Biomedical subjects

Katrien Koppo

Publications and source records attributed to Katrien Koppo.

12 recordsLinked to original sources

PubMed2005

Prior arm exercise speeds the VO2 kinetics during arm exercise above the heart level.

PURPOSE: To test the hypothesis that the initial O2 uptake kinetics during exercise where the rise in blood flow (and, by implication, O2 delivery) to the working muscles during an abrupt increase in exercise intensity is reduced (i.e., arm exercise performed above the level of the heart) would be faster when preceded by a bout of high-intensity exercise. METHODS: Eleven physically active males completed two protocols, each consisting of two consecutive bouts of 6 min of high-intensity arm crank exercise separated by 6 min of recovery. In one protocol, the arm crank exercise was performed with the arms below the level of the heart ( HL). RESULTS: In the HL protocol, the amplitudes of the VO2 fast and slow component were unaffected by prior exercise, whereas the VO2 fast component time constant was significantly reduced in the second bout (49.8+/-22.1 vs 40.7+/-13.2 s; P<0.05). CONCLUSION: The results of this study demonstrate that prior high-intensity exercise caused a significant speeding of the VO2 fast component response during subsequent high-intensity arm crank exercise performed above, and not below, the level of the heart.

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

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

Effects of training status and exercise intensity on phase II VO2 kinetics.

PURPOSE: To test the hypotheses that: 1) the time constant for the fast component of .VO2 kinetics (tau1) at exercise onset would be faster in trained than in untrained subjects for both moderate and heavy exercise, and that 2) tau1 would become progressively slower in untrained subjects at higher power outputs but be invariant in trained subjects. METHODS: Eight untrained subjects (.VO2peak: 42.9 +/- 5.1 mL.kg-1.min-1) and seven trained cyclists (.VO2peak: 66.6 +/- 2.5 mL.kg-1.min-1) completed square-wave transitions to power outputs requiring 60% and 80% of gas exchange threshold (GET), and 50% of the difference between GET and .VO2 peak (50%Delta) from a baseline of "unloaded" cycling. .VO2 was measured breath-by-breath and individual responses were modeled using nonlinear regression techniques. RESULTS: A repeated measures ANOVA revealed that the tau1 was significantly smaller (i.e., the kinetics were faster) in the trained compared with the untrained subjects and that tau1 became significantly greater (i.e., the kinetics were slowed) at higher power outputs both in the untrained (60%GET: 17.8 +/- 3.8 s, 80%GET: 21.5 +/- 6.6 s, and 50%Delta: 23.5 +/- 2.8 s) and the trained (60%GET: 8.9 +/- 1.3 s, 80%GET: 11.7 +/- 2.5 s, and 50%Delta: 15.2 +/- 2.0 s) subjects (P < 0.05). CONCLUSION: Phase II .VO2 kinetics became progressively slower at higher power outputs in both trained and untrained subjects. That a greater tau1 was evident at a higher power output within the moderate exercise intensity domain (<GET), where O2 availability is presumed not to be limiting, indicates that the slowing of the phase II .VO2 kinetics may be attributed to other factors besides O2 availability such as the recruitment of higher threshold motor units.

Adult↗

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

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↗

PubMed2003

Effects of prior exercise on metabolic and gas exchange responses to exercise.

'Warm-up' activity is almost universally performed by athletes prior to their participation in training or competition. However, relatively little is known about the optimal intensity and duration for such exercise, or about the potential mechanisms primed by warm-up that might enhance performance. Recent studies demonstrate that vigorous warm-up exercise that normally results in an elevated blood and presumably muscle lactate concentration has the potential to increase the aerobic energy turnover in subsequent high-intensity exercise. The reduced oxygen deficit is associated with a reduction in both the depletion of the intramuscular phosphocreatine stores and the rate at which lactic acid is produced. Furthermore, the oxygen uptake 'slow component' that develops during high-intensity, ostensibly submaximal, exercise is attenuated. These factors would be hypothesised to predispose to increased exercise tolerance. Interestingly, the elevation of muscle temperature by prior exercise does not appear to be implicated in the altered metabolic and gas exchange responses observed during subsequent exercise. The physiological mechanism(s) that limit the rate and the extent to which muscle oxygen uptake increases following the onset of exercise, and which are apparently altered by the performance of prior heavy exercise, are debated. However, these mechanisms could include oxygen availability, enzyme activity and/or availability of metabolic substrate, and motor unit recruitment patterns. Irrespective of the nature of the control mechanisms that are influenced, 'priming' exercise has the potential to significantly enhance exercise tolerance and athletic performance. The optimal combination of the intensity, duration and mode of 'warm-up' exercise, and the recovery period allowed before the criterion exercise challenge, remain to be determined.

