Abstract
Aging is associated with a decline in autophagy and a state of low-grade inflammation which further affects apoptosis and autophagy. Importantly, these alterations could reverse with regular physical activity. This study assessed the effects of a resistance exercise training program on autophagy, NLRP3 inflammasome, and apoptosis in peripheral blood mononuclear cells (PBMCs) from old subjects. Twenty-six healthy women and men (age, 69.6±1.5 yr) were randomized to a training (TG) or a control (CG) group. TG performed an 8-week resistance training program, while CG followed their daily routines. Protein expression of beclin-1, Atg12, Atg16 and LAMP-2 increased following the training program, while expression of p62/SQSTM1 and phosphorylation of ULK-1 at Ser757 were significantly lower. Resistance exercise also induced a decrease in NLRP3 expression and in the caspase-1/procaspase-1 ratio. Expression of Bcl-2 and Bcl-xL, as well as the Bad/BcL-2 ratio were reduced, and there was a significant decrease in the protein content of caspase-3. The results obtained seem to indicate that 8-week resistance training stimulates autophagy, prevents NLRP3 inflammasome activation, and reduces apoptosis in PBMCs from elderly subjects. These data could have a significant impact in prevention and rehabilitation programs currently employed in elderly population.
Highlights
Autophagy is a catabolic process of eukaryotic cells, contributing to the degradation in lysosomes of unwanted or damaged components [1]
This study investigated the potential of an 8-week resistance training program to prevent age-related decline in autophagy, chronic low-grade inflammation and apoptosis in peripheral blood mononuclear cells (PBMCs) from old subjects
The current study shows that an 8-week resistance training program induces an activation of the autophagy machinery in PBMCs from elderly subjects
Summary
Autophagy is a catabolic process of eukaryotic cells, contributing to the degradation in lysosomes of unwanted or damaged components [1]. Autophagy proceeds through a series of cellular events, including induction of the formation of autophagic isolated membranes (called phagophore), elongation of the phagophore and sequestration of cytosolic components through formation of the autophagosome, transport to the lysosome, degradation, and use of the products of degradation [2]. The nucleation of the autophagosomal membrane is controlled by a molecular complex containing Bcl-2-interacting protein (beclin)-1 [3]. Autophagosome formation is under the control of autophagy related genes (Atg). The first, the Atg12-Atg complex interacts with Atg to participate in the formation of autophagosome membrane. The second system involves the mammalian protein 1 light chain 3 (LC3), with formation of the LC3II isoform, which binds to the adaptor protein p62 sequestrosome 1 (p62/SQSTM1), facilitating the autophagic degradation of ubiquitinated protein aggregates in lysosomes [5]
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