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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.)

To examine differences in objective and subjective outcomes in outpatients undergoing percutaneous coronary intervention (PCI) performed for acute myocardial infarction versus cardiac surgery (CS) following a phase II cardiac rehabilitation (CR). Longitudinal observational study of 437 consecutive cardiac outpatients after 8 weeks of phase II CR. Patients were divided into the PCI group (n = 281) and CS group (n = 156). Handgrip and knee extensor muscle strength, peak oxygen uptake VO₂, upper- and lower-body self-efficacy for physical activity (SEPA), and physical component summary (PCS) and mental component summary (MCS) scores as assessed by Short Form-36 were measured at 1 and 3 months after PCI or CS. All outcomes increased significantly between months 1 and 3 in both groups. However, increases were greater in the CS versus PCI group in handgrip strength (+12.3 % vs. +8.1%, P < 0.01), knee extensor muscle strength (+19.3% vs. +17.5%, P = 0.008), peak VO₂ (+20.9% vs. +16.9%, P < 0.01), upper-body SEPA (+27.7% vs. +9.2 vs. , P = 0.001), and PCS score (+6.5% vs. +4.1%, P = 0.001). Although this relatively short-term phase II CR increased all outcomes for both groups, outcomes showed the recovery process was different between the PCI and CS groups, slightly favoring CS patients. Furthermore, patents in the field of CR are presented.

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.

Objective: To evaluate the effect of the self-monitoring approach (SMA) on self-efficacy for physical activity (SEPA), exercise maintenance, and objective physical activity level over a 6-mo period after a supervised 6-mo cardiac rehabilitation (CR) program., Design: We conducted a randomized, controlled trial with 45 myocardial infarction patients (38 men, seven women; mean age, 64.2 yrs) recruited after completion of an acute-phase, exercise-based CR program. Patients were randomly assigned to an SMA group (n = 24) or control group (n = 21). Along with CR, the subjects in the SMA group self-monitored their weight and physical activity for 6 mos. The SMA used in this study was based on Bandura's self-efficacy theory and was designed to enhance confidence for exercise maintenance. The control group participated in CR only. All patients were evaluated with the SEPA assessment tool. Exercise maintenance, SEPA scores, and objective physical activity (average steps per week) as a caloric expenditure were assessed at baseline and during a 6-mo period after the supervised CR program., Results: Mean period from myocardial infarction onset did not differ significantly between the SMA and control groups (12.1 +/- 1.3 vs. 12.2 +/- 1.2 mos, P = 0.692). All patients maintained their exercise routine in the SMA group. Mean SEPA score (90.5 vs. 72.7 points, P < 0.001) and mean objective physical activity (10,458.7 vs. 6922.5 steps/wk, P < 0.001) at 12 mos after myocardial infarction onset were significantly higher in the SMA than control group. SEPA showed significant positive correlation with objective physical activity (r = 0.642, P < 0.001)., Conclusions: SMA during supervised CR may effectively increase exercise maintenance, SEPA, and objective physical activity at 12 mos after myocardial infarction onset.

Objective: The purpose of this study was to determine exercise maintenance rate, leisure-time objective physical activity level, and health-related quality of life in relation to exercise maintenance over the 6-mo period after a supervised 5-mo recovery-phase cardiac rehabilitation program in acute myocardial infarction patients. The study also investigated whether exercise maintenance resulted in reproducible health-related quality-of-life outcomes comparable with those of the Japanese normal population., Design: This observational study comprised 109 acute myocardial infarction patients (89 men, 20 women; mean age, 63.5 +/- 10.1 yrs). Physiologic outcomes (peak oxygen uptake, handgrip, and knee-extension strength) measured at 1 and 6 mos after acute myocardial infarction onset were compared. Completed exercise maintenance and health-related quality-of-life questionnaires and results of electronic pedometer recordings to evaluate leisure-time objective physical activity level were assessed 6 mos after cardiac rehabilitation., Results: The mean period from acute myocardial infarction to evaluation of outcomes was 18.8 +/- 3.4 mos. Ninety of 109 patients (82.6%) continued exercise for >6 mos after cardiac rehabilitation (exercise group); 19 patients (17.4%) quit exercise after cardiac rehabilitation (nonexercise group). Improvement in physiologic outcomes was noted at 6 mos vs. those at 1 mo, but outcomes were not significantly different between groups. The exercise group performed significantly better than the nonexercise group for leisure-time objective physical activity level and scored significantly higher than the nonexercise group for seven of eight health-related quality of life measures, attaining scores similar to those of the Japanese normal population., Conclusions: At >18 mos after acute myocardial infarction, the exercise maintenance rate in our patients remains high, and exercise maintenance may be one of the factors contributing to improvement of health-related quality of life and leisure-time objective physical activity level.