Acidosis, Lactic↗

PubMed2002

Effect of prior heavy arm and leg exercise on VO2 kinetics during heavy leg exercise.

The aim of the present study was to examine the effect of prior exercise at a remote site on the VO(2) kinetics during subsequent heavy cycle exercise using a model that allowed us to discriminate between the VO(2) fast and slow component responses. Ten male subjects completed a constant-load exercise of 6 min cycling at 90% of the VO(2)peak in three conditions: without prior exercise (LE-C), after heavy cycling exercise (6 min at 90% of the VO(2)peak) (LE-L) and after heavy arm-cranking exercise (6 min at 90% of the arm VO(2)peak) (LE-A). Subjects performed four repetitions of each exercise protocol, separated by at least 1 day. VO(2) was measured on a breath-by-breath basis and VO(2) kinetics were determined with a biexponential model. There were no significant differences in the VO(2) fast component parameters between LE-C, LE-L and LE-A. However, the VO(2) slow component amplitude was significantly reduced in LE-L and LE-A compared to LE-C, but the reduction was less pronounced in LE-A [the value of the VO(2) slow exponential term at the end of exercise, A(2)', was 657 (SD 200) ml x min(-1) in LE-C versus 384 (SD 136) ml x min(-1) in LE-L and 551 (SD 169) m x min(-1) in LE-A; P<0.05]. The results of this study demonstrate that prior heavy arm exercise alters VO(2) kinetics during cycling exercise by reducing the VO(2)slow component amplitude, though this reduction is smaller than the reduction observed following prior heavy leg exercise. These data indicate that the primary factor causing changes in the VO(2) kinetics is probably located in the involved muscle.

Adaptation, Physiological↗

PubMed2002

Oxygen uptake kinetics during high-intensity arm and leg exercise.

The purpose of the present study was to examine the oxygen uptake kinetics during heavy arm exercise using appropriate modelling techniques, and to compare the responses to those observed during heavy leg exercise at the same relative intensity. We hypothesised that any differences in the response might be related to differences in muscle fibre composition that are known to exist between the upper and lower body musculature. To test this, ten subjects completed several bouts of constant-load cycling and arm cranking exercise at 90% of the mode specific V(O(2)) peak. There was no difference in plasma [lactate] at the end of arm and leg exercise. The time constant of the fast component response was significantly longer in arm exercise compared to leg exercise (mean+/-S.D., 48+/-12 vs. 21+/-5 sec; P < 0.01), while the fast component gain was significantly greater in arm exercise (12.1+/-1.0 vs. 9.2+/-0.5 ml min(-1) W(-1); P < 0.01). The V(O(2)) slow component emerged later in arm exercise (126+/-27 vs. 95+/-20 sec; P < 0.01) and, in relative terms, increased more per unit time (5.5 vs. 4.4% min(-1); P < 0.01). These differences between arm crank and leg cycle exercise are consistent with a greater and/or earlier recruitment of type II muscle fibres during arm crank exercise.

Adult↗

PubMed2002

Effect of prior exercise on VO(2) slow component is not related to muscle temperature.

INTRODUCTION: It has been widely reported that the VO(2) slow component is reduced in the second of two bouts of heavy exercise. It has also been shown that an increase in muscle temperature (Tm) produced by wearing hot-water-perfused pants causes a reduction in the VO(2) slow component. Therefore, the aim of this study was to investigate whether the effect of prior heavy exercise on the VO(2) slow component of subsequent heavy exercise is related to the warming-up of the exercising limbs. METHODS: Six male subjects completed an exercise protocol consisting of two constant-load exercise bouts (EX-1 and EX-2) at 90% VO(2peak), separated by 6 min of rest. The Tm of the m. vastus lateralis was measured with an indwelling thermistor. Seven days later, the subjects completed a second exercise protocol consisting of a passive warming-up of the upper legs until the same Tm was reached as after EX-1, followed by a constant-load work bout (EX-3) identical to EX-1 and EX-2. RESULTS: Tm reached comparable levels at the start of EX-2 and EX-3 (37.3 +/- 0.6 degrees C and 37.2 +/- 0.3 degrees C, respectively). The VO(2) slow component (measured as deltaVO(2)(6-2 min)) was reduced by 57% after prior heavy exercise ( < 0.05), whereas no significant reduction was observed after prior passive warming-up. CONCLUSIONS: The results of this study indicate that the reduction in VO(2) slow component observed after prior heavy exercise cannot be explained by an increase in muscle temperature of the upper legs.

Adaptation, Physiological↗