%0 Journal Article
%T The mitochondrial multi-omic response to exercise training across rat tissues.
%A Amar D
%A Gay NR
%A Jimenez-Morales D
%A Jean Beltran PM
%A Ramaker ME
%A Raja AN
%A Zhao B
%A Sun Y
%A Marwaha S
%A Gaul DA
%A Hershman SG
%A Ferrasse A
%A Xia A
%A Lanza I
%A Fernández FM
%A Montgomery SB
%A Hevener AL
%A Ashley EA
%A Walsh MJ
%A Sparks LM
%A Burant CF
%A Rector RS
%A Thyfault J
%A Wheeler MT
%A Goodpaster BH
%A Coen PM
%A Schenk S
%A Bodine SC
%A Lindholm ME
%A  
%J Cell Metab
%V 36
%N 6
%D 2024 Jun 4
%M 38701776
%F 31.373
%R 10.1016/j.cmet.2023.12.021
%X Mitochondria have diverse functions critical to whole-body metabolic homeostasis. Endurance training alters mitochondrial activity, but systematic characterization of these adaptations is lacking. Here, the Molecular Transducers of Physical Activity Consortium mapped the temporal, multi-omic changes in mitochondrial analytes across 19 tissues in male and female rats trained for 1, 2, 4, or 8 weeks. Training elicited substantial changes in the adrenal gland, brown adipose, colon, heart, and skeletal muscle. The colon showed non-linear response dynamics, whereas mitochondrial pathways were downregulated in brown adipose and adrenal tissues. Protein acetylation increased in the liver, with a shift in lipid metabolism, whereas oxidative proteins increased in striated muscles. Exercise-upregulated networks were downregulated in human diabetes and cirrhosis. Knockdown of the central network protein 17-beta-hydroxysteroid dehydrogenase 10 (HSD17B10) elevated oxygen consumption, indicative of metabolic stress. We provide a multi-omic, multi-tissue, temporal atlas of the mitochondrial response to exercise training and identify candidates linked to mitochondrial dysfunction.