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Biomedical subjects

Daryl P Wilkerson

Publications and source records attributed to Daryl P Wilkerson.

18 recordsLinked to original sources
PubMed2006

Effects of baseline metabolic rate on pulmonary O2 uptake on-kinetics during heavy-intensity exercise in humans.

We hypothesised that initiating heavy-intensity exercise from an elevated baseline metabolic rate would result in slower Phase II O2 uptake V(O2) kinetics and a greater overall 'gain' in V(O2) per unit increase in work rate. Seven healthy males performed a series of like-transitions on a cycle ergometer: (1) from light exercise to 'moderate' exercise (80% of the gas exchange threshold, GET; L-->M); (2) from light exercise to 'heavy' exercise (40% of the difference between GET and V(O2) peak; L-->H); (3) from moderate exercise to heavy exercise (M-->H). The Phase II time constant (tau) was significantly (P<0.01) greater in the M-->H condition (48+/-11 s) compared to the L-->M and L-->H conditions (26+/-6 s versus 27+/-4 s, respectively). Moreover, the end-exercise 'gain' values were significantly different between the three conditions (L-->M, 8.1+/-0.7 mL min-1 W-1; L-->H, 9.7+/-0.4 mL min-1 W-1; M-->H, 10.7+/-0.7 mL min-1 W-1; P<0.05). This 'non-linearity' in the pulmonary V(O2) response to exercise might be attributed, at least in part, to differences in the metabolic properties of the muscle fibres recruited in the abrupt transition from a lower to a higher work rate.

Adult↗
PubMed2006

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) 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 tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 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 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 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 VO2 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.

Adaptation, Physiological↗
PubMed2006

Influence of acute plasma volume expansion on VO2 kinetics, VO2 peak, and performance during high-intensity cycle exercise.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V(O2max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O(2) content, APVE had no effect on V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O(2) pulse was also enhanced by the treatment (Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

Adult↗
PubMed2006

Sodium bicarbonate ingestion alters the slow but not the fast phase of VO2 kinetics.

PURPOSE: The influence of metabolic alkalosis (ALK) on pulmonary O2 uptake (pVO2) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO2 kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. METHODS: Seven healthy males completed step tests to a work rate requiring 80% pVO2max on six separate occasions: three times after ingestion of 0.3 g x kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO2 was measured breath-by-breath. RESULTS: NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO2 response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO2 slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 +/- 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO2 (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L x min(-1); P < 0.05). CONCLUSIONS: Metabolic alkalosis has no effect on phase II pVO2 kinetics but alters the pVO2 slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

Acid-Base Imbalance↗
PubMed2005

Influence of initial metabolic rate on pulmonary O2 uptake on-kinetics during severe intensity exercise.

We hypothesised that the fundamental (Phase II) component of pulmonary oxygen uptake (VO(2)) kinetics would be significantly slower when step transitions to severe intensity cycle exercise were initiated from elevated baseline metabolic rates, and that this would be associated with evidence for a greater activation of higher-order (i.e. type II) muscle fibres. Seven male subjects (age 22-34 years) completed repeat step transitions to a severe (S) work rate, estimated to require 100% VO(2) peak, from a baseline of: (1) 3 min of unloaded cycling (L-->S); (2) 6 min of moderate exercise (M-->S); (3) 6 min of heavy exercise (H-->S). Pulmonary gas exchange and the electromyogram (EMG) of the m. vastus lateralis were measured throughout all exercise tests. The Phase II VO(2) kinetics became progressively slower at higher baseline metabolic rates (tau was 37 +/- 6, 59 +/- 23, and 93 +/- 50 s for L-->S, M-->S, and H-->S, respectively; P < 0.05 between L-->S and H-->S). Both the integrated EMG and the mean power frequency were significantly higher immediately before the step transition to severe exercise when it was initiated from higher metabolic rates. Although indirect, these data suggest that the slower Phase II VO(2) kinetics observed at higher baseline metabolic rates was related to alterations in muscle activation and fibre recruitment patterns.

Adult↗
PubMed2005

Influence of hyperoxia on pulmonary O2 uptake kinetics following the onset of exercise in humans.

