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Background: Insulin resistance (IR) is characterized as a metabolic disorder syndrome that is upstream of hypertension, dyslipidemia, and diabetes mellitus (DM). This study investigated exercise training effects on the exercise tolerance and heart rate dynamics in patients with IR or pancreatic β-cell dysfunction., Methods: Seventy patients (mean age, 60.1 years) with myocardial infarction (MI) participating in a phase II cardiac rehabilitation program were studied. Patients diagnosed with DM were excluded. Homeostasis model-assessment indices were used to divide patients into three groups - A: IR; B: normal; and C: β-cell dysfunction. A cardiopulmonary exercise test (CPX) was performed and peak oxygen uptake (V˙O2) was measured. After baseline testing, subjects participated in a supervised, combined aerobic and resistance exercise program., Results: Peak V˙O2 at baseline was comparable among the three groups, and it improved after training in all groups (p<0.05). However, both the increase and percentage increase in peak V˙O2 were smaller in Group C than in Group A (p<0.05). Heart rate (HR) reserve (peak HR-rest HR), and HR recovery immediately 1min after exercise during CPX were calculated in 45 patients who were not taking negative chronotropic agents. Group C alone did not show any significant increase in HR reserve. HR reserve at both baseline and after training had significant positive correlations with peak V˙O2. HR recovery was 1.9 beats/min lower in group C than group A, but this was not significant. HR recovery in group C did not increase after cardiac rehabilitation., Conclusion: Impaired HR reserve increase after training in patients with pancreatic β-cell dysfunction attenuates exercise training effects on functional capacity. Comprehensive treatment including vigorous exercise training will be needed in such prediabetic patients., (Copyright © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Background: The goal of the present study was to determine knee extensor muscle strength (KEMS) and degree of renal dysfunction associated with an exercise capacity of ≥5 metabolic equivalents (METs) in male chronic heart failure (CHF) patients with chronic kidney disease (CKD)., Methods: In this cross-sectional study of 75 male CHF patients with CKD (65.3 ± 11.6 years), we measured clinical characteristics, peak [Formula: see text], estimated glomerular filtration rate (eGFR), and KEMS. Patients were divided into two groups by exercise capacity: ≥5 METs group (n = 41) and <5 METs group (n = 34). Cutoff values for KEMS and eGFR resulting in an exercise capacity of ≥5 METs were selected with ROC curves. Patients were divided into four groups according to cutoff values, and numbers of patients attaining an exercise capacity of ≥5 METs were compared between groups., Results: Age was significantly higher although eGFR, Hb, and KEMS were lower in the <5 METs versus ≥5 METs group (P < 0.001). Multiple logistic regression analysis revealed a positive significant relation between KEMS and eGFR and exercise capacity of ≥5 METs. Exercise capacity of ≥5 METs was associated with KEMS of approximately 1.69 Nm/kg and an eGFR of 45.7 mL/min/1.73 m(2). The number of patients attaining an exercise capacity of ≥5 METs in the patients who did not reach both cutoff values was significantly lower than that in any other patients (P < 0.001)., Conclusion: KEMS and eGFR may be useful indices for predicting attainment of exercise capacity of ≥5 METs in male CHF patients with CKD.

