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. To investigate whether the effects of acute exercise on smoking behavior and HPA axis activation in smokers are intensity-dependent. 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 β-endorphin (β-E), adrenocorticotropic hormone (ACTH), cortisol and catecholamines], were obtained prior to and immediately after each trial. β-E, ACTH, catecholamines and cortisol responses to exercise were intensity-dependent and differed in smokers and non-smokers. Resting β-E levels were 2-2.5 times lower in smokers compared to non-smokers. HI resulted in increased β-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. HPA axis activation in response to exercise may differ between smokers and non-smokers. Smokers have lower resting levels of β-E compared to non-smokers and, since HI exercise increases β-E to similar levels to those of non-smokers and delays smoking, this may be used as an adjunct in smoking cessation.

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