Galanin, a neuropeptide, is found in the central nervous system and in a number of nonbrain areas including adrenal sympathetic medullar tissue and pancreas. Several studies involve galanin in the regulation of GH, which responds to stressful stimuli. This study refers to the investigation of the effect of a 20-min exercise on plasma human galanin (hGAL) and GH in middle-aged healthy volunteer adults. Thirteen individuals, 5 males and 8 females aged 40-50 years (44.7 +/- 2.95) were selected on the basis of normal body mass index (22.5 +/- 2.3 kg/m2) and the absence of endocrine or any other abnormality. Basal concentrations of GH and hGAL were measured between 0800 and 0900h after an overnight fast. Post exercise levels were recorded after termination of the stressful test and 15 min thereafter. GH and hGAL were determined by an immunoradiometric and radioimmunoassay, respectively. The exercise-potentiated GH response in all subjects with post-exercise levels significantly higher (11.09 +/- 1.8 ng/ml vs 1.27 +/- 0.7 ng/ml, p<0.0001, F=32.44) with the peak in the hormone level detected 15 min after the end of exercise (12.09 +/- 1.96 ng/ml). Plasma hGAL levels were also substantially affected by the acute exercise test, in that post exercise peripheral blood concentration was significantly higher from the basal values (21.51 +/- 9.94 vs 13.46 +/- 7.2 pg/ml, p<0.02, F=5.50). Again the hGAL values peaked 15 min after the end of exercise (24.0 +/- 10.5 pg/ml, P<0.015, F = 4.68). However, the time-correlation of the increments of GH and hGAL did not reach a statistically significant level (20 min: r=0.41, p=0.161., 35 min: r=-0.095, P=0.758). These results clearly show an independence of the two hormones. The responsivity of hGAL of middle-aged individuals to the exercise stimulus might be due to the higher releasable pool of the hormone.

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This study investigated the leptin response to vigorous exercise. We examined 12 sedentary subjects (7 males and 5 females) aged 45-59 yr (53 +/- 6.3) with body mass index of 26.1 +/- 8 Kg/m2. The selection of the population was based on the absence of endocrine or any other pathological anomaly. Basal concentrations of leptin, cortisol, insulin and glucose were measured at 08:00 h after an overnight fast. After that the individuals were placed on a computer-controlled ergometer performing a 20-min run at 70% VO2 max under controlled environmental conditions. Blood samples were obtained immediately after the completion of the test. For the following hour, all subjects were placed in the supine position and blood samples were taken at the end of the time period. Statistical evaluation was performed using analysis of variance (ANOVA) for independent variables. Plasma leptin levels exhibited a statistically significant decrease at the end of the 20 min running period (1.5 +/- 0.1 ng/ml vs 3.2 +/- 0.4 ng/ml, p<0.005). Interestingly, after 1 h in the supine position, leptin levels reached the basal values (3.17 +/- 0.1 ng/ml). The concentration of insulin, glucose and cortisol were unaltered during the exercise test (9.8 +/- 1.3 vs 8.85 +/- 1.27 microIU/ml, 95.58 +/- 6.71 mg/dl vs 98.4 +/- 0.78 mg/dl and 10.35 +/- 0.74 microg/dl vs 9.5 +/- 0.7 microg/dl respectively). In conclusion, our data demonstrate a relationship between stressful physical activity and plasma leptin levels in middle-aged subjects.

Rat cortical synaptosomes prepared on four-step discontinuous Percoll density gradients were loaded with the fluorescent Ca2+-indicator fura-2 to allow measurement of the intrasynaptosomal free calcium concentration ([Ca2+]i). When P1-purinergic, alpha 2-adrenergic, or kappa-opiate agonists were incubated with these synaptosomes for 1 min, there was a highly significant, dose-dependent reduction in [Ca2+]i. The effects of these agonists were blocked by inclusion of appropriate specific antagonists. When alpha 2-adrenergic and P1-purinergic agonists were coincubated, a mutual antagonism of their effects was observed, and, in fact, an increase rather than a decrease in [Ca2+]i was apparent. This mutual antagonism was reversed by addition of either a P1-purinergic or a alpha 2-adrenergic antagonist. Parallel studies in which kappa-opiate and P1-purinergic agonists were coincubated also demonstrated a mutual antagonism between the individual effects that was reversed by prior inclusion of either a kappa-opiate or P1-purinergic antagonist. As these mutually antagonistic effects have been observed between alpha 2-adrenergic, kappa-opiate, and P1-purinergic receptor-mediated events, we suggest that this may be a general phenomenon and may be a regulatory mechanism at nerve endings.

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