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Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans.
- Source :
- Journal of Applied Physiology; Sep2021, Vol. 131 Issue 3, p1035-1042, 8p
- Publication Year :
- 2021
-
Abstract
- Mitochondrial-derived peptides (MDPs) humanin (HN) and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and metabolism. Circulating levels of MDPs are altered in chronic diseases such as diabetes type 2 and chronic kidney disease. Whether acute resistance (RE) or endurance (EE) exercise modulates circulating levels of HN and MOTS-c in humans is unknown. Following familiarization, subjects were randomized to EE (n = 10, 45 min cycling at 70% of estimated VO<subscript>2</subscript>max), RE (n = 10, 4 sets x 7RM, leg press and knee extension), or control (CON, n = 10). Skeletal muscle biopsies and blood samples were collected before and at 30 min and 3 h following exercise. Plasma concentration of HN and MOTS-c, skeletal muscle MOTS-c as well as gene expression of exercise-related genes were analyzed. Acute EE and RE promoted changes in skeletal muscle gene expression typically seen in response to each exercise modality (c-Myc, 45S prerRNA, PGC-1a-total, and PGC-1a-ex1b). At rest, circulating levels of HN were positively correlated to MOTS-c levels and age. Plasma levels of MDPs were not correlated to fitness outcomes [VO<subscript>2</subscript>max, leg strength, or muscle mitochondrial (mt) DNA copy number]. Circulating levels of HN were significantly elevated by acute EE but not RE. MOTS-C levels showed a trend to increase after EE. These results indicate that plasma MDP levels are not related to fitness status but that acute EE increases circulating levels of MDPs, in particular HN. [ABSTRACT FROM AUTHOR]
- Subjects :
- TYPE 2 diabetes
CELL survival
SKELETAL muscle
CHRONIC kidney failure
PEPTIDES
Subjects
Details
- Language :
- English
- ISSN :
- 87507587
- Volume :
- 131
- Issue :
- 3
- Database :
- Complementary Index
- Journal :
- Journal of Applied Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 152644431
- Full Text :
- https://doi.org/10.1152/japplphysiol.00706.2019