Lifelong football training: Effects on autophagy and healthy longevity promotion

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Dokumenter

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

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.

OriginalsprogEngelsk
Artikelnummer132
TidsskriftFrontiers in Physiology
Vol/bind10
Antal sider12
ISSN1664-042X
DOI
StatusUdgivet - 2019

Bibliografisk note

CURIS 2019 NEXS 090

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