Objectives: This study investigated whether myocardial infarction patients with diabetes mellitus had lower heart rate reserve to exercise by measuring the increment in heart rate (HR) divided by the increment of norepinephrine (NE) concentration from rest to peak exercise (delta HR/log delta NE). The difference in exercise training effects was also investigated., Methods: The 148 patients after myocardial infarction were divided into two groups, the DM group (n = 34) and the non-DM group (n = 114). Cardiopulmonary exercise testing was performed in each subject at 1 and 3 months after the onset. Blood samples were taken at rest and immediately after peak exercise, rest brain natriuretic peptide, rest and peak norepinephrine were analyzed. Exercise training was performed from 1 to 3 months after the onset., Results: Resting heart rates were significantly higher in the DM group than in the non-DM group both at 1 and 3 months although peak heart rates were not significantly different. Peak oxygen uptake were lower in the DM group both at 1 and 3 months after onset of myocardial infarction compared to the non-DM group. End-tidal carbon dioxide pressure was lower and the rate of increase of minute ventilation to carbon dioxide output was higher in the DM group. Plasma brain natriuretic peptide was higher in the DM group. delta HR/log delta NE was 19.4 +/- 4.0 in the DM group and 22.2 +/- 5.6 in the non-DM group (p < 0.01), and increased in only the non-DM group. delta HR/log delta NE was more closely correlated with peak oxygen uptake in the DM group than in the non-DM group., Conclusions: Impaired response to exercise training may be caused, in part, by impaired heart rate reserve to exercise in patients with diabetes mellitus.

This study was undertaken in acute myocardial infarction (AMI) patients with non-insulin-dependent diabetes mellitus (type 2 DM) to investigate their impaired chronotropic response to exercise. Seventy-one AMI subjects entered the study, 30 with type 2 DM and 41 age- and body mass index-matched non-DM (control) patients. One month after the onset of AMI, these patients underwent cardiopulmonary exercise testing on a treadmill under a ramp protocol. Anaerobic threshold (AT) and peak oxygen uptake (peak VO2) were determined as indicators of exercise capacity. Plasma norepinephrine (NE) concentration was measured in blood samples obtained at 2 time points: during pre-exercise rest and immediately after peak exercise. The change in NE concentration during exercise, as an index of sympathetic nervous activity, was calculated as a percentage: deltaNE = [(NE during exercise) - (resting value)]/(resting value) x 100. The change in heart rate (HR) during exercise was calculated as a simple difference: deltaHR = [(peak HR) - (rest HR)]. Index of chronotropic response to exercise was then quantified as the deltaHR/deltaNE during exercise. No significant intergroup differences in ejection fraction at rest or HR at peak exercise were observed. However, VO2 at AT, peak VO2, deltaHR, and deltaHR/deltaNE were significantly lower in the type 2 DM group than in the non-DM group. DeltaHR correlated with VO2 at AT (r = 0.49, P<0.001) and with peak VO2 (r = 0.53, P<0.001) in all subjects. Also, deltaHR/deltaNE correlated with VO2 at AT (r = 0.42, P<0.001) and with peak VO2 (r = 0.44, P<0.001) in all subjects. AMI patients with type 2 DM had impaired cardiopulmonary responses to maximal and submaximal exercise testing and impaired chronotropic response to exercise, even though their cardiac function at rest was similar to that of non-DM AMI patients. The data suggest that one mechanism of impaired cardiopulmonary response to exercise in AMI patients with type 2 DM groups is an impaired chronotropic response.

