Different thresholds of myocardial ischemia in ramp and standard bruce protocol exercise tests in patients with positive exercise stress tests and angiographically demonstrated coronary arterial narrowing.

Gradual instead of abrupt increases in workload favor a more physiologic response in terms of hemodynamic and gas exchange parameters. Therefore, we investigated whether myocardial ischemia is attenuated with a ramp compared with a standard Bruce exercise protocol in patients with coronary artery disease. We compared electrocardiographic ischemic parameters on the standard Bruce protocol treadmill and the individualized ergocycle ramp protocol in 18 men with coronary artery disease and a reproducible ischemic electrocardiographic exercise test. Oxygen consumption (VO2), ischemic threshold (rate-pressure product [RPP]=systolic blood pressure x heart rate at 1-mm ST-segment depression), and maximum ST-segment depression corresponding to the highest RPP common to the 2 tests were determined. Ischemic threshold was higher with the ramp than with the Bruce protocol (23,420+/-5,732 vs 20,018+/-3,542 beats.min/mm Hg, p=0.007). Peak RPP was higher during the ramp than during the Bruce protocol (28,492+/-6,450 vs 25,519+/-6,067 beats.min/mm Hg, respectively, p=0.02) despite similar peak VO2 (25.59+/-5.05 vs 26.39+/-4.65 mlO2.kg-1.min-1, respectively, p=0.6). Maximum ST-segment depression corresponding to the highest RPP common to the 2 tests was less with the ramp than with the Bruce protocol (-1.2+/-0.9 vs -1.9+/-0.7 mm, p=0.003). In conclusion, exercise-induced myocardial ischemia is markedly attenuated on the more gradually increasing workload of the individualized ramp ergocycle compared with the standard Bruce treadmill protocol. This effect is unexplained by energy expenditure (VO2) or myocardial work (RPP) and is consistent with a "warm-up" ischemic mechanism.

Impact of diabetes, chronic heart failure, congenital heart disease and chronic obstructive pulmonary disease on acute and chronic exercise responses.

Several chronic diseases are known to negatively affect the ability of an individual to perform exercise. However, the altered exercise capacity observed in these patients is not solely associated with the heart and lungs dysfunction. Exercise has also been shown to play an important role in the management of several pathologies encountered in the fields of cardiology and pneumology. Studies conducted in our institution regarding the influence of diabetes, chronic heart failure, congenital heart disease and chronic pulmonary obstructive disease on the acute and chronic exercise responses, along with the beneficial effects of exercise training in these populations, are reviewed.

Influence of glycemic control on pulmonary function and heart rate in response to exercise in subjects with type 2 diabetes mellitus.

Conflicting results exist regarding the impact of glycemic control on peak oxygen uptake (VO2peak) in subjects with type 2 diabetes mellitus. The influence of glycemic control on submaximal oxygen uptake (VO2) in these subjects is unknown. The aim of this study was to evaluate the impact of fasting blood glucose (FBG) (short-term glycemic control) and glycated hemoglobin (HbA1c) (long-term glycemic control) on submaximal VO2 and VO2peak during exercise in subjects with type 2 diabetes mellitus without cardiovascular disease. FBG and HbA1c levels and exercise tolerance in 30 sedentary men with type 2 diabetes mellitus treated with oral hypoglycemic agents and/or diet were evaluated. VO2, carbon dioxide production (VCO2), heart rate, pulmonary ventilation (VE), and the respiratory exchange ratio (RER) were measured throughout the exercise protocol. Subjects were separated into 2 groups of the same age, weight, and body mass index according to median FBG and HbA1c levels (6.5 mmol/L and 6.1%, respectively). Per protocol design, there was a significant difference in FBG and HbA1c levels (P < .001), but not for age, weight, or body mass index. There was no significant difference in peak exercise parameters between the 2 groups according to median FBG or median HbA1c levels. However, the subjects with elevated HbA1c level had lower submaximal V e throughout the exercise protocol (P < .03), and the subjects with elevated FBG concentration had a blunted heart rate pattern during submaximal exercise (P < .03). Although relatively small abnormalities in the control of glycemia do not affect VO2peak in subjects with type 2 diabetes mellitus without cardiovascular disease, they may influence pulmonary function and the chronotropic response during submaximal exercise in these subjects.

