  
Janos Porszasz ◽  
Marshall Riley ◽  
Karlman Wasserman ◽  
Kazuhira Maehara ◽  
...  
Keyword(s):  
Heart Rate ◽  
Time Constant ◽  
Slow Component ◽  
Hypoxic Hypoxia ◽  
Baseline Heart Rate ◽  
Heavy Exercise ◽  
Rate Kinetics ◽  
Lactic Acidosis Threshold ◽  
Kinetics Of ◽  
Heart Rate Kinetics

Engelen, Marielle, Janos Porszasz, Marshall Riley, Karlman Wasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. J. Appl. Physiol. 81(6): 2500–2508, 1996.—It is unclear whether hypoxia alters the kinetics of O2 uptake (V˙o 2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise inV˙o 2 (period of first 2–3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slowV˙o 2 component (beginning 2–3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant forV˙o 2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component ofV˙o 2 is unaffected.

Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise

2009 ◽  
Vol 297 (3) ◽  
pp. R615-R621 ◽  
Author(s):  
Tadashi Saitoh ◽  
Leonardo F. Ferreira ◽  
Thomas J. Barstow ◽  
David C. Poole ◽  
Anna Ooue ◽  
...  
Keyword(s):  
Spatial Heterogeneity ◽  
Time Constant ◽  
Near Infrared ◽  
Slow Component ◽  
Rectus Femoris ◽  
Primary Component ◽  
Heavy Exercise ◽  
Muscle Deoxygenation ◽  
Prior Exercise ◽  
Heavy Work

We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O2 uptake (pV̇o2) kinetics during subsequent heavy exercise. Seven healthy men completed two 6-min bouts of heavy work rate cycling exercise, separated by 6 min of unloaded exercise. The changes in the concentration of deoxyhemoglobin/myoglobin (Δdeoxy-[Hb+Mb]) were assessed simultaneously at 10 different sites on the rectus femoris muscle using multichannel near-infrared spectroscopy. Prior exercise had no effect on either the time constant or the amplitude of the primary component pV̇o2, whereas it reduced the amplitude of the slow component (SC). ΔDeoxy-[Hb+Mb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 ± 1.3 vs. 9.3 ± 1.4 s; P < 0.01) and slower primary component time constant (τ: 9.3 ± 1.3 vs. 17.8 ± 1.0 s; P < 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the τ of Δdeoxy-[Hb+Mb] (26.6 ± 11.8 vs. 13.7 ± 5.6%; P < 0.01) and the point-by-point heterogeneity [root mean square error (RMSE)] during the primary component in the second bout. However, neither the change in the CV for τ nor RMSE of Δdeoxy-[Hb+Mb] correlated with the reduction in the SC in pV̇o2 kinetics during subsequent heavy exercise. In conclusion, prior exercise reduced the spatial heterogeneity of the primary component of muscle deoxygenation kinetics. This effect was not correlated with alterations in the pV̇o2 response during subsequent heavy exercise.

scholarly journals Influence of l-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise

2004 ◽  
Vol 96 (3) ◽  
pp. 1033-1038 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Sally Wilmshurst ◽  
Iain T. Campbell
Keyword(s):  
Nitric Oxide ◽  
Gas Exchange ◽  
Phase Ii ◽  
Slow Component ◽  
Muscle Blood Flow ◽  
Primary Component ◽  
Cycle Exercise ◽  
The Difference ◽  
Component Amplitude ◽  
Oxide Synthase

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.

scholarly journals Prolonged ischaemia impairs muscle blood flow and oxygen uptake dynamics during subsequent heavy exercise

2010 ◽  
Vol 588 (19) ◽  
pp. 3785-3797 ◽  
Author(s):  
Azmy Faisal ◽  
Kenneth S. Dyson ◽  
Richard L. Hughson
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Muscle Blood Flow ◽  
Heavy Exercise

Principles, Techniques, and Limitations of Near Infrared Spectroscopy

2004 ◽  
Vol 29 (4) ◽  
pp. 463-487 ◽  
Author(s):  
Marco Ferrari ◽  
Leonardo Mottola ◽  
Valentina Quaresima
Keyword(s):  
Blood Flow ◽  
Near Infrared ◽  
Dynamic Balance ◽  
Exercise Physiology ◽  
Muscle Blood Flow ◽  
Subcutaneous Fat ◽  
Nir Spectroscopy ◽  
Radical Change ◽  
Cortical Activation ◽  
Muscle Energetics

In the last decade the study of the human brain and muscle energetics underwent a radical change, thanks to the progressive introduction of noninvasive techniques, including near-infrared (NIR) spectroscopy (NIRS). This review summarizes the most recent literature about the principles, techniques, advantages, limitations, and applications of NIRS in exercise physiology and neuroscience. The main NIRS instrumentations and measurable parameters will be reported. NIR light (700-1000 nm) penetrates superficial layers (skin, subcutaneous fat, skull, etc.) and is either absorbed by chromophores (oxy- and deoxyhemoglobin and myoglobin) or scattered within the tissue. NIRS is a noninvasive and relatively low-cost optical technique that is becoming a widely used instrument for measuring tissue O2 saturation, changes in hemoglobin volume and, indirectly, brain/muscle blood flow and muscle O2 consumption. Tissue O2 saturation represents a dynamic balance between O2 supply and O2 consumption in the small vessels such as the capillary, arteriolar, and venular bed. The possibility of measuring the cortical activation in response to different stimuli, and the changes in the cortical cytochrome oxidase redox state upon O2 delivery changes, will also be mentioned. Key words: tissue oximetry, oxidative metabolism, optical imaging, blood flow, oxygen consumption, exercise physiology

Pulmonary oxygen uptake kinetics

2017 ◽  
Author(s):  
Alan R Barker ◽  
Neil Armstrong
Keyword(s):  
Oxygen Uptake ◽  
Oxidative Phosphorylation ◽  
Children And Adolescents ◽  
Phase Ii ◽  
Slow Component ◽  
Moderate Intensity ◽  
Heavy Exercise ◽  
Moderate Intensity Exercise ◽  
Pulmonary Oxygen Uptake ◽  
Age Related

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.

Sign in / Sign up

Export Citation Format

Share Document