Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

Urea kinetics in humans at two levels of exercise intensity

A primed constant infusion of [15N2]urea was used to quantify the response of urea production to exercise at 40 and 70% maximal oxygen consumption on a treadmill. Total urea production, urea production from recycled N, urea production from nonrecycled N, and urea N recycled back into body protein were calculated. Most components of urea kinetics were unaffected by exercise at either intensity. The rate of urea reincorporated into protein was significantly increased during exercise and recovery at both levels of exercise. We conclude that exercise does not stimulate urea production but that there may be an accelerated reincorporation of urea N back into body protein.     

Alanine and glutamine kinetics at rest and during exercise in humans

PURPOSE: The purpose of this study was to quantify both alanine and glutamine kinetics during exercise of moderate intensity to determine the sum total of alanine and glutamine flux. METHODS: Tracer methods were used to quantify alanine and glutamine rates of appearance (Ra) in plasma at rest and during 180 min of approximately 45% VO2max treadmill exercise in six normal volunteers (25 +/- 2 yr, 68 +/- 2.5 kg, VO2max 43 +/- 2.4 mL.min-1.kg-1; means +/- SE). Bolus injections (N = 3) or primed-constant infusions (N = 3) of 2H5-glutamine and 3-13C-alanine were given at rest on 1 d and 10-15 min after the onset of exercise on a separate day less than 2 wk later. Plasma enrichment decay curves and plateau enrichments were used to estimate alanine and glutamine kinetics. RESULTS: Whereas alanine Ra increased significantly from rest to exercise (5.72 +/- 0.31 vs 13.5 +/- 1.9 mumol.min-1.kg-1, respectively; P < 0.01), glutamine Ra was not significantly altered by exercise (6.11 +/- 0.44 and 6.40 +/- 0.69 mumol.min-1.kg-1 at rest and during exercise, respectively). The total of alanine and glutamine flux increased from 17.93 +/- 0.88 to 25.98 +/- 3.04 (P < 0.05). CONCLUSIONS: Since most muscle amino-N is released as alanine and glutamine, these findings provide strong evidence that amino-N delivery from muscle to the liver is increased during exercise. In addition, it appears that alanine, rather than glutamine, is the predominant N carrier involved in the transfer of N from muscle to the liver during moderate intensity exercise.     

Comparison of femoral blood gases and muscle near-infrared spectroscopy at exercise onset in humans

We hypothesized that near-infrared spectroscopy (NIRS) measures of hemoglobin and/or myoglobin O2 saturation (IR-SO2) in the vascular bed of exercising muscle would parallel changes in femoral venous O2 saturation (SfvO2) at the onset of leg-kicking exercise in humans. Six healthy subjects performed transitions from rest to 48 +/- 3 (SE)-W two-legged kicking exercise while breathing 14, 21, or 70% inspired O2. IR-SO2 was measured over the vastus lateralis muscle continuously during all tests, and femoral venous and radial artery blood samples were drawn simultaneously during rest and during 5 min of exercise. In all gas-breathing conditions, there was a rapid decrease in both IR-SO2 and SfvO2 at the onset of moderate-intensity leg-kicking exercise. Although SfvO2 remained at low levels throughout exercise, IR-SO2 increased significantly after the first minute of exercise in both normoxia and hyperoxia. Contrary to the hypothesis, these data show that NIRS does not provide a reliable estimate of hemoglobin and/or O2 saturation as reflected by direct femoral vein sampling.     

