Regular aerobic exercise-ameliorated troponin I carbonylation to mitigate aged rat soleus muscle functional recession

What is the central question of this study? What is the biological role of carbonylation in muscle age-related functional decline and how might exercise affect the carbonylation process differently compared to habitual sedentary behaviour? What is the main finding and its importance? The carbonylation of troponin I (TNNI1), tropomyosin α-1 chain and α-actinin-1 demonstrated a relationship with muscle age-related functional decline. Exercise attenuated the decline by slowing the rate of carbonylation and promoting antioxidant reactions within the muscle. As exercise demonstrated the greatest effect on TNNI1, quantification of protein carbonyls in TNNI1 may be used as a potential biomarker of muscle age-related functional decline.

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 ( $$ ) 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.