Transient changes to metabolic homeostasis initiate mitochondrial adaptation to endurance exercise

Jessica R. Dent, Ben Stocks, Dean G. Campelj, Andrew Philp*

*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskriftReviewForskningpeer review

6 Citationer (Scopus)

Abstract

Endurance exercise is well established to increase mitochondrial content and function in skeletal muscle, a process termed mitochondrial biogenesis. Current understanding is that exercise initiates skeletal muscle mitochondrial remodeling via modulation of cellular nutrient, energetic and contractile stress pathways. These subtle changes in the cellular milieu are sensed by numerous transduction pathways that serve to initiate and coordinate an increase in mitochondrial gene transcription and translation. The result of these acute signaling events is the promotion of growth and assembly of mitochondria, coupled to a greater capacity for aerobic ATP provision in skeletal muscle. The aim of this review is to highlight the acute metabolic events induced by endurance exercise and the subsequent molecular pathways that sense this transient change in cellular homeostasis to drive mitochondrial adaptation and remodeling.

OriginalsprogEngelsk
TidsskriftSeminars in Cell and Developmental Biology
Vol/bind143
Sider (fra-til)3-16
ISSN1084-9521
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
A.P. is supported by an Al and Val Rosenstrauss Fellowship from the Rebecca Cooper Medical Foundation. J.R.D was supported by a Lottery Health Research Council , New Zealand Project grant 2019-101565 . B.S is supported by a European Foundation for the Study of Diabetes Rising Star Fellowship.

Funding Information:
A.P. is supported by an Al and Val Rosenstrauss Fellowship from the Rebecca Cooper Medical Foundation. J.R.D was supported by a Lottery Health Research Council, New Zealand Project grant 2019-101565. B.S is supported by a European Foundation for the Study of Diabetes Rising Star Fellowship.

Publisher Copyright:
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