Exercise-induced changes in pulmonary function of healthy, elite long-distance runners in cold air and pollen season exercise challenge tests.

Exercise-induced changes in postexercise pulmonary function have not been studied in healthy elite athletes in normal training conditions. Twelve healthy elite runners volunteered. They showed normal resting spirometry and bronchial responsiveness to histamine, and were non-atopic. They performed free running exercise challenge tests (ECT) at subzero temperature and immediately after highest birch pollen season. The mean maximal postexercise changes in FEV(1), PEF, FVC, and FEV(1)/FVC did not differ between the cold air and pollen season ECTs. Compared with pre-exercise values, FEV(1)increased significantly at 10 min (p = 0.028) and 20 min (p = 0.033) postexercise in the cold air ECT, as well as at 10 min (p = 0.024) and 20 min (p = 0.010) postexercise in the pollen season ECT. The mean (SEM) maximal postexercise change in FEV(1) was mostly small + 2.6 (0.6)% in the winter and + 2.7 (0.9)% in the pollen season. In contrast, significant decreases in PEF, compared with baseline, were found at 10 min (p = 0.071) and 20 min (p = 0.0029) postexercise in the cold air ECT, as well as at 10 min (p = 0.060) and 20 min (p = 0.010) postexercise in the pollen season ECT (p = 0.0076). The mean (SEM) maximal postexercise fall in PEF was 5.9 (1.0)% in the winter and 6.0 (1.8)% in the pollen season. Heavy exercise challenge tests in extreme conditions increased FEV(1) post-exercise, while PEF decreased as compared with pre-exercise values. Thus, even small postexercise falls in FEV(1) may be considered as deviate exercise responses in elite athletes.

Expression of nitric oxide synthase in hypothalamic nuclei following axonal injury or colchicine treatment.

Nitric oxide (NO) has recently gained much attention due to its apparently double-edged role in neuronal injury. This study was aimed at elucidating neuronal nitric oxide synthase (nNOS) expression in the brain after two types of injury, namely axonal transection and colchicine treatment. The neurosecretory hypothalamo-pituitary pathway served as a model for the reaction of central neurons to these two types of injury. Axonal transection, i.e., pituitary stalk section, resulted in a qualitative increase in NOS content in the supraoptic and paraventricular nuclei. In these nuclei, there was also an increase in the number of NOS-expressing neurons after the operation. Surprisingly, in the periventricular nucleus, a strong decrease in the number of NOS-positive magnocellular neurons was observed in the anterior part of the nucleus. Intracerebroventricular injection of colchicine resulted in an increase in the cell count in the paraventricular nucleus, while the other nuclei remained unchanged. Our results suggest that axonal injury results in an increase in nNOS expression in the major neurosecretory nuclei, while the periventricular nucleus shows the opposite reaction. Colchicine treatment has an effect similar to that of axotomy in the major neurosecretory nuclei, suggesting that an increase in NOS expression may be induced by interrupted axonal transport. In the periventricular nucleus, the decrease in the number of NOS-containing neurons suggests differences among hypothalamic NOS-containing neuron groups in response to neuronal injury.