al . Biomechanical and skeletal muscle determinants of maximum running speed with aging . Med Sci Sports Exerc . 2009 ; 41 ( 4 ): 844 – 856 . PubMed doi:10.1249/MSS.0b013e3181998366 19276848 10.1249/MSS.0b013e3181998366 19. Nakatani M , Takai Y , Akagi R , et al . Validity of muscle thickness
Norihide Sugisaki, Kai Kobayashi, Hiroyasu Tsuchie and Hiroaki Kanehisa
Nicola Giovanelli, Lea Biasutti, Desy Salvadego, Hailu K. Alemayehu, Bruno Grassi and Stefano Lazzer
the skeletal muscle, as the exercise they analyzed was not isolated to a single muscle group (cycling at 1 and 1.5 W·kg −1 ). Thus, the purpose of the present study was to evaluate the effects of a trail-running race on muscle oxidative function by measuring pulmonary gas exchange variables and muscle
Ildus I. Ahmetov, Olga L. Vinogradova and Alun G. Williams
The ability to perform aerobic or anaerobic exercise varies widely among individuals, partially depending on their muscle-fiber composition. Variability in the proportion of skeletal-muscle fiber types may also explain marked differences in aspects of certain chronic disease states including obesity, insulin resistance, and hypertension. In untrained individuals, the proportion of slow-twitch (Type I) fibers in the vastus lateralis muscle is typically around 50% (range 5–90%), and it is unusual for them to undergo conversion to fast-twitch fibers. It has been suggested that the genetic component for the observed variability in the proportion of Type I fibers in human muscles is on the order of 40–50%, indicating that muscle fiber-type composition is determined by both genotype and environment. This article briefly reviews current progress in the understanding of genetic determinism of fiber-type proportion in human skeletal muscle. Several polymorphisms of genes involved in the calcineurin–NFAT pathway, mitochondrial biogenesis, glucose and lipid metabolism, cytoskeletal function, hypoxia and angiogenesis, and circulatory homeostasis have been associated with fiber-type composition. As muscle is a major contributor to metabolism and physical strength and can readily adapt, it is not surprising that many of these gene variants have been associated with physical performance and athlete status, as well as metabolic and cardiovascular diseases. Genetic variants associated with fiber-type proportions have important implications for our understanding of muscle function in both health and disease.
Stefan M. Pasiakos, Holly L. McClung, James P. McClung, Maria L. Urso, Matthew A. Pikosky, Gregory J. Cloutier, Roger A. Fielding and Andrew J. Young
This study examined alterations in skeletal-muscle growth and atrophy-related molecular events after a single bout of moderate-intensity endurance exercise. Muscle biopsies were obtained from 10 men (23 ± 1 yr, body mass 80 ± 2 kg, and VO2peak 45 ± 1 ml · kg−1 · min−1) immediately (0 hr) and 3 hr after a 60-min bout of cycle exercise (60% ± 5% VO2peak). Corresponding muscle biopsies were also obtained under resting conditions. The phosphorylation status of insulin/IGF-PI3K molecular-signaling proteins, ubiquitin-proteasome-related gene expression, FOXO transcription factors, and myogenic regulatory factors in muscle samples was analyzed using multiplex analysis, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). A condition–time interaction was observed for Akt phosphorylation (p < .05) with multiplexing. Regardless of endurance exercise, Akt phosphorylation decreased and ERK phosphorylation increased at 3 hr compared with 0 hr (p < .05). Levels of p70S6K phosphorylation were 110% greater (p < .05) at 3 hr than at 0 hr using Western blots. MuRF mRNA expression postexercise increased; levels were 4.7- and 5.7-fold greater (p < .05) at 0 hr and 3 hr, respectively, than at rest with qRT-PCR. Atrogin mRNA expression was up-regulated 3.2-fold 3 hr postexercise compared with rest. These findings demonstrate modest changes in the molecular responses to moderate endurance exercise in the absence of nutrition. This study provides the groundwork for future investigations designed to optimize the metabolic conditions necessary to positively influence the cellular mechanisms specific to skeletal-muscle protein turnover during recovery from endurance exercise.