Elevated peak exercise systolic blood pressure is not associated with reduced exercise capacity in subjects with Type 2 diabetes.

Subjects with Type 2 diabetes without cardiovascular disease have a reduced exercise capacity compared with nondiabetic subjects. However, the mechanisms responsible for this phenomenon are unknown. The purpose of this study was to evaluate the impact of exercise systolic blood pressure (SBP) response on diverse exercise tolerance parameters in Type 2 diabetic subjects. Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. Subjects were treated with oral hypoglycemic agents and/or diet. Evaluation of glycemic control and peak exercise capacity were performed for each subject. The subjects were divided into two groups according to the median value of peak SBP (210 mmHg) measured in each subject. We observed a 13, 13, and 16% reduction in the relative peak oxygen uptake (V(O2 peak)), absolute V(O2 peak), and peak work rate in the low- compared with the high-peak SBP group [26.95 (SD 5.35) vs. 30.96 (SD 3.61) ml.kg(-1).min(-1), 2.5 (SD 0.4) vs. 2.8 (SD 0.6) l/min, and 169 (SD 34) vs. 202 (SD 32) W; all P < 0.05]. After adjusting for age, relative V(O2 peak) was still significantly different (P < 0.05). There were similar peak respiratory exchange ratio (RER) [1.20 (SD 0.08) vs. 1.16 (SD 0.07); P = 0.24] and peak heart rate [160 (SD 20) vs. 169 (SD 15) beats/min; P = 0.18] between the low- compared with the high-SBP group. No difference in glycemic control was observed between the two groups. The results reported in this study suggest that in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and its modulation is probably not related to glycemic control.

Impact of exercise training on muscle function and ergoreflex in Fontan patients: a pilot study.

BACKGROUND: Several studies have demonstrated persistent reduced exercise capacity in Fontan patients even after surgical intervention. The purpose of this study was to evaluate if the skeletal muscle function of these patients is abnormal, if it correlates with exercise tolerance and if it can be improved by exercise training. METHODS: We evaluated the functional capacity of seven patients who underwent Fontan procedure (age:16+/-5 years, mean+/-SD) and seven healthy children (19+/-7 years) paired for age, sex, height and weight. Evaluation included pulmonary evaluation, neuromuscular function and exercise tolerance. Secondly, an 8-week exercise training program was performed by five of these patients. RESULTS: The ergoreflex contribution to absolute diastolic blood pressure was higher (12.5+/-4.8 vs. 5.6+/-4.2 mmHg; p=0.04) in Fontan patients vs. healthy subjects whereas a trend was encountered regarding the ergoreflex contribution to absolute systolic blood pressure (9.0+/-7.0 vs. 0.4+/-9.0 mmHg; p=0.09). Furthermore, time to fatigue of the non-dominant forearm muscles was shorter in Fontan patients vs. healthy subjects (431+/-290 vs. 847+/-347 s; p=0.03). Following exercise training, there was a significant reduction of the ergoreflex contribution to absolute values of systolic blood pressure (9.8+/-0.9 vs. 0.3+/-2.7 mmHg; p<0.05). There was an association between muscle strength and VO2 peak in Fontan patients (upper limb: r=0.895; p<0.01; lower limb: r=0.838; p<0.05, respectively). CONCLUSIONS: Skeletal muscle function in Fontan patients is abnormal which may have an impact in the reduced exercise tolerance encountered in these patients. Exercise training may have beneficial impacts on the skeletal muscle function in this population.

Exercise capacity and impact of exercise training in patients after a Fontan procedure: a review.

