Katrien Koppo

Effects of Prior Exercise on Metabolic and Gas Exchange Responses to Exercise

Abstract‘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.

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.

Inhibition of Nitric Oxide Synthase by L‐NAME Speeds Phase II Pulmonary V̇O2 Kinetics in the Transition to Moderate‐Intensity Exercise in Man

There is evidence that the rate at which oxygen uptake (V̇O2) 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 V̇O2 by nitric oxide and result in a speeding of V̇O2 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 V̇O2 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 V̇O2 (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 V̇O2 above baseline (1000 ± 83 vs. 990 ± 85 ml min−1), respectively. However, the phase II time constant of the V̇O2 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 V̇O2 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 V̇O2 by nitric oxide at cytochrome c oxidase, although other mechanisms for the effect of L‐NAME on V̇O2 kinetics remain to be explored.

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.

In humans the oxygen uptake slow component is reduced by prior exercise of high as well as low intensity

Abstract The aim of the study was to examine to what extent prior high- or low-intensity cycling, yielding the same amount of external work, influenced the oxygen uptake (V˙O2) slow component of subsequent high-intensity cycling. The 12 subjects cycled in two protocols consisting of an initial 3 min period of unloaded cycling followed by two periods of constant-load exercise separated by 3 min of rest and 3 min of unloaded cycling. In protocol 1 both periods of exercise consisted of 6 min cycling at a work rate corresponding to 90% peak oxygen uptake (V˙O2peak). Protocol 2 differed from protocol 1 in that the first period of exercise consisted of a mean of 12.1 (SD 0.8) min cycling at a work rate corresponding to 50% V˙O2peak. The difference between the 3rd min V˙O2 and the end V˙O2 (ΔV˙O2(6−3)) was used as an index of the V˙O2 slow component. Prior high-intensity exercise significantly reduced ΔV˙O2(6−3). The ΔV˙O2(6−3) was also reduced by prior low-intensity exercise despite an unchanged plasma lactate concentration at the start of the second period of exercise. The reduction was more pronounced after prior high- than after prior low-intensity exercise (59% and 28%, respectively). The results of this study show that prior exercise of high as well as low intensity reduces the V˙O2 slow component and indicate that a metabolic acidosis is not a necessary condition to elicit a reduction in ΔV˙O2(6−3).

Adrenaline but not noradrenaline is a determinant of exercise-induced lipid mobilization in human subcutaneous adipose tissue

The relative contribution of noradrenaline (norepinephrine) and adrenaline (epinephrine) in the control of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise was evaluated in men treated with a somatostatin analogue, octreotide. Eight lean and eight obese young men matched for age and physical fitness performed 60 min exercise bouts at 50% of their maximal oxygen consumption on two occasions: (1) during i.v. infusion of octreotide, and (2) during placebo infusion. Lipolysis and local blood flow changes in SCAT were evaluated using in situ microdialysis. Infusion of octreotide suppressed plasma insulin and growth hormone levels at rest and during exercise. It blocked the exercise‐induced increase in plasma adrenaline while that of noradrenaline was unchanged. Plasma natriuretic peptides (NPs) level was higher at rest and during exercise under octreotide infusion in lean men. Under placebo, no difference was found in the exercise‐induced increase in glycerol between the probe perfused with Ringer solution alone and that with phentolamine (an α‐adrenergic receptor antagonist) in lean subjects while a greater increase in glycerol was observed in the obese subjects. Under placebo, propranolol infusion in the probe containing phentolamine reduced by about 45% exercise‐induced glycerol release; this effect was fully suppressed under octreotide infusion while noradrenaline was still elevated and exercise‐induced lipid mobilization maintained in both lean and obese individuals. In conclusion, blockade of β‐adrenergic receptors during exercise performed during infusion of octreotide (blocking the exercise‐induced rise in adrenaline but not that of noradrenaline) does not alter the exercise‐induced lipolysis. This suggests that adrenaline is the main adrenergic agent contributing to exercise‐induced lipolysis in SCAT. Moreover, it is the combined action of insulin suppression and NPs release which explains the lipolytic response which remains under octreotide after full local blockade of fat cell adrenergic receptors. For the moment, it is unknown if results apply specifically to SCAT and exercise only or if conclusions could be extended to all forms of lipolysis in humans.

