Competitive dynamics underlie cognitive improvements during sleep

We provide evidence that human sleep is a competitive arena in which cognitive domains vie for limited resources. Using pharmacology and effective connectivity analysis, we demonstrate that long-term memory and working memory are served by distinct offline neural mechanisms that are mutually antagonistic. Specifically, we administered zolpidem to increase central sigma activity and demonstrated targeted suppression of autonomic vagal activity. With effective connectivity, we determined the central activity has greater causal influence over autonomic activity, and the magnitude of this influence during sleep produced a behavioral trade-off between offline long-term and working memory processing. These findings suggest a sleep switch mechanism that toggles between central sigma-dependent long-term memory and autonomic vagal-dependent working memory processing.

Single Slow-Paced Breathing Session at Six Cycles per Minute: Investigation of Dose-Response Relationship on Cardiac Vagal Activity

The practice of slow-paced breathing (SPB) has been linked to a range of positive outcomes, such as decreasing symptoms of depression, anxiety, and stress, as well as increasing well-being. Among the suggested mechanisms of action, SPB has been shown to increase cardiac vagal activity (CVA). The present study aimed to investigate whether there is a dose-response relationship modulating the effects of SPB on CVA. A total of 59 participants were involved in this study. In a within-subject design, participants attended the lab five times, and realized SPB at six cycles per minute with different durations (5, 10, 15, and 20 min), as well as a control condition without SPB. CVA was indexed via the root mean square of successive differences (RMSSD). During SPB, findings showed an increase in RMSSD in all conditions compared to the control condition. However, no differences were found in RMSSD among the different session durations, during SPB or during the resting measurement completed immediately after SPB. Noteworthily, session duration showed an influence on the spontaneous respiratory frequency in the resting measurement occurring immediately after SPB. Specifically, respiratory frequency appears to decrease with session duration, thus potentially contributing to additional relaxing effects.

Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

The renin–angiotensin–aldosterone system (RAAS) impacts cardiovascular homeostasis via direct actions on peripheral blood vessels and via modulation of the autonomic nervous system. To date, research has primarily focused on the actions of the RAAS on the sympathetic nervous system. Here, we review the critical role of the RAAS on parasympathetic nerve function during normal physiology and its role in cardiovascular disease, focusing on hypertension. Angiotensin (Ang) II receptors are present throughout the parasympathetic nerves and can modulate vagal activity via actions at the level of the nerve endings as well as via the circumventricular organs and as a neuromodulator acting within brain regions. There is tonic inhibition of cardiac vagal tone by endogenous Ang II. We review the actions of Ang II via peripheral nerve endings as well as via central actions on brain regions. We review the evidence that Ang II modulates arterial baroreflex function and examine the pathways via which Ang II can modulate baroreflex control of cardiac vagal drive. Although there is evidence that Ang II can modulate parasympathetic activity and has the potential to contribute to impaired baseline levels and impaired baroreflex control during hypertension, the exact central regions where Ang II acts need further investigation. The beneficial actions of angiotensin receptor blockers in hypertension may be mediated in part via actions on the parasympathetic nervous system. We highlight important unknown questions about the interaction between the RAAS and the parasympathetic nervous system and conclude that this remains an important area where future research is needed.

Autonomic Responses during Labor: Potential Implications for Takotsubo Syndrome

Takotsubo syndrome is a serious complication of labor. Although the pathophysiologic role of excessive sympathetic activation is established in this process, concurrent vagal responses have not been adequately described. Moreover, it remains unclear whether autonomic activity depends on the mode of delivery. Here, we explored the hypothesis that the different management of cesarean and vaginal delivery may elicit diverse responses affecting both autonomic arms. For this aim, continuous electrocardiographic recording was performed in 20 women during labor, and non-invasive indices of sympathetic and vagal activity were compared between the two modes of delivery. We report sympathetic prevalence during cesarean delivery, caused by marked vagal withdrawal, whereas autonomic activity was rather stable during vaginal delivery. These differences may be attributed to the effects of anesthesia during cesarean delivery, along with the protective effects of oxytocin administration during vaginal delivery. Our results provide further insights on autonomic responses during labor that may prove useful in the prevention of complications, such as takotsubo syndrome.