Background: Patients with chronic heart failure (CHF) commonly fatigue easily due to low peak oxygen uptake (peak VO(2)), an important index of exercise capacity. Maximum phonation time (MPT) is widely used to evaluate maximum vocal capabilities because it is non-invasive, quick, and inexpensive., Aim: The aim of this study was to determine the relation between MPT and exercise capacity, and MPT required to attain an exercise capacity of ≥5 metabolic equivalents (METs) in CHF outpatients., Design: Cross-sectional study., Setting: Outpatient cardiac rehabilitation unit., Population: We enrolled 111 CHF outpatients (mean age 54.2±10.1 years)., Methods: Peak VO(2) was assessed during cardiopulmonary exercise testing (CPX) as the index of exercise capacity. After CPX, we divided the patients into two groups according to exercise capacity: ≥5 METs group (N.=68) and <5 METs group (N.=43). Measurements of MPT were taken in the seated position. All patients were asked to produce a sustained vowel /a:/ for as long as possible and were verbally encouraged during respiratory effort., Results: After adjustment for patient clinical characteristics, MPT in the CHF patients was found to be significantly higher in the ≥5 METs group than in the <5 METs group (22.1±8.4 vs. 17.0±11.6 s, F=13.5, P<0.001). Receiver-operating characteristic curve analysis of exercise capacity of ≥5 METs extracted a cutoff value for MPT of 18.27 s, with a sensitivity of 0.76, 1-specificity of 0.33, and AUC value of 0.81 (95% CI: 0.70-0.87, P<0.001)., Conclusion: There were differences in MPT in relation to an exercise capacity threshold of ≥5 METs in CHF outpatients. A MPT of 18.27 sec may be the best cutoff value to identify people with or without exercise capacity of ≥5 METs., Clinical Rehabilitation Impact: Measurement of MPT may be a useful method for estimating exercise capacity in CHF outpatients.

Purpose: Exercise capacity of fewer than 5 metabolic equivalents (METs) has been associated with high risk of death and poor physical functioning in male patients with heart failure (HF). Therefore, we aimed to determine upper and lower extremity muscle strength levels required to attain an exercise capacity of 5 or more METs in male outpatients with HF., Methods: We enrolled 148 male HF patients (age 60.1 ± 1.0 years). Peak oxygen uptake (peak (Equation is included in full-text article.)o2) was assessed by cardiopulmonary exercise testing (CPX). After CPX, we further divided the patients into groups according to exercise capacity: 5 or more METs (group A, n = 85) and fewer than 5 METs (group B, n = 63). Handgrip strength and knee extensor and flexor muscle strengths were assessed as indices of upper and lower extremity muscle strength, respectively. Receiver operating characteristic curves were used to select cutoff values for upper and lower extremity muscle strength resulting in an exercise capacity of 5 or more METs in these patients., Results: Exercise capacity of 5 or more METs in male HF patients was equivalent to approximately 35.2 kgf of handgrip strength and 1.70 Nm/kg of knee extensor and 0.90 Nm/kg of knee flexor muscle strengths., Conclusions: These upper and lower extremity muscle strength values may be useful target goals for improvement of exercise capacity, risk management, and activities of daily living in male HF patients.

Purpose: Patients with exercise capacity of <5 metabolic equivalents (METs) are considered to have a high risk of death. The aim of this study was to determine age-related differences in physical activity associated with an exercise capacity of ≥5 METs in chronic heart failure (CHF) outpatients., Methods: We enrolled 157 stable CHF patients (79.6% men, age 60.3 ± 11.5 years). Patients were divided into two age-based groups (middle-aged, <65 years, n = 97) and (older-aged, ≥65 years, n = 60). Peak oxygen uptake (peak (V)O(2)) was assessed by cardiopulmonary exercise testing. We further divided patients into groups according to exercise capacity: ≥5 METs and <5 METs. Physical activity was assessed by measuring the average number of steps/day for 1 week with an electronic pedometer., Results: Receiver-operating characteristic curves were used to select cutoff values for steps associated with an exercise capacity of ≥5 METs in the middle- and older-aged patients. Cutoff values of 6045 steps in the middle-aged and 6070 steps in the older-aged patients were determined., Conclusions: Both middle- and older-aged CHF patients with exercise capacity of ≥5 METs completed approximately 6000 steps/day. This could become a target amount for minimal physical activity that could contribute to increased exercise capacity in CHF patients., Implications for Rehabilitation: • Middle-aged and older-aged chronic heart failure (CHF) patients with a measured exercise capacity of ≥5 METs completed approximately 6000 steps/day as measured by electronic pedometer. • This amount of steps could become a target amount for minimal physical activity that could contribute to increased exercise capacity in CHF patients.

