Impact of Protein Supplements on Muscle Recovery After Exercise-induced Muscle Soreness

The intent of this study was to determine whether nutritional supplements [protein (0.4 g·kg−1) vs. carbohydrate (0.4 g·kg−1) vs. placebo] would affect muscle recovery differently after eccentric exercise-induced muscle soreness in untrained healthy young men (n = 21) aged 20-28 years. During this double-blind randomized block study design, each subject completed three, 3-day trials (separated by = 2 weeks), identical except for treatment, with each subject serving as his own control. Trials began with a bout of right-leg eccentric exercise (Biodex), followed directly by treatment. At 0 (baseline), 24 and 48 hours, data were collected: creatine phosphokinase from pre-exercise blood samples, subjective muscle soreness questions, and strength tests (power, torque, work). ANOVA indicated that exercise caused mild muscle damage, as evidenced by an overall day effect (p = 0.0001) for muscle soreness, with the lowest median values (0-10 scale) on day 1 (0.7), increasing (p = 0.0001) on day 2 (3.2), and remaining elevated on day 3 (3.4). We also noted an overall day effect (p = 0.0001) for creatine phosphokinase, with the lowest median values on day 1 (136 U·L-1), increasing (p = 0.0001) on day 2 (235 U·L-1), and remaining elevated on day 3 (189 U·L-1). ANOVA revealed no significant treatment effect on indicators of soreness or damage during recovery. Our results indicated that protein or carbohydrate supplement after exercise that caused mild muscle damage did not facilitate muscle recovery in adequately nourished, healthy young men

beta-Hydroxy-beta-methylbutyrate free acid reduces markers of exercise-induced muscle damage and improves recovery in resistance-trained men

The purpose of the present study was to determine the effects of short-term supplementation with the free acid form of beta-hydroxy-beta-methylbutyrate (HMB-FA) on indices of muscle damage, protein breakdown, recovery and hormone status following a high-volume resistance training session in trained athletes. A total of twenty resistance-trained males were recruited to participate in a high-volume resistance training session centred on full squats, bench presses and dead lifts. Subjects were randomly assigned to receive either 3 g/d of HMB-FA or a placebo. Immediately before the exercise session and 48 h post-exercise, serum creatine kinase (CK), urinary 3-methylhistadine (3-MH), testosterone, cortisol and perceived recovery status (PRS) scale measurements were taken. The results showed that CK increased to a greater extent in the placebo (329%) than in the HMB-FA group (104%) (P=0.004, d=1.6). There was also a significant change for PRS, which decreased to a greater extent in the placebo (9.1 (SEM 0.4) to 4.6 (SEM 0.5)) than in the HMB-FA group (9.1 (SEM 0.3) to 6.3 (SEM 0.3)) (P=0.005, d = -0.48). Muscle protein breakdown, measured by 3-MH analysis, numerically decreased with HMB-FA supplementation and approached significance (P=0.08, d = 0.12). There were no acute changes in plasma total or free testosterone, cortisol or C-reactive protein. In conclusion, these results suggest that an HMB-FA supplement given to trained athletes before exercise can blunt increases in muscle damage and prevent declines in perceived readiness to train following a high-volume, muscle-damaging resistance-training session

Adenosine-5'-triphosphate (ATP) supplementation improves low peak muscle torque and torque fatigue during repeated high intensity exercise sets

Abstract Background Intracellular concentrations of adenosine-5’-triphosphate (ATP) are many times greater than extracellular concentrations (1–10 mM versus 10–100 nM, respectively) and cellular release of ATP is tightly controlled. Transient rises in extracellular ATP and its metabolite adenosine have important signaling roles; and acting through purinergic receptors, can increase blood flow and oxygenation of tissues; and act as neurotransmitters. Increased blood flow not only increases substrate availability but may also aid in recovery through removal of metabolic waste products allowing muscles to accomplish more work with less fatigue. The objective of the present study was to determine if supplemental ATP would improve muscle torque, power, work, or fatigue during repeated bouts of high intensity resistance exercise. Methods Sixteen participants (8 male and 8 female; ages: 21–34 years) were enrolled in a double-blinded, placebo-controlled study using a crossover design. The participants received either supplemental ATP (400 mg/d divided into 2 daily doses) or placebo for 15 d. After an overnight fast, participants underwent strength and fatigue testing, consisting of 3 sets of 50 maximal knee extensions performed on a Biodex® leg dynamometer. Results No differences were detected in high peak torque, power, or total work with ATP supplementation; however, low peak torque in set 2 was significantly improved (p Conclusions Supplementation with 400 mg ATP/d for 15 days tended to reduce muscle fatigue and improved a participant’s ability to maintain a higher force output at the end of an exhaustive exercise bout.</p

L-leucine, beta-hydroxy-beta-methylbutyric acid (HMB) and creatine monohydrate prevent myostatin-induced Akirin-1/Mighty mRNA down-regulation and myotube atrophy

Background: The purpose of this study was to examine if L-leucine (Leu), β-hydroxy-β-methylbutyrate (HMB), or creatinemonohydrate (Crea) prevented potential atrophic effects of myostatin (MSTN) on differentiated C2C12 myotubes. Methods: After four days of differentiation, myotubes were treated with MSTN (10 ng/ml) for two additional days and four treatment groups were studied: 1) 3x per day 10 mM Leu, 2) 3x per day 10 mM HMB, 3) 3x per day 10 mM Crea,4) DM only. Myotubes treated with DM without MSTN were analyzed as the control condition (DM/CTL). Following treatment, cells were analyzed for total protein, DNA content, RNA content, muscle protein synthesis (MPS, SUnSET method), and fiber diameter. Separate batch treatments were analyzed for mRNA expression patterns of myostatin-relatedgenes (Akirin-1/Mighty, Notch-1, Ski, MyoD) as well as atrogenes (MuRF-1, and MAFbx/Atrogin-1). Results: MSTN decreased fiber diameter approximately 30% compared to DM/CTL myotubes (p < 0.001). Leu, HMB and Crea prevented MSTN-induced atrophy. MSTN did not decrease MPS levels compared to DM/CTL myotubes, but MSTN treatment decreased the mRNA expression of Akirin-1/Mighty by 27% (p < 0.001) and MyoD by 26% (p < 0.01) compared to DM/CTL myotubes. shRNA experiments confirmed that Mighty mRNA knockdown reduced myotube size, linkingMSTN treatment to atrophy independent of MPS. Remarkably, MSTN + Leu and MSTN + HMB myotubes had similar Akirin-1/Mighty and MyoD mRNA levels compared to DM/CTL myotubes. Furthermore, MSTN + Crea myotubes exhibiteda 36% (p < 0.05) and 86% (p < 0.001) increase in Akirin-1/Mighty mRNA compared to DM/CTL and MSTN-only treated myotubes, respectively. Conclusions: Leu, HMB and Crea may reduce MSTN-induced muscle fiber atrophy by influencing Akirin-1/Mighty mRNAexpression patterns. Future studies are needed to examine if Leu, HMB and Crea independently or synergistically affectAkirin-1/Mighty expression, and how Akirin-1/Mighty expression mechanistically relates to skeletal muscle hypertrophyin vivo