α-lipoic acid has been found to enhance glucose uptake into skeletal muscle in animal models. Studies have also found that the co-ingestion of carbohydrate along with creatine increases muscle creatine uptake by a process related to insulin-stimulated glucose disposal. The purpose of this study was to determine the effect of α-lipoic acid on human skeletal muscle creatine uptake by directly measuring intramuscular concentrations of creatine, phosphocreatine, and ad-enosine triphosphate when creatine monohydrate was co-ingested with α-lipoic acid. Muscle biopsies were acquired from the vastus lateralis m. of 16 male subjects (18–32 y) before and after the experimental intervention. After the initial biopsy, subjects ingested 20 g · d−1 of creatine monohydrate, 20 g · d−1 of creatine monohydrate + 100 g · d−1 of sucrose, or 20 g · d−1 of creatine monohydrate + 100 g · d−1 of sucrose + 1000 mg · d−1 of α-lipoic acid for 5 days. Subjects refrained from exercise and consumed the same balanced diet for 7 days. Body weight increased by 2.1% following the nutritional intervention, with no differences between the groups. There was a significant increase in total creatine concentration following creatine supplementation, with the group ingesting α-lipoic acid showing a significantly greater increase (p < .05) in phosphocreatine (87.6 → 106.2 mmol · kg−1 dry mass [dm]) and total creatine (137.8 → 156.8 mmol · kg−1 dm). These findings indicate that co-ingestion of α-lipoic acid with creatine and a small amount of sucrose can enhance muscle total creatine content as compared to the ingestion of creatine and sucrose or creatine alone.
Darren G. Burke, Philip D. Chilibeck, Gianni Parise, Mark A. Tarnopolsky and Darren G. Candow
Nai-Hsin Meng, Chia-Ing Li, Chiu-Shong Liu, Wen-Yuan Lin, Chih-Hsueh Lin, Chin-Kai Chang, Tsai-Chung Li and Cheng-Chieh Lin
To compare muscle strength and physical performance among subjects with and without sarcopenia of different definitions.
A population-based cross-sectional study.
857 community residents aged 65 years or older.
Sarcopenia was defined according to the European Working Group of Sarcopenia in Older People consensus criteria. Dual-energy X-ray absorptiometry measured lean soft tissue mass. Sarcopenic participants with low height-adjusted or weight-adjusted skeletal muscle index (SMI) were classified as having h-sarcopenia or w-sarcopenia, respectively. Combined sarcopenia (c-sarcopenia) was defined as having either h- or w-sarcopenia. The participants underwent six physical performance tests: walking speed, timed up-and-go, six-minute walk, single-leg stance, timed chair stands, and flexibility test. The strength of five muscle groups was measured.
Participants with h-sarcopenia had lower weight, body mass index (BMI), fat mass, and absolute muscle strength (p ≤ .001); those with w-sarcopenia had higher weight, BMI, fat mass (p < .001), and low relative muscle strength (p ≤ .003). Participants with c-sarcopenia had poorer performance in all physical performance tests, whereas h-sarcopenia and w-sarcopenia were associated with poor performance in four tests.
Subjects with h- and w-sarcopenia differ significantly in terms of obesity indicators. Combining height- and weight-adjusted SMIs can be a feasible method to define sarcopenia.
Trent M. Guess, Swithin Razu, Amirhossein Jahandar, Marjorie Skubic and Zhiyu Huo
The Microsoft Kinect is becoming a widely used tool for inexpensive, portable measurement of human motion, with the potential to support clinical assessments of performance and function. In this study, the relative osteokinematic Cardan joint angles of the hip and knee were calculated using the Kinect 2.0 skeletal tracker. The pelvis segments of the default skeletal model were reoriented and 3-dimensional joint angles were compared with a marker-based system during a drop vertical jump and a hip abduction motion. Good agreement between the Kinect and marker-based system were found for knee (correlation coefficient = 0.96, cycle RMS error = 11°, peak flexion difference = 3°) and hip (correlation coefficient = 0.97, cycle RMS = 12°, peak flexion difference = 12°) flexion during the landing phase of the drop vertical jump and for hip abduction/adduction (correlation coefficient = 0.99, cycle RMS error = 7°, peak flexion difference = 8°) during isolated hip motion. Nonsagittal hip and knee angles did not correlate well for the drop vertical jump. When limited to activities in the optimal capture volume and with simple modifications to the skeletal model, the Kinect 2.0 skeletal tracker can provide limited 3-dimensional kinematic information of the lower limbs that may be useful for functional movement assessment.
