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Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training
Desy Salvadego, R. Domenis, Stefano Lazzer, Simone Porcelli, Joern Rittweger, Giovanna Rizzo, I. Mavelli, Boštjan Šimunič, Rado Pišot, Bruno Grassi, 2013, original scientific article

Abstract: Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA, body mass 102.67.3 kg, meanSD) and 11 controls (CTRL, body mass 77.86.0). Pulmonary O2 uptake (V'O2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross sectional area, volume (determined by magnetic resonance imaging) and strength were greater in RTA vs. CTRL (by ~40%, ~33% and ~20%, respectively). V'O2peak during CE was higher in RTA vs. CTRL (4.050.64 L min-1 vs. 3.560.30); no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE) V'O2peak was lower (by 15-20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, both during CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.723.7 pmolO2s-1mg-1 ww) vs. CTRL (35.710.2), and a tighter coupling of oxidative phosphorylation. In RTA the greater muscle mass and maximal force, and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mass
Keywords: skeletal muscle, hypertrophy, mitochondrial respiration, oxidative metabolism, exercise
Published in RUP: 15.10.2013; Views: 3950; Downloads: 151
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16.
Cancer cachexia-anorexia syndrome and skeletal muscle wasting
Mihaela Jurdana, 2009, review article

Abstract: Cachexia-anorexia syndrome is a common and important indicator of cancer. It occurs in 30% to 80% of cancer patients. Cachexia means "bad condition" and may be present in the early stages of tumor growth, before any signs of malignancy. Cancer cachexia is a syndrome of progressive body wasting, characterized by loss of adipose tissue and skeletal muscle mass. In most cancer patients, cachexia is characteriyed by anorexia, which implies a failure of food intake, regulated through a complex system of hormones and neuropeptides. A decline in food intake relative to energy expenditure is a fundamental physiologic derangement leading to cancer associated weight loss. The weight loss in patients with cachexia-anorexia syndrome differs from that in caloric starvation or anorexia nervosa. The pathophysiology of cancer cachexia is not fully understood; however, studies have shown that cytokines are important in the alteration of the carbohydrate, lipid and protein metabolism. Cancer, prolonged bed rest, HIV infection and aging are conditionsin which muscle wasting is a common feature. An intervention that may potentially attenuate the progression of muscle wasting in cancer patientsis resistance exercise training, defined as multiple repetitions of static or dynamic muscular contractions that increase muscle mass. The main components of the pathological state of cachexia are anorexia and metabolic abnormalities such as fat depletion and muscle protein catabolism. Future developments may concentrate on the molecular abnormalities of cachexia and on examination of the functional benefit of resistance exercise training for cancer related muscle wasting.
Keywords: cancer cachexia, muscle wasting, cytokines, muscle
Published in RUP: 15.10.2013; Views: 3982; Downloads: 94
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