The aim of this study was to clarify the mechanism of impaired exercise tolerance in chronic sleep-restricted conditions by investigating variables related to heart-rate (HR) response to sympathetic nervous stimulation. Sixteen healthy men (mean age 21.5 years) were tested in a control state, acute sleep-loss state, and chronic sleep-restricted state. Participants underwent cardiopulmonary exercise testing in each state. Their norepinephrine (NE) concentration was measured before and immediately after exercise. Intracellular magnesium (Mg) concentration was measured in a resting state. Exercise duration was shorter and the ratio of HR response to the percentage increase in NE was higher in the chronic sleep-restricted state than in the control state. Intracellular Mg gradually decreased from control to chronic sleep restriction. There was a negative correlation between peak exercise duration and the ratios of HR response to the rate of increase in NE. Intracellular Mg was positively correlated with the ratios of HR response to the increase in NE both in control and in acute sleep loss. The authors conclude that the impaired exercise tolerance in a chronic sleep-restricted state is caused by hypersensitivity of the HR response to sympathetic nervous stimulation, which showed a compensation for decreased intracellular Mg concentration.

Background: No previous studies have fully investigated the exercise training effect on the skeletal muscle strength and volume to improve the exercise capacity in patients with myocardial infarction (MI). The present study was performed based on a hypothesis that the relationship between exercise capacity, skeletal muscle strength and volume might be changed by the amount of skeletal muscle volume in MI patients up to 3 months after the onset., Methods: Seventy patients with MI underwent symptom-limited cardiopulmonary exercise testing using a treadmill. The lower limb muscle volume (MV) was evaluated according to electrical impedance analysis and the maximal knee extension strength (Peak torque: PT) was measured by a Biodex. All patients participated in 12-week exercise training program. The subjects were divided into 2 groups on the basis of MV: Group H, MV>==22 kg; Group L, MV<22 kg. Delta values were calculated as follows: the value at 3 months minus the value at 1 month., Results: A positive and significant correlation was observed between the delta PT and delta peak VO(2) (r=0.50, p<0.005) only in the L group. No significant correlation was observed between the delta peak VO(2) and the delta lower limb MV or between the delta lower limb MV and the delta PT in the 2 groups., Conclusions: Cardiac rehabilitation program combined with resistance and aerobic training improved exercise capacity and increased not the skeletal muscle volume but the skeletal muscle strength in patients with MI in their recovery phase. It was presumed that the improvement of exercise capacity was determined by the skeletal muscle strength not by the muscle volume especially in MI patients with low muscle volume.

Previous studies have reported that skeletal muscle strength is closely related to exercise capacity in patients with myocardial infarction (MI). However, none of the previous studies have fully investigated the correlation between exercise capacity and the skeletal muscle volume (MV). Seventy patients with MI underwent symptom-limited cardiopulmonary exercise testing using a treadmill. The MV was evaluated by electrical impedance analysis and the maximal knee extension strength (Peak torque: PT) was measured by a Biodex. The subjects were divided into 2 groups according to the MV (group L, MV < 22 kg; group H, MV > or = 22 kg). The PT was positively and significantly correlated with the peak V(.)O(2) in both the L and H groups (r = 0.70 versus r = 0.71). The MV of the lower limbs was positively correlated with the peak V(.)O(2) in the L group (r = 0.57), but not in the H group. The lower limb MV was positively and significantly correlated with PT in the L group (r = 0.48), but not in the H group. The exercise capacity of patients with MI is thought to depend on both the strength and volume of the skeletal muscle. In MI patients with high muscle volume, exercise capacity was determined by skeletal muscle strength alone.

Background: The aim of this study was to clarify the influence of sympathetic and parasympathetic nerve (SN and PN) dysfunction on the heart rate (HR) response to exercise and the exercise capacity of patients with acute myocardial infarction (AMI) and diabetes mellitus (DM)., Methods and Results: Fifty-two male patients who underwent cardiopulmonary exercise testing (CPX) 1 month after onset of AMI were divided into 2 groups: (DM (+) group, n=20; DM (-) group, n=32). HR, peak oxygen uptake (VO2peak), and plasma norepinephrine (NE) levels were measured during CPX. The high-frequency power (HF) was analyzed by HR variability. The DeltaHR/logDeltaNE obtained from changes of HR and NE from rest to peak exercise and HR change from baseline to the minimum HF (DeltaHRHF) were calculated as parameters of HR response derived from SN and PN activities, respectively. DeltaHR, VO2peak, DeltaHR/logDeltaNE, and DeltaHRHF were significantly lower in the DM (+) group than in the DM (-) group, and both of them showed positive correlations with VO2peak., Conclusion: An inadequate HR response to exercise is a major factor causing a decline of exercise capacity, which is derived from both of SN and PN dysfunction, in AMI patients with DM.

