RESUMEN
The mechanisms responsible for the similar muscle growth attained with high- and low-load resistance training (RT) have not yet been fully elucidated. One mechanism is related to the mechanical stimulus and the level of motor unit recruitment; another mechanism is related to the metabolic response. We investigated the electromyographic signal amplitude (sEMG) and the general metabolic response to high-load RT (HL) and low-load resistance training (LL). We measured muscle thickness by ultrasound, sEMG amplitude by electromyography, and analysis of metabolites expressed through metabolomics. No differences were observed between the HL and LL groups for metabolic response and muscle thickness. A greater amplitude of sEMG was observed in the HL group. In addition, a correlation was observed between changes in muscle thickness of the vastus lateralis muscle in the HL group and levels of the metabolites carnitine, creatine, 3-hydroxyisovalerate, phenylalanine, asparagine, creatine phosphate, and methionine. In the LL group, a correlation was observed between changes in muscle thickness of the vastus lateralis muscle and levels of the metabolites acetoacetate, creatine phosphate, and oxypurinol. These correlations seem to be related to the characteristics of activated muscle fibers, the metabolic demand of the training protocols used, and the process of protein synthesis.
RESUMEN
The present study aimed to compare the early metabolic response between high-load resistance exercise (HL-RE) and low-load resistance exercise with blood flow restriction (LL-BFR). Nine young, well-trained men participated in a randomized crossover design in which each subject completed LL-BFR, HL-RE, or condition control (no exercise) with a 1-week interval between them. Blood samples were taken immediately before and 5 min after the exercise sessions. Nuclear magnetic resonance spectroscopy identified and quantified 48 metabolites, 6 of which presented significant changes among the exercise protocols. The HL-RE promoted a higher increase in pyruvate, lactate, and alanine compared with the LL-BFR and the control. HL-RE and LL-BFR promoted a higher increase in succinate compared with the control; however, there was no difference between HL-RE and LL-BFR. Also, while there was no difference in acetoacetate between HL-RE and LL-BFR, a greater decrease was observed in both compared with the control. Finally, LL-BFR promoted a greater decrease in choline compared with the control. In conclusion, this study provides by metabolomics a new insight in metabolic response between LL-BFR and HL-RE by demonstrating a distinct response to some metabolites that are not commonly analyzed.