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Exercise is assumed to have a positive effect on migraine. However, none of the few studies on this topic can prove the expected positive influence of exercise. Therefore, the aim of this pilot study was to develop a training program suitable for migraine patients and to examine its effect on migraine. 16 patients were examined. 8 migraine patients completed a 10-week aerobic running exercise program consisting of 3 workouts per week. The program was developed by sports scientists especially to increase the fitness level. Physical fitness, i. e., physical working capacity, was assessed using a PWC 150 test. There was also a control group of 8 patients without any special physical training. Migraine patients of the exercise group showed both a reduction in the number of migraine days per month (p=0.048) and the intensity of the attacks (p=0.028). An increase in fitness level resulted in a lowered stress level. Stress strategies like "displacement activity" (r=-0.715; p=0.046), "looking for self-affirmation" (r=-0.742; p=0.035) and "feelings of aggression" (r=-0.802; p=0.017) were reduced. Increasing the level of fitness (PWC 150) is one predictor for migraine improvement (r=0.409, p=0.031). Aerobic exercise which leads to a better fitness level is an alternative therapy method for migraine.

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Previous pharmacological and pathological studies have reported negative relationships between circulating testosterone and certain stress hormones (i.e., cortisol and prolactin) in humans. These relationships have subsequently been used in hypotheses explaining the subclinical resting testosterone levels often found in some endurance-trained males, but as of yet no one has specifically examined these relationships as they relate to exercise. Thus, we examined the relationship between total and free testosterone levels and cortisol, and between total and free testosterone and prolactin following prolonged endurance exercise in trained males. Twenty-two endurance-trained males volunteered to run at 100% of their ventilatory threshold (VT) on a treadmill until volitional fatigue. Blood samples were taken at pre-exercise baseline (B0); volitional fatigue (F0); 30 min (F30), 60 min (F60), and 90 min (F90) into recovery; and at 24 h post-baseline (P24 h). At F0 [mean running time = 84.8 (3.8) min], exercise induced significant changes (P<0.05) from B0 in total testosterone, cortisol and prolactin. All three of these hormones were still significantly elevated at F30; but at F60 only cortisol and prolactin were greater than their respective B0 values. Free testosterone displayed no significant changes from B0 at F0, F30, or the F60 time point. At F90, neither cortisol nor prolactin was significantly different from their B0 values, but total and free testosterone were reduced significantly from B0. Cortisol, total testosterone and free testosterone at P24 h were significantly lower than their respective B0 levels. Negative relationships existed between peak cortisol response (at time F30) versus total testosterone (at F90, r=-0.53, P<0.05; and at P24 h, r=-0.60, P<0.01). There were no significant relationships between prolactin and total or free testosterone. In conclusion, the present findings give credence to the hypothesis suggesting a linkage between the low resting testosterone found in endurance-trained runners and stress hormones, with respect to cortisol.

Increased adiposity is associated with insulin resistance (IR) and an inflammatory response in adults. We tested the hypotheses that cytokines associated with adiposity are also correlated with IR in early adolescents and that these relationships are moderated by weight status, levels of vigorous physical activity (VPA), or maximal aerobic power (pVO 2 max). Body mass, stature, and a fasting blood sample were obtained from 120 mid-pubertal adolescents (60 girls & 60 boys). Habitual VPA was obtained by a survey. Predicted VO 2 max was determined using a cycle-ergometer test. Weight status was based on body mass index percentiles (normal weight = BMI < 75 th %tile and overweight = BMI > 95th %tile). Glucose, insulin, adiponectin, resistin, tumor necrosis factor-α, and interleukin-6 were measured, and IR index was based on the Homeostatic Model Assessment (HOMA). Adiponectin, resistin and TNF-α were associated with IR in all adolescents (R 2 =0.329, p<0.001, R 2 =0.152, p=0.001, R 2 =0.141, p=0.002; respectively), but IL-6 was not (R 2 =0.148, p=0.114). The degree of association between adiponectin and IR was stronger in overweight than in normal weight adolescents (p<0.050). When regression models included weight status, neither TNF-α nor resistin were significantly related to IR (p>0.050). Exercise did not moderate the association between these cytokines and IR. However, higher levels of VPA and/or pVO 2 max were associated with higher adiponectin, lower resistin and lower TNF-α in at least one of the genders. Our results indicate that the pathophysiology of obesity is already established in early adolescents. Increased adiposity, resulting in reduced adiponectin and increased resistin and TNF-α may link these cytokines with insulin resistance in adolescents.