Skeletal muscle mass independently predicts peak oxygen consumption and ventilatory response during exercise in noncachectic patients with chronic heart failure

Cicoira, Mariantonietta; Zanolla, Luisa; Franceschini, Lorenzo; Rossi, Andrea; Golia, Giorgio; Zamboni, Mauro; Tosoni, Paolo; Zardini, Piero

doi:10.1016/s0735-1097(01)01306-7

Cited by 137 publications

(93 citation statements)

References 39 publications

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“…Our finding contrasts with previous studies that found selected peripheral components rather than central hemodynamic parameters to be better predictors of V O 2 peak in HF (5,8,9,13,23). For example, Cicoira et al (5) demonstrated that skeletal muscle is an important determinant of exercise capacity independent of central hemodynamics in noncachectic patients with HF. Leg muscle cross-sectional area has also been shown to be significantly correlated with and serve as an independent predictor of V O 2 peak in male patients with HF (13).…”

Section: Discussioncontrasting

confidence: 99%

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Meyer¹,

Karamanoglu²,

Kovács

2004

Journal of Applied Physiology

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. Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction. J Appl Physiol 97: 1667-1672. First published June 18, 2004 doi:10.1152/japplphysiol.00078.2004.-Impaired exercise tolerance, determined by peak oxygen consumption (V O2 peak), is predictive of mortality and the necessity for cardiac transplantation in patients with chronic heart failure (HF). However, the role of left ventricular (LV) diastolic function at rest, reflected by chamber stiffness assessed echocardiographically, as a determinant of exercise tolerance is unknown. Increased LV chamber stiffness and limitation of V O2 peak are known correlates of HF. Yet, the relationship between chamber stiffness and V O2 peak in subjects with HF has not been fully determined. Forty-one patients with HF New York Heart Association [(NYHA) class 2.4 Ϯ 0.8, mean Ϯ SD] had echocardiographic studies and V O2 peak measurements. Transmitral Doppler E waves were analyzed using a previously validated method to determine k, the LV chamber stiffness parameter. Multiple linear regression analysis of V O2 peak variance indicated that LV chamber stiffness k (r 2 ϭ 0.55) and NYHA classification (r 2 ϭ 0.43) were its best independent predictors and when taken together account for 59% of the variability in V O2 peak. We conclude that diastolic function at rest, as manifested by chamber stiffness, is a major determinant of maximal exercise capacity in HF. diastole; echocardiography; oxygen consumption CHRONIC HEART FAILURE (HF) is a major health problem that carries a high mortality rate despite continued significant advances in medical therapy. With ϳ400,000 new cases of HF diagnosed each year, 4.7 million Americans suffer from this debilitating disease (1). It has been established that patients with HF have impaired exercise tolerance that is predictive of mortality and the need for cardiac transplantation (10). Characteristically, the failing heart demonstrates an inability to maintain an adequate cardiac output, first during effort and later also at rest. Cardiac decompensation ultimately leads to impaired exercise capacity, fatigue, and exertional dyspnea. Patients with HF thus may have a decreased left ventricular (LV) ejection fraction (LVEF), large end-diastolic volume, and impaired contractile reserve (33, 34). Ventricular dysfunction as quantitated by a decreased LVEF is the main manifestation of HF that ultimately results in circulatory failure. Advanced LV dysfunction is associated with a variety of neurohumoral, peripheral circulatory, skeletal muscle, and respiratory adaptations that determine the syndrome's overall clinical presentation and prognosis (33, 34). The known mechanisms that lead to HF are highly complex, involving chamber enlargement and remodeling and decreased LV contractile reserve (10). The factor common to all types of HF regardless of etiology is increased LV end-diastolic pressure (LVEDP), which compromises LV filling, diminishes stroke volume and cardiac outpu...