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans

We tested the hypothesis that the slower increase in alveolar oxygen uptake (VO2) at the onset of supine, compared with upright, exercise would be accompanied by a slower rate of increase in leg blood flow (LBF). Seven healthy subjects performed transitions from rest to 40-W knee extension exercise in the upright and supine positions. LBF was measured continuously with pulsed and echo Doppler methods, and VO2 was measured breath by breath at the mouth. At rest, a smaller diameter of the femoral artery in the supine position (P < 0. 05) was compensated by a greater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of 6 min of exercise, femoral artery diameter was larger in the upright position and there were no differences in VO2, MBV, or LBF between upright and supine positions. The rates of increase of VO2 and LBF in the transition between rest and 40 W exercise, as evaluated by the mean response time (time to 63% of the increase), were slower in the supine [VO2 = 39.7 +/- 3.8 (SE) s, LBF = 27.6 +/- 3.9 s] than in the upright positions (VO2 = 29.3 +/- 3.0 s, LBF = 17.3 +/- 4.0 s; P < 0.05). These data support our hypothesis that slower increases in alveolar VO2 at the onset of exercise in the supine position are accompanied by a slower increase in LBF.     

Velocity of oxygen uptake response at the onset of exercise: A comparison between children after cardiac surgery and healthy boys

A comparison was carried out concerning maximal oxygen uptake, oxygen uptake adjustment at the onset of high-intensity exercise, and maximal blood lactate between 10 healthy prepubertal boys and 35 children after repair of cardiac malformations or after Fontan operation. Mean maximal oxygen uptake (VO2) was moderately reduced in children after repair of tetralogy of Fallot or after Mustard or Senning operations and severely reduced after Fontan operations. Conversely, mean half-time of VO2 response was moderately prolonged in children after repair of tetralogy of Fallot or after Senning and Mustard operations and considerably prolonged after Fontan operations. According to our results unfavorable kinetics of VO2 response to physical exercise are present in addition to reduced aerobic power in many of the operated children. Besides being less qualified for endurance performance, these children are also less prepared for short, high-intensity exercise.     

Progressive effect of endurance training on VO2 kinetics at the onset of submaximal exercise

The rates of increase in O2 uptake (VO2) after step changes in work rate from 25 W to 60% of pretraining peak VO2 (VO2 peak) were measured at various times during an endurance training program (2 h/day at 60% pretraining VO2 peak). Seven untrained males [23 +/- 1 (SE) yr] performed a series of repeated step changes in work rate before training (PRE) and after 4 days (4D), 9 days (9D), and 30 days (30D) of training. VO2 kinetic responses were determined from breath-by-breath data averaged across four repetitions and analyzed using a two-component exponential model. Mean response time (time taken to reach 63% of steady-state VO2) was faster (P < 0.01) than PRE (38.1 +/- 2.6 s) at both 4D (34.9 +/- 2.4 s) and 9D (32.5 +/- 1.8 s) and was faster (P < 0.01) at 30D than at all other times (28.3 +/- 1.0 s). Blood lactate concentrations (after 6 min of cycling) were also lower at 4D and 9D than PRE (P < 0.01) and were lower at 30D than at all other times (P < 0.01). VO2 peak was unchanged from PRE (3.52 +/- 0.20 l/min) at 8D (3.55 +/- 0.20 l/min) but was increased (P < 0.01) at 30D (3.89 +/- 0.18 l/min). Muscle oxidative capacity (maximal citrate synthase activity) was not significantly increased until 30D (P < 0.01). It is concluded that at least part of the acceleration of whole body VO2 kinetics with endurance training is a rapid phenomenon, occurring before changes in VO2 peak and/or muscle oxidative potential.     

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.     

Determinants of oxygen uptake. Implications for exercise testing

For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.     

Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans

The activation of MAPKs is controlled by the balance between MAPK kinase and MAPK phosphatase activities. The latter is mediated by a subset of phosphatases with dual specificity (VH-1 family). Here, we describe a new member of this family encoded by the puckered gene of Drosophila. Mutations in this gene lead to cytoskeletal defects that result in a failure in dorsal closure related to those associated with mutations in basket, the Drosophila JNK homolog. We show that puckered mutations result in the hyperactivation of DJNK, and that overexpression of puc mimics basket mutant phenotypes. We also show that puckered expression is itself a consequence of the activity of the JNK pathway and that during dorsal closure, JNK signaling has a dual role: to activate an effector, encoded by decapentaplegic, and an element of negative feedback regulation encoded by puckered.     

