Resistance exercise (RE) is broadly recommended to prevent or attenuate obesity, type 2 diabetes and other comorbidities, avoiding premature death. However, several aspects involved in resistance training (RT) prescription and the mechanisms that are affected with acute RE and chronic RT practice are not well understood, precluding an RT design that provides a stimuli to promote optimized and continued gains in muscle strength and hypertrophy in humans. Our group successfully investigated (FAPESP funded) some of the mechanisms involved in RT-induced hypertrophy, such as the relation between acute integrated myofibrillar protein synthesis, muscle damage and chronic hypertrophy in different RT phases in young men. In this proposal, we want to progress and try to continue to understand the mechanisms that underpin RE aiming a prescription that provides the best stimuli to promote human health and improve performance. One important aspect of RT that is far from being understood is how to maximize RT-induced muscle hypertrophy individually, since human biological variability of RT-related outcomes (i.e., muscle strength and hypertrophy) is fairly large. Therefore, an important current unanswered question is raised: is there any importance of manipulating RT variables (e.g., load, number of sets, repetitions, type of contraction, rest between sets) when applying RT up to muscle fatigue; or is it that fatigue is really enough to maximize gains independent of other RT modulations and how each individual capacity to adapt is the key to understand variability in RT-induced muscle hypertrophy? This would allow to determine if the magnitude of muscle hypertrophy is dependent on RT manipulations or if is related to an individual's biological capacity, independent from RT manipulations, when it is performed to muscle failure. The objectives of the present study are: 1) understand if RT to fatigue is enough to promote an intra-individual maximized hypertrophic response, or if random manipulations in RT variables throughout RT produce a greater effect in muscle hypertrophy than an individualized RT volume progression when all training paradigms are performed to fatigue; 2) if inter-individual differences in responsivity to RT (compared to manipulations of RT variables) would explain the variability in muscle hypertrophy; and 3) if individual biologic variability can be explained by previous suggested mechanisms, such as changes in satellite cells and myonuclei quantity and differential gene expression. We propose to use a 10wk unilateral RT design (2·wk-1) in resistance-trained young men to analyze biological individual responsivity to different RT to muscle fatigue paradigms (individual RT (IRT) progression - leg 1; random RT (RRT) - leg 2). IRT will serve as an internal control for testing fatigue/individual responsivity, as it is based on each individual capacity to progress RT fatiguing most of their fibres at each RT session. This will be compared within-subjects to the RRT leg, which will perform in a random sequence different types of RE all also to muscle fatigue, but varying load, number of sets, type of RE (eccentric exercise) and rest intervals. We hypothesize that when RT is designed to allow training to 'real' muscle fatigue, intra-individual hypertrophic responses are already maximized, independent of other RT-variables. Further, individual biologic responsivity to RT will explain the variability in muscle hypertrophy inter-individuals and satellite cell pool, the number of myonuclei and gene expression will be differentially modulated in high-responders, independent of the type of RT realized.
News published in Agência FAPESP Newsletter about the scholarship: