Lifelong Football Training: Effects on Autophagy and Healthy Longevity Promotion.

Annamaria Mancini,Daniela Vitucci,Annalisa Mandola,Esther Imperlini,Stefania Orrù,Jakob Friis Schmidt,Morten Bredsgaard Randers,Peter Krustrup,Marie Hagman,Thomas Rostgaard Andersen,Pasqualina Buono

doi:10.3389/fphys.2019.00132

Abstract

Aging is a physiological process characterized by a progressive decline of biological functions and an increase in destructive processes in cells and organs. Physical activity and exercise positively affects the expression of skeletal muscle markers involved in longevity pathways. Recently, a new mechanism, autophagy, was introduced to the adaptations induced by acute and chronic exercise as responsible of positive metabolic modification and health-longevity promotion. However, the molecular mechanisms regulating autophagy in response to physical activity and exercise are sparsely described. We investigated the long-term adaptations resulting from lifelong recreational football training on the expression of skeletal muscle markers involved in autophagy signaling. We demonstrated that lifelong football training increased the expression of messengers: RAD23A, HSPB6, RAB1B, TRAP1, SIRT2, and HSBPB1, involved in the auto-lysosomal and proteasome-mediated protein degradation machinery; of RPL1, RPL4, RPL36, MRLP37, involved in cellular growth and differentiation processes; of the Bcl-2, HSP70, HSP90, PSMD13, and of the ATG5-ATG12 protein complex, involved in proteasome promotion and autophagy processes in muscle samples from lifelong trained subjects compared to age-matched untrained controls. In conclusion, our results indicated that lifelong football training positively influence exercise-induced autophagy processes and protein quality control in skeletal muscle, thus promoting healthy aging.

Highlights

Aging is a physiological process characterized by a progressive decline of biological functions and a progressive increase of destructive processes in cells and organs, eventually leading to death (LópezOtín et al, 2013; Aunan et al, 2016; Flatt and Partridge, 2018).This process affects the homeostasis within organs and the tissue response to injury, but, at a molecular level, it is associated with accumulation of DNA and protein damage (Soares et al, 2014; Boros and Freemont, 2017)
We found significant up-expression of RAD23A, HSPB6, RAB1B, TRAP1, SIRT2 (p < 0.01), HSPB1 (p < 0.05) messengers, which are involved in the auto-lysosomal and proteasome-mediated protein degradation machinery and maintenance of protein quality control and significant up-expression of RPLP1, RPL4, RPL36, MRLP37 (p < 0.05) messengers that are involved in cellular growth and proliferation in skeletal muscle from VPG compared to CG (Figure 3)
We demonstrated that lifelong football training is able to induce transcriptional activation of key markers involved in pathways of protein quality control, in particular autophagy, and associated to improvement of intermediate metabolism and cardiovascular capacity in elderly VPG compared to untrained subjects

Summary

Introduction

Aging is a physiological process characterized by a progressive decline of biological functions and a progressive increase of destructive processes in cells and organs, eventually leading to death (LópezOtín et al, 2013; Aunan et al, 2016; Flatt and Partridge, 2018) This process affects the homeostasis within organs and the tissue response to injury, but, at a molecular level, it is associated with accumulation of DNA and protein damage (Soares et al, 2014; Boros and Freemont, 2017). Aging acts on the metabolically active bone and muscle tissues by triggering events that eventually impair their cross-talk determining low body mass density (BMD) and/or sarcopenia (Boirie, 2009) At this regard, fatty infiltration in both tissues is considered an age-related hallmark leading to osteosarcopenia, a recently defined geriatric syndrome, which is associated to increased morbidity and mortality risk among older people (Hirschfeld et al, 2017). HSPs induction is requested for the maintenance of cellular homeostasis and promotion of longevity (Lindquist and Craig, 1988; Hartl, 2016)

Objectives

Methods

Results

Discussion

Conclusion