We investigated the correlations between exercise intolerance and the plasma levels of neurohormonal factors and proinflammatory cytokines in chronic heart failure (CHF) patients. Sixty-two CHF patients who underwent cardiopulmonary exercise testing (CPX) were enrolled in this study. Peak oxygen uptake (peak VO2) and the plasma concentrations of noradrenaline (NA), brain natriuretic peptide (BNP), and soluble tumor necrosis factor receptors I and II (TNFR-I and -II) were all measured during the CPX. The patients were divided into three groups according to their peak VO2; a severe exercise intolerance group (severe group; peak VO2 < 18 mL/min/kg), moderate exercise intolerance group (moderate group; 18 24). There were no significant differences in left ventricular ejection fraction (EF) among the three groups. NA and BNP both increased gradually in parallel with the worsening of exercise intolerance (NA, 211.5 +/- 75.7 pg/mL, 331.8 +/- 163.7, 441.9 +/- 202.9, respectively; BNP, 37.9 +/- 25.4 pg/mL, 148.9 +/- 117.1, 247.9 +/- 150.0, respectively). TNFR-I and II were significantly higher in the severe group than in the moderate group (1746.1 +/- 950.7 versus 1085.2 +/- 370.5 pg/mL and 2855.3 +/- 1550.9 versus 2047.7 +/- 648.7 pg/mL, respectively), while the values in the moderate group were not significantly different from those in the mild group. EF showed no significant correlations with NA, BNP, TNFR-I, or TNFR-II, whereas peak VO2 exhibited significant negative correlations with NA (r = -0.50, P < 0.0001), BNP (r = -0.53, P < 0.0001), TNFR-I (r = -0.50, P < 0.0001), and TNFR-II (r = -0.45, P < 0.0001). It is concluded that NA and BNP rise in parallel with the degree of exercise intolerance, while TNFR-I and -II rise only when exercise intolerance reaches severe levels.

Objectives: Physical training in cardiac patients can increase exercise capacity and reduce plasma brain natriuretic peptide(BNP) concentration, but these effects may depend on the etiology of cardiac disease. The change in exercise capacity and BNP during the training period were investigated in patients with different cardiac diseases., Methods: Ninety-one patients after coronary artery bypass grafting(CABG) and 78 patients after valve replacement (VR) underwent a symptom-limited incremental cardiopulmonary exercise test before (1 month) and 6 months after physical training. Anaerobic threshold and peak oxygen uptake(peak-Vo2) were measured during the cardiopulmonary exercise test. Before each cardiopulmonary exercise test, a blood sample was obtained in the resting condition for measuring BNP., Results: Anaerobic threshold and peak-Vo2 were increased significantly from 1 month to 6 months in both groups. BNP in the CABG group indicated a tendency to decrease (194.6 +/- 155.3-->144.2 +/- 232.2 pg/ml, p < 0.1) from 1 month to 6 months. BNP in VR group was significantly decreased (159. 9 +/- 115.5-->112.8 +/- 131.7 pg/ml, p < 0.05) during the training period. The CABG group showed a significant negative correlation between peak-Vo2 and BNP at 1 month(r = -0.28, p < 0.01) and at 6 months(r = -0.39, p = 0.001). The VR group showed a significant negative correlation between peak-Vo2 and BNP at 6 months(r = -0.32, p < 0.01), but not at 1 month., Conclusions: Six months of physical training in patients after cardiac surgery may improve exercise capacity and reduce BNP. BNP concentration in the VR group before physical training did not reflect functional capacity.

