Correlation between heart rate variability and pulmonary function adjusted by confounding factors in healthy adults

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.

Correlation between heart rate variability and pulmonary function adjusted by confounding factors in healthy adults.

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.

Effect of testosterone on the response of young rat vas deferens to norepinephrine.

1. Following in vitro treatment with 12 microM 6-hydroxy-dopamine, 2 microM B-oestradiol, 0.1 microM propranolol and 10 microM cocaine vasa deferentia isolated from young rats (21-23 days old) showed supersensitivity to norepinephrine (NE) compared to those from adult (3 months old) rats. 2. The pA2 values for prazosin were higher in young (9.6 +/- 0.1) than in adult (8.3 +/- 0.1) rat vas deferens, with the slopes of the Schild plots not different from 1.0 (0.78 +/- 0.26 and 1.14 +/- 0.14, respectively). 3. The treatment of young rats with a single dose of testosterone abolished the supersensitivity to NE and the higher affinity for prazosin. 4. We conclude that there is a reduction of neuronal NE uptake and a decrease in the sensitivity to NE in the vas deferens as the rat matures sexually. 5. Testosterone induces a decrease in the sensitivity to NE, probably via an action on the alpha 1-adrenoceptor population and the sympathetic nerve discharge in this organ.

Footshock stress-induced supersensitivity to isoprenaline in the isolated pacemaker of the rat: effects of the compounds RU-38486 and RU-28362.

1. Three daily sessions of inescapable footshock stress of 30 min duration each increased the sensitivity of the isolated pacemaker of the rat to the chronotropic effect of isoprenaline. 2. The effect of inescapable footshock stress on the sensitivity of the isolated rat pacemaker to the chronotropic effect of isoprenaline was prevented by the daily administration of the compound RU-38486, a potent antiglucocorticoid which blocks the cytosolic receptor for corticosterone. 3. The administration of the compound RU-28362, a potent agonist of the cytosolic receptor for corticosterone, during 3 days to rats which were not submitted to footshock stress induces supersensitivity to the chronotropic effect of isoprenaline. 4. It is concluded that corticosterone plays an important role in the qualitative control of the rat pacemaker beta-adrenoceptor population during adaptation to repeated footshock stress.

Subsensitivity to beta-adrenoceptor agonists in pacemakers isolated from senescent rats.

1. The effects of aging on the responsiveness of the isolated pacemaker of the rat to the chronotropic effect of norepinephrine, isoproterenol and soterenol were studied. 2. Pacemakers isolated from senescent rats (22-24 months old) showed subsensitivity to norepinephrine, isoproterenol and soterenol, when compared with pacemakers isolated from young rats (3-4 months old). The maximum response to the partial agonist soterenol was reduced. 3. Determination of the pA2 value of metoprolol in pacemakers isolated from senescent and young rats showed that the chronotropic response is mediated by a homogeneous beta 1-adrenoceptor population. 4. Inhibition of extraneuronal uptake did not potentiate the chronotropic effect of isoproterenol in pacemakers isolated from senescent rats. Addition of cocaine shifted the concentration-effect curve for norepinephrine only 2.2-fold to the left in senescent rats. 5. It is concluded that, during aging, impairment of the extraneuronal and neuronal uptake mechanisms has an important role in the control of chronotropic responsiveness to catecholamines.

Stress-induced desensitization of the cardiovascular response to noradrenaline in unanesthetized rats.

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. Swimming induced a desensitization of the blood pressure response to NA which was not blocked by previous 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.

Stress-induced desensitization of the cardiovascular response to noradrenaline in unanesthetized rats

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

Supersensitivity to isoprenaline and epinephrine in right atria isolated from rats submitted to a single swimming session.

1. The effects of swim-induced stress on rat atrial norepinephrine content, plasma corticosterone level and pacemaker sensitivity to catecholamines were studied. 2. Swimming for 50 min reduced the atrial norepinephrine content and induced a long-lasting increase in the plasma corticosterone level. 3. Pacemakers isolated from swim stressed rats showed supersensitivity to the chronotropic effect of isoprenaline. Sensitivity to norepinephrine was not significantly altered. Bilateral adrenalectomy or metyrapone pretreatment prevented the development of swimming-induced supersensitivity to isoprenaline. After in vitro denervation and addition of cocaine supersensitivity to epinephrine was demonstrated. 4. It is concluded that corticosterone, at least partially, mediates the supersensitivity to isoprenaline and epinephrine in pacemaker isolated from acutely swim stressed rats.

Repeated swimming stress and responsiveness of the isolated rat pacemaker to the chronotropic effect of noradrenaline and isoprenaline: role of adrenal corticosteroids.

1. Repeated swimming stress (three daily sessions) resulted in an increased plasma corticosterone level and subsensitivity of the isolated rat pacemaker to noradrenaline and isoprenaline. 2. Repeated swimming stress was found to decrease the affinity of beta 1-adrenoreceptors for metoprolol. 3. Bilateral adrenalectomy performed 2 days before repeated swimming stress abolished the development of pacemaker subsensitivity to noradrenaline and isoprenaline and the decrease in beta 1-adrenoreceptors affinity for metoprolol. 4. It is concluded that adrenal corticosteroids, at least partially, mediate the swimming stress-induced subsensitivity of the isolated rat pacemaker to noradrenaline and isoprenaline.

The effects of acute reserpine administration on the sensitivity of the isolated pacemaker from rat heart to isoprenaline and noradrenaline.

The effects of reserpine on the sensitivity of the isolated pacemaker from rat heart to the chronotropic effect of isoprenaline and noradrenaline were studied. A single large dose of reserpine (2.5 mg kg-1) administered to rats 24 h before killing induces supersensitivity of the isolated pacemaker to isoprenaline, leaving unaltered the responsiveness of the pacemaker to noradrenaline. Reserpine at the dose of 1.0 mg kg-1 did not alter the sensitivity of the pacemaker to the catecholamines. Only the larger dose of reserpine raised the corticosterone plasma level. It is possible that a corticosterone-mediated inhibition of the extraneuronal uptake process is responsible for the supersensitivity to isoprenaline. Large doses of reserpine should not be used in experiments aimed to study cardiac sensitivity to isoprenaline or extraneuronal uptake and metabolism of the catecholamine.

Aging and rat pacemaker sensitivity to beta-adrenoceptor agonists.

Sympathetic control of cardiac function is known to decrease with age. This report deals with the sensitivity of pacemakers isolated from young, adult and senescent rats to isoprenaline and noradrenaline. Pacemaker sensitivity to the catecholamines decreases from young to adult rats, the effect remaining unaltered after in vitro denervation and inhibition of the catecholamine dissipating mechanisms. Pacemakers isolated from senescent rats showed subsensitivity to the chronotropic effect of isoprenaline and noradrenaline after in vitro inhibition of the catecholamine dissipating mechanisms. This suggests that the efficiency of the extraneuronal uptake process may be physiologically reduced in the pacemaker of senescent rats.