HPA axis responses to acute exercise differ in smokers and non-smokers.

Physical exercise has been proposed as an adjunct in addiction treatment, including tobacco cigarette smoking. The physiological and biochemical mechanisms that could be affected by physical exercise in smokers and that could help quit smoking have not been investigated yet. OBJECTIVE: To investigate whether the effects of acute exercise on smoking behavior and HPA axis activation in smokers are intensity-dependent. METHODS: Healthy, non-systematically exercising individuals [25 smokers (age: 33±1.4 years) and 10 non-smokers (age: 34±2.1 years)] underwent three trials [moderate intensity (MI), high intensity (HI) exercise, control (C)] in a counterbalanced order, after an overnight fast and smoking abstinence, separated by at least six days. MI involved cycling at 50-60% of Heart Rate Reserve (HRR) for 30 min, HI involved cycling at 65-75% HRR for 30 min, while in C participants rested for 30 min. Time till the first cigarette following each trial was recorded. Smoking urge was evaluated and blood samples, [analyzed for ß-endorphin (ß-E), adrenocorticotropic hormone (ACTH), cortisol and catecholamines], were obtained prior to and immediately after each trial. RESULTS: ß-E, ACTH, catecholamines and cortisol responses to exercise were intensity-dependent and differed in smokers and non-smokers. Resting ß-E levels were 2-2.5 times lower in smokers compared to non-smokers. HI resulted in increased ß-E levels in both groups, with smokers exhibiting similar levels to that observed in non-smokers. Although smoking urge did not change post-exercise in smokers, time till first cigarette increased following both MI (64.6%) and HI (77.9%) compared to C. CONCLUSIONS: HPA axis activation in response to exercise may differ between smokers and non-smokers. Smokers have lower resting levels of ß-E compared to non-smokers and, since HI exercise increases ß-E to similar levels to those of non-smokers and delays smoking, this may be used as an adjunct in smoking cessation.

Enhanced erythrocyte antioxidant status following an 8-week aerobic exercise training program in heavy drinkers.

Alcohol-induced oxidative stress is involved in the development and progression of various pathological conditions and diseases. On the other hand, exercise training has been shown to improve redox status, thus attenuating oxidative stress-associated disease processes. The purpose of the present study was to evaluate the effect of an exercise training program that has been previously reported to decrease alcohol consumption on blood redox status in heavy drinkers. In a non-randomized within-subject design, 11 sedentary, heavily drinking men (age: 30.3 ± 3.5 years; BMI: 28.4 ± 0.86 kg/m2) participated first in a control condition for 4 weeks, and then in an intervention where they completed an 8-week supervised aerobic training program of moderate intensity (50-60% of the heart rate reserve). Blood samples were collected in the control condition (pre-, post-control) as well as before, during (week 4 of the training program), and after intervention (week 8 of the training program). Samples were analyzed for total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), protein carbonyls (PC), uric acid (UA), bilirubin, reduced glutathione (GSH), and catalase activity. No significant change in indices of redox status in the pre- and post-control was observed. Catalase activity increased (p < 0.05) after 8 weeks of intervention compared to week 4. GSH increased (p < 0.05) after 8 weeks of intervention compared to the control condition and to week 4 of intervention. TAC, UA, bilirubin, TBARS, and PC did not significantly change at any time point. Moreover, concentrations of GSH, TBARS, and catalase activity negatively correlated with alcohol consumption. In conclusion, an 8-week aerobic training program enhanced erythrocyte antioxidant status in heavy drinkers, indicating that aerobic training may attenuate pathological processes caused by alcohol-induced oxidative stress.

Effects of acute exercise on liver function and blood redox status in heavy drinkers.

Excessive alcohol consumption can induce oxidative stress, resulting in the development of several diseases. Exercise has been reported to prevent and/or improve a number of health issues through several mechanisms, including an improvement in redox status. It has also been previously suggested that exercise can help individuals with alcohol use disorders reduce their alcohol intake; however, research in this field is limited. The aim of the present study was to investigage the effects of acute exercise of moderate intensity on the liver function and blood redox status in heavy drinkers. For this purpose, a total of 17 heavy drinkers [age, 31.6±3.2 years; body mass index (BMI), 27.4±0.8 kg/m2; experimental group (EG)] and 17 controls [age, 33.5±1.3 years; BMI, 26.1±1.4 kg/m2; control group (CG), who did not exceed moderate alcohol consumption], underwent one trial of acute exercise of moderate intensity (50-60% of the heart rate reserve) for 30 min on a cycle ergometer, following an overnight fast, and abstaining from smoking and alcohol consumption. Blood samples were obtained before and immediately after exercise for later determination of the indices of liver function and blood redox status. The subjects in the EG had significantly higher (p<0.05) baseline γ-glutamyl transferase (γ-GT) levels compared to the subjects in the CG. Exercise thus resulted in significantly higher γ-GT levels (p<0.005) only in the EG. No significant differences in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) baseline levels were observed between the 2 groups. Following exercise, the AST levels increased significantly (p<0.001) in both groups, whereas the ALT levels increased significantly (p<0.01) only in the EG. The baseline glutathione (GSH) levels were significantly lower (p<0.05) and remained low following exercise in the EG. In addition, we observed a trend for higher (p=0.07) baseline levels of thiobarbituric acid-reactive substances (TBARS), which remained elevated post-exercise in the EG compared to the CG. Significantly increased post-exercise total antioxidant capacity (TAC; p<0.01) and uric acid (UA; p<0.05) levels were noted in the CG, whereas the TAC (p=0.06) and UA (p=0.08) levels increased and approached significance post-exercise in the EG. No significant differences in the baseline levels of total bilirubin and protein carbonyl were observed between the 2 groups, even post-exercise. Thus, the findings of the present study indicate that even though heavy drinkers may be prone to oxidative stress, their exercise-induced antioxidant response is similar to that of individuals who do not drink heavily.

Effect of exercise on oxidative stress in individuals with glucose-6-phosphate dehydrogenase deficiency.

UNLABELLED: The effect of exercise on oxidative stress in glucose-6-phosphate dehydrogenase (G6PD)-deficient individuals was investigated. MATERIALS AND METHODS: Nine G6PD-deficient males and nine males with normal G6PD activity were selected and requested to run at approximately 75% their maximum heart rate for 45 min. Blood samples were collected prior to and immediately after exercise. Several hematological parameters, reduced glutathione (GSH), oxidized glutathione (GSSG), lipid hydroperoxides, thiobarbituric acid reactive substances (TBARS), protein carbonyls, catalase and total antioxidant capacity (TAC) were measured in the blood before and after each exercise bout. RESULTS: GSH was significantly (more than two-fold) higher in the control group compared to the G6PD-deficient group at baseline, whereas GSSG, GSH/GSSG and lipid hydroperoxides were not different between the two groups. Exercise did not affect the levels of any oxidative stress marker. There was no evidence of Heinz body formation neither at rest nor after exercise in either group. Exercise of moderate intensity and duration did not result in an increase of blood oxidative-stress biomarkers in G6PD-deficient males nor in matched controls. It appears that G6PD-deficient individuals may exercise without experiencing a rise in oxidative stress at an exercise intensity approximately 75% of their maximum heart rate.