The present study was undertaken to investigate the relationship between the extent of impaired chronotropic response and cardiac output during exercise, and exercise tolerance in patients with chronic heart failure. The subjects consisted of 24 patients (mean 60.1 +/- 14.0 years) who had mild chronotropic incompetence. Cardiopulmonary exercise testing was performed in all patients, and heart rate (HR), anaerobic threshold (AT), maximum oxygen uptake (peak VO2), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO2 slope), and exercise time were measured. Cardiac output (CO) was measured by a thoracic bioimpedance method and cardiac index (CI) was calculated. Plasma norepinephrine (NE) was measured at rest and immediately after the exercise test. The changes in HR, NE, and CI from the resting state to immediately after exercise were calculated as deltaHR, deltaNE, and deltaCI, respectively. The deltaNE was converted to a logarithmic scale and deltaHR/log deltaNE was used as a parameter of HR response to sympathetic nerve stimulation. The results were as follows: HR and NE in the resting state had no correlation with AT and with peak VO2. DeltaHR/log deltaNE correlated positively with both AT and peak VO2, and negatively with the VE/CO2 slope. DeltaHR/log deltaNE correlated positively with peak CI, %deltaCI, and deltaCI/exercise time. The data suggest that one of the mechanisms of low exercise tolerance in chronic heart failure patients was due to an inadequate increase in CO response against exercise caused by an impaired HR response to increased NE.

Recent observations have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlate with cardiac function or prognosis in heart failure patients. However, relatively little is known about changes in their plasma concentration during commonly occurring physiological states such as fatigue. Therefore, this study was designed to examine the physiological changes of plasma ANP and BNP concentrations using a chronic sleep-deprivation model. Bicycle ergometer cardiopulmonary exercise tests were performed in 10 healthy volunteers (mean age: 22.7 years). Blood samples for measuring ANP and BNP were drawn during the resting state and immediately after each exercise test. Cardiac output (CO) was measured during the exercise test by the impedance method. The study conditions were designed as follows: (A) a day following a period of normal sleep (control state) and (B) a day preceded by 1 month during which sleep lasted <60% of normal (chronic sleep-deprived state). Results were as follows. (1) Peak oxygen uptake and peak CO decreased during the sleep-deprived state compared with the control state. (2) There was no difference between peak heart rates measured during exercise under the 2 conditions. (3) Plasma ANP concentration during exercise increased significantly during the control state, whereas only a tendency toward increase was observed during the sleep-deprived state. (4) Plasma BNP concentration during exercise tended to increase in the control state compared with the resting state, whereas there was no difference in plasma BNP between after exercise and resting state in the sleep-deprived state. These results indicate that changes of ANP or BNP induced by exercise tended to be decreased by chronic sleep deprivation.

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.

Cardiac index is widely used as a parameter of cardiac function for cardiovascular patients, but its value is limited when measured in the resting supine position, because it never demonstrates the maximal cardiac index performance. The incremental increase in cardiac index (delta CI) was evaluated during incremental exercise (delta work rate: delta WR), delta CI/delta WR, in patients with chronic congestive heart failure, and compared to brain natriuretic peptide (BNP), which is known to be increased in patients with chronic left ventricular dysfunction. The subjects were 18 heart failure patients (16 males and 2 females, mean age [+/-SD] 63.8 +/- 8.9 years). Symptom-limited cardiopulmonary exercise test using cycle ergometer was performed. Cardiac index was calculated with the Benchmark Exercise Test device using oxygen uptake, carbon dioxide output and respired flow. Blood samples were taken in the resting state before the exercise test. A positive correlation was obtained between delta CI/delta WR and peak oxygen uptake (peak VO2) (r = 0.71, p < 0.01), and delta CI/delta WR and peak oxygen pulse (r = 0.66, p < 0.01). A negative correlation was obtained between delta CI/delta WR and BNP (r = 0.45) in the resting state. Peak VO2 (20.9 +/- 7.5 vs 13.9 +/- 2.7 ml/min/kg, p < 0.05), peak cardiac index (7.2 +/- 1.7 vs 5.5 +/- 0.9 l/min/m2, p < 0.05), and delta CI/delta WR (20.1 +/- 8.1 vs 12.4 +/- 2.5 ml/m2/W, p < 0.05) were significantly higher in the group with normal BNP (mean [+/-SD] 11.0 +/- 3.2 pg/ml) than in the group with high BNP (40.7 +/- 22.7 pg/ml). Delta CI/delta WR reflects the grade of exercise tolerance and may be useful for evaluating exercise capacity in patients with congestive heart failure.