A closed-loop approach to the study of the baroreflex dynamics during posture changes at rest and at exercise in humans

We hypothesized that during rapid up-tilting at rest, due to vagal withdrawal, arterial baroreflex sensitivity (BRS) may decrease promptly and precede the operating point (OP) resetting, whereas different kinetics are expected during exercise steady state, due to lower vagal activity than at rest. To test this, eleven subjects were rapidly (< 2s) tilted from supine (S) to upright (U) and vice versa every 3 minutes, at rest and during steady state 50W pedaling. Mean arterial pressure (MAP) was measured by finger cuff (Portapres) and R-to-R interval (RRi) by electrocardiography. BRS was computed with the sequence method both during steady and unsteady states. At rest, BRS was 35.1ms∙mmHg-1 (SD17.1) in S and 16.7ms∙mmHg-1 (SD6.4) in U (p<0.01), RRi was 901ms (SD118) in S and 749ms (SD98) in U (p<0.01), and MAP was 76mmHg (SD11) in S and 83mmHg (SD8) in U (p<0.01). During up-tilt, BRS decreased promptly [first BRS sequence was 19.7ms∙mmHg-1 (SD5.0)] and was followed by an OP resetting (MAP increase without changes in RRi). At exercise, BRS and OP did not differ between supine and upright positions [respectively, BRS was 7.7ms∙mmHg-1 (SD3.0) and 7.7ms∙mmHg-1 (SD3.5), MAP was 85mmHg (SD13) and 88mmHg (SD10), and RRi was 622ms (SD61) and 600ms (SD70)]. The results support the tested hypothesis. The prompt BRS decrease during up-tilt at rest may be ascribed to a vagal withdrawal, similarly to what occurs at exercise onset. The OP resetting may be due to a slower control mechanism, possibly an increase in sympathetic activity.

ISCHEMIC PRECONDITIONING IMPROVES AUTONOMIC MODULATION AFTER SESSION OF RESISTANCE EXERCISE

The aim of this study was to investigate the acute effect of ischemic preconditioning (IPC) in a session of resistance exercise (RE) for upper and lower limbs on the heart rate variability (HRV) in normotensive and trained men. sixteen normotensive and trained men visit the laboratory in five sessions in non-consecutive days. The first two sessions subjects performed one repetition maximum (RM) test and retest, and the next three visits they performed the experimental protocols: a) RE (CON), b) IPC+RE (IPC), c) SHAM+RE (SHAM). RE were performed in 3 sets at 80% 1RM until concentric failure. IPC consisted of 4x5-mins of vascular occlusion at 220 mmHg alternating with 5-min of reperfusion. SHAM protocol followed the same IPC method with 20mmHg vascular occlusion. A significant decrease in LF­nu and RMSSDms (p=0.001) was found from baseline for IPC, SHAM, and CON. A significant increase in HFnu and LF/HF (p=0.001) was found from baseline for IPC, SHAM, and CON. A significant decrease in LF­nu and LF/HF was observed from 60-min post for IPC vs. SHAM and IPC vs. CON (p<0.05). A significant increase in HFnu was observed from 60-min post for IPC vs. SHAM and IPC vs. CON (p<0.05). A significant increase in RMSSDms was found from post-60 for IPC vs. SHAM (p < 0.05). RE followed IPC shows significantly improvements in the autonomic cardiac modulation, accelerating the autonomic recovery after the RE session, by increasing the vagal activity and reducing the sympathetic activation when compared to RE and SHAM protocols.

