Abstract：
:The loss of skeletal muscle mass with energy deficit is thought to be due to protein breakdown by the autophagy-lysosome and the ubiquitin-proteasome systems. We studied the main signaling pathways through which exercise can attenuate the loss of muscle mass during severe energy deficit (5500 kcal/day). Overweight men followed four days of caloric restriction (3.2 kcal/kg body weight day) and prolonged exercise (45 min of one-arm cranking and 8 h walking/day), and three days of control diet and restricted exercise, with an intra-subject design including biopsies from muscles submitted to distinct exercise volumes. Gene expression and signaling data indicate that the main catabolic pathway activated during severe energy deficit in skeletal muscle is the autophagy-lysosome pathway, without apparent activation of the ubiquitin-proteasome pathway. Markers of autophagy induction and flux were reduced by exercise primarily in the muscle submitted to an exceptional exercise volume. Changes in signaling are associated with those in circulating cortisol, testosterone, cortisol/testosterone ratio, insulin, BCAA, and leucine. We conclude that exercise mitigates the loss of muscle mass by attenuating autophagy activation, blunting the phosphorylation of AMPK/ULK1/Beclin1, and leading to p62/SQSTM1 accumulation. This includes the possibility of inhibiting autophagy as a mechanism to counteract muscle loss in humans under severe energy deficit.
journal_name
Nutrientsjournal_title
Nutrientsauthors
Martin-Rincon M,Pérez-López A,Morales-Alamo D,Perez-Suarez I,de Pablos-Velasco P,Perez-Valera M,Perez-Regalado S,Martinez-Canton M,Gelabert-Rebato M,Juan-Habib JW,Holmberg HC,Calbet JALdoi
10.3390/nu11112824subject
Has Abstractpub_date
2019-11-19 00:00:00issue
11issn
2072-6643pii
nu11112824journal_volume
11pub_type
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