The present study was conducted to investigate the effects of cilazapril on exercise tolerance and the hormone kinetics of catecholamines, the reninangiotensin-aldosterone system and alpha-atrial natriuretic peptide (ANP) in patients in the chronic phase of acute myocardial infarction (AMI). The subjects consisted of 19 cases of AMI. Cardiopulmonary exercise testing was performed 1 month after the onset of AMI, and patients were randomly assigned to either a group treated with 1 mg/day of cilazapril (9 cases) and or an untreated group (10 cases). After the completion of 2 months of exercise training at the anaerobic threshold (AT), blood samples were taken during a cardiopulmonary exercise test and various hormones were measured. In comparing the parameters of exercise tolerance before and after the completion of exercise training there were no significant differences between the 2 groups with respect to oxygen uptake, oxygen pulse, or exercise time at AT or at peak exercise. With regard to temporal changes in exercise tolerance, oxygen uptake, oxygen pulse and exercise time all tended to increase in both groups. With regard to hormone kinetics, the alpha-ANP concentration at peak exercise was significantly lower, and the noradrenaline secretions also tended to be lower, in the cilazapril-treated group, even though the peak exercise time was similar in both groups. These results may be support the hypothesis that cilazapril mitigates the left ventricular load during exercise therapy in patients in the chronic phase of AMI.

The effect of combined aerobic and weight training on indexes of muscle strength and exercise capacity was investigated in 59 patients after myocardial infarction. Subjects were randomly assigned into three groups: group I performing combined aerobic and weight training (n = 22), group II performing ordinary aerobic training alone (n = 19) and group III not performing physical training (n = 18). Before and after the training, isokinetic knee extension strength was measured and cardiopulmonary exercise testing was performed. Physical training was prescribed for 8 weeks. Weight training of knee extensors was performed at 60% of 1 repetition maximum and aerobic training was prescribed at the heart rate of anaerobic threshold (AT) level. After 8 weeks, the increase of isokinetic knee extension strength was significantly greater in group I (26 +/- 14%) than group II (6 +/- 8%) and III (4 +/- 8%). Increases in peak VO2, exercise time, AT and peak O2 pulse were greater in groups I and II than group III. Furthermore, increase of exercise time was greater in group I (25 +/- 14%) than group II (16 +/- 9%). The rating of perceived exertion in submaximal exercise decreased significantly only for group I. In patients with myocardial infarction, combined aerobic and weight training is a more effective method for increasing muscle strength and exercise capacity than only ordinary aerobic training.

To predict exercise tolerance in the chronic phase of myocardial infarction (MI), cardiopulmonary exercise testing was performed using a ramp treadmill protocol in 25 patients at 1 and 3 months after the onset of MI. Oxygen uptake, heart rate and O2 pulse were estimated at rest, during a warm-up period, and at the levels of anaerobic threshold (AT), respiratory compensation (RC) and peak exercise. Results were as follows: 1) AT and peak oxygen uptake at 3 months after the onset of MI were 14.1 +/- 2.8 and 21.8 +/- 5.2 ml/min/Kg, respectively. 2) The subjects were divided into 2 groups according to peak oxygen uptake at 3 months: one showing peak oxygen uptake > 22 ml/min/Kg and the other < 22 ml/min/Kg. The former group (n = 13) was referred to as the good tolerance group, and the latter group (n = 12) was referred to as the poor tolerance group. Oxygen uptake at AT, RC and peak exercise was lower in the poor tolerance group than in the good tolerance group (11.2 vs 14.7, 15.1 vs 20.4, 17.1 vs 23.4 ml/min/Kg, respectively). 3) The increases in oxygen uptake from AT to RC and from AT to peak exercise were less in the poor tolerance group than in the good tolerance group. 4) O2 pulse at rest, warm-up, AT, RC and peak exercise were also lower in the poor tolerance group.2+ tolerance in the chronic phase of MI.