. Ghrelin regulates mitochondrial-lipid metabolism gene expression and tissue fat distribution in liver and skeletal muscle.

BackgroundAs muscle capillarization is related to the oxidative capacity of the muscle and the size of muscle fibres, capillary rarefaction may contribute to sarcopenia and functional impairment in older adults. Therefore, it is important to assess how ageing affects muscle capillarization and the interrelationship between fibre capillary supply with the oxidative capacity and size of the fibres.MethodsMuscle biopsies from healthy recreationally active young (22 years; 14 men and 5 women) and older (74 years; 22 men and 6 women) people were assessed for muscle capillarization and the distribution of capillaries with the method of capillary domains. Oxidative capacity of muscle fibres was assessed with quantitative histochemistry for succinate dehydrogenase (SDH) activity.ResultsThere was no significant age‐related reduction in muscle fibre oxidative capacity. Despite 18% type II fibre atrophy (P = 0.019) and 23% fewer capillaries per fibre (P < 0.002) in the old people, there was no significant difference in capillary distribution between young and old people, irrespective of sex. The capillary supply to a fibre was primarily determined by fibre size and only to a small extent by oxidative capacity, irrespective of age and sex. Based on SDH, the maximal oxygen consumption supported by a capillary did not differ significantly between young and old people.ConclusionsThe similar quantitative and qualitative distribution of capillaries within muscle from healthy recreationally active older people and young adults indicates that the age‐related capillary rarefaction, which does occur, nevertheless maintains the coupling between skeletal muscle fibre size and capillarization during healthy ageing.

Background: Muscle inactivity and low energy intake commonly occur in persons with acute or chronic disease, in astronauts during space flight, and during aging. Objective: We used a crossover design to investigate the effects of the interactions of inactivity and calorie restriction on whole-body composition and protein kinetic regulation in 9 healthy volunteers. Design: Lean body mass (LBM) was measured by using dual-energy X-ray absorptionmetry before and at the end of 14-d periods of bed rest (B) and controlled ambulation (A) in patients receiving eucaloric (E) or hypocaloric (H) (Ȃ80% of total energy expenditure) diets. Whole-body leucine kinetics were determined at the end of the 4 study periods by using a standard stable-isotope technique in the postabsorptive state and during a 3-h infusion of a 0.13 g ⅐ kg LBM Ҁ1 ⅐ h Ҁ1 amino acid mixture. Results: In the postabsorptive state, we found a significant (P ҃ 0.04) bed rest ҂ hypocaloric diet interaction for the rate of leucine oxidation, an index of net protein catabolism (AѿE: 0.23 Ȁ 0.01; BѿE: 25 Ȁ 0.01; AѿH: 0.23 Ȁ 0.01; BѿH: 0.28 Ȁ 0.01 mol ⅐ min Ҁ1 ⅐ kg LBM Ҁ1 ). Bed rest significantly (P 0.01) decreased amino acid-mediated stimulation of nonoxidative leucine disappearance, an index of protein synthesis (AѿE: 35 Ȁ 2%; BѿE: 30 Ȁ 2%; AѿH: 41 Ȁ 3%; BѿH: 32 Ȁ 2%). BѿH decreased LBM by 1.10 Ȁ 0.1 kg, which is significantly (P 0.01) greater than the decrease seen with AѿE, AѿH, or BѿE. Conclusion: Calorie restriction enhanced the catabolic response to inactivity by combining greater protein catabolism in the postabsorptive state with an impaired postprandial anabolic utilization of free amino acids.Am J Clin Nutr 2007;86:366 -72.