Skeletal Muscle Function and Its Relation to Exercise Tolerance in Chronic Heart Failure

Objectives. This study sought to define the relation between muscle function and bulk in chronic heart failure (HF) and to explore the association between muscle function and bulk and exercise capacity.Background. Skeletal muscle abnormalities have been postulated as determinants of exercise capacity in chronic HF. Previously, muscle function in chronic HF has been evaluated in relatively small numbers of patients and with variable results, with little account being taken of the effects of muscle wasting.Methods. One hundred male patients with chronic HF and 31 healthy male control subjects were studied. They were matched for age (59.0 ± 1.0 vs. 58.7 ± 1.7 years [mean ± SEM]) and body mass index (26.6 ± 0.4 vs. 26.3 ± 0.7 kg/m²). We assessed maximal treadmill oxygen consumption (

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₂), quadriceps maximal isometric strength, fatigue (20-min protocol, expressed in baseline maximal strength) and computed tomographic cross-sectional area (CSA) at midthigh.Results. Peak

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₂ was lower in patients (18.0 ± 0.6 vs. 33.3 ± 1.4 ml/min per kg, p < 0.0001), although both groups achieved a similar respiratory exchange ratio at peak exercise (1.15 ± 0.01 vs. 1.19 ± 0.03, p = 0.13). Quadriceps (582 vs. 652 cm², p < 0.05) and total leg muscle CSA (1,153 vs. 1,304 cm², p < 0.005) were lower in patients with chronic HF. Patients were weaker than control subjects (357 ± 12 vs. 434 ± 18 N, p < 0.005) and also exhibited greater fatigue at 20 min (79.1% vs. 92.1% of baseline value, p < 0.0001). After correcting strength for quadriceps CSA, significant differences persisted (5.9 ± 0.2 vs. 7.0 ± 0.3 N/cm², p < 0.005), indicating reduced strength per unit muscle. In patients, but not control subjects, muscle CSA significantly correlated with peak absolute

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₂ (R = 0.66, p < 0.0001) and is an independent predictor of peak absolute

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₂.Conclusions. Patients with chronic HF have reduced quadriceps maximal isometric strength. This weakness occurs as a result of both quantitative and qualitative abnormalities of the muscle. With increasing exercise limitation there is increasing muscle weakness. This progressive weakness occurs predominantly as a result of loss of quadriceps bulk. In patients, this muscular atrophy becomes a major determinant of exercise capacity.     

Dietary Nitrate and Skeletal Muscle Contractile Function in Heart Failure

Current Heart Failure Reports - Heart failure (HF) patients suffer from exercise intolerance that diminishes their ability to perform normal activities of daily living and hence compromises their...     

Skeletal Muscle Myopathy in Heart Failure: the Role of Ejection Fraction

Purpose of Review

This review summarizes: (1) the structural and functional features coupled with pathophysiological factors responsible of skeletal muscle myopathy (SMM) in both heart failure with reduced (HFrEF) and preserved (HFpEF) ejection fraction and (2) the role of exercise as treatment of SMM in these HF-related phenotypes.

Recent Findings

The recent literature showed two main phenotypes of heart failure (HF): (1) HFrEF primarily due to a systolic dysfunction of the left ventricle and (2) HFpEF, mainly related to a diastolic dysfunction. Exercise intolerance is one of most disabling symptoms of HF and it is shown that persists after the normalization of the central hemodynamic impairments by therapy and/or cardiac surgery including heart transplant. A specific skeletal muscle myopathy (SMM) has been defined as one of the main causes of exercise intolerance in HF.

Summary

The SMM has been well described in the last 20 years in the HFrEF; on the contrary, few studies are available in HFpEF. Recent evidences have revealed that exercise training counteracts HF-related SMM and in turn ameliorates exercise intolerance.

     

Impaired Exercise Tolerance in Heart Failure: Role of Skeletal Muscle Morphology and Function

Purpose of Review

To discuss the impact of deleterious changes in skeletal muscle morphology and function on exercise intolerance in patients with heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF), as well as the utility of exercise training and the potential of novel treatment strategies to preserve or improve skeletal muscle morphology and function.

Recent Findings

Both HFrEF and HFpEF patients exhibit a reduction in percent of type I (oxidative) muscle fibers and oxidative enzymes coupled with abnormal mitochondrial respiration. These skeletal muscle abnormalities contribute to impaired oxidative metabolism with an earlier shift towards glycolytic metabolism during exercise that is strongly associated with exercise intolerance. In both HFrEF and HFpEF patients, peripheral “non-cardiac” factors are important determinants of the improvement in exercise tolerance following aerobic exercise training. Adjunctive strategies that include nutritional supplementation with amino acids and/or anabolic drugs to stimulate anabolic molecular pathways in skeletal muscle show great promise for improving exercise tolerance and treating heart failure-associated sarcopenia, but these efforts remain early in their evolution, with no immediate clinical applications.

Summary

There is consistent evidence that heart failure is associated with multiple skeletal muscle abnormalities which impair oxygen uptake and utilization and contribute greatly to exercise intolerance. Exercise training induces favorable adaptations in skeletal muscle morphology and function that contribute to improvements in exercise tolerance in patients with HFrEF. The contribution of skeletal muscle adaptations to improved exercise tolerance following exercise training in HFpEF remains unknown and warrants further investigation.

