ABSTRACT
Sarcopenia and sleep problems share common physiopathology. We aimed to investigate the association of sleep disturbances with sarcopenia and its defining components in Brazilian middle-aged and older adults. In this cross-sectional analysis of the second wave of the ELSA-Brasil study, we included data from 7948 participants aged 50 years and older. Muscle mass was evaluated by bioelectrical impedance analysis and muscle strength by hand-grip strength. Sarcopenia was defined according to the Foundation for the National Institutes of Health criteria. Sleep duration and insomnia complaint were self-reported. Short sleep duration was considered as ≤6 h/night and long sleep duration as >8 h/night. High risk of obstructive sleep apnea (OSA) was assessed using the STOP-Bang questionnaire. Possible confounders included socio-demographic characteristics, lifestyle, clinical comorbidities, and use of sedatives and hypnotics. The frequencies of sarcopenia, low muscle mass, and low muscle strength were 1.6, 21.1, and 4.1%, respectively. After adjustment for possible confounders, high risk of OSA was associated with low muscle mass (OR=2.17, 95%CI: 1.92-2.45). Among obese participants, high risk of OSA was associated with low muscle strength (OR=1.68, 95%CI: 1.07-2.64). However, neither short nor long sleep duration or frequent insomnia complaint were associated with sarcopenia or its defining components. In conclusion, high risk of OSA was associated with low muscle mass in the whole sample and with low muscle strength among obese participants. Future studies are needed to clarify the temporal relationship between both conditions.
ABSTRACT
The autonomic nervous system plays an important role in physiological and pathological conditions, and has been extensively evaluated by parametric and non-parametric spectral analysis. To compare the results obtained with fast Fourier transform (FFT) and the autoregressive (AR) method, we performed a comprehensive comparative study using data from humans and rats during pharmacological blockade (in rats), a postural test (in humans), and in the hypertensive state (in both humans and rats). Although postural hypotension in humans induced an increase in normalized low-frequency (LFnu) of systolic blood pressure, the increase in the ratio was detected only by AR. In rats, AR and FFT analysis did not agree for LFnu and high frequency (HFnu) under basal conditions and after vagal blockade. The increase in the LF/HF ratio of the pulse interval, induced by methylatropine, was detected only by FFT. In hypertensive patients, changes in LF and HF for systolic blood pressure were observed only by AR; FFT was able to detect the reduction in both blood pressure variance and total power. In hypertensive rats, AR presented different values of variance and total power for systolic blood pressure. Moreover, AR and FFT presented discordant results for LF, LFnu, HF, LF/HF ratio, and total power for pulse interval. We provide evidence for disagreement in 23 percent of the indices of blood pressure and heart rate variability in humans and 67 percent discordance in rats when these variables are evaluated by AR and FFT under physiological and pathological conditions. The overall disagreement between AR and FFT in this study was 43 percent.