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Section: Discussioncontrasting

confidence: 99%

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Meyer¹,

Karamanoglu²,

Kovács

2004

Journal of Applied Physiology

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“…Relationship between skeletal muscle volume and exercise capacity: Several previous studies have provided results consistent with our own by recognizing significant correlations between skeletal muscle volume and exercise capacity in patients with MI 3) and CHF. 15,[20][21][22][23] As in our study, Murabayashi, et al 3) found a significant correlation between skeletal muscle volume and exercise capacity in patients with MI.…”

Section: Discussionsupporting

confidence: 78%

“…19) Several others revealed correlations between skeletal muscle volume and exercise capacity in patients with CHF. 15,[20][21][22][23] If a similar correlation exists in patients with MI, it remains uncertain whether such a correlation could be found to influence the exercise capacity of the patient. The present study had two objectives: first, to evaluate skeletal muscle volume as a determinant of skeletal muscle strength in a population of MI patients, and second, to evaluate the correlation between skeletal muscle volume and skeletal muscle strength in relation to exercise capacity in the same patients.…”

mentioning

confidence: 99%

Functional Capacity, Skeletal Muscle Strength, and Skeletal Muscle Volume in Patients With Myocardial Infarction

et al. 2006

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SUMMARYPrevious studies have reported that skeletal muscle strength is closely related to exercise capacity in patients with myocardial infarction (MI). However, none of the previous studies have fully investigated the correlation between exercise capacity and the skeletal muscle volume (MV). Seventy patients with MI underwent symptom-limited cardiopulmonary exercise testing using a treadmill. The MV was evaluated by electrical impedance analysis and the maximal knee extension strength (Peak torque: PT) was measured by a Biodex. The subjects were divided into 2 groups according to the MV (group L, MV < 22 kg; group H, MV ≥ 22 kg). The PT was positively and significantly correlated with the peak VO 2 in both the L and H groups (r = 0.70 versus r = 0.71). The MV of the lower limbs was positively correlated with the peak VO 2 in the L group (r = 0.57), but not in the H group. The lower limb MV was positively and significantly correlated with PT in the L group (r = 0.48), but not in the H group. The exercise capacity of patients with MI is thought to depend on both the strength and volume of the skeletal muscle. In MI patients with high muscle volume, exercise capacity was determined by skeletal muscle strength alone. (Int Heart J 2006; 47: 727-738)

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“…Muscle mass is the major determinant of both resting energy expenditure (50) and exercise capacity (51) . The muscle hypothesis (52) holds that many factors are involved in the development of reduced peak oxygen uptake (peak VO 2 ) in HF.…”

Section: Muscle Loss In Heart Failurementioning

confidence: 99%

The wasting continuum in heart failure: from sarcopenia to cachexia

Haehling

2015

Proc. Nutr. Soc.

101

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Conference on 'Nutrition and age-related muscle loss, sarcopenia and cachexia' Symposium 2: Mechanisms for loss of muscle mass, strength and clinical measurement of malnutrition and cachexiaThe wasting continuum in heart failure: from sarcopenia to cachexiaStephan von Haehling Sarcopenia (muscle wasting) and cachexia share some pathophysiological aspects.Sarcopenia affects approximately 20 %, cachexia <10 % of ambulatory patients with heart failure (HF). Whilst sarcopenia means loss of skeletal muscle mass and strength that predominantly affects postural rather than non-postural muscles, cachexia means loss of muscle and fat tissue that leads to weight loss. The wasting continuum in HF implies that skeletal muscle is lost earlier than fat tissue and may lead from sarcopenia to cachexia. Both tissues require conservation, and therapies that stop the wasting process have tremendous therapeutic appeal. The present paper reviews the pathophysiology of muscle and fat wasting in HF and discusses potential treatments, including exercise training, appetite stimulants, essential amino acids, growth hormone, testosterone, electrical muscle stimulation, ghrelin and its analogues, ghrelin receptor agonists and myostatin antibodies.

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Skeletal muscle mass independently predicts peak oxygen consumption and ventilatory response during exercise in noncachectic patients with chronic heart failure

Abstract: Skeletal muscle mass is an independent predictor of peak Vo2 and VE/VCo2 slope in stable noncachectic patients with CHF. Future studies will determine whether an increase in skeletal muscle mass in the individual patient might result in an improvement in parameters of exercise capacity.

Cited by 137 publications

References 39 publications

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Functional Capacity, Skeletal Muscle Strength, and Skeletal Muscle Volume in Patients With Myocardial Infarction

The wasting continuum in heart failure: from sarcopenia to cachexia

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