The purpose of this study was to investigate the effect of compensatory hypertrophy (CH), heavy-resistance exercise training (HRET), and simultaneous CH and HRET on fast-twitch skeletal-muscle myofibrillar-protein synthesis, myosin heavy-chain (MHC) turnover rate, and MHC-isoform composition in young and old rats. In young animals all treatments intensified myofibrillar-protein synthesis, whereas in old animals with CH protein synthesis remained unchanged. The relative content of MHC I and IID in plantaris muscle increases with age, and the relative content of MHC IIB decreases. HRET and simultaneous CH and HRET decreased the proportion of MHC IIB and IIA and increased that of MHC IID in young rat muscle. In old rat muscle, relative content of MHC IID decreased and that of MHC IIB increased. CH decreased relative content of MHC IIB in both age groups and of MHC IIA in old animals. Relative content of MHC IID increased in both groups, and of MHC IIA, in young animals. MHC in plantaris of young rats turned over much faster in all types of mechanical loading but in old rats only during HRET and its combination with CH.
Ando Pehme, Karin Alev, Priit Kaasik and Teet Seene
Heather M. Logan-Sprenger, George J. F. Heigenhauser, Graham L. Jones and Lawrence L. Spriet
This study investigated the effects of progressive mild dehydration during cycling on whole-body substrate oxidation and skeletal-muscle metabolism in recreationally active men. Subjects (N = 9) cycled for 120 min at ~65% peak oxygen uptake (VO2peak 22.7 °C, 32% relative humidity) with water to replace sweat losses (HYD) or without fluid (DEH). Blood samples were taken at rest and every 20 min, and muscle biopsies were taken at rest and at 40, 80, and 120 min of exercise. Subjects lost 0.8%, 1.8%, and 2.7% body mass (BM) after 40, 80, and 120 min of cycling in the DEH trial while sweat loss was not significantly different between trials. Heart rate was greater in the DEH trial from 60 to 120 min, and core temperature was greater from 75 to 120 min. Rating of perceived exertion was higher in the DEH trial from 30 to 120 min. There were no differences in VO2, respiratory-exchange ratio, total carbohydrate (CHO) oxidation (HYD 312 ± 9 vs. DEH 307 ± 10 g), or sweat rate between trials. Blood lactate was significantly greater in the DEH trial from 20 to 120 min with no difference in plasma free fatty acids or epinephrine. Glycogenolysis was significantly greater (24%) over the entire DEH vs. HYD trial (433 ± 44 vs. 349 ± 27 mmol · kg−1 · dm−1). In conclusion, dehydration of <2% BM elevated physiological parameters and perceived exertion, as well as muscle glycogenolysis, during exercise without affecting whole-body CHO oxidation.
Resistance exercise can effectively result in an increase in muscle mass, or hypertrophy, which generally becomes apparent after several weeks of training. Muscle hypertrophy requires muscle protein synthesis to exceed protein breakdown during an extended time period. It has been firmly established that the interaction between exercise and nutrition (i.e., protein intake) is necessary to attain net protein accretion in skeletal muscle. The stimulation of protein synthesis is caused in part by stimulation of mRNA translation initiation. There is relatively little information on the response of intracellular signaling controlling mRNA translation to exercise and nutrition, especially in humans, but the available data in humans seem to suggest that a single bout of resistance exercise does not substantially enhance PI-3 kinase/mTOR signaling during the first 2 h after exercise. Moreover, it is demonstrated that the ingestion of protein or amino acids after exercise is crucial to further stimulate molecular signaling that controls translation initiation. The aim of this review is to provide an overview of the intracellular signaling related to translational control and to provide a summary of the current knowledge about the response of the signaling pathways controlling the anabolic response to exercise and nutrient intake in vivo in humans.
