Sarcopenia is defined as a loss of skeletal muscle mass, quality, and strength that occurs as a result of normal aging ( Rosenberg, 1997 ). The loss of skeletal muscle mass and strength caused by sarcopenia lowers people’s ability to do daily activities like standing up and walking and may weaken
Farnoosh Mafi, Soheil Biglari, Alireza Ghardashi Afousi and Abbas Ali Gaeini
Alexandre M. Lehnen, Graziela H. Pinto, Júlia Borges, Melissa M. Markoski and Beatriz D. Schaan
subsequently transmitted through the cell by a series of interactions, which ensues through two major cascades of protein–protein interactions ( Lebovitz, 2001 ). Considering that skeletal muscle is the major tissue for insulin-mediated glucose disposal (70–80%; Ng et al., 2012 ; Zierath et al., 2000
Donald A. Bailey and Alan D. Martin
A considerable amount of research into osteoporosis has focused on the management and treatment of bone loss in later life. More recently, a limited amount of research has been directed toward the development of an optimal level of peak bone mass during the adolescent and early adult years. While genetics is a major determinant of bone status, there is considerable evidence that physical activity is an important nonhereditary factor. Studies on adults suggest that the positive effect of physical activity on bone is modest in the short term but may be quite powerful with more intense activity that overloads the muscular system for a longer time period. In children, however, our knowledge about the long-term effects of physical activity on bone accretion is incomplete. This paper presents a review of the pediatric literature dealing with the relationship of physical activity to bone mineral density status in the adolescent population.
Walter R. Frontera, Virginia A. Hughes, Lisa S. Krivickas and Ronenn Roubenoff
J.J.F.P. Luiken, D. Miskovic, Y. Arumugam, J.F.C. Glatz and A. Bonen
While it has long been assumed that long chain fatty acids (LCFA) can freely diffuse across the plasma membrane, recent work has shown that LCFA uptake also involves a protein-mediated mechanism. Three putative LCFA transporters have been identified (FABPpm, FATP, and FAT/CD36), and all are expressed in rodent and human muscles. In a new model system (giant vesicles), we have demonstrated that (a) LCFA transport rates are scaled with the oxidative capacity of heart and muscle, (b) only FABPpm and FAT/CD36, but not FATP1, correlate with vesicular LCFA transport, and (c) LCFA transport can be increased by increasing (1) the FAT/CD36 protein of muscle (chronic adaptation) or (2) via the translocation of FAT/CD36 from an intracellular pool to the plasma membrane during muscle contraction (acute adaptation).
Yasuo Kawakami and Tetsuo Fukunaga
John C. Lawrence Jr.
Muscle mass is influenced by many factors including genetically programmed changes, hormonal state, level of activity, and disease processes. Ultimately, whether or not a muscle hypertrophies or atrophies is determined by a simple relationship between the rates of protein synthesis and degradation. When synthesis exceeds degradation, the muscle hypertrophies, and vice versa. In contrast to this simple relationship, the processes that control muscle protein synthesis and degradation are complex. Recently, significant progress has been made in understanding the biochemical mechanisms that control the rate of translation initiation, which is generally the limiting phase in protein synthesis.