A community approach to assessments of exercise tolerance in health and disease.
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A reduction in muscle blood flow caused by central vascular or peripheral vascular disease, or both, invariably leads to a reduction in exercise tolerance. Exercise conditioning programs have been shown to be an effective means of improving exercise tolerance in many patients with cardiovascular disease. However, improvements can be found without detectable changes in total muscle blood flow during activity. This suggests that peripheral adaptations induced within active muscles by exercise training exert a beneficial influence. These adaptations could include (1) a redistribution of blood flow within the active muscle or limb, or both; (2) an enhanced capillary density within the active muscle; and (3) an increased mitochondrial content within the active muscle. Evaluation of these adaptations, in an animal model of peripheral arterial insufficiency, suggests that all 3 factors potentially serve to enhance exercise tolerance after training. The improved ability of trained muscle to accommodate the metabolic stress during contractions is noteworthy. These factors could contribute to the marked increase in endurance during mild submaximal exercise observed in patients after training.
Although the haemodynamic response during submaximal supine exercise in mitral stenosis has been well described, the determinants of peak oxygen uptake during maximal upright exercise are poorly characterized and may differ in sinus rhythm and atrial fibrillation. Seventy patients with isolated mitral stenosis underwent Doppler-echocardiography and bicycle exercise with respiratory gas analysis. Forty-two patients were in sinus rhythm (Group I) and 28 in atrial fibrillation (Group II). Peak oxygen uptake was 21.3 +/- 5.6 ml.min-1.kg-1 in group I and 18.1 +/- 5.1 ml.min-1.kg-1 in group II (P < 0.05). There was no significant correlation between indices of exercise tolerance (exercise duration, ventilatory threshold, peak oxygen uptake, indexed peak oxygen uptake, peak oxygen pulse) and valve area or gradient in either group. Indexed peak oxygen uptake was not correlated to delta oxygen pulse but was linearly related (r = 0.43) to delta heart rate (delta heart rate = peak heart rate/rest heart rate) in Group I but not in Group II. Thus, in patients with mitral stenosis, no correlation was found between the mitral valve area or the gradient at rest and maximal upright exercise tolerance, suggesting that peripheral adaptation and, in sinus rhythm, chronotropic reserve, are important compensatory mechanisms.
BACKGROUND: Although exercise training improves exercise tolerance in most patients with chronic obstructive pulmonary disease (COPD), some patients with severe disease may not be able to tolerate exercise training due to incapacitating breathlessness. Transcutaneous electrical muscle stimulation (TCEMS) has been shown to improve muscle strength, muscle mass, and performance in paraplegics, patients with knee ligament injury, and patients with peripheral vascular disease. We hypothesised that TCEMS of the lower extremities can improve muscle strength and exercise tolerance in patients with moderate to severe COPD. METHODS: A randomised controlled trial of TCEMS of the lower extremities was performed in 18 medically stable patients of mean (SD) age 60.0 (1.5) years with a mean forced expiratory volume in 1 second (FEV(1)) of 1.03 (0.10) l (38% predicted) and residual volume/total lung capacity (RV/TLC) of 59 (2)%. Stimulation of the lower extremities was performed three times a week, 20 minutes each session, for six continuous weeks. Quadriceps and hamstring muscle strength, exercise capacity, and peak oxygen uptake were measured at baseline and after 6 weeks of stimulation. RESULTS: TCEMS improved both the quadriceps strength (by 39.0 (20.4)% v 9.0 (8.1)%, p=0.046) and hamstring muscle strength (by 33.9 (13.0)% v 2.9 (4.7)%, p=0.038) in the treated (n=9) and sham treated (n=9) groups, respectively. The improvement in muscle strength carried over to better performance in the shuttle walk test in the treated group (36.1% v 1.6% in the treated and sham groups respectively, p=0.007, Mann-Whitney U test). There was no significant change in lung function, peak workload, or peak oxygen consumption in either group. Muscle stimulation was well tolerated by the patients with no dropouts and better than 95% compliance with the protocol. CONCLUSIONS: TCEMS of peripheral muscles can be a useful adjunct to the comprehensive pulmonary rehabilitation of patients with COPD.
Abnormal blood rheology is a known characteristics of coronary artery disease. The authors evaluated the effects of pentoxifylline on the exercise capacity ejection fraction and symptoms of 9 patients with ischemic cardiomyopathy. All patients had signs and symptoms of left ventricular dysfunction. All had at least two major vessels obstructed as determined by coronary angiography. Pentoxifylline 400 mg three times daily was administered for twelve weeks. Seven of 9 patients responded with increases in ejection fraction and exercise tolerance. Exercise tolerance correlated with improvement or lack of improvement in ejection fraction. For all patients at twelve weeks post-therapy mean ejection fraction increased 9.8% over baseline (p = .07), total treadmill time increased 15% (p = .27), and mean double product increased 13% (p = .03). Anginal symptoms were significantly improved over baseline at twelve weeks of therapy (p greater than .001), as well as dyspnea on exertion (p = .03). Pentoxifylline was well tolerated. Pentoxifylline may benefit ischemic cardiomyopathy by improving coronary perfusion owing to favorable alterations in hemorheologic properties.