Attained METS were 6.2 +/- 2.5 and Borg RPE was 15.2 +/- 1.7. Borg RPE was negatively related to intensity and duration of exercise. Females, patient with a lower level of education and patients on diuretics perceived higher efforts. Patients who stopped exercising because of dyspnea or angina reached a lower level of METs (4.7 +/- 1.7 vs 6.3 +/- 2.7 METs; P<0.001) but the perceived effort was similar

(15.5 +/- 1.7 vs 15.2 +/- 1.7; P=0.252). The subjective method would have yielded a significantly higher training workload: 5.4 +/- 2.3 vs 4.3 +/- 1.8 (P<0.001). In conclusion, in obese patients, Borg RPE is not MI-503 supplier equivalent to attained METs in exercise prescription and it influenced by educational level. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Decramer

M. Response of the respiratory muscles to rehabilitation in COPD. J Appl Physiol 107: 971-976, 2009. First published April 2, 2009; doi:10.1152/japplphysiol.91459.2008.-Respiratory rehabilitation is known to improve outcomes in patients with chronic obstructive pulmonary disease (COPD). The question addressed in the present review is whether these beneficial effects are related to improvements in inspiratory muscle function. Respiratory muscle fatigue often did not occur during Selleck Liproxstatin-1 exercise in patients with COPD, since exercise limitation usually occurred when significant force reserve in the inspiratory muscles was still present. Notwithstanding, a number of observations may provide indirect evidence that respiratory muscle fatigue may occur during exercise. Some evidence is present that, in normal humans, whole body exercise training improved inspiratory muscle endurance, but no studies are available in patients with COPD. Animal studies invariably demonstrated that exercise training increased the number of oxidative fibers and oxidative enzyme activity in inspiratory muscles. These effects, however, were considerably smaller than the effects found on peripheral muscles with similar fiber composition. Clear evidence indicated that inspiratory muscle training (IMT) improved inspiratory muscle function. Two large meta-analyses indicated that, if the training load was properly controlled, Galardin manufacturer IMT alone or combined

with general exercise reconditioning improved inspiratory muscle strength and endurance and dyspnea. The combination did not result in greater improvements in functional exercise capacity. Animal studies and one patient study confirmed the occurrence of structural remodeling of the inspiratory muscles in response to IMT. The final question is whether improvements in inspiratory muscle function produced by IMT lead to improved outcomes in COPD. In all five studies in which training load was adequately controlled, a significant reduction of dyspnea during activities of daily living was found. Eight randomized studies examined the effects of the combination. Greater improvements in exercise capacity were only found in three studies, and none showed a greater reduction in dyspnea.