RESUMO
BACKGROUND: Sarcopenia is a musculoskeletal disease characterized by a significant reduction in muscle mass, strength, and performance. As it mostly affects older adults, it is often recognized as a disease of old age. However, sleep is also closely related to its development. Hence, it becomes critical to explore the relationship between sleep and sarcopenia in populations under 60 years of age to develop strategies for preventing sarcopenia. We here aim to explore the specific association between sleep duration and sleep quality with pre-sarcopenia in the non-elderly population using large population samples. METHODS: This study involved 7,187 participants aged 20-59 years from the National Health and Nutrition Examination Survey (NHANES) conducted between 2005 and 2014. Pre-sarcopenia is defined based on the appendicular skeletal muscle mass (ASM) adjusted for body mass index (BMI). Self-reported sleep duration was categorized into three groups: <6 h (short sleep), 6-8 h (normal sleep), and > 8 h (long sleep). Sleep quality was assessed based on the Sleep Disorder and Trouble Sleeping Questionnaire. Univariate analysis and multivariate logistic regression were used to examine the relationship between sleep duration and sleep quality with pre-sarcopenia. RESULTS: Sleep quality was significantly linked with the risk of pre-sarcopenia (OR 1.72, 95% CI 1.36-2.18, P < 0.01). Longer or shorter sleep duration did not affect the risk of pre-sarcopenia, in contrast to normal sleep duration. Subgroup analysis demonstrated a more pronounced association in individuals who are > 40 years old (P < 0.01), non-Hispanic (P ≤ 0.01), overweight (P < 0.01), have a higher income (P < 0.01), and are more educated (P ≤ 0.01). Moreover, this association was noted in populations with or without smoking (P < 0.01) and alcohol consumption (P < 0.01), hypertension (P < 0.01) and diabetes (P ≤ 0.02). CONCLUSION: Sleep quality is associated with an increased risk of pre-sarcopenia, while sleep duration is not in the population aged 20-59 years. Further prospective cohort studies with a large sample size are needed to determine causality and develop effective interventions for preventing sarcopenia in the population aged 20-59 years.
RESUMO
BACKGROUND: A higher body mass index (BMI) is associated with shorter telomeres. The loss of muscle mass with aging is associated with adverse outcomes. The appendicular skeletal muscle index (ASMI) is currently used to quantify muscle mass. OBJECTIVE: We investigated the association of the ASMI with leukocyte telomere length in adult Americans. METHODS: This cross-sectional study used the National Health and Nutrition Examination Survey (NHANES) 1999-2002 dataset. Body composition was measured by dual-energy X-ray absorptiometry. Low muscle mass was defined using sex-specific thresholds of the appendicular skeletal muscle mass index (ASMI). The telomere-to-single-copy gene ratio (T/S ratio) was converted to base pairs. Generalized linear models were performed to evaluate the association of ASMI with telomere length. RESULTS: In multivariable adjustment regression models, higher ASMI was associated with longer telomeres in US adults (ß = 70.2, P < 0.001, P trend<0.001). In participants with preserved muscle mass, the ASMI was related to longer telomere length (ß = 75.1, P < 0.001), but not significantly in low muscle mass participants (ß = 68.7, P = 0.30). Further subgroup analysis by a combination of age groups and muscle mass status showed positive association with young-preserved muscle mass (ß = 82.6, P < 0.001), old-preserved muscle mass (ß = 44.4, P = 0.12), young-low muscle mass (ß = 135.4, P = 0.20), and old-low muscle mass (ß = 52.7, P = 0.55). Because each additional year of chronological age was associated with telomeres that were 15.3 base pairs shorter, on average, this would equate to 5.4 fewer years of biological aging (82.6 ÷ 15.3) in the young-preserved muscle mass participants. CONCLUSIONS: A higher ASMI is associated with longer telomeres. The prevention of skeletal muscle loss has the potential to delay telomere shortening and account for less biological aging.