After a successful Fontan procedure, children and adolescents should improve their exercise capacity. However, several studies have shown that these children have a reduced maximal oxygen consumption compared with healthy children. The lower exercise performance in these patients was mainly explained by a reduced cardiorespiratory functional capacity. However, it has recently been reported that the lower exercise performance may also be related to altered skeletal muscle function. Moreover, exercise training had a beneficial impact on several parameters related to exercise tolerance in these patients. The main studies supporting these observations are reviewed, with a focus on the physiological adaptation and limitation of the exercise performance as well as the benefits of exercise training in patients after a Fontan procedure.

Skeletal muscle endurance and muscle metabolism in patients with chronic heart failure.

BACKGROUND: Alterations in skeletal muscle function are known to contribute to exercise intolerance in patients with chronic heart failure (CHF). OBJECTIVES: To evaluate whether muscle isometric endurance can be objectively measured and whether it is related to skeletal muscle metabolism in CHF. METHODS: Isometric endurance of the vastus lateralis, measured as time to fatigue (T(F)), was evaluated in 25 patients with CHF (55+/-8 years of age [mean +/- SD]) and 18 healthy subjects (HS) (62+/-6 years of age [mean +/- SD]). Median frequency of surface electromyography was obtained from spectral analysis using a fast Fourier transformation. Citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase (HADH), hexokinase (HK) and phosphofructokinase (PFK) activities were determined from the right vastus lateralis muscle. RESULTS: T(F) was lower in CHF patients than in HS (49+/-4 s and 80+/-7 s, respectively; P<0.01). Muscle fatigue was present at the end of the endurance test in both groups (median frequency breakpoint at mid-exercise for both groups [P<0.05]). CS (P<0.01) and HK (P<0.01) activities were lower in CHF patients than in HS, but PFK activity was higher (P<0.05). T(F) correlated significantly with CS (r=0.50), HADH (r=0.42), PFK (r=-0.47) and HK (r=0.41) activities and the PFK/CS ratio (r=-0.39) when both groups were considered, and with HADH (r=0.47) and PFK (r=-0.57) activities for the CHF group alone (all P<0.05). CONCLUSIONS: These results suggest that isometric endurance of the vastus lateralis muscle is reduced in patients with CHF and that it is related to a reduced muscle oxidative capacity.

What induces the warm-up ischemia/angina phenomenon: exercise or myocardial ischemia?

BACKGROUND: The relation of the warm-up ischemia phenomenon to the presence and intensity of initial myocardial ischemia is unclear. We sought to determine whether the warm-up ischemia phenomenon requires initial myocardial ischemia or can be induced by exercise without ischemia and whether there is a relation between the intensity of initial ischemia and the attenuation of ischemia on reexercise. METHODS AND RESULTS: Twelve subjects with exertional myocardial ischemia performed 2 exercise ECG tests (1 and 2) at a +/-10-minute interval on 3 occasions (A, B, C) 1 month apart. A1 and A2 were symptom-limited. B1 was kept as long as A1, but its intensity was held under the ischemic threshold (heart ratexsystolic pressure at 1-mm ST depression [STD]) noted at A1. B2 was symptom-limited. C1 was also kept as long as A1 but with an intensity adjusted to maintain one-half maximum STD of A1. C2 was symptom-limited. Exercise duration of A2, B2, and C2 increased similarly compared with A1 (P=0.009). However, the ischemic threshold (x10-3) increased at A2 (23.5+/-6.0) compared with A1 (20.3+/-4.8; P<0.0001) but not at B2 (19.8+/-5.0) or C2 (21.5+/-5.8). Similarly, maximum STD adjusted to the highest heart rate-systolic pressure product common to A1, A2, B2, and C2 decreased at A2 (1.4+/-0.7 mm) compared with A1 (2.5+/-0.9 mm; P<0.0001) but not at B2 (2.7+/-0.9 mm) or C2 (2.3+/-0.9 mm). CONCLUSIONS: Exercises under the ischemic threshold and of intermediate ischemic intensity increase short-term exercise capacity, but myocardial ischemia of more than moderate intensity is needed to induce the warm-up ischemia phenomenon.