There have been no previous studies that clearly demonstrate the effects of training on the relation between exercise capacity and vasodilatory capacity in skeletal muscle. This study was performed to clarify the effects of short-term, moderate-intensity physical training on exercise tolerance and vasodilatory capacity in cardiac patients. We studied 21 patients after acute myocardial infarction, coronary artery bypass grafting, or valve replacement. Each patient performed symptom-limited incremental exercise tests before and after a 2-week training program of moderate-intensity exercise. A cycle ergometer was used for both the training and exercise tests. Blood pressure measurement and respiratory gas analysis were continuously performed during the tests. Cardiac output was also measured using a dye-dilution method at rest and every 2 minutes during incremental exercise. Reactive hyperemic calf blood flow was measured at rest. After the training program, the subjects attained a significant decrease in systemic vessel resistance and significant increases in oxygen uptake and cardiac output at peak exercise. Changes in reactive hyperemic calf blood flow were significantly correlated with the changes in cardiac output, systemic vascular resistance, and the kinetics of oxygen uptake during warm-up exercise. By improving the peripheral vasodilatory capacity in these patients, short-term, moderate-intensity physical training was found to improve the cardiovascular adaptation not only at peak exercise, but also during the onset of exercise.

Heart rate (HR) response during exercise in patients with ischemic heart disease was evaluated, and the appropriateness of Karvonen's method for determining rehabilitation exercise target HR was investigated. The study group comprised 24 patients with acute myocardial infarction (AMI) and 37 patients who had undergone coronary artery bypass grafting (CABG). Cardiopulmonary exercise testing (CPX) was performed with a cycle ergometer and changes in HR (deltaHR)/changes in work rate (deltaWR) and interval changes of the coefficient of Karvonen's formula were evaluated. In the AMI group and the CABG group, deltaHR/deltaWR were significantly lower than those of age-matched control subjects (p<0.01). Karvonen's coefficients ranged from 0.37 to 0.54 when calculated from actual peak HR and 0.21 to 0.32 calculated from the predicted peak HR. An impaired HR response was found in patients with AMI and those who had had CABG up to 6 months previously. Because the Karvonen's coefficient values, which ranged from 0.6 to 0.8, were elevated for these patients, and considering the data from the CPX, increased exercise is recommended for such cases.

Objectives: Sympathetic heart rate response decreases in patients with left ventricular dysfunction. Angiotensin converting enzyme (ACE) inhibitors effectively prevent heart failure after myocardial infarction. However, the effect of ACE inhibitors on heart rate response is not well known. The present study investigated the effect of ACE inhibitors on sympathetic heart rate response in the early phase of acute myocardial infarction., Methods: Sixty-five patients with acute myocardial infarction receiving no beta-blocking agents participated in the study. The subjects consisted of 25 patients (mean age 60.2 +/- 10.7 years) treated with ACE inhibitor lisinopril from the initial stage and 40 control subjects (mean age 57.7 +/- 7.6 years). Cardiopulmonary exercise testing with a treadmill was performed using the ramp protocol in the first month and the third month after the onset of the disease. Heart rate (HR) was measured in the resting state (rest) and immediately after peak exercise (peak). At the same time, blood samples were obtained to investigate the changes in the plasma level of norepinephrine (NE). The degree of sympathetic heart rate response was evaluated as follows: (peak HR - rest HR)/¿(peak NE - rest NE)/rest NE¿ x 100., Results: There were no significant differences between the 2 groups in the first month in anaerobic threshold, peak oxygen uptake and plasma brain natriuretic peptide concentration. Though the change of heart rate was not significant, the change in the plasma level of norepinephrine was significantly lower in the lisinopril group (9.3 +/- 4.4 vs 5.7 +/- 2.8, p < 0.01). In the first month, the heart rate response in the control group was markedly lower than that in the lisinopril group (8.7 +/- 3.5 vs 15.2 +/- 8.5 beats/min/%, p < 0.01). In the third month, the significant difference between the 2 groups disappeared (10.7 +/- 7.9 vs 14.0 +/- 9.7 beats/min/%, NS) due to the increase of the value in the control subjects., Conclusions: From these results, we conclude that ACE inhibitors are effective to improve sympathetic heart rate response during exercise in the early phase of myocardial infarction.