Han C.G. Kemper
This paper reviews the growth and development of skeletal mass in youth and the effects of physical activity upon the bone mass in young people. The different methods to measure the bone mass are described such as anthropometrics, radiographics, dual energy X-ray absorptiometry, quantitative computed tomography, and ultrasound. Two different mechanisms are important for the formation and plasticity of bone: a central hormonal mechanism (with estrogen production) and a local mechanism (based on mechanical forces of gravity and muscle contractions). This local mechanism is closely connected to physical activity patterns and therefore discussed in more detail. Thereafter the natural course of the development of the bone mass during youth is described, taking into account the pubertal stages of boys and girls and also the age at which the maximal bone mass (peak bone mineral density) will be reached. The last part is devoted to the effects of physical activity on bone mass based on results of randomized controlled trials. Although the number of experimental studies are scarce, significant effects of weight bearing activity and high impact strength training programs are shown on the side specific bone mineral density in both boys and girls.
Hermann Zbinden-Foncea, Luc J. C. van Loon, Jean-Marc Raymackers, Marc Francaux and Louise Deldicque
Mitogen-activated protein kinase (MAPK) pathways are activated in skeletal muscle during endurance exercise, but the upstream molecular events are incompletely resolved. As an increase in plasma nonesterified fatty acids (NEFA) is a common feature of long-lasting exercise, the authors tested the hypothesis that NEFA contribute to the activation of MAPK during endurance exercise. Acipimox was used before and during endurance exercise to prevent the elevation of plasma NEFA levels in healthy subjects and patients with diabetes. In 2 separate studies, healthy subjects cycled for 2 hr and patients with diabetes for 1 hr at 50% Wmax. In control conditions, plasma NEFA concentrations increased from 0.35 to 0.90 mM during exercise in healthy subjects and from 0.55 to 0.70 mM in patients with diabetes (p < .05). Phosphorylation states of extracellularly regulated kinase 1 and 2 (ERK1/2), p38, and c-Jun NH2-terminal kinases (JNK) were significantly increased after exercise in the vastus lateralis in both groups. Acipimox blocked the increase in plasma NEFA concentrations and almost completely repressed any rise in ERK1/2 and p38 but not in JNK. In conclusion, the data support a role for plasma NEFA in the activation of p38 and ERK1/2 in skeletal-muscle tissue of healthy and diabetic subjects during endurance exercise. Further investigation will be required to determine the molecular link between NEFA and MAPK activation during exercise in human skeletal muscle.
Charles L. Stebbins, Lauren E. Hammel, Benjamin J. Marshal, Espen E. Spangenberg and Timothy I. Musch
The polyunsaturated fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) affect vascular relaxation and involve factors (e.g., nitric oxide) that contribute to exercise-induced increases in skeletal-muscle blood flow (Q). The authors investigated whether DHA and EPA supplementation augments skeletal-muscle Q and vascular conductance (VC) and attenuates renal and splanchnic Q and VC in exercising rats. Rats were fed a diet of 5% lipids by weight, of which 20% was DHA and 30% EPA (PUFA group, n = 9), or 5% safflower oil (SO group, n = 8) for 6 wk. Heart rate (HR), blood pressure (MAP), and hind-limb, renal, and splanchnic Q were measured at rest and during moderate treadmill running. MAP, HR, and renal and splanchnic Q and VC were similar between the 2 groups at rest and during exercise. In the PUFA group, Q (158 ± 27 vs. 128 ± 28 ml · min−1 · 100 g−1) and VC (1.16 ± 0.21 vs. 0.92 ± 0.23 ml · min−1 · 100 g−1 · mm Hg−1) were greater in the exercising hind-limb muscle. Q and VC were also higher in 8 of 28 and 11 of 28 muscles and muscle parts, respectively. These increases were positively correlated to the percent sum of Types I and IIa fibers. Results suggest that DHA+EPA (a) enhances Q and VC in active skeletal muscle (especially Type I and IIa fibers) and that the increase in Q is due to an increase in cardiac output secondary to increases in VC and (b) has no apparent influence on vasoconstriction in renal and splanchnic tissue.
Andrew J.R. Cochran, Michael E. Percival, Sara Thompson, Jenna B. Gillen, Martin J. MacInnis, Murray A. Potter, Mark A. Tarnopolsky and Martin J. Gibala
Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.
