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It is widely established throughout the literature that skeletal muscle can induce hypertrophic adaptations following progressive overload of moderate to high-intensity resistance training. However, there has recently been a growing body of research that shows that the combination of blood flow restriction (BFR) with low intensity resistance exercise can induce similar gains in muscular strength and hypertrophic adaptations. The implementation of external pressure cuffs over the most proximal position of the limb extremities with the occlusion of venous outflow of blood distal to the occlusion site defines the BFR methodological protocol. There are various mechanisms through which BFR training may cause the stimulations for skeletal muscle hypertrophy and increases in strength. These may include increases in hormonal concentrations, increases within the components of the intracellular signaling pathways for muscle protein synthesis such as the mTOR pathway, increases within biomarkers denoting satellite cell activity as well as apparent patterns in fiber type recruitment. There have also been scientific findings demonstrating hypertrophic effects within both blood-flow restricted limbs and non-blood flow-restricted muscles during BFR training programs. The purpose behind this critical review will be to provide a comprehensive discussion on relevant literature that can help elucidate the potential underlying mechanisms leading to hypertrophic adaptations following BFR training programs. This review will also explicate the various findings within the literature that focalizes on both blood flow-restricted limb and non-blood flow-restricted muscle hypertrophy following bouts of BFR training. Furthermore, this critical review will also address the various needs for future research in the many components underlying the novel modality of BFR training.

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McKinley-Barnard, SK, Andre, TL, Gann, JJ, Hwang, PS, and Willoughby, DS. Effectiveness of fish oil supplementation in attenuating exercise-induced muscle damage in females during midfollicular and midluteal menstrual phases. J Strength Cond Res 32(6): 1601-1612, 2018-The purpose of this study was to determine whether the differences in estrogen levels during the female menstrual cycle and fish oil supplementation would attenuate eccentric exercise-induced muscle damage and delayed-onset muscle soreness (DOMS). In a double-blind fashion, 22 physically active females (20.9 ± 1.4 years, 63.5 ± 9.0 kg, 165.2 ± 7.5 cm) were randomly assigned to ingest either 6 g of fish oil (n = 11) or placebo (n = 11) daily for 21 days. Participants underwent an eccentric exercise bout of the knee extensors on 2 occasions during the midfollicular (MF) and midluteal (ML) phases of the 28-day menstrual cycle. Before (PRE), at 6 (6HRPOST), and at 24 hours postexercise (24HRPOST) for each session, participants underwent assessments of DOMS, muscle strength, and had venous blood samples and muscle biopsies obtained. Data were analyzed using a 2 × 2 × 3 repeated-measures multivariate analysis of variance for each criterion variable (p ≤ 0.05). Further analysis of the main effects for the test was performed using separate 1-way analyses of variance. Delayed-onset muscle soreness was significantly greater at the 6HRPOST and 24HRPOST timepoints compared with PRE (p < 0.001). Superoxide dismutase and tumor necrosis factor-alpha (TNF-α) concentrations were significantly higher at the MF phase compared with the ML phase (p < 0.001 and p = 0.05, respectively). There were no statistically significant differences observed for muscle strength, myoglobin, NF-Kβ p50, or NF-Kβ p65. This study demonstrates that higher levels of estrogen may exert a cytoprotective effect on the sarcolemma.

PURPOSE: Curcumin is a natural polyphenolic compound with antioxidant and anti-inflammatory properties. In vitro and in vivo animal studies have demonstrated that exposure to curcumin leads to dysregulation of the ubiquitin-proteasome system (UPS). However, to date, no study has investigated curcumin's ability to influence UPS activity in a human model. Therefore, the purpose of this study was to investigate the effects of curcumin supplementation on markers of UPS activity in the presence of elevations in UPS activity due to exercise-induced muscle damage. METHODS: Twenty-three recreationally active male and female participants between the ages of 18-30 were randomized into a curcumin (CUR; n=11) or placebo (PLA; n=12) group. Both groups were instructed to consume 2 g of their respective supplement and 20 mg of piperine for 11 consecutive days. Following 8 consecutive days of supplementation, participants performed a 45 minute eccentrically-biased muscle damaging treadmill protocol at 60% VO2max. Muscle biopsies and delayed onset muscle soreness (DOMS) analyses were performed 30 minutes prior and 3, 24, 48, and 72 hours following exercise-induced muscle damage. Skeletal muscle ubiquitin, MAFbx/Atrogin-1, ubiquitin specific peptidase 19 (USP19), and chymotrypsinlike protease concentrations were measured using ELISA. A 3-way repeated measures ANOVA with pairwise comparisons was conducted with significance set at p≤0.05. RESULTS: Both groups had a significant time effect for DOMS (p < .001). Pairwise comparisons indicated DOMS was significantly greater from baseline at all time points except 72 hours following muscle damage. No significant differences were found for USP19 between groups. Regardless of time, a significant main effect for condition was observed for ubiquitin (p=.016) and MAFbx/Atrogin-1 (p=.006) where CUR was significantly lower than PLA. Additionally, a significant main effect for gender was observed for MAFbx/Atrogin-1 (p=.013) where females were greater than males. A significant group x gender interaction was found for chymotrypsin-like protease (p = .049) where males had lower values with curcumin supplementation while females had slightly higher. CONCLUSION: Curcumin supplementation in humans does appear to dysregulate UPS activity in the presence of exercise-induced muscle damage. Specifically, curcumin's ability to suppress protein ubiquination provides preliminary evidence of curcumin supplementation's potential therapeutic role in decreasing protein degradation associated with skeletal muscle damage and perhaps other atrophic scenarios.