The present study investigated the serial changes in serum magnesium (Mg) and erythrocyte concentration of Mg in patients with acute myocardial infarction (AMI) and the relationship between these changes and left ventricular ejection fraction (LVEF) at 1 month after the onset of infarction. The study group comprised 26 patients with AMI (mean age, 57.9+/-8.9 years). Serum Mg and erythrocyte Mg were measured on hospital days 1, 2, 4, 7 and 21. The change in erythrocyte Mg during the acute phase was calculated as a ratio: [(erythrocyte Mg at day 2)-(erythrocyte Mg at day 1)]/(erythrocyte Mg at day 1). The change in serum Mg was calculated similarly. The following results were obtained. (1) Serum Mg tended to increase from the onset of myocardial infarction (day 1: 1.86+/-0.19, day 2: 1.93+/-0.22, day 4: 2.17+/-0.23; day 7: 2.25+/-0.20; day 21: 2.12+/-0.15 mg/dl). (2) Erythrocyte Mg on day 2 and day 4 showed a significant decrease compared with day 1 (day 1: 2.45+/-0.40, day 2: 2.09+/-0.41, day 4: 2.07+/-0.37, day 7: 2.22+/-0.33, day 7: 2.34+/-0.28 mg/dl per 400x10(4)/mm3 cells). (3) A significant positive correlation was observed between the change in serum Mg and LVEF (r=0.55, p<0.05), and a significant negative correlation was observed between the change in erythrocyte Mg and LVEF (r=-0.57, p<0.05). Thus, it was concluded that an extracellular shift in intracellular Mg occurred during the first 2 days after the onset of myocardial infarction. This responsive increase in the extracellular Mg level may be an important factor for maintaining left ventricular function in patients 1 month after the onset of AMI.

It is generally accepted in clinical electrocardiography that a right bundle branch block (RBBB) does not interfere with the electrocardiographic (ECG) diagnosis of myocardial infarction (MI). The basic assumption is that the initial excitation wavefronts are relatively unchanged in RBBB. This study compared serial changes in Q wave duration in inferior leads II, III, and aVF in 9 patients who developed RBBB within 3 weeks after myocardial revascularization procedure (RBBB group) and in 41 revascularized patients without RBBB in the same observation period (control group). Q wave durations in the electrocardiograms obtained before the patients' procedures were not significantly different between the study and control groups. However, Q wave durations shortened significantly more in the RBBB group than in the control group. The most pronounced Q wave duration shortening took place in lead aVF, -18.2 ms in the RBBB group versus -3.8 ms in the control group (P = .0001). The shortening was less pronounced, although significant, in leads II and III: II, -7.6 +/- -10.9 ms in the RBBB group vs -2.3 +/- -3.5 ms in the control group (P = .01); III, -11.3 +/- -10.5 ms vs -2.6 +/- -6.5 ms (P = .002); aVF, -18.2 +/- -13.5 ms vs -3.8 +/- -5.3 ms (P < .0001). It is concluded that incident RBBB complicating revascularization procedures may cause significant alterations in spatial orientation of the initial excitation wavefronts. This may be a potential source of false-negative ECG diagnosis of inferior MI, particularly in clinical trials where serial ECG analysis is an important part in MI classification.

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.