The purpose of this study was to examine the influence of hyperoxic gas (50% O2 in N2) inspiration on pulmonary oxygen uptake (V(O2)) kinetics during step transitions to moderate, severe and supra-maximal intensity cycle exercise. Seven healthy male subjects completed repeat transitions to moderate (90% of the gas exchange threshold, GET), severe (70% of the difference between the GET and V(O2) peak) and supra-maximal (105% V(O2) peak) intensity work rates while breathing either normoxic (N) or hyperoxic (H) gas before and during exercise. Hyperoxia had no significant effect on the Phase II V(O2) time constant during moderate (N: 28+/-3s versus H: 31+/-7s), severe (N: 32+/-9s versus H: 33+/-6s) or supra-maximal (N: 37+/-9s versus H: 37+/-9s) exercise. Hyperoxia resulted in a 45% reduction in the amplitude of the V(O2) slow component during severe exercise (N: 0.60+/-0.21 L min(-1) versus H: 0.33+/-0.17 L min(-1); P < 0.05) and a 15% extension of time to exhaustion during supra-maximal exercise (N: 173+/-28 s versus H: 198+/-41 s; P < 0.05). These results indicate that the Phase II V(O2) kinetics are not normally constrained by (diffusional) O2 transport limitations during moderate, severe or supra-maximal intensity exercise in young healthy subjects performing upright cycle exercise.

Adult↗
PubMed2005

Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans.

We hypothesized that 4 weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in haemoglobin concentration ([Hb]) and arterial blood O(2)-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake during ramp incremental exercise, and (2) speed kinetics during 'severe'-, but not 'moderate'- or 'heavy'-intensity, step exercise. Fifteen subjects (mean +/- s.d. age 25 +/- 4 years) were randomly assigned to either an experimental group which received a weekly subcutaneous injection of RhEPO (150 IU kg(-1); n = 8), or a control group (CON) which received a weekly subcutaneous injection of sterile saline (10 ml; n = 7) as a placebo, for four weeks. The subjects and the principal researchers were both blind with respect to the group assignment. Before and after the intervention period, all subjects completed a ramp test for determination of the gas exchange threshold (GET) and , and a number of identical 'step' transitions from 'unloaded' cycling to work rates requiring 80% GET (moderate), 70% of the difference between the GET and (heavy), and 105% (severe) as determined from the initial ramp test. Pulmonary gas exchange was measured breath-by-breath. There were no significant differences between the RhEPO and CON groups for any of the measurements of interest ([Hb], kinetics) before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON. RhEPO had no significant effect on kinetics for moderate (Phase II time constant, from 28 +/- 8 to 28 +/- 7 s), heavy (from 37 +/- 12 to 35 +/- 11 s), or severe (from 33 +/- 15 to 35 +/- 15 s) step exercise. Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetics, suggesting that the latter is principally regulated by intracellular (metabolic) factors, even during exercise where the requirement is greater than the , at least in young subjects performing upright cycle exercise.

Double-Blind Method↗
PubMed2005

Pulmonary O2 uptake on-kinetics in rowing and cycle ergometer exercise.

The purpose of this study was to characterise, for the first time, the pulmonary O2 uptake (V(O2)) on-kinetic responses to step transitions to moderate and heavy intensity rowing ergometer exercise, and to compare the responses to those observed during upright cycle ergometer exercise. We hypothesised that the recruitment of a greater muscle mass in rowing ergometer exercise (Row) might limit muscle perfusion and result in slower Phase II V(O2) kinetics compared to cycle exercise (Cyc). Eight healthy males (aged 28+/-5 years) performed a series of step transitions to moderate (90% of the mode-specific gas exchange threshold, GET) and heavy (50% of the difference between the mode-specific GET and V(O2) max) work rates, for both Row and Cyc exercise. Pulmonary V(O2) was measured breath-by-breath and the V(O2) on-kinetics were described using standard non-linear regression techniques. With the exception of delta V(O2)delta WR which was approximately 12% greater for Row, the V(O2) kinetic responses were similar between the exercise modes. There was no significant difference in the time constant describing the Phase II V(O2) kinetics between the exercise modes for either moderate (rowing: 25.9+/-6.8 s versus cycling: 25.7+/-8.6 s) or heavy (rowing: 26.5+/-3.0 s versus cycling: 27.8+/-5.1s) exercise. Furthermore, there was no significant difference in the amplitude of the V(O2) slow component between the exercise modes (rowing: 0.34+/-0.13 L min(-1) versus cycling: 0.35+/-0.12 L min(-1)). These data suggest that muscle V(O2) increases towards the anticipated steady-state requirement at essentially the same rate following a step increase in ATP turnover in the myocytes, irrespective of the mode of exercise, at least in subjects with no particular sport specialism. The recruitment of a greater muscle mass in rowing compared to cycling apparently did not compromise muscle perfusion sufficiently to result either in slower Phase II V(O2) kinetics or a greater V(O2) slow component amplitude during heavy exercise.

