Emerson Ferreira Martins

Exercise, Occupational Activity, and Risk of Sleep Apnea: A Cross-Sectional Study.

STUDY OBJECTIVES To investigate whether structured exercise and occupational activity are associated with obstructive sleep apnea (OSA) severity. METHODS The International Physical Activity Questionnaire was answered by 5,453 individuals who underwent full-night polysomnography. Participants were classified as exercisers or non-exercisers and also as occupationally active or non-active. The apnea-hypopnea index (AHI), minimum oxygen saturation (SaO2min), and time with saturation below 90% (TB90%) during polysomnography were used as indicators of OSA severity. RESULTS The sample included mostly men (59%), non-exercisers (56%), and occupationally non-active individuals (75%). Mean age (± standard deviation) was 44 ± 14 years, and mean body mass index was 29.9 ± 7.3 kg/m2. Non-exercisers had higher AHI (median 14, 25-75% interquartile range 4-34) than exercisers (8 [2-24]), lower SaO2min (83 ± 9 vs. 86 ± 8%), and longer TB90% (2 [0-18] vs. 0 [0-7] minutes), with p < 0.001 for all comparisons. AHI was higher in active (16 [6-34]) vs. non-active occupations (10 [3-27]; p < 0.001). Multinomial logistic regression with control for age, sex, overweight, obesity, and occupational activity showed that structured exercise was significantly associated with a 23% lower odds ratio for moderate OSA and 34% lower odds ratio for severe OSA. Active occupation was not associated with OSA. CONCLUSIONS Structured physical exercise is associated with lower odds for OSA, independently of confounders. Occupational activity does not seem to replace the effects of regular exercise. Compensatory behaviors may be involved in these diverging outcomes. Our results warrant further research about the effect of occupational activity on OSA severity.

Melatonin prevents hyperglycemia in a model of sleep apnea.

OBJECTIVE Obstructive sleep apnea is a common disorder associated with aging and obesity. Apneas cause repeated arousals, intermittent hypoxia, and oxidative stress. Changes in glucolipidic profile occur in apnea patients, independently of obesity. Animal models of sleep apnea induce hyperglycemia. This study aims to evaluate the effect of the antioxidants melatonin and N-acetylcysteine on glucose, triglyceride, and cholesterol levels in animals exposed to intermittent hypoxia. MATERIALS AND METHODS Two groups of Balb/c mice were exposed to intermittent hypoxia (n = 36) or sham intermittent hypoxia (n = 36) for 35 days. The intermittent hypoxia group underwent a total of 480 cycles of 30 seconds reducing the inspired oxygen fraction from 21% to 7 ± 1% followed by 30 seconds of normoxia, during 8 hours daily. Melatonin or N-acetylcysteine were injected intraperitonially daily from day 21 on. RESULTS At day 35, glucose levels were significantly higher in the intermittent hypoxia group than in the control group. The intermittent hypoxia groups receiving N-acetylcysteine and vehicle showed higher glucose levels than the group receiving melatonin. The lipid profile was not affected by intermittent hypoxia or antioxidant administration. CONCLUSIONS The present results suggest that melatonin prevents the well-recognized increase in glucose levels that usually follows exposure to intermittent hypoxia. Further exploration of the role of melatonin in sleep apnea is warranted.

The effect of caffeine supplementation on exercise performance evaluated by a novel animal model

Introduction: Caffeinated drinks are used for improve performance. Animal models represent investigational strategy that circumvents most of the drawbacks of research in humans, including motivational factors and the placebo effect. No animal model that could test whether different forms of administering caffeine affect exercise propensity was found in the literature. Methods: An animal model of grouped voluntary exercise was tested. Two-month-old male C57/bl mice were housed in a cage fitted with one running wheel and a monitoring system. Six animals per cage were introduced individually. To assess the sensitivity of the model, the effect of different caffeinated drinks was observed in mice exercising ad libitum . During 2 days, the mice received: 1) pure anhydrous caffeine 0.125 mg/mL (PC), 2) cola drink (CC), and 3) caffeine-taurine-glucuronolactone drink (CTG), intercalating wash-out periods of 2 days, receiving pure water. Results: The distance run during the periods of water ingestion was significantly lower than during the periods of stimulant drinks ingestion: PC (5.6±1.3 km; p = 0.02), of CC ingestion (7.6±0.6 km; p = 0.001), and of CTG ingestion (8.3±1.6 km; p = 0.009). The performances when ingesting the three caffeinated drinks do not follow a dose-response curve. Conclusions: The model described here was able to measure the effect of caffeine intake on voluntary exercise of mice. The sensitivity of the model to the effect of caffeine needs to be further validated. The action of each component of the drinks on exercise performance needs to be clarified in future research. The present model is adequate for such investigation. Key words: Exercise; caffeine; energy drinks; running

Uncoupling protein-2 mRNA expression in mice subjected to intermittent hypoxia

Objective: To investigate the effect of intermittent hypoxia-a model of obstructive sleep apnea (OSA)-on pancreatic expression of uncoupling protein-2 (UCP2), as well as on glycemic and lipid profiles, in C57BL mice. Methods: For 8 h/day over a 35-day period, male C57BL mice were exposed to intermittent hypoxia (hypoxia group) or to a sham procedure (normoxia group). The intermittent hypoxia condition involved exposing mice to an atmosphere of 92% N and 8% CO2 for 30 s, progressively reducing the fraction of inspired oxygen to 8 ± 1%, after which they were exposed to room air for 30 s and the cycle was repeated (480 cycles over the 8-h experimental period). Pancreases were dissected to isolate the islets. Real-time PCR was performed with TaqMan assays. Results: Expression of UCP2 mRNA in pancreatic islets was 20% higher in the normoxia group than in the hypoxia group (p = 0.11). Fasting serum insulin was higher in the hypoxia group than in the normoxia group (p = 0.01). The homeostasis model assessment of insulin resistance indicated that, in comparison with the control mice, the mice exposed to intermittent hypoxia showed 15% lower insulin resistance (p = 0.09) and 21% higher pancreatic β-cell function (p = 0.01). Immunohistochemical staining of the islets showed no significant differences between the two groups in terms of the area or intensity of α- and β-cell staining for insulin and glucagon. Conclusions: To our knowledge, this is the first report of the effect of intermittent hypoxia on UCP2 expression. Our findings suggest that UCP2 regulates insulin production in OSA. Further study of the role that UCP2 plays in the glycemic control of OSA patients is warranted.