Usefulness of measuring net atrioventricular compliance by Doppler echocardiography in patients with mitral stenosis.

Twenty-six patients with severe pure mitral stenosis underwent Doppler echocardiographic examination and cardiac catheterization within the same day before the realization of mitral valve balloon valvuloplasty. Net atrioventricular compliance estimated by Doppler echocardiography from the ratio of mitral valve effective orifice area and E-wave downslope was a major independent determinant of left atrial and pulmonary arterial pressures measured by catheterization.

Reaching recommended lipid and blood pressure targets with amlodipine/atorvastatin combination in patients with coronary heart disease.

The effects of combined atorvastatin and amlodipine on blood pressure (BP) and low-density lipoprotein (LDL) cholesterol levels were investigated in 134 patients with documented coronary heart disease treated for 1 year. BP at baseline was 128 +/- 15/79 +/- 9 mm Hg and was controlled by the treating physician; no calcium channel blockers were allowed. Baseline means for plasma cholesterol were 6.4 +/- 1.1 mmol/L (147 +/- 39 mg/dl), triglycerides 2.0 +/- 0.9 mmol/L (177 +/- 88 mg/dl), LDL cholesterol 4.4 +/- 1.0 mmol/L (170 +/- 39 mg/dl), and high-density lipoprotein cholesterol 1.2 +/- 0.3 mmol/L (46 +/- 12 mg/dl). Patients were all given atorvastatin 10 mg, then increased to 80 mg if the LDL cholesterol was <2.5 mmol/L (100 mg/dl). At 3 months, patients were randomized to amlodipine 10 mg or placebo. Plasma LDL cholesterol was decreased by 50%, and the LDL cholesterol target of <2.5 mmol/L was achieved in 81% of the patients. BP targets were achieved in 69% of the atorvastatin + placebo group, versus 96% in the atorvastatin + amlodipine group (p = 0.0002). With use of combination atorvastatin + amlodipine at doses ranging from 10 to 80 mg and 5 to 10 mg, respectively, recommended therapeutic goals were reached in most select subjects with coronary artery disease who were concomitantly receiving aspirin and antihypertensive therapy.

Post-exercise heart rate recovery and mortality in chronic obstructive pulmonary disease.

Abnormal heart rate recovery (HRR) after exercise, a marker of cardiac autonomic dysfunction, is associated with poor prognosis in various populations. As chronic obstructive pulmonary disease (COPD) is associated with cardiac autonomic dysfunction, we tested the hypothesis that patients with COPD have a lower HRR than healthy people, and evaluated whether a delay in HRR is associated with an increased risk of mortality in COPD. The records of 147 COPD patients were reviewed (65.1+/-9.1 years, mean+/-sd, 42 women/105 men, forced expiratory volume in 1s (FEV1): 42+/-15% predicted) and compared to 25 healthy subjects (61.6+/-4.5 years, 5 women/20 men, FEV1: 100+/-14% predicted) during recovery after an exercise test. Heart rate was measured at peak exercise and at 1-min recovery, the difference between the two being defined as HRR (11+/-9 beats in COPD patients vs. 20+/-9 beats in healthy subjects, P < 0.0001). During a mean follow-up of 43.1+/-22.0 months, 32 patients died. Abnormal HRR (14 beats) was a strong predictor of mortality in COPD patients (adjusted hazard ratio: 5.12, 95% CI [1.54-17.00]). In conclusion, COPD patients have a lower HRR than healthy subjects, and have a worse prognosis when presenting abnormal HRR.

[French-Canadian validation of the MOS Social Support Survey]. / Validation canadienne-francaise du "MOS Social Support Survey".

