ABSTRACT
The autonomic nervous system maintains homeostasis, which is the state of balance in the body. That balance can be determined simply and noninvasively by evaluating heart rate variability (HRV). However, independently of autonomic control of the heart, HRV can be influenced by other factors, such as respiratory parameters. Little is known about the relationship between HRV and spirometric indices. In this study, our objective was to determine whether HRV correlates with spirometric indices in adults without cardiopulmonary disease, considering the main confounders (e.g., smoking and physical inactivity). In a sample of 119 asymptomatic adults (age 20-80 years), we evaluated forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). We evaluated resting HRV indices within a 5-min window in the middle of a 10-min recording period, thereafter analyzing time and frequency domains. To evaluate daily physical activity, we instructed participants to use a triaxial accelerometer for 7 days. Physical inactivity was defined as <150 min/week of moderate to intense physical activity. We found that FVC and FEV1, respectively, correlated significantly with the following aspects of the RR interval: standard deviation of the RR intervals (r =0.31 and 0.35), low-frequency component (r =0.38 and 0.40), and Poincaré plot SD2 (r =0.34 and 0.36). Multivariate regression analysis, adjusted for age, sex, smoking, physical inactivity, and cardiovascular risk, identified the SD2 and dyslipidemia as independent predictors of FVC and FEV1 (R2=0.125 and 0.180, respectively, for both). We conclude that pulmonary function is influenced by autonomic control of cardiovascular function, independently of the main confounders.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Aged, 80 and over , Heart Rate/physiology , Lung/physiology , Smoking/physiopathology , Autonomic Nervous System/physiology , Cross-Sectional Studies , Dyslipidemias/physiopathology , Forced Expiratory Volume/physiology , Sedentary Behavior , Spirometry , Vital Capacity/physiologyABSTRACT
The present study was undertaken in order to analyse the effect of swimming stress on the blood pressure response to noradrenaline (NA) in unanesthetized rats. Suwimming induced a desensitization of the blood pressure response to NA which was not blocked by previnous animal treatment with prazosin (0.1 mg/Kg). However, rats submitted to stress showed increased sensitivity to the prazosin blocking effect. The results suggest that swimming-induced desensitization of the cardiovascular response to NA is mediated by alpha rather than beta-1 adrenoceptors