Moderate Exercise Training Induces ROS-Related Adaptations to Skeletal Muscles

Abstract

Aim of the present work was the evaluation of the effects of moderate exercise training on 2 skeletal muscles differing in fibre-type composition, Tibialis Anterior (TA) and Soleus (SOL). Fibre adaptations, including their metabolic shift and mechanisms underlying proliferation and differentiation, oxidative stress markers, antioxidant and cytoprotective molecules, activity of Ca2+-handling molecules were examined. 6 male 2-month-old rats trained on a treadmill for 1 h/day, 3 days/week, for 14 weeks, reaching 30 m/min at the end of training. 6 age-matched sedentary rats served as controls. Rats were sacrificed 24 h after the last training session. Muscle regulatory factors increased in both muscles, activating satellite cell proliferation, which led to moderate hypertrophy in SOL and to moderate hyperplasia in TA, where the upregulation of desmin and TNFR2 expression suggests that myotube formation by proliferating myoblasts is somehow delayed. Changes leading to a more oxidative metabolism together with the upregulation of a number of antioxidant enzymes occurred in TA. HSP70i protein was upregulated in both SOL and TA, while oxidative stress markers increased in SOL alone. The status of ionic channels and pumps was preserved. We suggest that the increase in ROS, known to be associated with exercise, underlies most observed results.

High intensity interval training favourably affects antioxidant and inflammation mRNA expression in early-stage chronic kidney disease

“…In rats, moderate-(65% VO 2max ) and high-intensity (75% VO 2max ) chronic aerobic exercise resulted in significantly increased SOD activity, compared to low-intensity (55% VO 2max ) and sedentary conditions [11] in the right ventricle of the heart. In addition, treadmill running performed for 8 weeks (50 min/day, 5 days/wk, 17 m/min) [24] and 14 weeks (60 min/day, 3 days/wk, 30 m/min) [25] resulted in significant increases in kidney-specific SOD activity [24] and CAT activity in the tibialis anterior [25], compared to sedentary rats. Although research suggests increases in exercise intensity results in increased levels of OS and INF, it is the repeated exposure to increased oxidative and inflammatory insult that seems to be responsible for positive exercise-induced adaptations, namely increases in eAO activity [11,25].…”

“…In addition, treadmill running performed for 8 weeks (50 min/day, 5 days/wk, 17 m/min) [24] and 14 weeks (60 min/day, 3 days/wk, 30 m/min) [25] resulted in significant increases in kidney-specific SOD activity [24] and CAT activity in the tibialis anterior [25], compared to sedentary rats. Although research suggests increases in exercise intensity results in increased levels of OS and INF, it is the repeated exposure to increased oxidative and inflammatory insult that seems to be responsible for positive exercise-induced adaptations, namely increases in eAO activity [11,25]. At present, much of the work focusing on the effects of exercise on eAO utilises blood markers and skeletal muscle tissue.…”

Exercise-Induced Skeletal Muscle Remodeling and Metabolic Adaptation: Redox Signaling and Role of Autophagy

“…Interestingly, PGC-1a up-regulation occurs during differentiation (88,130). Other signalings triggered by endurance exercise, such as p38 MAPK and Akt, contribute to satellite cell differentiation (1,153,183). Therefore, muscle wasting might be counteracted by endurance training through enhancement of myoblast differentiation and fusion.…”

Vitamin A Oral Supplementation Induces Oxidative Stress and Suppresses IL-10 and HSP70 in Skeletal Muscle of Trained Rats

“…Due to high oxygen demand by skeletal muscle, exercise increases the generation of reactive oxygen species (ROS), such as the superoxide anion radical, hydrogen peroxide, and the hydroxyl radical [4,5]. At physiological concentrations, ROS act as signaling molecules that lead to positive adaptations induced by exercise, such as upregulation of endogenous antioxidant defenses, skeletal muscle hypertrophy, and mitochondrial biogenesis [6,7,8]. When the redox imbalance intensifies towards an excessive pro-oxidant state, ROS may cause DNA damage, functional loss of protein structures, such as enzymes and membrane receptors, and structural damage of the cell lipid bilayer [9].…”