BACKGROUND: The MOS Social Support Survey was developed for patients who participated in the Medical Outcomes Study (MOS), a two-year study on persons who suffered from chronic illness. There are a number of advantages to using the MOS Social Support Survey, especially with those persons who suffer from chronic illness: it is easy to understand, is relatively short, is multidimensional, can be completed by the patient without assistance and has good psychometric properties. OBJECTIVE: The goal of this study was to establish a French-Canadian version of the MOS Social Support Survey and to verify its psychometric properties following the cross-cultural translation and validation procedures proposed by Vallerand. METHODS: A first draft of the MOS Social Support Survey was achieved by following the back-to-back translation technique. Next, a committee of four bilingual people reviewed and evaluated the preliminary versions of the questionnaire (English and French) to establish a French experimental version. A pre-test was done with 10 francophone persons. The Haccoun method was used to evaluate the construct validity and test-retest reliability, as well as the internal consistency of the questionnaire. The test-retest was performed with 20 students from the School of Languages from Laval University, Sainte-Foy, Quebec. The present research was approved by the ethics committee of the institution. RESULTS: The results showed acceptable internal consistency and good reliability. The psychometric properties were found to be acceptable and comparable with those obtained by Sherbourne and Stewart with the English version. CONCLUSION: The French-Canadian version of the MOS Social Support Survey should be useful in evaluating social support among patients to allow medical staff to plan rehabilitation programs that would include the necessary consultations and interventions needed to establish a better quality of life for the patient.

Effect of atorvastatin on exercise-induced myocardial ischemia in patients with stable angina pectoris.

To investigate whether marked and sustained lipid-lowering in subjects with stable angina pectoris and dyslipidemia reduces exercise-induced myocardial ischemia, 17 subjects were treated with dose-adjusted atorvastatin over 1 year and underwent serial evaluation of exercise electrocardiographic ischemic parameters, serum biomarkers, and brachial artery endothelial function. Endothelial function improved progressively and C-reactive protein, P-selectin, and tissue plasminogen activator inhibitor levels decreased, but there was no decrease in exercise electrocardiographic ischemia.

Positive pleiotropic effects of HMG-CoA reductase inhibitor on vitiligo.

BACKGROUND: HMG-CoA reductase inhibitors (statins) are commonly used in medicine to control blood lipid disorder. Large clinical trials have demonstrated that statins greatly reduces cardiovascular-related morbidity and mortality in patients with and without coronary artery disease. Also, the use of HMG-CoA reductase inhibitors has been reported to have immunosuppressive effects. CASE PRESENTATION: We describe an unusual case of regression of vitiligo in a patient treated with high dose simvastatin. The relation between simvastatin and regression of vitiligo in this case report may be related to the autoimmune pathophysiology of the disease. CONCLUSION: This unexpected beneficial impact provides another scientific credence to the hypothesis that immune mechanisms play a role in the development of vitiligo and that the use of statins as immuno-modulator could be of use not only for treatment relative to organ transplant but in other pathologies such as vitiligo.

Comparison of myocardial ischemia on the ergocycle versus the treadmill in patients with coronary heart disease.

We previously observed an attenuation of exercise-induced myocardial ischemia on the ergocycle during a ramp protocol compared to the standard Bruce protocol treadmill test in patients with coronary heart disease. However, it was uncertain whether decreased ischemia on the ergocycle resulted from the warm-up effect of the more gradual ramp protocol or from the mode of exercise itself (cycling vs running). Sixteen stable patients, aged 64 +/- 5 years, with documented coronary heart disease (> or =70% coronary artery stenosis and/or reversible myocardial perfusion defects) performed 3 symptom-limited exercise tests: the standard Bruce protocol treadmill test and 2 individualized ramp protocols (treadmill and ergocycle). We measured the ischemic threshold (heart rate x systolic blood pressure product at 1-mm ST-segment depression) and oxygen consumption (VO(2)). The ischemic threshold was higher during cycling (ergocycle ramp, 24,009 +/- 5,769 beats/min x mm Hg) compared to running (Bruce treadmill, 20,429 +/- 3,508 beats/min x mm Hg; and ramp treadmill, 19,451 +/- 3,392 beats/min x mm Hg; p <0.001), independently of exercise intensity (VO(2)). The peak VO(2) did not significantly differ among all tests (p = 0.25) despite a greater peak rate-pressure product achieved with the ergocycle (29,378 +/- 6,291 beats/min x mm Hg) compared to either treadmill protocol (Bruce, 26,202 +/- 5,831 beats/min x mm Hg; ramp, 25,654 +/- 6,492 beats/min x mm Hg; p <0.001). In conclusion, the mode of exercise (ergocycle vs treadmill), rather than the type of protocol (ramp vs Bruce), is associated with an attenuation of electrocardiographic parameters of myocardial ischemia, independently of exercise intensity (VO(2)) and myocardial demand (rate-pressure product).