Adult↗
PubMed2004

Effect of work rate on the functional 'gain' of Phase II pulmonary O2 uptake response to exercise.

It has recently been reported that the 'gain' of Phase II increase in pulmonary oxygen uptake (i.e. the 'fundamental' increase in V(O(2)) per unit increase in work rate; G(p)) does not attain the anticipated value of approximately 10 ml min(-1)W(-1) following the onset of high-intensity exercise. In the present study, we hypothesised that G(p) would fall significantly below 10 ml min(-1)W(-1) only when the work rate exceeded the so-called 'critical power' (CP). Seven healthy males completed several 'square-wave' transitions from 'unloaded' cycling to work rates requiring 60 and 90% of the gas exchange threshold (GET), 40 and 80% of the difference between the GET and V(O(2)) peak (i.e. below and above the CP, respectively), and 100, 110 and 120% of V(O(2)) peak. Pulmonary V(O(2)) was measured breath-by-breath and V(O(2)) kinetics were determined using non-linear regression techniques. The asymptotic G(p) was significantly lower at work rates above (7.2-8.6 ml min(-1)W(-1)) compared to work rates below (9.3-9.7 ml min(-1)W(-1)) the CP (P < 0.05). We conclude that the gain of Phase II increase in V(O(2)) becomes significantly reduced when the work rate exceeds the CP.

Adult↗
PubMed2004

Influence of nitric oxide synthase inhibition on pulmonary O2 uptake kinetics during supra-maximal exercise in humans.

We have recently reported that inhibition of nitric oxide synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME) accelerates the 'phase II' pulmonary O2 uptake (VO2) kinetics following the onset of moderate and heavy intensity submaximal exercise in humans. These data suggest that the influence of nitric oxide (NO) on mitochondrial function is an important factor in the inertia to aerobic respiration that is evident in the transition from a lower to a higher metabolic rate. The purpose of the present study was to investigate the influence of L-NAME on pulmonary VO2 kinetics following the onset of supra-maximal exercise, where it has been suggested that O2 availability represents an additional limitation to VO2 kinetics. Seven healthy young men volunteered to participate in this study. Following an incremental cycle ergometer test for the determination of VO2max, the subjects returned on two occasions to perform a 'step' exercise test from a baseline of unloaded cycling to a work rate calculated to require 105% VO2max, preceded either by systemic infusion of L-NAME (4 mg kg(-1) in 50 ml saline) or 50 ml saline as a control (Con). Pulmonary gas exchange was measured on a breath-by-breath basis throughout the exercise tests. The duration of 'phase I' was greater with L-NAME (Con: 14.0 +/- 2.1 versus L-NAME: 16.0 +/- 1.6 s; P = 0.03), suggestive of a slower cardiovascular adaptation following the onset of exercise. However, the phase II VO2 time constant was reduced by 44% with L-NAME (Con: 36.3 +/- 17.3 versus L-NAME: 20.4 +/- 8.3 s; P = 0.01). The accumulation of blood lactate during exercise was also reduced with L-NAME (Con: 4.0 +/- 1.1 versus L-NAME: 2.7 +/- 2.1 mM; P = 0.04). These data indicate that skeletal muscle NO production represents an important limitation to the acceleration of oxidative metabolism following the onset of supra-maximal exercise in humans.

Adult↗
PubMed2004

Nitric oxide synthase inhibition with L-NAME reduces maximal oxygen uptake but not gas exchange threshold during incremental cycle exercise in man.