Maximal oxygen uptake during exercise with various combinations of arm and leg work

Oxygen uptake (VO2) was determined in 10 males during the following types of maximal exercise (work time: about 5 min): uphill running, bicycling, arm work (cranking), and combined arm work and bicycling (A + L). The A + L exercise was performed in four different ways, the arms doing 10%, 20%, 30%, or 40% of the same total rate of work; and also with the maximal bicycle work load plus either maximal or submaximal arm work. VO2 was the same in running as in all types of A + L exercise, except when the arm work load was 10% and 40% of the total rate of work, where VO2 was 2.5% (P less than 0.05) and 9.4% (P less than 0.001) lower, respectively. Bicycle VO2 was lower than VO2 in running but equal to A + L VO2 when arm work intensity was 40% of the total rate of work. It is concluded that VO2 during maximal exercise a) to a certain extent depends on the exercising muscle mass, b) is lower than the oxygen-consuming potential of the muscles involved in A + L exercise, and c) in A + L exercise is influenced by the ratio of arm work to total rate of work and the subject's fitness for arm work and bicycling.     

Oxygen uptake kinetics during low level exercise in patients with heart failure: relation to neurohormones, peak oxygen consumption, and clinical findings

OBJECTIVE: To investigate whether oxygen uptake (VO2) kinetics during low intensity exercise are related to clinical signs, symptoms, and neurohumoral activation independently of peak oxygen consumption in chronic heart failure. DESIGN: Comparison of VO2 kinetics with peak VO2, neurohormones, and clinical signs of chronic heart failure. SETTING: Tertiary care centre. PATIENTS: 48 patients with mild to moderate chronic heart failure. INTERVENTIONS: Treadmill exercise testing with "breath by breath" gas exchange monitoring. Measurement of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), and noradrenaline. Assessment of clinical findings by questionnaire. MAIN OUTCOME MEASURES: O2 kinetics were defined as O2 deficit (time [rest to steady state] x DeltaVO2 -sigmaVO2 [rest to steady state]; normalised to body weight) and mean response time of oxygen consumption (MRT; O2 deficit/DeltaVO2). RESULTS: VO2 kinetics were weakly to moderately correlated to the peak VO2 (O2 deficit, r = -0.37, p < 0.05; MRT, r = -0.49, p < 0.001). Natriuretic peptides were more closely correlated with MRT (ANF, r = 0.58; BNP, r = 0.53, p < 0.001) than with O2 deficit (ANF, r = 0.48, p = 0.001; BNP, r = 0.37, p < 0.01) or peak VO2 (ANF, r = -0.40; BNP, r = -0.31, p < 0.05). Noradrenaline was correlated with MRT (r = 0. 33, p < 0.05) and O2 deficit (r = 0.39, p < 0.01) but not with peak VO2 (r = -0.20, NS). Symptoms of chronic heart failure were correlated with all indices of oxygen consumption (MRT, r = 0.47, p < 0.01; O2 deficit, r = 0.39, p < 0.01; peak VO2, r = -0.48, p < 0. 01). Multivariate analysis showed that the correlation of VO2 kinetics with neurohormones and symptoms of chronic heart failure was independent of peak VO2 and other variables. CONCLUSIONS: Oxygen kinetics during low intensity exercise may provide additional information over peak VO2 in patients with chronic heart failure, given the better correlation with neurohormones which represent an index of homeostasis of the cardiovascular system.     

Validity of oxygen uptake measurements during exercise under moderate hyperoxia

PURPOSE: The validity of oxygen uptake in hyperoxia (FIO2 = 30%) measured by an automated system (MedGraphics, CPX/D system) was assessed during the simulation of gas exchanges during exercise with a mechanical system and during submaximal exercise by human subjects. METHODS: The simulation system reproduced a stable and accurate VO2 for 30 min (sim-test). This trial was repeated nine times in normoxia and nine times in hyperoxia. Ten subjects also performed two submaximal exercises (55% of normoxic VO2max) on a cycle ergometer at the same absolute power in normoxia and in hyperoxia (ex-test). RESULTS: There was a significant downward drift of the oxygen fraction measurement in hyperoxia (< or = 0.10% for FIO2 and FEO2) during sim-test, but VO2 measurement remained stable in the two conditions. There was also a downward drift of the oxygen fraction measurement in the two conditions (< or = 0.07% for FIO2) during ex-test. VO2 was significantly higher in hyperoxia (+4.6%), and this result was confirmed using a modified Douglas bag method. CONCLUSIONS: These findings show that the CPX/D system is stable and valid for assessing VO2 in moderate hyperoxia.     