Modulation of arterial reactivity using amlodipine and atorvastatin measured by ultrasound examination (MARGAUX).

OBJECTIVE: To evaluate the effect of the calcium channel blocker amlodipine on endothelial function in normotensive patients with coronary disease taking concomitant atorvastatin therapy. METHODS AND RESULTS: Atorvastatin was titrated (10-80 mg/day) to maintain LDL-C<2.5 mmol/L and patients were randomized to receive amlodipine (5-10mg/day, n=64) or placebo (n=70) for 12 months. Brachial artery flow-mediated vasodilation (FMD) was assessed using vascular ultrasound. Inflammatory markers were also measured. At 12 months there was a significant decrease in mean low-density lipoprotein cholesterol (LDL-C) (4.4-2.1 mmol/L, P<0.0001), high-sensitivity C-reactive protein (hsCRP) (3.8-2.3mg/L, P<0.0001) and soluble vascular cell adhesion molecule-1 (sVCAM-1) (710-665 ng/mL, P<0.0001) for all patients, compared with baseline. Amlodipine was associated with a mean blood pressure reduction of 8/3 mm Hg (P<0.0001) whereas patients on placebo had no significant change. In the atorvastatin-placebo group, mean FMD increased (7.3-9.5%, P<0.05) with no change in nitroglycerin-mediated dilation. No further benefit on FMD or inflammatory markers was observed with the addition of amlodipine. CONCLUSIONS: Intensive reduction of LDL-C with atorvastatin improves endothelium-dependent vasodilation and reduces markers of inflammation in patients with coronary disease. Amlodipine was not associated with a significant additional benefit on these variables.

Can prolonged exercise-induced myocardial ischaemia be innocuous?

AIMS: To evaluate the innocuousness of intense and prolonged exercise training above the threshold for myocardial ischaemia (1 mm ST-segment depression). METHODS AND RESULTS: Twenty-two patients with ischaemic heart disease (IHD) were randomized to exercise training either at a target intensity that induced myocardial ischaemia (ischaemic group) or that adhered to current guidelines (control group). Training was progressively increased to 60 min under continuous electrocardiographic (ECG) monitoring. Cardiac troponin T (cTnT) was measured at various intervals. Ambulatory ECG monitoring was performed before and after 6 weeks of training and left ventricular function was evaluated in the ischaemic group after at least 6 weeks of training. The ischaemic group had myocardial ischaemia during the first 20, 40, and 60 min exercise sessions for 12.3 +/- 6.8, 29.0 +/- 12.9, and 49.8 +/- 2.2 min, respectively, with ST-segment depression ranging from 1.0 to 2.1 mm. No patient in either group demonstrated significant arrhythmias or increased cTnT. The ischaemic group had preserved left ventricular function. CONCLUSION: In patients with IHD, prolonged and repeated ischaemic training sessions up to 60 min can be well tolerated without evidence of myocardial injury, significant arrhythmias, or left ventricular dysfunction.

Assessment of muscle fatigue during exercise in chronic obstructive pulmonary disease.