Martin J. Gibala
The contribution of amino acid oxidation to total energy expenditure is negligible during short-term intense exercise and accounts for 3–6% of the total adenosine triphosphate supplied during prolonged exercise in humans. While not quantitatively important in terms of energy supply, the intermediary metabolism of several amino acids—notably glutamate, alanine, and the branched-chain amino acids—afreets other metabolites .including the intermediates within the tricarboxylic acid (TCA) cycle. Glutamate appears to be a key substrate for the rapid increase in muscle TCA cycle intermediates (TCAI) that occurs at the onset of moderate to intense exercise, due to a rightward shift of the reaction catalyzed by alanine aminotransferase (glutamate + pyruvate <-> alanine + 2-oxoglutarate). The pool of muscle TCAI declines during prolonged exercise, and this has been attributed to an increase in leucine oxidation that relies on one of the TCAI. However, this mechanism does not appear to be quantitatively important due of the relatively low maximal activity of branched-chain oxoacid dehydrogenase, the key enzyme involved. It has been suggested that an increase in TCAI is necessary to attain high rates of aerobic energy production and that a decline in TCAI may be a causative factor in local muscle fatigue. These topics remain controversial, but recent evidence suggests that changes in TCAI during exercise are unrelated to oxidative energy provision in skeletal muscle.
Gianluca Vernillo, Alfredo Brighenti, Eloisa Limonta, Pietro Trabucchi, Davide Malatesta, Grégoire P. Millet and Federico Schena
To quantify changes in skeletal-muscle oxygenation and pulmonary O2 uptake (V̇O2) after an extreme ultratrail running bout.
Before (PRE) and after (POST) the race (330-km, 24000 D±), profiles of vastus lateralis muscle oxygenation (ie, oxyhemoglobin [O2Hb], deoxyhemoglobin [HHb], and tissue oxygenation index [TOI]) and V̇O2 were determined in 14 athletes (EXP) and 12 control adults (CON) during two 4-min constant-load cycling bouts at power outputs of 1 (p1) and 1.5 (p1.5) W/kg performed in randomized order.
At POST, normalized [HHb] values increased (p1, +38.0%; p1.5, +27.9%; P < .05), while normalized [O2Hb] (p1, –20.4%; p1.5, –14.4%; P < .05) and TOI (p1, –17.0%; p1.5, –17.7%; P < .05) decreased in EXP. V̇O2 values were similar (P > 0.05). An “overshoot“ in normalized [HHb]:V̇O2 was observed, although the increase was significant only during p1.5 (+58.7%, P = .003). No difference in the aforementioned variables was noted in CON (P > .05).
The concentric and, particularly, the eccentric loads characterizing this extreme ultratrail-running bout may have led to variations in muscle structure and function, increasing the local muscle deoxygenation profile and the imbalance between O2 delivery to working muscles and muscle O2 consumption. This highlights the importance of incorporating graded training, particularly downhill bouts, to reduce the negative influence of concentric and severe eccentric loads to the microcirculatory function and to enhance the ability of runners to sustain such loading.
Christopher C. Webster, Kathryn M. van Boom, Nur Armino, Kate Larmuth, Timothy D. Noakes, James A. Smith and Tertius A. Kohn
in heart disease, obesity, and T2D ( Ludwig et al., 2018 ). A few days of consuming the LCHF diet can increase postprandial blood glucose concentrations in healthy individuals and reduce the capacity of skeletal muscle to oxidize a carbohydrate load, suggesting a typical state of poor glucose
Sunhyo Jeong and Michung Yoon
Ovariectomy leads to weight gain primarily in the form of adipose tissue in rodents. The authors investigated whether swimming improves ovariectomy-induced obesity through activation of peroxisome proliferatoractivated receptor α (PPARα) in the skeletal muscle of female ovariectomized (OVX) mice, an animal model of postmenopausal women. Female mice were randomly divided into 3 groups (n = 8/group): a sedentary sham-operated group, a sedentary OVX group, and a swim-trained OVX group. After mice were subjected to swim training or kept sedentary for 6 wk, the authors studied the effects of swimming on not only bodyweight gain, white adipose tissue (WAT) mass, adipocyte size, and skeletal-muscle lipid accumulation but also the expression of skeletal-muscle PPARα target genes. Sedentary OVX mice had significantly higher body weight and WAT than sedentary sham mice. However, swim training reduced body-weight gain, WAT mass, and adipocyte size of OVX mice. Swim-trained OVX mice had significantly lower levels of serum triglycerides and total cholesterol than sedentary OVX mice. Lipid accumulation in skeletal muscle was also markedly decreased by swimming. Concomitantly, swim training significantly increased mRNA levels of skeletal-muscle PPARα and its target enzymes, as well as uncoupling protein 3 (UCP3) responsible for fattyacid oxidation. These results suggest that swimming can effectively prevent weight gain, adiposity, adipocyte hypertrophy, and lipid disorders caused by ovariectomy, in part through the activation of PPARα and UCP3, in the skeletal muscle of female mice and may contribute to the alleviation of metabolic syndrome, including obesity, hyperlipidemia, and Type 2 diabetes in postmenopausal women.
