THE INFLUENCE OF MUSCLE MASS, STRENGTH, FATIGABILITY AND BLOOD-FLOW ON EXERCISE CAPACITY IN CACHECTIC AND NON-CACHECTIC PATIENTS WITH CHRONIC HEART-FAILURE

Citation
Sd. Anker et al., THE INFLUENCE OF MUSCLE MASS, STRENGTH, FATIGABILITY AND BLOOD-FLOW ON EXERCISE CAPACITY IN CACHECTIC AND NON-CACHECTIC PATIENTS WITH CHRONIC HEART-FAILURE, European heart journal, 18(2), 1997, pp. 259-269
Citations number
47
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
18
Issue
2
Year of publication
1997
Pages
259 - 269
Database
ISI
SICI code
0195-668X(1997)18:2<259:TIOMMS>2.0.ZU;2-P
Abstract
Background The influence of age, skeletal muscle function and peripher al blood flow on exercise capacity in chronic heart failure patients i s controversial, possibly due to variations in skeletal muscle atrophy . Methods and results To assess predictors of exercise capacity in pat ients with clinical cardiac cachexia, we studied 16 cachectic and 39 n on-cachectic male chronic heart failure patients of similar age and ej ection fraction. All cachectic patients were wasted (% ideal body weig ht: 81.2 +/- 1.9 vs 105.2 +/- 2.1, P<0.0001, mean +/- SEM) and had doc umented weight loss (5-30 kg). Peak oxygen consumption (14.9 +/- 1.4 v s 16.3 +/- 0.6 ml.kg(-1). min(-1), resting, and peak blood flow (pleth ysmography) and 20 min fatigability (% baseline strength) were all sim ilar between the two groups. Quadriceps strength, muscle size (all P<0 .0001), strength per unit muscle (right: P<0.05; left: P<0.001) and 5 min fatigability (P<0.05) were all lower in cachectic patients. In non -cachectic patients, age (R=0.48) and quadriceps strength (R=0.43, all P<0.01) predicted peak oxygen consumption. Only in cachectic patients did peak blood flow predict peak oxygen consumption significantly (R= 0.72, P=O.OO5), whereas age and strength did not. Similar findings wer e confirmed using other previously published definitions of cardiac ca chexia. Conclusions The predictors of exercise capacity change with th e development of cardiac cachexia from age and strength to peak blood flow. This shift may be caused by additional endocrine or catabolic ab normalities active in end stage heart failure.