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Fernandez-Garcia, B.

Publications and source records attributed to Fernandez-Garcia, B..

2 recordsLinked to original sources

miR-29a-3p, a new myokine orchestrating resistance exercise via coordinated metabolic responses

It remains unclear whether the adaptive response to different exercise models is mediated by EV miRNAs released from skeletal muscle and their functional metabolic role. We sequenced miRNA-loaded plasma EVs obtained from resting mice after 4-weeks endurance or resistance training. Resistance exercise increased the expression of a 11-miRNA profile grouped into two functional clusters. Using both genetically modified animal models and in vitro approaches, we have identified miR-29a-3p as a novel myokine secreted into the bloodstream as EV cargo by contracting skeletal muscle. It is a cornerstone in the adaptation to resistance training by mediating the coordinated expression and secretion of other miRNAs and affecting muscle mass development and energy metabolism in muscle and liver. Taken together, our study suggests a coordinating and determinant role of miR-29a-3p in the response and adaptation to resistance training, possibly due to its role as a myokine through its regulatory role in energy metabolism.

molecular biology↗

Autophagy alterations in white and brown adipose tissues of mice exercised under different training protocols

Autophagy is a conserved catabolic process that promotes cellular homeostasis and health. Although exercise is a well-established inducer of this pathway, little is known about the effects of different types of training protocols on the autophagy levels of tissues that are tightly linked to the obesity pandemic (like brown adipose tissue) but not easily accessible in humans. Here, we take advantage of animal models to assess the effects of short- and long-term resistance and endurance training in both white and brown adipose tissue, reporting distinct alterations on autophagy proteins LC3B and p62. For instance, both short-term endurance and resistance training protocols increased the levels of these proteins in white adipose tissue before this similarity diverges during long training, while autophagy regulation appears to be far more complex in brown adipose tissue. Additionally, we also analyzed the repercussion of these interventions in fat tissues of mice lacking autophagy protease ATG4B, further assessing the impact of exercise in these dynamic, regulatory organs (which are specialized in energy storage) when autophagy is limited. In this regard, only resistance training could slightly increase the presence of lipidated LC3B, while p62 levels increased in white adipose tissue after short-term training but decreased in brown adipose tissue after long-term training. Altogether, our study suggests an intricated regulation of exercise-induced autophagy in adipose tissues that is dependent on the training protocol and the autophagy competence of the organism.

molecular biology↗