     

骨骼肌成肌细胞移植对慢性心力衰竭犬左心室功能的影响

目的:观察自体骨骼肌成肌细胞移植对慢性心力衰竭犬的左心室重塑及左心室功能的影响.方法:19只慢性心力衰竭犬模型建立后随机分为实验组(n=9):采用开胸直接心肌内注射自体骨骼肌成肌细胞;对照组(n=10):开胸心肌内注射等量生理盐水.移植前及移植后5周行超声心动图检查,病理组织标本行Desmin和Brd-U免疫荧光双重染色.结果:①移植后较移植前,实验组收缩末期心室腔面积(ESA)、舒张末期心室腔面积(EDA)均明显下降(P<0.05),射血分数显著升高(P<0.05),差异有统计学意义;而对照组ESA和EDA在移植前、移植后差异无统计学意义(P>0.05);②实验组心肌注射部位可见存活细胞,经Desmin和Brd-U免疫荧光双重染色证实来自于移植的骨骼肌成肌细胞.结论:自体骨骼肌成肌细胞对慢性心力衰竭犬的左心室重塑及功能有明显改善作用.     

Pharmacologic Approaches to Electrolyte Abnormalities in Heart Failure

Current Heart Failure Reports - Electrolyte abnormalities are common in heart failure and can arise from a variety of etiologies. Neurohormonal activation from ventricular dysfunction, renal...     

慢性心力衰竭的免疫学研究进展

慢性心力衰竭是一种常见的综合征,它的发病机制很多,最近的研究表明免疫激活影响慢性心力衰竭的发生与发展。现就慢性心力衰竭与免疫学的关系作一综述。     

Enhanced Echo Intensity of Skeletal Muscle Is Associated With Exercise Intolerance in Patients With Heart Failure

BackgroundSkeletal muscle is quantitatively and qualitatively impaired in patients with heart failure (HF), which is closely linked to lowered exercise capacity. Ultrasonography (US) for skeletal muscle has emerged as a useful, noninvasive tool to evaluate muscle quality and quantity. Here we investigated whether muscle quality based on US-derived echo intensity (EI) is associated with exercise capacity in patients with HF.Methods and ResultsFifty-eight patients with HF (61 ± 12 years) and 28 control subjects (58 ± 14 years) were studied. The quadriceps femoris echo intensity (QEI) was significantly higher and the quadriceps femoris muscle thickness (QMT) was significantly lower in the patients with HF than the controls (88.3 ± 13.4 vs 81.1 ± 7.5, P= .010; 5.21 ± 1.10 vs 6.54 ±1.34 cm, P< .001, respectively). By univariate analysis, QEI was significantly correlated with age, peak oxygen uptake (VO₂), and New York Heart Association class in the HF group. A multivariable analysis revealed that the QEI was independently associated with peak VO₂ after adjustment for age, gender, body mass index, and QMT: β-coefficient = −11.80, 95%CI (−20.73, −2.86), P= .011.ConclusionEnhanced EI in skeletal muscle was independently associated with lowered exercise capacity in HF. The measurement of EI is low-cost, easily accessible, and suitable for assessment of HF-related alterations in skeletal muscle quality.     

慢性心力衰竭中的贫血

近年来研究发现,慢性心力衰竭患者中常常伴有贫血,而且贫血会加重心力衰竭患者的临床症状,使生存率下降。用促红细胞生成素治疗心力衰竭中的贫血,能够使心力衰竭患者的心功能和临床症状明显改善。     

Micronutrients in Chronic Heart Failure

Heart failure (HF)-associated mortality remains high, despite guideline-recommended medical therapies. Poor nutritional status and unintentional cachexia have been shown to have a strong association with worse survival in HF patients. Importantly, micronutrient deficiencies are potential contributing factors to the progression of HF. This review aims to summarize contemporary evidence on the role of micronutrients in the pathophysiology and outcome of HF patients. Emphasis will be given to the most well-studied micronutrients, specifically, vitamin D, vitamin B complex, coenzyme Q10 and L-carnitine.     

Digoxin Therapy in Chronic Heart Failure

Digitalis has been used for more than 250 years, but its role in the treatment of chronic heart failure has been intensively investigated only during the past two decades. Digoxin increases cardiac output both at rest and during exercise, alone or in combination with ACE inhibitors, and these hemodynamic effects are sustained during chronic therapy. A daily dose of digoxin that achieves a serum concentration of approximately 1.2 ng/ml is associated with a significant improvement in central hemodynamics, particularly in patients with impaired cardiac function despite pretreatment with diuretics and ACE inhibitors. Acute administration of digoxin in patients with chronic heart failure has an immediate sympathoinhibitory effect, and chronic therapy is associated with a sustained decrease in serum norepinephrine concentration. Discontinuation of digoxin in patients with chronic heart failure resulted in hemodynamic deterioration, which was reversed when the drug was readministered. Randomized withdrawal of digoxin in patients receiving only diuretics (PROVED study), or its withdrawal in patients receiving diuretics and ACE inhibitors (RADIANCE study), was associated with worsening of the clinical evidence of heart failure and a decrease in left ventricular systolic function in both studies. In the only large-scale, placebo-controlled mortality study reported thus for (DIG Trial), 7788 patients received standard drug treatment for chronic heart failure in addition to either digoxin or placebo. Digoxin had no impact on survival over the 37 months of follow-up, but the incidence of hospitalizations due to worsening heart failure was significantly reduced in patients receiving the drug compared with those receiving placebo.