Objectives: In this study, we investigated the influence of the differences in exercise duration on alveolar and cytokines.

　Methods: We randomly allocated 28 wild type mice into four groups: the exercise, non-exercise, four weeks (4W), and twelve weeks (12W). We induced the chronic obstructive pulmonary disease (COPD) in mice of all groups, when they were 12-14 weeks old, then disuse muscle atrophy was induced when they were 15-16 weeks old, to develop the COPD muscle atrophy model mice. Then, the exercises were performed until mice were 20 or 28 weeks old. The mRNA expression levels were analyzed by real-time PCR, the morphological analysis of the histological image was obtained from general staining, the macrophage expression level was examined using immunostaining, and pulmonary function was measured using spirometry.

　Results: IL-13 in the lungs decreased in the exercise (4W) group, and IL-4 and TNF-α decreased in the exercise (12W) group. On the other hand, cathepsin-L increased in the non-exercise group (12W) (p ＜ 0.01-0.05). The differences in the exercise duration also affected TNF-α and cathepsin-L expressions. Mean alveolar diameter and the number of macrophages decreased in the exercise group (p ＜ 0.01-0.05).

　Conclusions: Given this, it was elucidated that the difference in exercise duration affected the cytokines and macrophages, resulting in morphological changes.

　Objectives: Long-term exposure to heat-not-burn cigarette smoke can serve as a risk factor for smoking-related diseases such as chronic obstructive pulmonary disease (COPD), similar to the exposure to conventional cigarettes. In this study, we evaluated the effects of heat-not-burn cigarettes on the alveoli and the cytokine expression in COPD muscle atrophy model mice treated with heat-not-burn cigarettes.

　Methods: We used 17 wild-type mice (C57BL6, male, 12 weeks old) and divided them into heat-not-burn cigarette and control groups; next, we randomly divided them into three groups depending on whether they were subjected/not subjected to hind limb suspension. The COPD muscle atrophy mice model was developed through the intratracheal administration of a solution of heat-not-burn cigarettes along with hind limb suspension of mice. The mRNA expression levels were analyzed by real-time PCR, the morphological analysis of the histological image was obtained from general staining, the macrophage expression level was examined using immunostaining, and pulmonary function was measured using spirometry.

　Results: The results indicated increases in the mean linear intercept, inflammatory cytokine expression, and macrophage count in the lungs in the COPD muscle atrophy model treated with heat-not-burn cigarettes. Besides, a decrease in the mRNA levels of optic atrophy 1 was observed during mitochondrial fusion in the muscle tissues.

　Conclusions: These results indicate that the heat-not-burn model can be used as a COPD model, and that the use of heat-not-burn cigarettes affects pulmonary tissues, inflammatory cytokine expression, macrophage count, and muscle mitochondrial dynamics in the lung.

　Impairment of cardiac impulse conduction contributes to arrhythmogenesis in diabetes mellitus (DM) patients. Which active or passive property contributes to impairment of ventricular impulse conduction in type 2 DM rats was investigated. Electrocardiograms were obtained from type 2 DM model Otsuka Long-Evans Tokushima Fatty (OLETF) and healthy Long-Evans Tokushima Otsuka (LETO) rats. The active properties were evaluated by measuring ion channel currents, such as fast Na^＋ channel current, L-type Ca^2＋ channel current, transient outward current, and delayed rectifier K^＋ current, in freshly-isolated single myocytes using the patch-clamp technique. The size of isolated myocytes was measured. Fibrosis was determined by Azan staining of formalinfixed ventricular sections. Connexin 43 protein (Cx43) expression was determined by Western blotting. The QRS duration in the OLETF rats was significantly longer than in the LETO rats (P ＜ 0.01). Current density/voltage relationships in the ion channels showed no difference between the LETO and OLETF ventricular myocytes. The length and width of the right ventricular myocytes was 7.5％ and 11.9％ greater, respectively, in the OLETF rats (each P ＜ 0.01). The width of the left ventricular myocytes was 10.3％ greater in the OLETF rats (P ＜ 0.01). The degree of perivascular and interstitial fibrosis showed no difference between the LETO and OLETF ventricles. Connexin 43 showed a significant decrease in the OLETF rat compared to in the LETO rats (P ＜ 0.05). Impulse conduction in type 2 diabetic rat ventricle may not be caused by dysfunction of ion channels, but decreased expression of Cx43.

Purpose: The impact of cessation of functional training-specific rehabilitation on physical fitness due to the COVID-19 emergency was investigated.

Participants: A total of 83 participants who were required to cease exercise therapy were included. They were divided into the following 3 groups for a comparison: 17 who did not exercise during the cessation period (group I); 46 who exercised or walked twice a week (group II); and 20 who exercised or walked daily (group III).

Results: There were no significant differences in age or sex and between the 3 groups. No significant differences were observed between the 3 groups in body weight, skeletal muscle index score, body fat percentage, basal metabolic rate, grip strength, or walk speed prior to cessation of therapy. Both the skeletal muscle index score and strength showed a reduction in group I. Grip strength showed a significant reduction in group I in comparison with in group III. The 5-meter walk speed showed a significant decrease in group I compared to in groups II and III.

Conclusion: These results indicate that alternative exercise routines should be prepared for patients no longer able to undergo exercise therapy due to the danger of re-spreading of the COVID-19 virus.