Arlette Delamarche

Aerobic Training Suppresses Exercise-induced Lipid Peroxidation and Inflammation in Overweight/Obese Adolescent Girls

This study aimed to determine whether aerobic training could reduce lipid peroxidation and inflammation at rest and after maximal exhaustive exercise in overweight/obese adolescent girls. Thirty-nine adolescent girls (14-19 years old) were classified as nonobese or overweight/obese and then randomly assigned to either the nontrained or trained group (12-week multivariate aerobic training program). Measurements at the beginning of the experiment and at 3 months consisted of body composition, aerobic fitness (VO2peak) and the following blood assays: pre- and postexercise lipid peroxidation (15F2a-isoprostanes [F2-Isop], lipid hydroperoxide [ROOH], oxidized LDL [ox-LDL]) and inflammation (myeloperoxidase [MPO]) markers. In the overweight/ obese group, the training program significantly increased their fat-free mass (FFM) and decreased their percentage of fat mass (%FM) and hip circumference but did not modify their VO2peak. Conversely, in the nontrained overweight/obese group, weight and %FM increased, and VO2peak decreased, during the same period. Training also prevented exercise-induced lipid peroxidation and/or inflammation in overweight/obese girls (F2-Isop, ROOH, ox-LDL, MPO). In addition, in the trained overweight/obese group, exercise-induced changes in ROOH, ox-LDL and F2-Isop were correlated with improvements in anthropometric parameters (waist-to-hip ratio, %FM and FFM). In conclusion aerobic training increased tolerance to exercise-induced oxidative stress in overweight/obese adolescent girls partly as a result of improved body composition.

Acute Electrical Pulse Stimulation and Hyperglycemia Regulates RCAN1-4 in C2C12 myotubes through Oxidative Stress.

Regulator of Calcineurin1 (RCAN1) controls the Sr/Thr phosphatase, Calcineurin. RCAN1 has never been studied in-vitro in myotubes following acute Electrical Pulse Stimulation (EPS) which recapitulates the physiological effect of exhaustive exercise and hyperglycemia (HG). 144 h differentiated C2C12 myotubes were treated either with high glucose (HG) at 15mM or kept as control for 48 h. The myotubes were subjected to EPS for 1second followed by 1second of pause for 90min. Two separate Non-EPS controls with and without HG were performed simultaneously. The protein level of RCAN1-4 increased immediately after EPS up to 6hours in HG myotubes and in control. Non-EPS myotubes treated with HG exhibited a higher level of RCAN1-4 compare to Non-EPS control. RCAN1-1L and 1-S did not show any significant change after EPS in both groups. Calcineurin level decreased immediately after EPS. The levels of CuZn SOD and MnSOD were increased immediately after EPS whereas Catalase level increased significantly only 3hours after EPS in both groups. CuZn SOD and MnSOD showed higher level in HG control compare to control while the level of Catalase was lesser in HG control. NFATc4 level decreased at 3Hr post EPS in both groups. PGC1-? remained unchanged in all the samples. 4HNE increased significantly in both groups after EPS and was higher in HG control than in control. Protein Carbonyl (PC) increased significantly 3hours after EPS in normal cells and returned to basal level at 6 h. However in HG myotubes, PC level increased immediately after EPS and no further modification until 6Hr was observed. HG samples exhibited much higher PC than normal samples. We have already shown than exhaustive exercise regulates RCAN1-4 in rat skeletal muscle through involvement of oxidative stress. The acute EPS of C2C12 myotubes in normal condition or under hyperglycemia, served as an in-vitro model of exercise and diabetic regulation of RCAN1 through oxidative stress in-vitro.