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.

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.

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.

Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline

2008 ◽  
Vol 105 (2) ◽  
pp. 538-546 ◽  
Author(s):  
Fred J. DiMenna ◽  
Daryl P. Wilkerson ◽  
Mark Burnley ◽  
Andrew M. Jones
Keyword(s):  
Gas Exchange ◽  
Metabolic Rate ◽  
Phase Ii ◽  
Slow Component ◽  
Vastus Lateralis ◽  
Moderate Intensity ◽  
Severe Intensity ◽  
Severe Exercise ◽  
Priming Exercise ◽  
The Difference

It has been suggested that the slower O2 uptake (V̇o2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that “priming” exercise would significantly reduce the phase II time constant (τ) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak V̇o2 from a moderate-intensity baseline (90% GET) on three occasions in each of the “unprimed” and “primed” conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II V̇o2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean ± SD τ, 42 ± 15 vs. 33 ± 8 s; P < 0.05), but were not accelerated by priming exercise (42 ± 17 s; P > 0.05). The amplitude of the V̇o2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (V̇o2 slow component: from 0.47 ± 0.09 to 0.27 ± 0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51 ± 35 to 26±43% of baseline; P < 0.05 for both comparisons). These results indicate that the slower phase II V̇o2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced V̇o2 slow component may be linked to changes in muscle fiber activation.

Endothelial nitric oxide synthase polymorphism and venous thromboembolism: A meta-analysis of 9 studies involving 3993 subjects

2021 ◽  
pp. 026835552110166
Author(s):  
Guangbin Huang ◽  
Xuejun Deng ◽  
Yanan Xu ◽  
Pan Wang ◽  
Tao Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Venous Thromboembolism ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Meta Analysis ◽  
Enos Polymorphism ◽  
The Difference ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Intron 4

Background Endothelial nitric oxide synthase (eNOS) polymorphism may influence the risk of venous thromboembolism (VTE). However, data from published studies with low statistical power are inconclusive. The present meta-analysis aimed to assess the relationship between eNOS polymorphism and the risk of VTE. Method Case-control studies evaluating the association between the eNOS polymorphism and VTE were searched in PubMed, Embase, Web of Science, Google Scholar, Wanfang, Chinese National Knowledge Infrastructure (CNKI), the Chongqing VIP Chinese Science and Technology Periodical Database (VIP), and Chinese Biomedical Literature Database (CBM). Results A total of 1588 cases and 2405 controls from 9 studies were included in the analysis. The results showed that eNOS G894T polymorphism was related to VTE susceptibility and the difference was statistically significant [T vs G: OR = 1.41, 95% CI (1.13, 1.75), P = 0.002; TT + GG vs TG: OR = 0.71, 95% CI (0.60, 0.84), P = 0.000; TT + TG vs GG: OR = 1.45, 95% CI (1.23, 1.70), P = 0.000]. Additionally, eNOS Intron 4 VNTR polymorphism was related to VTE susceptibility and the difference was statistically significant [4b4b vs 4a4a + 4a4b: OR = 2.77, 95% CI (1.01, 7.61), P = 0.048]. Conclusion ENOS G894T and eNOS Intron 4 VNTR polymorphisms were associated with VTE susceptibility, especially in Asian populations. However, multicenter studies with larger samples should be conducted to further clarify this association and verify our findings.

Longitudinal changes in the kinetic response to heavy-intensity exercise in children

2004 ◽  
Vol 97 (2) ◽  
pp. 460-466 ◽  
Author(s):  
Samantha G. Fawkner ◽  
Neil Armstrong
Keyword(s):  
Slow Component ◽  
Phase 1 ◽  
Exponential Model ◽  
Cycle Ergometer ◽  
Primary Component ◽  
Total Change ◽  
Exercise Tests ◽  
Longitudinal Changes ◽  
Dependent Change ◽  
The Difference

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.

scholarly journals Inhibition of Nitric Oxide Synthase by L‐NAME Speeds Phase II Pulmonary V̇ O2 Kinetics in the Transition to Moderate‐Intensity Exercise in Man

2003 ◽  
Vol 552 (1) ◽  
pp. 265-272 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Katrien Koppo ◽  
Sally Wilmshurst ◽  
Iain T. Campbell
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Phase Ii ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Oxide Synthase

scholarly journals Inhibitor of neuronal nitric oxide synthase improves gas exchange in ventilator-induced lung injury after pneumonectomy

2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Evgeny V Suborov ◽  
Alexey A Smetkin ◽  
Timofey V Kondratiev ◽  
Andrey Y Valkov ◽  
Vsevolod V Kuzkov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gas Exchange ◽  
Lung Injury ◽  
Neuronal Nitric Oxide Synthase ◽  
Ventilator Induced Lung Injury ◽  
Oxide Synthase
Sign in / Sign up

Export Citation Format

Share Document