Sirtuin 3 enzyme (SIRT3) is involved in the regulation of mitochondrial energy homeostasis by activating Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α). Murine models have shown that the protein SIRT3 was modified by exercise and diet, however, the effect of exercise without diet in humans has not been examined. Propose of this paper was to analyze the effect of aerobic training on SIRT3 and PGC-1α in skeletal muscle of overweight adolescents without change in caloric intake. Fourteen overweight or obese male adolescents (15.5 ± 0.8 years) trained 3 days-week/50 min x session, at 70-80% of maximal heart rate for 12 weeks. Anthropometrics and skeletal muscle biopsies from the vastus lateralis were taken before and after the exercise program to measure adiposity, SIRT3, and PGC-1α proteins. Peak aerobic capacity (VO2peak) was estimated before and after training. The participants did not change their eating habits during the intervention. SIRT3 (1.05 ± 0.11 vs. 1.25 ± 0.14 AU, p = .014) and PGC-1a (1.06 ± 0.15 Vs 1.39 ± 0.20 AU, p = .009) increased. Fat percentage and waist circumference decreased (p < .05). VO2peak increased after training (p < .001). There was a significant association between SIRT3 and PGC-1α after training program. These data suggest that aerobic training increased SIRT3 and PGC-1a expression levels in sedentary, overweight, or obese adolescents.
Katya Vargas-Ortiz, Victoriano Perez-Vazquez, Francisco J. Diaz-Cisneros, Arturo Figueroa, Lizbeth M. Jiménez-Flores, Gustavo Rodriguez-DelaRosa and Maciste H. Macias
Yanmei Niu, Hong Yuan and Li Fu
Insulin resistance (IR) is a common pathophysiological feature of Type 2 diabetes. Although the mechanisms leading to IR are still elusive, evidence has shown that aerobic exercise can reverse this process. To investigate the effects of aerobic exercise on IR, the authors created an IR animal model by feeding C57BL/6 mice a high-fat diet for 8 wk. They then compared the effect of 6 wk of treadmill training (60 min/d) at 75% VO2max on mice in normal-diet (NE) and high-fat-diet (HE) groups with their sedentary control groups. Levels of skeletal-muscle AMPKα (AMP-activated protein kinase α), ACC (acetyl-CoA carboxylases), and CPT1 (carnitine palmitoyltransferase 1) mRNA and AMPKα, pAMPK-Thr172, ACC, pACC-Ser79, and CPT1 protein expressions were analyzed. In addition, fasting serum levels of insulin, triglyceride, and cholesterol were measured. The results demonstrate that 6 wk of exercise increased AMPKα mRNA expression by 11% and 25 % (p < .01) in the NE and HE groups, respectively, and AMPKα protein expression by 37.9% and 20.1% (p < .01) in NE and HE compared with their sedentary control. In addition, ACC mRNA and protein expressions declined, whereas CPT1 mRNA and protein expressions were elevated in both exercise groups compared with sedentary control groups. In addition, pAMPK-Thr172 and pACC-Ser79 expression increased significantly in the NE and HE groups compared with sedentary control groups. In conclusion, our results demonstrate that 6 wk of aerobic exercise can effectively ameliorate IR by increasing the expression of AMPKα and pAMPK-Thr172, thereby activating the key enzymes that facilitate lipid metabolism.
Farnoosh Mafi, Soheil Biglari, Alireza Ghardashi Afousi and Abbas Ali Gaeini
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
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
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).
Walter R. Frontera, Virginia A. Hughes, Lisa S. Krivickas and Ronenn Roubenoff
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.
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.