We hypothesized that the effective inhibition of nitric oxide synthase (NOS), achieved via systemic infusion of N(G)-nitro-l-arginine methyl ester (l-NAME), would reduce the gas exchange threshold (GET) and the maximal oxygen uptake (V(.)(O(2)max)) during incremental cycle exercise in man if NO is important in the regulation of muscle vasodilatation. Seven healthy males, aged 18-34 years, volunteered to participate in this ethically approved study. On two occasions, the subjects completed an incremental exercise test to exhaustion on an electrically braked cycle ergometer following the infusion of either l-NAME (4 mg kg(-1) in 50 ml saline) or placebo (50 ml saline, CON). At rest, the infusion of l-NAME resulted in a significant increase in mean arterial pressure (MAP; CON vs. l-NAME, 89 +/- 8 vs. 103 +/- 11 mmHg (mean +/- s.d.; P < 0.05)) and a significant reduction in heart rate (HR; CON vs. l-NAME, 60 +/- 12 vs. 51 +/- 8 beats min(-1); P < 0.01). At submaximal work rates, there was no significant difference in V(.)(O(2)) between the conditions and no difference in the GET (CON vs. l-NAME, 1.94 +/- 0.47 vs. 2.01 +/- 0.41 l min(-1)). However, at higher work rates, differences in V(.)(O(2)) between the conditions became more pronounced such that V(.)(O(2)max) was significantly lower with l-NAME (CON vs. l-NAME, 4.02 +/- 0.41 vs. 3.80 +/- 0.34 l min(-1); P < 0.05). The reduction in V(.)(O(2)max) was associated with a reduction in HR(max) (CON vs. l-NAME, 186 +/- 10 vs. 178 +/- 7 beats min(-1); P < 0.01). These results demonstrate that NOS inhibition with l-NAME has no effect on GET but reduces V(.)(O(2)max) during large muscle group exercise in man, presumably by direct or indirect effects on cardiac output and muscle blood flow.

Adult↗
PubMed2004

Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise.

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.

Adaptation, Physiological↗
PubMed2004

Influence of DCA on pulmonary (.-)V(O2) kinetics during moderate-intensity cycle exercise.

PURPOSE: To test the hypothesis that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) with dichloroacetate (DCA) would speed phase II pulmonary oxygen uptake ((.-)V(O2)) kinetics after the onset of subsequent moderate-intensity (40-45% ((.-)V(O2)) peak) cycle exercise. METHODS: Seven healthy males (mean +/- SD age 25 +/- 4 yr, body mass 75.3 +/- 9.4 kg) performed four "square-wave" transitions from unloaded cycling to a work rate requiring 90% of the predetermined gas exchange threshold either with or without prior infusion of DCA (50 mg x kg body mass in 50 mL saline). Pulmonary ((.-)V(O2)) was measured breath-by-breath in all tests and ((.-)V(O2)) kinetics were determined from the averaged individual response to each condition using nonlinear regression techniques. RESULTS: The blood [lactate] measured immediately before the onset of exercise was significantly reduced in the DCA condition (C: 1.1 +/- 0.3 vs DCA: 0.6 +/- 0.3 mM; P < 0.01) consistent with successful activation of the PDC. However, DCA had no discernible effect on the rate at which ((.-)V(O2)) increased toward the steady state after the onset of exercise as reflected in the phase II time constant (C: 28.5 +/- 11.8 vs DCA: 29.4 +/- 14.9 s). CONCLUSIONS: The results suggest that PDC activation does not represent a principal intramuscular limitation to ((.-)V(O2)) kinetics after the onset of moderate-intensity exercise.

Adult↗
PubMed2003

Dichloroacetate does not speed phase-II pulmonary VO2 kinetics following the onset of heavy intensity cycle exercise.

We hypothesised that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) by dichloroacetate (DCA) would speed phase-II pulmonary O2 uptake (VO2) kinetics following the onset of high-intensity, sub-maximal exercise. Eight healthy males (aged 19-33 years) completed two "square-wave" transitions of 6 min duration from unloaded cycling to a work-rate equivalent to approximately 80% of peak VO2 either with or without prior i.v. infusion of DCA (50 mg kg(-1) body mass in 50 ml saline). Pulmonary VO2 was measured breath-by-breath throughout all tests, and VO2 kinetics were determined using non-linear regression techniques from the averaged individual response to each of the conditions. Infusion of DCA resulted in significantly lower blood [lactate] during the baseline cycling period (means+/-SEM: control 0.9+/-0.1, DCA 0.5+/-0.1 mM; P<0.01) consistent with successful activation of PDC. However, DCA had no discernible effect on the rate at which VO2 increased towards the initially anticipated steady state following the onset of exercise as reflected in the time constant of the fundamental VO2 response (control 26.7+/-4.1, DCA 27.7+/-2.8 s). These results indicate that the principal limitation to oxidative metabolism following the onset of high-intensity, sub-maximal cycle exercise lies downstream from PDC and/or that muscle O2 consumption is primarily under "feedback" control via the concentration of one or more of the reactants associated with ATP hydrolysis.

