Objectives: To evaluate effects of Hatha yoga and Omkar meditation on cardiorespiratory performance, psychologic profile, and melatonin secretion.Subjects and methods: Thirty healthy men in the age group of 25-35 years volunteered for the study. They were randomly divided in two groups of 15 each. Group 1 subjects served as controls and performed body flexibility exercises for 40 minutes and slow running for 20 minutes during morning hours and played games for 60 minutes during evening hours daily for 3 months. Group 2 subjects practiced selected yogic asanas (postures) for 45 minutes and pranayama for 15 minutes during the morning, whereas during the evening hours these subjects performed preparatory yogic postures for 15 minutes, pranayama for 15 minutes, and meditation for 30 minutes daily, for 3 months. Orthostatic tolerance, heart rate, blood pressure, respiratory rate, dynamic lung function (such as forced vital capacity, forced expiratory volume in 1 second, forced expiratory volume percentage, peak expiratory flow rate, and maximum voluntary ventilation), and psychologic profile were measured before and after 3 months of yogic practices. Serial blood samples were drawn at various time intervals to study effects of these yogic practices and Omkar meditation on melatonin levels.Results: Yogic practices for 3 months resulted in an improvement in cardiorespiratory performance and psychologic profile. The plasma melatonin also showed an increase after three months of yogic practices. The systolic blood pressure, diastolic blood pressure, mean arterial pressure, and orthostatic tolerance did not show any significant correlation with plasma melatonin. However, the maximum night time melatonin levels in yoga group showed a significant correlation (r 5 0.71, p , 0.05) with well-being score.Conclusion: These observations suggest that yogic practices can be used as psychophysiologic stimuli to increase endogenous secretion of melatonin, which, in turn, might be responsible for improved sense of well-being.
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These observations suggest that Antarctic residency during austral summer results in gradual attenuation of sympathetic tone and a shift of autonomic balance toward the parasympathetic side. However, WOT members showed a predominance of sympathetic and adrenal activity compared with initial responses of ST members, suggesting deconditioning or possible resetting of the autonomic nervous system.
Cerebral and pulmonary syndromes may develop in unacclimatized individuals shortly after ascent to high altitude resulting in high altitude illness, which may occur due to extravasation of fluid from intra to extravascular space in the brain, lungs and peripheral tissues. The objective of the present study was to evaluate the potential of seabuckthorn (SBT) (Hippophae rhamnoides L.) leaf extract (LE) in curtailing hypoxia-induced transvascular permeability in the lungs by measuring lung water content, leakage of fluorescein dye into the lungs and further confirmation by quantitation of albumin and protein in the bronchoalveolar lavage fluid (BALF). Exposure of rats to hypoxia caused a significant increase in the transvascular leakage in the lungs. The SBT LE treated animals showed a significant decrease in hypoxia-induced vascular permeability evidenced by decreased water content and fluorescein leakage in the lungs and decreased albumin and protein content in the BALF. The SBT extract was also able to significantly attenuate hypoxia-induced increase in the levels of proinflammatory cytokines and decrease hypoxia-induced oxidative stress by stabilizing the levels of reduced glutathione and antioxidant enzymes. Pretreatment of the extract also resulted in a significant decrease in the circulatory catecholamines and significant increase in the vasorelaxation of the pulmonary arterial rings as compared with the controls. Further, the extract significantly attenuated hypoxia-induced increase in the VEGF levels in the plasma, BALF (ELISA) and lungs (immunohistochemistry). These observations suggest that SBT LE is able to provide significant protection against hypoxia-induced pulmonary vascular leakage.
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