Contractile fatigue is associated with exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). Contractile fatigue may be assessed by quantifying the decline in strength after a fatiguing protocol but this may pose practical problems. The purpose of this study was to investigate the relationship between the decline in quadriceps strength, quadriceps electrical activity, perception of leg fatigue, and arterial lactate level in patients with COPD during constant work-rate cycling exercise. The decline in quadriceps strength was significantly associated with the decrease in electromyographic median frequency (r = 0.606), leg fatigue perception (r = 0.453), and arterial lactate level (r = 0.384). Using the receiver-operating-characteristic curve, it was found that a 4% decline in electromyographic median frequency had a 94% sensitivity and a 75% specificity to predict contractile fatigue. We conclude that contractile fatigue commonly occurs during cycling exercise in COPD. The electromyographic median frequency appears to be a valuable indirect marker to predict contractile leg fatigue.

Long-term effects of cardiac rehabilitation and the paradigms of cardiac rehabilitation.

BACKGROUND: The benefits of exercise training for postmyocardial infarction and postcoronary artery bypass surgery patients are well established, but little is known about the effects of rehabilitation in the months or years following the program. The purpose of this study was to assess exercise capacity, blood lipids, and physical activity patterns 2 years after completing a concentrated residential rehabilitation program in Switzerland. METHODS: Seventy-eight patients (86% males, mean age = 56 +/- 10, mean ejection fraction = 64% +/- 12%) were referred to a residential rehabilitation program after a myocardial infarction or coronary artery bypass surgery between January 2001 and June 2001. Patients lived at the center for 1 month, during which time they underwent educational sessions, consumed a low-fat diet, and exercised 2 hours daily. Two years after completing the program, patients returned to the hospital and underwent a maximal exercise test, an assessment of recent and adulthood physical activity patterns, and evaluation of blood lipids. RESULTS: During the 2-year follow-up period, there were 5 deaths, and 70 of the remaining 73 patients returned for repeat testing. Mean exercise capacity increased 27% during the rehabilitation program (P < .01). Gains in exercise capacity during rehabilitation were maintained after the follow-up period; mean exercise capacity after 2 years was 34% higher compared with that at baseline (P < .01). At the 2-year evaluation, patients were expending a mean of 3127 +/- 1689 kcals/wk during recreational activities compared with 977 +/- 842 kcals/wk during adulthood prior to their cardiac event (P < .001). Between the completion of rehabilitation and the 2-year follow-up, total cholesterol, total cholesterol/high-density lipoprotein ratio, and triglycerides increased significantly. CONCLUSIONS: Two years after a cardiac event and participation in a concentrated residential rehabilitation program, patients maintained their exercise capacity and engaged in physical activities that exceed the levels recommended by guidelines for cardiovascular health. These observations suggest that a relatively intensive rehabilitation program provided a catalyst to maintain physical activity patterns and exercise tolerance in the 2 years following a cardiac event.

Contractile fatigue, muscle morphometry, and blood lactate in chronic obstructive pulmonary disease.

We hypothesized that patients with chronic obstructive pulmonary disease developing contractile fatigue of the quadriceps during cycle exercise may have characteristic metabolic and muscle features that could increase their susceptibility to fatigue, thus differentiating them from those who do not develop fatigue. We examined, in 32 patients, the fiber-type proportion, enzymatic activities, and capillary density in the vastus lateralis and the arterial blood lactate level during constant work-rate cycling exercise. Contractile fatigue was defined as a postexercise fall in quadriceps twitch force greater than 15% of resting values. Twenty-two patients developed contractile fatigue after exercise. No significant differences were found between fatiguers and non-fatiguers for the endurance time, fiber-type proportion, and oxidative enzyme activities. The lactate dehydrogenase activity was significantly higher (p < 0.05) and muscle capillarization significantly reduced in fatiguers (p < 0.05). Compared with non-fatiguers, the arterial lactate level during exercise was significantly higher in fatiguers (p < 0.001). A significant relationship was found between the fall in quadriceps twitch force and lactate dehydrogenase activity, capillary/fiber ratio, and blood lactate level. We conclude that changes in muscle enzymatic profile and capillarization with a greater reliance on glycolytic metabolism during exercise are associated with contractile fatigue in patients with chronic obstructive pulmonary disease.