Adult↗
PubMed2003

Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) 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 Vo(2) 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 Vo(2) 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 Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) 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 Vo(2) 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 Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) 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 Vo(2) by nitric oxide. The cause of the larger Vo(2) 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.

Adult↗
PubMed2003

Inhibition of nitric oxide synthase by L-NAME speeds phase II pulmonary .VO2 kinetics in the transition to moderate-intensity exercise in man.

There is evidence that the rate at which oxygen uptake (.VO2) rises at the transition to higher metabolic rates within the moderate exercise intensity domain is modulated by oxidative enzyme inertia, and also that nitric oxide regulates mitochondrial function through competitive inhibition of cytochrome c oxidase in the electron transport chain. We therefore hypothesised that inhibition of nitric oxide synthase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial .VO2 by nitric oxide and result in a speeding of .VO2 kinetics at the onset of moderate-intensity exercise. Seven males performed square-wave transitions from unloaded cycling to a work rate requiring 90 % of predetermined gas exchange threshold with and without prior intravenous infusion of L-NAME (4 mg kg-1 in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath-by-breath and .VO2 kinetics were determined from the averaged response to four exercise bouts performed in each condition using a mono-exponential function following elimination of the phase I response. There were no significant differences between the control and L-NAME conditions for baseline .VO2 (means +/- S.E.M. 797 +/- 32 vs. 794 +/- 29), the duration of phase I (15.4 +/- 0.8 vs. 17.2 +/- 0.6), or the steady-state increment in .VO2 above baseline (1000 +/- 83 vs. 990 +/- 85 ml min-1), respectively. However, the phase II time constant of the .VO2 response was significantly smaller following L-NAME infusion (22.1 +/- 2.4 vs. 17.9 +/- 2.3; P < 0.05). These data indicate that inhibition of NOS by L-NAME results in a significant (19 %) speeding of pulmonary .VO2 kinetics in the transition to moderate-intensity cycle exercise in man. At least part of the intrinsic inertia to oxidative metabolism at the onset of moderate-intensity exercise may result from competitive inhibition of mitochondrial .VO2 by nitric oxide at cytochrome c oxidase, although other mechanisms for the effect of L-NAME on .VO2 kinetics remain to be explored.

Adult↗
PubMed2003

Prior heavy exercise enhances performance during subsequent perimaximal exercise.

PURPOSE: To test the hypothesis that prior heavy exercise increases the time to exhaustion during subsequent perimaximal exercise. METHODS: Seven healthy males (mean +/- SD 27 +/- 3 yr; 78.4 +/- 0.7 kg) completed square-wave transitions from unloaded cycling to work rates equivalent to 100, 110, and 120% of the work rate at VO2peak (W-[VO2peak) after no prior exercise (control, C) and 10 min after a 6-min bout of heavy exercise at 50% Delta (HE; half-way between the gas exchange threshold (GET) and VO2peak), in a counterbalanced design. RESULTS: Blood [lactate] was significantly elevated before the onset of the perimaximal exercise bouts after prior HE (approximately 2.5 vs approximately 1.1 mM; P < 0.05). Prior HE increased time to exhaustion at 100% (mean +/- SEM. C: 386 +/- 92 vs HE: 613 +/- 161 s), 110% (C: 218 +/- 26 vs HE: 284 +/- 47 s), and 120% (C: 139 +/- 18 vs HE: 180 +/- 29 s) of W-VO2peak, (all P < 0.01). VO2 was significantly higher at 1 min into exercise after prior HE at 110% W-VO2peak (C: 3.11 +/- 0.14 vs HE: 3.42 +/- 0.16 L x min(-1); P < 0.05), and at 1 min into exercise (C: 3.25 +/- 0.12 vs HE: 3.67 +/- 0.15; P < 0.01) and at exhaustion (C: 3.60 +/- 0.08 vs HE: 3.95 +/- 0.12 L x min(-1); P < 0.01) at 120% of W-VO2peak. CONCLUSIONS: This study demonstrate that prior HE, which caused a significant elevation of blood [lactate], resulted in an increased time to exhaustion during subsequent perimaximal exercise presumably by enabling a greater aerobic contribution to the energy requirement of exercise.

Adult↗