Matthew S. Palmer, George J.F. Heigenhauser, MyLinh Duong and Lawrence L. Spriet
This study determined whether mild dehydration influenced skeletal muscle glycogen use, core temperature or performance during high-intensity, intermittent cycle-based exercise in ice hockey players vs. staying hydrated with water. Eight males (21.6 ± 0.4 yr, 183.5 ± 1.6 cm, 83.9 ± 3.7 kg, 50.2 ± 1.9 ml·kg-1·min-1) performed two trials separated by 7 days. The protocol consisted of 3 periods (P) containing 10 × 45-s cycling bouts at ~133% VO2max, followed by 135 s of passive rest. Subjects drank no fluid and dehydrated during the protocol (NF), or maintained body mass by drinking WATER. Muscle biopsies were taken at rest, immediately before and after P3. Subjects were mildly dehydrated (-1.8% BM) at the end of P3 in the NF trial. There were no differences between the NF and WATER trials for glycogen use (P1+P2; 350.1 ± 31.9 vs. 413.2 ± 33.2, P3; 103.5 ± 16.2 vs. 131.5 ± 18.9 mmol·kg dm-1), core temperature (P1; 37.8 ± 0.1 vs. 37.7 ± 0.1, P2; 38.2 ± 0.1 vs. 38.1 ± 0.1, P3; 38.3 ± 0.1 vs. 38.2 ± 0.1 °C) or performance (P1; 156.3 ± 7.8 vs. 154.4 ± 8.2, P2; 150.5 ± 7.8 vs. 152.4 ± 8.3, P3; 144.1 ± 8.7 vs. 148.4 ± 8.7 kJ). This study demonstrated that typical dehydration experienced by ice hockey players (~1.8% BM loss), did not affect glycogen use, core temperature, or voluntary performance vs. staying hydrated by ingesting water during a cycle-based simulation of ice hockey exercise in a laboratory environment.
Thomas M. Doering, Peter R. Reaburn, Stuart M. Phillips and David G. Jenkins
Participation rates of masters athletes in endurance events such as long-distance triathlon and running continue to increase. Given the physical and metabolic demands of endurance training, recovery practices influence the quality of successive training sessions and, consequently, adaptations to training. Research has suggested that, after muscle-damaging endurance exercise, masters athletes experience slower recovery rates in comparison with younger, similarly trained athletes. Given that these discrepancies in recovery rates are not observed after non–muscle-damaging exercise, it is suggested that masters athletes have impairments of the protein remodeling mechanisms within skeletal muscle. The importance of postexercise protein feeding for endurance athletes is increasingly being acknowledged, and its role in creating a positive net muscle protein balance postexercise is well known. The potential benefits of postexercise protein feeding include elevating muscle protein synthesis and satellite cell activity for muscle repair and remodeling, as well as facilitating muscle glycogen resynthesis. Despite extensive investigation into age-related anabolic resistance in sedentary aging populations, little is known about how anabolic resistance affects postexercise muscle protein synthesis and thus muscle remodeling in aging athletes. Despite evidence suggesting that physical training can attenuate but not eliminate age-related anabolic resistance, masters athletes are currently recommended to consume the same postexercise dietary protein dose (approximately 20 g or 0.25 g/kg/meal) as younger athletes. Given the slower recovery rates of masters athletes after muscle-damaging exercise, which may be due to impaired muscle remodeling mechanisms, masters athletes may benefit from higher doses of postexercise dietary protein, with particular attention directed to the leucine content of the postexercise bolus.
Sijie Tan, Jianxiong Wang and Shanshan Liu
The purpose of this study was to establish the one-repetition maximum (1RM) prediction equations of a biceps curl, bench press, and squat from the submaximal skeletal muscle strength of 4–10RM or 11–15RM in older adults. The first group of 109 participants aged 60–75 years was recruited to measure their 1RM, 4–10RM, and 11–15RM of the three exercises. The 1RM prediction equations were developed by multiple regression analyses. A second group of participants with similar physical characteristics to the first group was used to evaluate the equations. The actual measured 1RM of the second group correlated significantly to the predicted 1RM obtained from the equations (r values were from .633–.985), and standard error of estimate ranged from 1.08–5.88. Therefore, the equations can be used to predict 1RM from submaximal skeletal muscle strength accurately for older adults.
Katya Vargas-Ortiz, Victoriano Perez-Vazquez, Francisco J. Diaz-Cisneros, Arturo Figueroa, Lizbeth M. Jiménez-Flores, Gustavo Rodriguez-DelaRosa and Maciste H. Macias
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.
Manu V. Chakravarthy, Frank W. Booth and Espen E. Spangenburg
Approximately 50% of humans older than 85 years have physical frailty due to weak skeletal muscles. This indicates a need for determining mechanisms to combat this problem. A critical cellular factor for postnatal muscle growth is a population of myogenic precursor cells called satellite cells. Given the complex process of sarcopenia, it has been postulated that, at some point in this process, a limited satellite cell proliferation potential could become rate-limiting to the regrowth of old muscles. It is conceivable that if satellite cell proliferative capacity can be maintained or enhanced with advanced age, sarcopenia could potentially be delayed or prevented. Therefore, the purposes of this paper are to describe whether IGF-I can prevent muscular atrophy induced by repeated cycles of hindlimb immobilization, increase the in vitro proliferation in satellite cells from these muscles and, if so, the molecular mechanisms by which IGF-1 mediates this increased proliferation. Our results provide evidence that IGFI can enhance aged muscle regrowth possibly through increased satellite cell proliferation. The results also suggest that IGF-I enhances satellite cell proliferation by decreasing the cell cycle inhibitor, p27Kip1, through the PI3’-K/Akt pathway. These data provide molecular evidence for IGF-I’s rescue effect upon aging-associated skeletal muscle atrophy.
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