To investigate the effect of intense exercise on immunological factors in saliva, we measured secretory immunoglobulin A (sIgA), lactoferrin and fibronectin. We used a reliable saliva collection method that has already been reported. Timed saliva samples were obtained from 16 healthy young males. Samples were collected before, immediately after, 1 day after and 5 days after endurance running (42.195 km) . The concentrations (μg/ml) of sIgA, lactoferrin and fibronectin were measured by ELISA, and the secretion rates (μg/min) of each were calculated. Immediately after the exercise, the concentration of total protein in saliva increased significantly, but the sIgA secretion rate decreased to 53%. The secretion rates of both lactoferrin and fibronectin did not change significantly. The local immune system plays an important role in mucosal surface defense against upper respiratory tract infection. The sIgA level in the oral cavity was temporarily decreased after intense exercise. A decreased sIgA secretion rate might partly explain the increased susceptibility to upper respiratory tract infection after endurance exercise.

It is generally accepted that secretory immunoglobulin A (sIgA) is a major effector of local immunity in the oral cavity. The salivary sIgA level is known to be temporarily decreased after an acute single bout of intense exercise. On the other hand, the effect of continuous exercise training on salivary sIgA has been controversial. In the present study, we collected timed saliva samples from collegiate kendoists using the reliable saliva collection method that has already been reported. The collection was performed before, during and after a traditional high-intensity 10-day training camp during the coldest part of the winter. We investigated the effect of repetitious intense exercise training on resting sIgA levels in saliva.
The subjects were 19 males and 8 females (age: 19.9±0.5 years) who took part in the camp. We obtained saliva samples before the camp, on the first and the 10th days of the camp, and 4 and 10 days after the camp at 5 p. m. The concentration of sIgA was measured by ELISA, and the sIgA secretion rate was calculated.
The resting sIgA secretion rate decreased significantly during the camp. It remained at a lower level 4 and 10 days after the camp compared to the initial level, although it tended to recover gradually. Prolonged suppression of the resting sIgA secretion rate during a traditional winter kendo training camp might be induced by repetition of high-intensity training.

Parkinson’s disease is often complicated by psychiatric symptoms. Psychiatrists are caught in a dilemma between such symptoms and physical treatment since Parkinson’s disease sometimes shows treatment resistance based on pharmacological treatment-induced dopamine dysfunction. Here, we report on a 64-year-old woman with a 15-year history of Parkinson’s disease with stage IV severity based on the Hoehn and Yahr scale. She was admitted to our hospital with a diagnosis of major depressive disorder with psychotic features. Unfortunately, her treatment course for depression was complicated by neuroleptic malignant syndrome. Because we were concerned about the persistence of her depressive symptoms, the risk of psychotropic drugs causing adverse effects, and progressive disuse syndrome, we administered modified electroconvulsive therapy. Her symptoms of neuroleptic malignant syndrome and depression sufficiently improved after five sessions of modified electroconvulsive therapy. Additionally, the primary motor symptoms of her Parkinson’s disease also markedly improved. The improvement of neuroleptic malignant syndrome and her motor symptoms based on dopamine dysfunction can be explained by electroconvulsive therapy’s effectiveness in activating dopamine neurotransmission. Besides, the marked improvement of her depressive episode with psychotic features was presumed to involve dopamine receptor activation and regulation. Because advanced Parkinson’s disease can sometimes be refractory to treatment based on pharmacological treatment-induced dopamine dysfunction, psychiatrists often have difficulty treating psychiatric symptoms; electroconvulsive therapy may stabilize the dopaminergic system in such cases, presenting a possible non-pharmacologic treatment option for Parkinson’s disease.

Parkinson’s disease is often complicated by psychiatric symptoms. Psychiatrists are caught in a dilemma between such symptoms and physical treatment since Parkinson’s disease sometimes shows treatment resistance based on pharmacological treatment-induced dopamine dysfunction. Here, we report on a 64-year-old woman with a 15-year history of Parkinson’s disease with stage IV severity based on the Hoehn and Yahr scale. She was admitted to our hospital with a diagnosis of major depressive disorder with psychotic features. Unfortunately, her treatment course for depression was complicated by neuroleptic malignant syndrome. Because we were concerned about the persistence of her depressive symptoms, the risk of psychotropic drugs causing adverse effects, and progressive disuse syndrome, we administered modified electroconvulsive therapy. Her symptoms of neuroleptic malignant syndrome and depression sufficiently improved after five sessions of modified electroconvulsive therapy. Additionally, the primary motor symptoms of her Parkinson’s disease also markedly improved. The improvement of neuroleptic malignant syndrome and her motor symptoms based on dopamine dysfunction can be explained by electroconvulsive therapy’s effectiveness in activating dopamine neurotransmission. Besides, the marked improvement of her depressive episode with psychotic features was presumed to involve dopamine receptor activation and regulation. Because advanced Parkinson’s disease can sometimes be refractory to treatment based on pharmacological treatment-induced dopamine dysfunction, psychiatrists often have difficulty treating psychiatric symptoms; electroconvulsive therapy may stabilize the dopaminergic system in such cases, presenting a possible non-pharmacologic treatment option for Parkinson’s disease.