After hind limb suspension, a remodeling of postural muscle phenotype is observed. This remodeling results in a shift of muscle profile from slow-oxidative to fast-glycolytic. These metabolic changes and fiber type shift increase muscle fatigability. Acetyl-L-carnitine (ALCAR) influences the skeletal muscle phenotype of soleus muscle suggesting a positive role of dietary supplementation of ALCAR during unloading. In the present study, we applied a 2-D DIGE, mass spectrometry and biochemical assays, to assess qualitative and quantitative differences in the proteome of rat slow-twitch soleus muscle subjected to disuse. Meanwhile, the effects of ALCAR administration on muscle proteomic profile in both unloading and normal-loading conditions were evaluated. The results indicate a modulation of troponin I and tropomyosin complex to regulate fiber type transition. Associated, or induced, metabolic changes with an increment of glycolytic enzymes and a decreased capacity of fat oxidation are observed. These metabolic changes appear to be counteracted by ALCAR treatment, which restores the mitochondrial mass and decreases the glycolytic enzyme expression, suggesting a normalization of the metabolic shift observed in unloaded animals. This normalization is accompanied by a maintenance of body weight and seems to prevent a switch of fiber type.

:The temporal structure, or complexity, of muscle torque output decreases with neuromuscular fatigue. The role of central fatigue in this process is unclear.

PURPOSE:We tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity.

METHODS:Eleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction (MVC), with a 60% duty factor (6 s contraction, 4 s rest), 60 min after ingesting 6 mg·kg caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central and peripheral fatigue were quantified using MVCs with femoral nerve stimulation.

RESULTS:Caffeine ingestion increased endurance by 30± 16% (mean ± SD, P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P<0.01), as global, central and peripheral fatigue developed (all P<0.01). Complexity decreased significantly more slowly following caffeine ingestion (ApEn, -0.04± 0.02 vs. -0.06 ± 0.01, P = 0.004; DFA α, 0.03 ± 0.02 vs. 0.04 ± 0.03, P = 0.024), as did the rates of global (-18.2 ± 14.1 vs. -23.0 ± 17.4 N.m.min, P = 0.004) and central (-3.5 ± 3.4 vs. -5.7 ± 3.9 %·min, P = 0.02) but not peripheral (-6.1 ± 4.1 vs. -7.9 ± 6.3 N.m.min, P = 0.06) fatigue.

CONCLUSION:Caffeine ingestion slowed the fatigue-induced loss of torque complexity and increased the time to task failure during intermittent isometric contractions, most likely through central mechanisms.

Cordyceps militaris is the one of the most important medicinal mushrooms, widely used in East Asian countries. Polysaccharide is considered to be the principal active component in C. militaris and has a wide range of biological and pharmacological properties. This study was undertaken to investigate the effect of polysaccharide from C. militaris (PCM) on physical fatigue induced in animals through a forced swimming test. The mice were divided into 4 groups receiving 28 days' treatment with drinking water (exercise control) or low-, medium-, and high-dose PCM (40, 80, and 160 mg/kg/day, respectively). After 28 days, the mice were subjected to the forced swimming test; the exhaustive swimming time was measured and fatigue-related biochemical parameters, including serum lactic acid, urea nitrogen, creatine kinase, alanine aminotransferase, aspartate aminotransferase, superoxide dismutase, glutathi- one peroxidase, catalase, malondialdehyde, liver glycogen, and muscle glycogen, were analyzed. The results showed that PCM could significantly prolong the exhaustive swimming time of mice; decrease concentrations of serum lactic acid, urea nitrogen, creatine kinase, aspartate aminotransferase, alanine aminotransferase, and malondialdehyde; and increase liver and muscle glycogen contents and the concentrations of serum superoxide dismutase, glutathione per- oxidase, and catalase. The data suggest that PCM has an antifatigue effect, and it might become a new functional food or medicine for fatigue resistance.

OBJECTIVE:The aim of this study was to verify how a pair of monozygotic twins would respond to light-emitting diode therapy (LEDT) or placebo combined with a strength-training program during 12 weeks.

DESIGN:This case-control study enrolled a pair of male monozygotic twins, allocated randomly to LEDT or placebo therapies. Light-emitting diode therapy or placebo was applied from a flexible light-emitting diode array (λ = 850 nm, total energy = 75 J, t = 15 seconds) to both quadriceps femoris muscles of each twin immediately after each strength training session (3 times/wk for 12 weeks) consisting of leg press and leg extension exercises with load of 80% and 50% of the 1-repetition maximum test, respectively. Muscle biopsies, magnetic resonance imaging, maximal load, and fatigue resistance tests were conducted before and after the training program to assess gene expression, muscle hypertrophy and performance, respectively. Creatine kinase levels in blood and visual analog scale assessed muscle damage and delayed-onset muscle soreness, respectively, during the training program.

RESULTS:Compared with placebo, LEDT increased the maximal load in exercise and reduced fatigue, creatine kinase, and visual analog scale. Gene expression analyses showed decreases in markers of inflammation (interleukin 1β) and muscle atrophy (myostatin) with LEDT. Protein synthesis (mammalian target of rapamycin) and oxidative stress defense (SOD2 [mitochondrial superoxide dismutase]) were up-regulated with LEDT, together with increases in thigh muscle hypertrophy.

CONCLUSIONS:Light-emitting diode therapy can be useful to reduce muscle damage, pain, and atrophy, as well as to increase muscle mass, recovery, and athletic performance in rehabilitation programs and sports medicine.

Hemmings, TJ, Kendall, KL, and Dobson, JL. Identifying dosage effect of light-emitting diode therapy on muscular fatigue in quadriceps. J Strength Cond Res 31(2): 395-402, 2017-The purpose of this study was to compare the effects of various dosages of light-emitting diode therapy (LEDT) on muscle fatigue while performing a single-leg extension to exhaustion. A total of 34 recreationally resistance-trained athletes between the ages of 18 and 26 participated in 4 trials. Each trial included pre-exercise/postexercise blood lactate measurements and 2 sets of 3 maximal voluntary isometric contractions (MVICs), followed by LEDT on 6 points across the superficial quadriceps. Each randomized trial consisted of a placebo, 30, 60, or 120 seconds on each point on the quadriceps. Three minutes after LEDT, the participants performed an eccentric leg extension with 120% of MVIC until fatigue. There was significant increase in the number of repetitions performed between the placebo treatment and 60 seconds (p = 0.023), as well as placebo and 120 seconds (p = 0.004) of irradiation on each point. There were no significant differences in blood lactate levels between any of the 4 trials. In conclusion, LEDT had a positive effect on performance when irradiating 6 points on the superficial quadriceps for 60 and 120 seconds before an eccentric leg extension.