Physical activity reduces oxidative stress and improves lipid profile made by smoking - Effectiveness of irregular and continuous training programs.

OBJECTIVE: The aim of the study was to identify the possible benefits of physical activity program in improving the antioxidant enzymes activity and lipid profile among smokers. PATIENTS AND METHODS: Fifteen cigarette smokers (CS), 14 hookah smokers (HS), and 14 non-smokers (NS) participated in the low-intensity continuous training (LCT). Eleven CS, 12 HS, and 12 NS participated in the moderate-intensity intermittent training (MIT). The LCT groups performed a 20 to 30-minute continuous exercise at 40% of the VO2max. The MIT groups performed 6 to 10 sets of 2-minute sprint at 70% of the VO2max interspersed by a 1-min recovery period. At baseline and after 12 weeks of intervention, the antioxidant defense activity and lipid profile were assessed. RESULTS: The improvement in antioxidant capacity under the effect of MIT program is statistically more significant than after LCT. The increase of glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR), malondialdehyde (MDA) and α-tocopherol was higher in smoker subjects participating in the MIT program compared to those participating in the LCT. In contrast, the LCT program has favorably altered lipid and lipoprotein profile of smokers and thus reduced their cardiovascular risk. CONCLUSIONS: The combination of the two training methods may have major implications in both defense and prevention programs.

Endurance training and insulin therapy need to be associated to fully exert their respective beneficial effects on oxidant stress and glycemic regulation in diabetic rats.

In type 1 diabetic subjects, hyperglycemia-induced oxidant stress (OS) plays a central role in the onset and development of diabetes complications. This study aimed to assess the benefits of an endurance training program and insulin therapy, alone or in combination, on the glycemic regulation, markers for OS, and antioxidant system in diabetic rats. Forty male Wistar rats were divided into diabetic (D), insulin-treated diabetic (D-Ins), diabetic trained (D-Tr), or insulin-treated diabetic trained (D-Ins+ Tr) groups. An additional healthy group served as control group. Insulin therapy (Lantus, insulin glargine, Sanofi) and endurance training (a treadmill run of 60 min/day, 25 m/min, 5 days/week) were initiated 1 week after streptozotocin-induced diabetes (45 mg/kg) and lasted for 8 weeks. At the end of the protocol, blood glucose and fructosamine levels, markers for skeletal muscle OS (CML, isoprostanes, GSH/GSSG) and antioxidant system (SOD and GPx activity, ORAC) were assessed. In diabetic rats, the glycemic control was altered and OS marker levels were increased, while the antioxidant system activity remained unchanged. Insulin treatment improved the glycemic regulation, the pro-antioxidant status, and contributed to the reduction of OS marker levels. Endurance training decreased OS marker levels without improving the antioxidant enzyme activity. Endurance training and insulin therapy acted independently (by different ways), but their association prolonged the insulin action and allowed a better adaptation of the antioxidant system. To conclude, our results demonstrate that combination of insulin treatment and endurance training leads to greater benefits on the glycemic regulation and oxidant status.

Superoxide production pathways in aortas of diabetic rats: beneficial effects of insulin therapy and endurance training.

Superoxide (O 2 (·-) ) overproduction, by decreasing the nitric oxide ((·)NO) bioavailability, contributes to vascular complications in type 1 diabetes. In this disease, the vascular O 2 (·-) can be produced by the NADPH oxidase (NOX), nitric oxide synthase (NOS), and xanthine oxidase (XO). This study aimed to determine the contribution of each enzymatic pathway in hyperglycemia-induced O 2 (·-) overproduction, and the effects of an endurance training program and insulin therapy, associated or not, on the O 2 (·-) production (amount and related enzymes) in diabetic rats. Forty male Wistar rats were divided into diabetic (D), diabetic treated with insulin (D-Ins), diabetic trained (D-Tr), or diabetic insulin-treated and trained (D-Ins + Tr) groups. An additional healthy group was used as control. Insulin therapy (Glargine Lantus, Sanofi) and endurance training (treadmill run: 60 min/day, 25 m/min, 5 days/week) started 1 week after diabetes induction by streptozotocin (45 mg/kg), and lasted for 8 weeks. At the end of the protocol, the O 2 (·-) production in aorta rings was evaluated by histochemical analyses (DHE staining). Each production pathway was studied by inhibiting NOX (apocynin), NOS (L-Name), or XO (allopurinol) before DHE staining. Diabetic rats exhibited hyperglycemia-induced O 2 (·-) overproduction, resulting from NOX, NOS, and XO activation. Insulin therapy and endurance training, associated or not, decreased efficiently and similarly the O 2 (·-) overproduction. Insulin therapy reduced the hyperglycemia and decreased the three enzymatic pathways implicated in the O 2 (·-) production. Endurance training decreased directly the NOS and XO activity. While both therapeutic strategies activated different pathways, their association did not reduce the O 2 (·-) overproduction more significantly.