The potential synergistic effect of combined blood flow restriction training and betaine supplementation on skeletal muscle mechanotransduction-associated cell signaling.

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Blood flow restriction (BFR) training and betaine supplementation both possibly facilitate myofibril-level mechanotransduction via intracellular cell swelling. Furthermore, the latter may augment the former through osmolyte-associated protein protection and subsequently attenuated fatigue. Therefore, the purpose of this randomized, double-blind, placebo-controlled investigation was to explore a potential extra-to-intracellular fluid flux-mediated BFR-betaine synergy on intramuscular phosphorylated signaling targets. The present investigation also examined the impacts of a possible BFR-betaine synergy and whether it may enhance total resistance load-volume accrued, which would ultimately promote greater metabolic stress and commensurate anabolic hormone concentrations. Erstwhile, a novel narrow-elastic BFR cuff was validated (against a commonly employed wide-rigid device) amongst 20 resistance trained subjects (25±5y) to demonstrate that these products could produce the previously standardized full-venous and partial-arterial occlusion that otherwise mediates BFR-associated adaptation. Eighteen resistance trained men (23±5y) visited the laboratory after supplementing with either 6g/day betaine anhydrous (BET) or equivalently dosed cellulose placebo (PLA) for 14-days. Following supplementation, all participants performed six sets (last two to muscular failure) in further randomized, counterbalanced, and crossover fashion of either high-load (HL; 70% one-repetition maximum [1RM]) or low-load BFR (LL-BFR; 20%1RM) leg press exercise. Participants underwent vastus lateralis muscle biopsies and venipuncture before (PRE) and 30-minutes post (POST30M) exercise to assess phosphorylated focal adhesion kinase (FAKTyr397), insulin receptor substrate 1 (PanTyrIRS1), and ribosomal protein S6 kinase beta-1 (p70S6KThr389), as well as serum hormone (growth hormone and insulin-like growth factor-1 [IGF-1-] levels. All statistical analyses were performed at a significance level of p<.05. Analyses revealed no significant main exercise or supplement effects, nor any interactions for FAKTyr397 or PanTyrIRS1. Furthermore, BFR combined with betaine yielded similarly equivocal main effects and failed to reveal any notable interactions for total load-volume, nor any metabolic or hormonal targets. There was nevertheless significant supplement-specific effects for p70S6KThr389 (p=.030) and IGF-1 (p=.042), whereby BET supplementation yielded higher relative levels versus PLA. Despite lacking evidence for a BFR-betaine synergy, these data further substantiate BFR as a suitable alternative to conventional high-load resistance training, as well as ultimately support betaine’s potential anabolic potential.

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Blood flow restriction (BFR). Betaine. Focal adhesion kinase (FAK). Ribosomal protein s6 beta-1 kinase (p70S6K). Insulin receptor substrate-1 (IRS1). Resistance training. Growth hormone (GH). Insulin-like growth factor 1 (IGF-1). Lactate.

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