Cardiovascular responses at the onset of static exercise in patients with dual-chamber pacemakers

Cardiac output (CO) responses to exercise can be altered by ventricular pacing in pacemaker-dependent patients. The relative contributions of CO and peripheral vascular resistance (PVR) toward the initial increase in blood pressure with the initiation of static exercise were investigated in eight otherwise healthy pacemaker-dependent subjects [age 24 +/- 2 yr (range 17-37 yr)]. Beat-by-beat measures of heart rate (HR; electrocardiography), mean arterial pressure (MAP), and CO derived from stroke volume (SV) (CO = HR.SV; 2-D echocardiography) were determined during the first 20 s of a one-legged static knee extension performed at 20% maximal voluntary effort by using three pacing modalities: dual pacing and sensing mode (DDD, i.e., normal physiological HR response), fixed at resting HR (DOO-R), and fixed at peak exercise HR (DOO-E), as previously achieved during 5 min of sustained contraction in the DDD mode. There were no differences in MAP, CO, or PVR (PVR = MAP/CO) between modes at rest (P > 0.05). With DOO-E pacing, SV was lower at rest compared with the other modes and increased with exercise (P < 0.05). Although there were no significant increase in MAP or CO during DOO-R pacing, both variables were elevated by leg contraction during DDD and DOO-E pacing (P < 0.05), with no significant change in PVR. Additionally, the CO and MAP increases were significantly greater with DOO-E pacing (P < 0.05). Thus the magnitude of the initial increase in arterial pressure at the onset of mild one-legged static exercise was dictated by the changes in CO as PVR remained unchanged.     

Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

Supplemental oxygen has acute beneficial effects on exercise performance in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate whether oxygen-supplemented training enhances the effects of training while breathing room air in patients with severe COPD. A randomized controlled trial was performed in 24 patients with severe COPD who developed hypoxaemia during incremental cycle exercise (arterial oxygen saturation (Sa,O2) <90% at peak exercise). All patients participated in an in-patient pulmonary rehabilitation programme of 10 weeks duration. They were assigned either to general exercise training while breathing room air (GET/RA group: forced expiratory volume in one second (FEV1) 38% of predicted; arterial oxygen tension (Pa,O2) 10.5 kPa at rest; Pa,O2 7.3 kPa at peak exercise), or to GET while breathing supplemental oxygen (GET/O2 group: FEV1 29% pred; Pa,O2 10.2 kPa at rest; Pa,O2 7.2 kPa at peak exercise). Sa,O2 was not allowed to fall below 90% during the training. The effects on exercise performance while breathing air and oxygen, and on quality of life were compared. Maximum workload (Wmax) significantly increased in the GET/RA group (mean (SD) 17 (15) W, p<0.01), but not in the GET/O2 group (7 (25) W). Six minute walking distance (6MWD), stair-climbing, weight-lifting exercise (all while breathing room air) and quality of life significantly increased in both groups. Acute administration of oxygen improved exercise performance before and after training. Training significantly increased Wmax, peak carbon dioxide production (V'CO2) and 6MWD while breathing oxygen in both groups. Differences between groups were not significant. Pulmonary rehabilitation improved exercise performance and quality of life in both groups. Supplementation of oxygen during the training did not add to the effects of training on room air.     

