Chronic heart failure and skeletal muscle catabolism: Effects of exercise training

Universität Leipzig, Herzzentrum GmbH, Klinik für Innere Medizin/Kardiologie, Russenstr. 19, 04289 Leipzig, Germany.
International Journal of Cardiology (Impact Factor: 4.04). 10/2002; 85(1):141-9. DOI: 10.1016/S0167-5273(02)00243-7
Source: PubMed


Although the clinical picture of cardiac cachexia is well-known in patients with advanced chronic heart failure (CHF) the factors that determine who is at risk for this progressive catabolic syndrome and who is not remain unclear. Different endocrine systems have been accused of being involved in this process: an imbalance between catabolic and anabolic steroids with an elevated cortisol/dihydroepiandrosterone ratio, an increased resting metabolic rate due to high levels of circulating catecholamines, various cytokines are activated in CHF (i.e. TNF-alpha, IL-6, IL-1beta and others), and elevated levels of growth hormone (GH) with inappropriately normal or low serum levels of insulin-like growth factor-I (IGF-I) have been described in cardiac cachexia. These catabolic factors contribute to peripheral muscle atrophy, augment the expression of the inducible nitric oxide synthase (iNOS), which in turn inhibits the aerobic cellular metabolism. The present review examines whether the catabolic factors can be influenced by a classical anabolic intervention: regular physical exercise training. Long-term training programs increase skeletal muscle cytochrome c oxidase activity and are associated with reduced local expression of pro-inflammatory cytokines as well as iNOS, and augment local IGF-I production. In concert, these beneficial effects of exercise training may help to retard the catabolic process in CHF finally leading to cardiac cachexia and death.

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    • "The protein synthesis is also essential to maintain muscle mass [42] [71] and it seems to be decreased in HF [82]. Further to the hypothesis that AET increases protein synthesis pathways in the skeletal muscle, our group is currently studying the effects of AET on cardiac cachexia animal model and humans. "
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    ABSTRACT: Aerobic exercise training (AET) induces several skeletal muscle changes, improving aerobic exercise capacity and health. Conversely, to the positive effects of AET, the cachexia syndrome is characterized by skeletal muscle wasting. Cachexia is a multifactorial disorder that occurs and is associated with other chronic diseases such as heart failure and cancer. In these diseases, an overactivation of ubiquitin-proteasome and autophagy systems associated with a reduction in protein synthesis culminates in severe skeletal muscle wasting and, in the last instance, patient's death. In contrast, AET may recycle and enhance many protein expression and enzyme activities, counteracting metabolism impairment and muscle atrophy. Therefore, the aim of the current review was to discuss the supposed therapeutic effects of AET on skeletal muscle wasting in both cardiac and cancer cachexia. Copyright © 2014. Published by Elsevier Inc.
    Full-text · Article · Dec 2014 · Life Sciences
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    • "Several reports described that myocardial infarction decreases the sectional area of slow-twitch type I fibres, which have a high potential for aerobic oxidation, and increases the area of fast-twitch type IIb fibres (Sullivan et al. 1990, 1991, Delp et al. 1997, Behnke et al. 2004, Bekedam et al. 2009). Moreover, it has been shown that apoptosis occurs in the skeletal muscle of individuals with heart failure, a phenomenon that may influence muscle contractility and the process of atrophy (Schulze et al. 2002). Our data show a decrease in crosssectional area and fibre area as a consequence of heart failure, derangements that were reversed by the ES protocol. "
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    ABSTRACT: Changes in skeletal muscle morphology and metabolism are associated with limited functional capacity in heart failure, which can be attenuated by neuromuscular electrical stimulation (ES). The purpose of the present study was to analyse the effects of ES upon GLUT-4 protein content, fibre structure and vessel density of the skeletal muscle in a rat model of HF subsequent to myocardial infarction. Forty-four male Wistar rats were assigned to one of four groups: sham (S), sham submitted to ES (S+ES), heart failure (HF) and heart failure submitted to ES (HF+ES). The rats in the ES groups were submitted to ES of the left leg during 20 days (2.5 kHz, once a day, 30 min, duty cycle 50%- 15 s contraction/15 s rest). After this period, the left tibialis anterior muscle was collected from all the rats for analysis. HF+ES rats showed lower values of lung congestion when compared with HF rats (P = 0.0001). Although muscle weight was lower in HF rats than in the S group, thus indicating hypotrophy, 20 days of ES led to their recovery (P < 0.0001). In both groups submitted to ES, there was an increase in muscle vessel density (P < 0.04). Additionally, heart failure determined a 49% reduction in GLUT-4 protein content (P < 0.03), which was recovered by ES (P < 0.01). In heart failure, ES improves morphological changes and raises GLUT-4 content in skeletal muscle.
    Full-text · Article · Feb 2011 · Acta Physiologica
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    • "Training reduces the activity of the sympathetic and renin– angiotensin systems (Coats et al., 1990; Coats et al., 1992; Kiilavuori et al., 1995; Working Group Report , 2001b). Furthermore, training induces skeletal muscle cytochrome C oxidase activity, which is associated with reduced local expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) and augmented local insulin-like growth factor-I (IGF-I) production (Schulze et al., 2002). Exercise training may thereby help retard the catabolic processes in patients with chronic heart failure and counteract muscle atrophy. "
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    ABSTRACT: Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.
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