No effect of the endurance training status on senescence despite reduced inflammation in skeletal muscle of older individuals

• Published in: American journal of physiology: endocrinology and metabolism Vol. 319; no. 2; pp. E447 - E454
• Main Authors: Balan, Estelle, De Groote, Estelle, Bouillon, Margot, Viceconte, Nikenza, Mahieu, Manon, Naslain, Damien, Nielens, Henri, Decottignies, Anabelle, Deldicque, Louise
• Format: Journal Article
• Language: English
• Published: 01.08.2020
• ISSN: 0193-1849; 1522-1555; 1522-1555
• DOI: 10.1152/ajpendo.00149.2020

The aim of the present study was to determine if the training status decreases inflammation, slows down senescence, and preserves telomere health in skeletal muscle in older compared with younger subjects, with a specific focus on satellite cells. Analyses were conducted on skeletal muscle and cultured satellite cells from vastus lateralis biopsies ( n = 34) of male volunteers divided into four groups: young sedentary (YS), young trained cyclists (YT), old sedentary (OS), and old trained cyclists (OT). The senescence state and inflammatory profile were evaluated by telomere dysfunction-induced foci (TIF) quantification, senescence-associated β-galactosidase (SA-β-Gal) staining, and quantitative (q)RT-PCR. Independently of the endurance training status, TIF levels (+35%, P < 0.001) and the percentage of SA-β-Gal-positive cells (+30%, P < 0.05) were higher in cultured satellite cells of older compared with younger subjects. p16 (4- to 5-fold) and p21 (2-fold) mRNA levels in skeletal muscle were higher with age but unchanged by the training status. Aging induced higher CD68 mRNA levels in human skeletal muscle (+102%, P = 0.009). Independently of age, both trained groups had lower IL-8 mRNA levels (−70%, P = 0.011) and tended to have lower TNF-α mRNA levels (−40%, P = 0.10) compared with the sedentary subjects. All together, we found that the endurance training status did not slow down senescence in skeletal muscle and satellite cells in older compared with younger subjects despite reduced inflammation in skeletal muscle. These findings highlight that the link between senescence and inflammation can be disrupted in skeletal muscle.