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The primary purpose was to determine the separate and combined effects of creatine and caffeine supplementation during resistance training on body composition and muscle performance in trained young adults. Twenty-eight participants were randomized to supplement with creatine and caffeine (CR-CAF; n = 9, 22 ± 4 years; 0.1 g·kg−1·d−1 of creatine monohydrate + 3 mg·kg−1·d−1 of caffeine anhydrous micronized powder); creatine (CR; n = 7, 22 ± 4 years, 0.1 g·kg−1·d−1 of creatine + 3 mg·kg−1·d−1 of micronized cellulose), caffeine (CAF; n = 6, 19 ± 1 years, 3 mg·kg−1·d−1 of caffeine + 0.1 g·kg−1·d−1 of maltodextrin) or placebo (PLA; n = 6, 23 ± 7 years, 0.1 g·kg−1·d−1 of maltodextrin + 3 mg·kg−1·d−1 micronized cellulose) one hour prior to performing resistance training for 6 weeks. Before and after training and supplementation, fat-free and fat mass (air-displacement plethysmography), muscle thickness (elbow and knee flexors and extensors; ultrasound), muscle strength (1-repetition maximum [1-RM] for the leg press and chest press), and endurance (one set of repetitions to volitional fatigue using 50% baseline 1-RM for leg press and chest press) were assessed. There was a group x time interaction (p = 0.049) for knee extensor muscle thickness with CR experiencing an increase over time with no changes in the other groups. There were no other between group differences for any variable. In conclusion, creatine supplementation and resistance training results in a small improvement in knee extensor muscle accretion in trained young adults. [ABSTRACT FROM AUTHOR]

Introduction: Caffeine has the athletic performance-enhancing effects, but its effect on concentrations of anabolic hormones is unclear. Therefore, this research examines the short–term effect of caffeine consumption on anabolic hormones of growth (GH) and testosterone (TS) after performing resistance exercise (RE). Materials and Methods: In this randomized double-blind, and placebo-controlled crossover study, 30 volunter men (mean age 21.72 ± 4.06, height 179.31 ± 5.08 centimeter, wight 77.31 ± 14.70 kilogram) who did resistance exercise consumed caffeine supplement (6 mg.k-1 of the body weight) and placebo (maltodextrine 6 mg.k-1 of the body weight) one hour before the RE, and the blood samples were taken before, after and 15 min after RE. Results: Analysis of data showed that GH concerntration showed a significant difference between the conditions of caffeine and placebo immediately and and 15 minutes after RE (P<0.05), but no significant diference was found in TS concentration caffeine and placebo groups at any times. Conclusion: In general, the present study indicated that caffeine (6 mg.k-1) leads to the significant increase in GH concentration after RE (85% of 1RM) in athletes, but, it had not any effect on the concentration of TS. [ABSTRACT FROM AUTHOR]

Caffeine is a highly catabolic dietary stimulant. High caffeine concentrations (1-10 mM) have previously been shown to inhibit protein synthesis and increase protein degradation in various mammalian cell lines. The purpose of this study was to examine the effect of short-term caffeine exposure on cell signaling pathways that regulate protein metabolism in mammalian skeletal muscle cells. Fully differentiated C2C12 skeletal myotubes either received vehicle (DMSO) or 5 mM caffeine for 6 h. Our analysis revealed that caffeine promoted a 40% increase in autolysosome formation and a 25% increase in autophagic flux. In contrast, caffeine treatment did not significantly increase the expression of the skeletal muscle specific ubiquitin ligases MAFbx and MuRF1 or 20S proteasome activity. Caffeine treatment significantly reduced mTORC1 signaling, total protein synthesis and myotube diameter in a CaMKKβ/AMPK-dependent manner. Further, caffeine promoted a CaMKII-dependent increase in myostatin mRNA expression that did not significantly contribute to the caffeine-dependent reduction in protein synthesis. Our results indicate that short-term caffeine exposure significantly reduced skeletal myotube diameter by increasing autophagic flux and promoting a CaMKKβ/AMPK-dependent reduction in protein synthesis. [ABSTRACT FROM AUTHOR]