Do different levels of lactate have an impact on mTORC1-signal and protein synthesis induced by resistance exercise?
Abstract: Aim: To investigate the role of lactate as a potential signaling molecule, for the molecular mechanisms underlying acute resistance exercise adaptation in the muscle cell. Method: Four women and four men recruited to perform two trials of unilateral leg extension exercise performed with either an infusion of sodium lactate or isotonic saline (placebo), in a randomized, blinded, crossover fashion. To enable measurement of muscle protein FSR, an oral dose of 2H2O was consumed the day before the trials. Sixteen blood samples were taken for direct analysis of lactate, glucose, Na+, K+ and pH. Five muscle biopsies were obtained from vastus lateralis during each trial and analyzed for 2H-protein incorporation using mass spectrometry. Furthermore, in sampled muscle tissue, the degree of protein phosphorylation in the mTORC1 signaling pathway was determined by immunoblotting and levels of lactate were determined spectrophotometrically. Results: There were no significant differences in load, repetitions or time under tension between the trials. Blood levels of lactate reached a maximal level of 3.00 ± 0.26 mmol/L post 6th set in the placebo trial (P<0.05 vs. Rest). In the lactate trial, a peak of 6.94 ± 0.47 mmol/L was reached post 6th set with levels significantly higher than placebo up to 45 min recovery (P<0.05 vs. Rest and Placebo). In both trials the muscle levels of lactate increased above rest both post exercise and following 90 min of recovery, with significantly higher levels in the lactate trial (P<0.05 vs. Rest and Placebo). The phosphorylation of mTOR at Ser2448, p70S6K1 at Thr389, and p44 at Thr202/Tyr204 increased immediately after resistance exercise and remained elevated throughout the entire recovery period (P<0.05). The phosphorylation of PRAS40 at Ser183, 4E-BP1 both at Ser65 and Thr37-46 decreased immediately after resistance exercise, whereas that of eEF2 at Thr56 decreased following 90 and 180 min of recovery (P<0.05). There were no differences between trials for any intracellular signaling protein on group basis. Conclusion: An infusion of a sodium lactate solution during resistance exercise increases whole venous blood and muscle levels of lactate, without altering time under tension, load or repetition lifted during exercise. Resistance exercised induced mTORC1-signaling is not altered by a sodium lactate infusion at the group level in this population but there are underpowered differences between men and women.
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