Interações entre sono e marcadores de padrões desfavoráveis de composição corporal

Detalhes bibliográficos
Ano de defesa: 2018
Autor(a) principal: Piovezan, Ronaldo Delmonte [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=6329206
https://repositorio.unifesp.br/handle/11600/52886
Resumo: Background: Evidence suggests that patterns of body composition such as obesity, sarcopenia and sarcopenic obesity (SO) are associated with sleep changes beginning in middle age. Circadian hormonal oscillations also undergo significant transformations along aging and may affect body composition. However, investigations into the associations between sleep and body composition are still scarce. Objectives: To investigate, using three studies, the interactions between sleep and its disturbances with unfavorable patterns of body composition in adults. First, we evaluated the effects of a pharmacological agent on sleep and the hormonal axes involved in body metabolism in older men. Second, we analyzed the association between sleep and serum levels of 25-hydroxyvitamin D (25(OH)D), a possible mediator of muscle and lipid metabolism, in a sample from a clinical setting. Finally, we investigated associations of poor sleep markers and sleep disturbances with adverse body composition patterns in a population-based sample. Methods: In study 1, a double-blind, randomized, placebo-controlled, crossover clinical trial tested the effects of gabapentin 300mg on serum hormone levels and sleep parameters in healthy older men (>60 years). Nocturnal growth hormone (GH), testosterone, and cortisol serum measures were collected every 20 minutes. Polysomnography (PSG) measured the effects of the intervention on sleep structure and respiratory parameters. In study 2, PSG data and serum quantification of 25 (OH)D were analyzed in adults from a clinically evaluated sample. Logistic regression models assessed the cross-sectional associations between the risk of 25 (OH) D deficiency (<30 ng / mL) and indicators of poor sleep and sleep disorders. In study 3, in a population-based adult sample, sleep was evaluated by several methods, and electrical bioimpedance (BIA) evaluated body composition. Appendicular skeletal muscle mass (ASMM) adjusted for body mass index (BMI) morphologically defined sarcopenia (men <0.789; women <0.512). Total body fat defined obesity (men> 30%, women> 40%) and SO was defined by the overlap between the two conditions. The cross-sectional associations between sleep and body composition were analyzed using multinomial logistic regression models. Results: In 8 older men, gabapentin 300mg did not increase the percentage of sleep stage 3 (N3) and total nocturnal GH secretion (median: 1.63 ng/mL, p = 0.21) did not differ from placebo (median 1.08 ng/mL). The apnea and hypopnea index (AHI) and the oxygen esaturation index (ODI) increased in the comparisons between placebo and gabapentin (median AHI: 6.90 vs. 21.4, p = 0.01; ODI: 6.45 vs. 15.2, p = 0.01). In the 657 participants in study 2, the risk of 25(OH)D deficiency was associated with obstructive sleep apnea (OSA) (OR: 1.89, 95%CI: 1.29-2.77), nocturnal hypoxemia (OR: 2.62, 95%CI 95 %: 1.56-4.32) and short duration of sleep (< 6hs) (OR: 1.56, 95%CI: 1.11-2.21). In the 707 participants in study 3, severe OSA (AHI>30) was associated with OS (OR: 3.23, 95%CI: 1.10-9.53) and nocturnal hypoxemia was associated with obesity (OR: 2.48, 95%CI: 1.45-4.25) and OS (OR = 2.12, 95%CI: 1.10-4.10). Conclusions: Taken together, our findings derived from different studies suggest an intricate pathophysiologic relationship between sleep disorders, especially OSA, and adverse body composition patterns, which may go beyond fat deposition and involve muscle metabolism. Likewise, vitamin D may play a modulatory role in the associations between sleep and body composition and, in older men, not only the increase in adipose tissue but also the morphofunctional muscle decline may be a risk factor for OSA.