Functional and morphological skeletal muscle abnormalities correlate with reduced electromyographic activity in chronic heart failure

Schulze, P. Christian; Linke, Axel; Schoene, Nina; Winkler, Sven Möbius; Adams, Volker; Conradi, Stefan; Busse, Martin; Schuler, Gerhard; Hambrecht, Rainer

doi:10.1097/01.hjr.0000124327.85096.a5

Cited by 35 publications

(22 citation statements)

References 38 publications

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“…Although we acknowledge that these relationships are not necessarily causal, previous studies (28,29) have demonstrated that exercise training induces a concomitant increase in muscle oxidative capacity and skeletal muscle endurance in patients with CHF, thus supporting the existence of a link between skeletal muscle endurance and oxidative capacity. Of note, we cannot exclude the possibility that the increased susceptibility to fatigue in CHF may, in part, be related to abnormal motor unit recruitment (30). However, the existing relationships between T F and various muscle enzyme activities also support the contention that the metabolic capacity of the vastus lateralis muscle was equally important in explaining reduced muscle endurance.…”

Section: Discussionmentioning

confidence: 80%

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

Brassard

Maltais

Noël

et al. 2006

Canadian Journal of Cardiology

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Section: Discussionmentioning

confidence: 80%

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

Brassard

Maltais

Noël

et al. 2006

Canadian Journal of Cardiology

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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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“…24 Excitation-contraction (E-C) coupling initiates the contraction of the myocardial muscle following the release of Ca 2+ from ryanodine receptors in the sarcoplasmic reticulum in response to voltage-gated Ca 2+ channels in the transverse tubules. 25,26 In HF, myocardial E-C coupling is impaired due to a variety of mechanisms such as a sarcoplasmic Ca 2+ leak, elevated cellular Na + levels, and structural remodeling.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Skeletal Muscle Torque Capacity and Circulating Ceramides in Patients with Advanced Heart Failure

Brunjes

Dunlop

et al. 2016

Journal of Cardiac Failure

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Background Heart failure (HF)-related exercise intolerance is thought to be perpetuated by peripheral skeletal muscle functional, structural, and metabolic abnormalities. We analyzed specific dynamics of muscle contraction in patients with HF compared with healthy, sedentary controls. Methods Isometric and isokinetic muscle parameters were measured in the dominant upper and lower limbs of 45 HF patients and 15 healthy age-matched controls. Measurements included peak torque normalized to body weight, work normalized to body weight, power, time to peak torque, and acceleration and deceleration to maximum strength times. Body morphometry (dual energy X-ray absorptiometry scan) and circulating fatty acids and ceramides (lipodomics) were analyzed in a subset of subjects (18 HF and 9 controls). Results Extension and flexion time-to-peak torque was longer in the lower limbs of HF patients. Furthermore, acceleration and deceleration times in the lower limbs were also prolonged in HF subjects. HF subjects had increased adiposity and decreased lean muscle mass compared with controls. Decreased circulating unsaturated fatty acids and increased ceramides were found in subjects with HF. Conclusions Delayed torque development suggests skeletal muscle impairments that may reflect abnormal neuromuscular functional coupling. These impairments may be further compounded by increased adiposity and inflammation associated with increased ceramides.

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Functional and morphological skeletal muscle abnormalities correlate with reduced electromyographic activity in chronic heart failure

Abstract: Our findings demonstrate an impaired electromyographic activity and muscular function in patients with CHF suggesting a new pathomechanism contributing to functional abnormalities of the skeletal muscle in advanced stages of this disease.

Cited by 35 publications

References 38 publications

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

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

An exploration of the association between frailty and muscle fatigue

Analysis of Skeletal Muscle Torque Capacity and Circulating Ceramides in Patients with Advanced Heart Failure

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