Effect of Exercise Protocol on Deoxy[Hb + Mb]: Incremental Step versus Ramp Exercise

PURPOSE The aim of the present study was to investigate whether the sigmoid pattern of deoxy[Hb + Mb] during incremental exercise is specific to non-steady-state conditions. METHODS Ten highly trained cyclists performed an incremental step (40 W x 3 min(-1)) and ramp (35 W x min(-1)) exercise. Deoxy[Hb + Mb] was measured at the distal and proximal sites of the musculus vastus lateralis throughout the exercises using near-infrared spectroscopy. Deoxy[Hb + Mb] was set out as a function of work rate (% peak power), and using curve-fitting techniques, the best-fitting model was determined. RESULTS These procedures showed that the sigmoid pattern also provided the best fit for the pattern of deoxy[Hb + Mb] in the step exercise. Furthermore, it was observed that the sigmoid model was similar for the ramp (d = 6.9% +/- 1.1% and 6.9% +/- 1.4% x %(-1) peak power; c/d = 52.1% +/- 3.8% and 52.1% +/- 4.5% peak power, for the proximal and distal measurement sites, respectively) and the step exercise (d = 7.4% +/- 1.5% and 6.4% +/- 1.5% x %(-1) peak power; c/d = 52.3% +/- 6.0% and 52.5% +/- 4.2% peak power, for the proximal and distal measurement sites, respectively). The pattern of deoxy[Hb + Mb] was not influenced by measurement site. CONCLUSIONS From the present study, it can be concluded that the sigmoid pattern of deoxy[Hb + Mb] during incremental exercise is not specific to non-steady-state conditions. It was hypothesized that this pattern is an expression of a nonlinear Q x m/V x O2m relationship, related to changes in muscle fiber-type recruitment.

The VO2 response to submaximal ramp cycle exercise: Influence of ramp slope and training status.

The aim of the study was to test whether ramp slope and training status interact in the oxygen uptake (VO2) response during submaximal ramp exercise. Eight cyclists (VO2 peak=67.8+/-3.7 ml min(-1)kg(-1)) and eight physically active students (PA students) (VO2 peak=49.1+/-4.3 ml min(-1)kg(-1)) performed several ramp protocols, respectively, 25 and 40 W min(-1) for the cyclists and 10, 25 and 40 W min(-1) for the PA students. Vo(2) was plotted as a function of time and work rate up to the gas exchange threshold (GET). Faster ramp elicited a significantly shorter mean response time (MRT) in both groups, and MRT was significantly longer for each ramp protocol in the PA students (126+/-32s, 76+/-15s and 50+/-6s for ramp 10, ramp 25 and ramp 40, respectively) compared to the cyclists (61+/-9s and 40+/-11s for ramp 25 and ramp 40, respectively). Ramp 40 showed less steep Delta VO2/Delta W than ramp 25 in both groups (p<0.01) and Delta VO2/Delta W was less steep for each ramp protocol in PA students (p<0.01) (9.82+/-0.30 ml min(-1)W(-1) and 9.33+/-0.45 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively) compared to cyclists (10.31+/-0.40 ml min(-1)W(-1) and 10.05+/-0.48 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively). In the PA students, Delta VO2/Delta W did not differ between ramp 10 and ramp 25. Statistical analysis showed no interaction effects between ramp slope and training status for MRT (p=0.62) and Delta VO2/Delta W (p=0.35).

Dietary arginine supplementation speeds pulmonary VO2 kinetics during cycle exercise.

PURPOSE To test the hypothesis that L-arginine (the substrate for nitric oxide synthase [NOS]) administration slows the VO2 kinetics at the onset of moderate-intensity exercise in humans. METHODS Seven physically active males were randomly assigned to receive either placebo (lactose) or L-arginine hydrochloride capsules (7.2 g x d(-1)) for 14 d in a double-blind crossover design, with a 7-d washout period between the two conditions. On day 11 and day 14 of each condition, the subjects completed two consecutive 6-min bouts of cycle exercise at 80% of the ventilatory threshold with a 12-min rest interval. VO2 was measured on a breath-by-breath basis, and VO2 kinetics were determined with a single exponential model from the averaged data derived from four repetitions. Capillary and venous blood samples were taken to determine plasma [La] and serum [arginine], respectively. RESULTS There were no differences in circulating lactate either before or during exercise. However, serum [arginine] was higher (P < 0.05) in the arginine condition at rest (119.0 +/- 12.6 vs 103.6 +/- 15.7 micromol x L(-1) in the control condition) and after exercise (113.3 +/- 26.0 vs 103.8 +/- 12.6 micromol x L(-1) in the control condition). With regard to the pulmonary VO2 kinetics, no significant difference was observed in the time at which the phase II response emerged or in the phase II amplitude between the two conditions. However, contrary to our hypothesis, the time constant was significantly reduced after arginine administration (i.e., 13.9 +/- 3.1 vs 15.8 +/- 2.6 s in the control condition, P < or = 0.014). CONCLUSION Exogenous L-arginine administration speeds the phase II pulmonary VO2 response by 12% at the onset of moderate-intensity exercise in humans.

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); in the other, the arms were above the level of the heart (>HL). RESULTS In the <HL protocol, the VO2 fast component time constant was not significantly affected by prior exercise (35.9+/-8.7 and 35.5+/-8.9 s in bouts 1 and 2, respectively). The amplitudes of the VO2 fast and slow component were respectively significantly higher and significantly lower in the second bout. 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.