Kian Peng Goh, Hwei Yee Lee, Dawn Pingxi Lau, Wilma Supaat, Yiong Huak Chan and Angela Fang Yung Koh
The primary aims of the study were to examine the effect of resveratrol on skeletal muscle SIRT1 expression and energy expenditure in subjects with Type 2 diabetes mellitus (T2DM).
Animal and in vivo studies indicate that resveratrol increases SIRT1 expression that stimulates PGC1α activity. Subsequent upregulation of AMPK and GLUT4 expression are associated with improved insulin sensitivity in peripheral tissues.
Ten subjects with T2DM were randomized in a double-blind fashion to receive 3g resveratrol or placebo daily for 12 weeks. Secondary outcomes include measures of AMPK, p-AMPK and GLUT4 expression levels, energy expenditure, physical activity levels, distribution of abdominal adipose tissue and skeletal muscle fiber type composition, body weight, HbA1c, plasma lipid subfraction, adiponectin levels, and insulin sensitivity.
There was a significant increase in both SIRT1 expression (2.01 vs. 0.86 arbitrary units [AU], p = .016) and p-AMPK to AMPK expression ratio (2.04 vs. 0.79 AU, p = .032) in the resveratrol group compared with the placebo group. Although the percentage of absolute change (8.6 vs. –13.9%, p = .033) and percentage of predicted resting metabolic rate (RMR; 7.8 vs. –13.9%, p = .013) were increased following resveratrol, there was a significant reduction in average daily activity (–38 vs. 43.2%, p = .028) and step counts (–39.5 vs. 11.8%, p = .047) when compared with placebo.
In patients with T2DM, treatment with resveratrol regulates energy expenditure through increased skeletal muscle SIRT1 and AMPK expression. These findings indicate that resveratrol may have beneficial exercise-mimetic effects in patients with T2DM.
Timo Byl, Jennifer A. Cole and Lori A. Livingston
Q-angle size has been found to correlate poorly with skeletal measures of pelvic breadth and femur length. Because the patella is exposed to the forces of quadriceps contraction, muscular forces might also affect Q-angle magnitude.
To compare bilateral measurements of the Q angle with selected skeletal and muscular strength measures.
In vivo study of anthropometric and quadriceps peak torque measures.
Thirty-four healthy men and women, mean age 20.9 ± 2.7 years.
Main Outcome Measures:
Q angles, pelvic breadths, femur lengths, and peak torque during dynamic knee-extension exercise, normalized to body weight.
Significant differences in Q-angle magnitude, femur length, and peak torqueBW were observed between sexes, but not between limbs. Pelvic breadth did not differ significantly between sexes. Correlational analysis revealed a weak, yet significant, linear relationship between Q angle and peak torqueBW in the right lower limb.
These findings lend some support to the notion that Q-angle magnitude is inversely related to quadriceps strength.
Aiping Chi, Liang Tang, Jing Zhang and Kunru Zhang
To investigate the effects of polysaccharide from Gynostemma pentaphyllum on antioxidant activity in skeletal muscle of mice exercised to exhaustion.
Three polysaccharide fractions were obtained from G. pentaphyllum polysaccharide (GPP) and termed GPP1-a, GPP2-b, and GPP3-a. Gas chromatography (GC) and infrared spectrum of the polysaccharides were determined. The fractions were orally administrated to mice once daily for 1 wk. The exercise time to exhaustion was assessed using a forced swim test of mice after a week. The glucose, creatine phosphokinase, and lactic dehydrogenase in serum; the activity of superoxide dismutase and glutathione peroxidase; and the levels of malondialdehyde (MDA) and glycogen in muscle were determined.
The results of GC demonstrated that GPP1-a, GPP2-b, and GPP3-a were composed of different monosaccharides with distinct molar ratios. Infrared spectrum showed that the main typicals of GPP1-a and GPP2-b were β-configuration and the main typical of GPP3-a was α-configuration. Among the 3 fractions of GPP, GPP1-a administration significantly prolonged exercise time to exhaustion of mice, increased glycogen level and some of antioxidant enzyme activities, and decreased MDA level in muscle.
The mechanism by which GPP1-a prolonged exercise time to exhaustion in mice may be associated with scavenging reactive oxygen species excessively produced and further increasing glycogen levels in skeletal muscle.