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

Brassard, Patrice; Maltais, François; Noël, Martin; Doyon, J F.; Leblanc, Pierre; Allaire, J.; Simard, C; Leblanc, Marie-Hélène; Poirier, Paul; Jobin, Jean

doi:10.1016/s0828-282x(06)70923-0

Cited by 22 publications

(16 citation statements)

References 26 publications

(47 reference statements)

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“…A similar trend can be seen in patients with heart failure (HF) with an accelerated level of muscle dysfunction (2). The absence of physical activity greatly increases muscle loss and decreases quality of life in both the aging and HF populations (3, 4).…”

Section: Introductionsupporting

confidence: 55%

Exercise capacity, physical activity, and morbidity

2017

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Section: Introductionsupporting

confidence: 55%

Exercise capacity, physical activity, and morbidity

2017

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“…Heart disease is one of the most common chronic conditions in older adults (National Advisory Council on Aging 2006). Patients with heart failure have greater muscle fatigue than healthy older adults (Brassard et al 2006;Schulze et al 2004) (Table 3). The impaired muscle function observed in heart failure patients may be explained by their reduced muscle strength, muscle mass, muscle blood flow, and muscle oxidative capacity, and increased proportion of type II muscle fibers, lactate accumulation, acidosis, and reliance on glycolytic metabolism (Brassard et al 2006;Schulze et al 2004).…”

Section: Diseasementioning

confidence: 99%

An exploration of the association between frailty and muscle fatigue

Theou

Jones

Overend

et al. 2008

Appl. Physiol. Nutr. Metab.

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Frailty is increasingly recognized as a geriatric syndrome that shares common biomedical determinants with rapid muscle fatigue: aging, disease, inflammation, physical inactivity, malnutrition, hormone deficiencies, subjective fatigue, and changes in neuromuscular function and structure. In addition, there is an established relationship between muscle fatigue and core elements of the cycle of frailty as proposed by Fried and colleagues (sarcopenia, neuroendocrine dysregulation and immunologic dysfunction, muscle weakness, subjective fatigue, reduced physical activity, low gait speed, and weight loss). These relationships suggest that frailty and muscle fatigue are closely related and that low tolerance for muscular work may be an indicator of frailty phenotype.

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“…Changes in the quantity or functional integrity (eg, oxidative modification; (11)) of specific proteins, or groups of proteins, could develop or be favored because of modifications in their synthesis or breakdown rates. In turn, these changes could lead to reduced muscle contractile function (12) or endurance (13) that contribute to exercise intolerance, the cardinal symptom of the disease.…”

Section: Skeletal Muscle Dysfunction and Protein Metabolism In Hfmentioning

confidence: 99%

“…Regarding myofilament proteins, animal and clinical studies suggest the loss of the most abundant contractile protein myosin (7, 14, 15), which contributes to diminished muscle function (7, 14, 15). Regarding mitochondrial proteins, studies have shown reduced mitochondrial content (16) and function (17) in HF patients, either of which could increase susceptibility to fatigue (13). Of note, recent studies have suggested that reduced mitochondrial density (18) and dysfunction (19) in HF may be related to muscle disuse that accompanies the disease, rather than a unique feature of the disease process (for review see (20)).…”

Section: Skeletal Muscle Dysfunction and Protein Metabolism In Hfmentioning

confidence: 99%

Skeletal muscle protein metabolism in human heart failure

Callahan

Toth

2013

Current Opinion in Clinical Nutrition and Metabolic Care

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Purpose of review This review considers evidence that the clinical condition of heart failure (HF) alters skeletal muscle protein synthesis and/or breakdown to promote skeletal muscle wasting and functional decrements that ultimately contribute to the symptomology of the disease. Recent findings Advanced heart failure is frequently accompanied by muscle atrophy and a cachectic phenotype. Protein metabolic derangements that promote this phenotype are understudied and poorly understood. Instead, most investigations have evaluated regulatory hormones/signaling pathways thought to be reflective of protein synthesis and breakdown. Several of these recent studies have provided exciting data suggesting that the dysfunctional myocardium releases catabolic agents that could promote the skeletal muscle myopathic phenotype either directly or through modulation of other regulatory systems (eg, energy balance). Summary While our understanding of skeletal muscle atrophy and dysfunction in heart failure is limited, recent studies have provided clues about the nature and timing of protein metabolic dysfunction. More specifically, skeletal muscle protein metabolic derangements likely evolve during periods of disease-related stress (ie, acute disease exacerbation and hospitalization) and potentially derive in part, from signals promoted in the damaged/dysfunctional myocardium. Despite these compelling studies, there is a surprising lack of data regarding the nature or timing of specific protein metabolic defects in HF.

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

Cited by 22 publications

References 26 publications

Exercise capacity, physical activity, and morbidity

Exercise capacity, physical activity, and morbidity

An exploration of the association between frailty and muscle fatigue

Skeletal muscle protein metabolism in human heart failure

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