David B. Preen, Brian T. Dawson, Carmel Goodman, John Beilby and Simon Ching
This study attempted to determine the relationship between creatine (Cr) accumulation in human skeletal muscle and erythrocytes following Cr supplementation. If a strong relationship exists, a blood test might provide a practical, less invasive alternative than muscle biopsy for evaluating cellular Cr accumulation. Eighteen active, but not well-trained males were supplemented with Cr (4 × 5g/d) for 5 d. Muscle biopsies (vastus lateralis) were obtained pre- and post-loading and analyzed for Cr, phosphocreatine (PCr), and total Cr (TCr) content. Venous blood was also drawn at these times to determine erythrocyte Cr concentrations. Muscle Cr, PCr, and TCr concentrations were elevated (P < 0.05) by 39.8%, 7.5%, and 20.1% respectively following supplementation. Erythrocyte Cr concentrations were also elevated (P < 0.01) following the loading period, although to a greater relative degree than tissue concentrations (129.6%). Pre- and post-loading erythrocyte Cr concentrations were poorly and nonsignificantly correlated with that observed in skeletal muscle. Further, loading-mediated increases in erythrocyte Cr concentrations were poorly correlated with elevations in muscle Cr (r = 0.07), PCr (r = 0.06) or TCr (r = 0.04) concentrations. Erythrocyte Cr concentrations can be augmented by 5 d of Cr supplementation, however, this elevation does not reflect that observed in skeletal muscle obtained by muscle biopsy. Consequently, erythrocyte response to Cr loading is not a reliable measure of skeletal muscle Cr/TCr accumulation.
Paul T. Reidy, Adam R. Konopka, J. Matthew Hinkley, Miranda K. Suer and Matthew P. Harber
We previously reported an increase in skeletal muscle protein synthesis during fasted and fed recovery from nonexhaustive aerobic exercise (Harber et al., 2010). The current study examined skeletal muscle intracellular signaling in the same subjects to further investigate mechanisms of skeletal muscle protein metabolism with and without feeding following aerobic exercise. Eight males (VO2peak: 52 ± 2 ml−1.kg−1.min−1) performed 60-min of cycle ergometry at 72 ± 1% VO2peak on two occasions in a counter-balanced design. Exercise trials differed only in the postexercise nutritional intervention: EX-FED (5kcal, 0.83g carbohydrate, 0.37g protein, 0.03g fat per kg body weight) and EX-FAST (noncaloric, isovolumic placebo) ingested immediately and one hour after exercise. Muscle biopsies were obtained from the vastus lateralis at rest (on a separate day) and two hours postexercise to assess intracellular signaling via western blotting of p70S6K1, eEF2, 4EBP1, AMPKα and p38 MAPK. p70S6K1 phosphorylation was elevated (p < .05) in EX-FED relative to REST and EX-FAST. eEF2, 4EBP1, AMPKα and p38 MAPK signaling were unaltered at 2h after exercise independent of feeding status when expressed as the ratio of phosphorylated to total protein normalized to actin. These data demonstrate that feeding after a nonexhaustive bout of aerobic exercise stimulates skeletal muscle p70S6K1 intracellular signaling favorable for promoting protein synthesis which may, as recent literature has suggested, better prepare the muscle for subsequent exercise bouts. These data provide further support into the role of feeding on mechanisms regulating muscle protein metabolism during recovery from aerobic exercise.