Regular aerobic exercise-ameliorated troponin I carbonylation to mitigate aged rat soleus muscle functional recession.
Wen-Feng LiuHeyu KuangYan XiaZachary C PopeZhiyuan WangChang Fa TangDazhong YinPublished in: Experimental physiology (2019)
This study investigated the biological role of carbonylation in muscle age-related functional decline and how regular aerobic exercise may affect the carbonylation process differently from habitual sedentary behaviour. Twenty-four healthy male Sprague-Dawley (SD) rats (mean age: 23 months) were randomly divided into an old-aged sedentary control group (O-SED) and an old-aged aerobic exercise group (O-EX). The O-EX group participated in regular aerobic exercise - treadmill running - with exercise intensity increased gradually from 50-55% to 65-70% of maximum oxygen consumption ( V ̇ O 2 max ) over 10 weeks. Rats' body weight, exercise behaviour index, morphology and oxidative stress were monitored. Avidin magnetic beads and electrospray ionization quadrupole time-of-flight mass spectrometry were used for gathering and separating carbonylated proteins while western blot tested for molecular targets. O-SED and O-EX rats both had 19 oxidative modification sites for protein carbonylation. In the O-SED group, 16 specific carbonylated proteins were identified, while 16 additional specific species were also found in the O-EX group, with all 28 species demonstrating oxidative modifications. The carbonylated proteins included troponin I (TNNI1; slow skeletal muscle), tropomyosin α1 and α-actinin 1. In particular, TNNI1 carbonylation modifications were found only in sedentary rats. Aerobic exercise increased TNNI1 and Ca2+ /calmodulin-dependent protein kinase IIα expression significantly. Observations suggested that quantification of TNNI1 carbonylation may be a potential biomarker of muscle age-related functional decline. Importantly, regular aerobic exercise appeared to have antioxidant effects in the muscle that reduced TNNI1 slow carbonylation and promoted Ca2+ /calmodulin-dependent protein kinase IIα (CAMK2) and TNNI1 expression for skeletal muscle contraction regulation, thus attenuating possible age-related skeletal muscle functional decline.