Prediction of maximum oxygen uptake during physical exercise on bicycle ergometer

Possibilities to predict maximum oxygen uptake (VO2max) during exercising on bicycle ergometer using the Russian Rating Perceived Exertion (RPE) was studied. Results of examination of 13 athletes demonstrate the possibility of predicting individual and group average VO2max on the basis of data from submaximum testing and the empirical formulas from the value of VO2max registered at RPE numbers 13 and 15. These VO2max values can serve as markers for assessing the dynamics of physical performance.     

O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise

Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La-]pl) during fatiguing exercise. We hypothesized that a lower [La-]pl may be associated with faster O2 uptake (V(O2)) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, VE(T). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (VE(T)). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La-]pl. MRT was similar during Con (31.2 +/- 2.6 and 32.7 +/- 1.2 s for on and off, respectively) and Acz (30.9 +/- 3.0 and 31.4 +/- 1.5 s for on and off, respectively) for work rates VE(T), MRT was similar between Con (69.1 +/- 6.1 and 50.4 +/- 3.5 s for on and off, respectively) and Acz (69.7 +/- 5.9 and 53.8 +/- 3.8 s for on and off, respectively). On- and off-MRTs were slower for >VE(T) than for VE(T) exercise but was lower at the end of the transition during Acz (1.4 +/- 0.2 and 7.1 +/- 0.5 mmol/l for VE(T) respectively) than during Con (2.0 +/- 0.2 and 9.8 +/- 0.9 mmol/l for VE(T), respectively). CA inhibition does not affect O2 utilization at the onset of VE(T) exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.     

Effect of voluntary exercise on maximal oxygen uptake in young female Fischer 344 rats

The effect of voluntary exercise on maximal oxygen uptake (VO2 max) was studied in young female Fischer 344 rats. After 10 weeks of wheel-running training, the absolute VO2 max and VO2 max relative to body mass increased without a decline in body mass. The running speed eliciting VO2 max, heart and soleus muscle mass, and succinate dehydrogenase (SDH) activity in the soleus muscle also increased. These results suggest that voluntary exercise is an effective means of increasing the aerobic exercise capacity of young female Fischer 344 rats.     

Effects of percutaneous balloon mitral valvuloplasty and exercise training on the kinetics of recovery oxygen consumption after exercise in patients with mitral stenosis

AIMS: Kinetics of recovery oxygen consumption after exercise plays an important role in determining exercise capacity. This study was performed to assess the kinetics of recovery oxygen consumption in mitral stenosis and evaluate the effects of percutaneous balloon mitral valvuloplasty and exercise training on the kinetics. METHODS AND RESULTS: Thirty patients with mitral stenosis (valve area < or =1.0 cm2) and same sized age- and size-matched healthy volunteers were included for this study. All subjects performed maximal upright graded bicycle exercise. Thirty consecutive patients who underwent successful percutaneous balloon mitral valvuloplasty (valve area > or =1.5 cm2 and mitral regurgitation grade < or =2), were randomized to an exercise training group or non-training group. The exercise group performed daily exercise training for 3 months. Half-recovery time of peak oxygen consumption was significantly delayed in mitral stenosis as compared to normal subjects (120+/-42 s vs 59+/-5, P<0.01). Peak oxygen consumption (ml x min(-1) x kg(-1)) was significantly increased in both the training (16.8+/-4.9 to 25.3+/-6.9) and non-training groups (16.3+/-5.1 to 19.6+/-6.0) 3 months after percutaneous balloon mitral valvuloplasty. Half-recovery time of peak oxygen consumption was significantly shortened in the training group (124+/-39 to 76+/-13, P<0.01), but not in the non-training group (114+/-46 to 109+/-44 s, P=0.12) at 3 months follow-up. The degrees of symptomatic improvement after percutaneous balloon mitral valvuloplasty were more closely correlated with the changes of the half-recovery time of peak oxygen consumption than those of peak oxygen consumption. CONCLUSION: Kinetics of recovery oxygen consumption was markedly delayed in mitral stenosis, which was improved after exercise training but not after percutaneous balloon mitral valvuloplasty alone. These results suggest that adjunctive exercise training may be useful for improvement of recovery kinetics and subjective symptoms after percutaneous balloon mitral valvuloplasty.