Cardiorespiratory Interaction and Autonomic Sleep Quality Improve during Sleep in Beds Made from Pinus cembra (Stone Pine) Solid Wood

Cardiorespiratory interactions (CRIs) reflect the mutual tuning of two important organismic oscillators—the heartbeat and respiration. These interactions can be used as a powerful tool to characterize the self-organizational and recreational quality of sleep. In this randomized, blinded and cross-over design study, we investigated CRIs in 15 subjects over a total of 253 nights who slept in beds made from different materials. One type of bed, used as control, was made of melamine faced chipboard with a wood-like appearance, while the other type was made of solid wood from stone pine (Pinus cembra). We observed a significant increase of vagal activity (measured by respiratory sinus arrhythmia), a decrease in the heart rate (as an indicator of energy consumption during sleep) and an improvement in CRIs, especially during the first hours of sleep in the stone pine beds as compared to the chipboard beds. Subjective assessments of study participants’ well-being in the morning and sub-scalar assessments of their intrapsychic stability were significantly better after they slept in the stone pine bed than after they slept in the chipboard bed. Our observations suggest that CRIs are sensitive to detectable differences in indoor settings that are relevant to human health. Our results are in agreement with those of other studies that have reported that exposure to volatile phytochemical ingredients of stone pine (α-pinene, limonene, bornyl acetate) lead to an improvement in vagal activity and studies that show a reduction in stress parameters upon contact with solid wood surfaces.

Salusin-β in Intermediate Dorsal Motor Nucleus of the Vagus Regulates Sympathetic-Parasympathetic Balance and Blood Pressure

The dorsal motor nucleus of the vagus (DMV) is known to control vagal activity. It is unknown whether the DMV regulates sympathetic activity and whether salusin-β in the DMV contributes to autonomic nervous activity. We investigated the roles of salusin-β in DMV in regulating sympathetic-parasympathetic balance and its underline mechanisms. Microinjections were carried out in the DMV and hypothalamic paraventricular nucleus (PVN) in male adult anesthetized rats. Renal sympathetic nerve activity (RSNA), blood pressure and heart rate were recorded. Immunohistochemistry for salusin-β and reactive oxidative species (ROS) production in the DMV were examined. Salusin-β was expressed in the intermediate DMV (iDMV). Salusin-β in the iDMV not only inhibited RSNA but also enhanced vagal activity and thereby reduced blood pressure and heart rate. The roles of salusin-β in causing vagal activation were mediated by NAD(P)H oxidase-dependent superoxide anion production in the iDMV. The roles of salusin-β in inhibiting RSNA were mediated by not only the NAD(P)H oxidase-originated superoxide anion production in the iDMV but also the γ-aminobutyric acid (GABA)A receptor activation in PVN. Moreover, endogenous salusin-β and ROS production in the iDMV play a tonic role in inhibiting RSNA. These results indicate that salusin-β in the iDMV inhibits sympathetic activity and enhances vagal activity, and thereby reduces blood pressure and heart rate, which are mediated by NAD(P)H oxidase-dependent ROS production in the iDMV. Moreover, GABAA receptor in the PVN mediates the effect of salusin-β on sympathetic inhibition. Endogenous salusin-β and ROS production in the iDMV play a tonic role in inhibiting sympathetic activity.

Heart Rate Variability in Elite Swimmers before, during and after COVID-19 Lockdown: A Brief Report on Time Domain Analysis

Background: Many athletes worldwide have endured home confinement during the COVID-19 pandemic, and their opportunities to train were strongly limited. This study describes the impact of lockdown on training volume and heart rate variability (HRV) in elite swimmers. Methods: HRV data of seven elite males were collected each Monday morning over 20 weeks, including 8 weeks of lockdown. The training volume was quantified retrospectively. Results: During the lockdown period (weeks 4–11) swimming was not allowed, and the total training volume was reduced by 55.2 ± 7.5% compared to the baseline volume (from 27.2 to 12.2 training hours). This drop was associated with a decrease in vagal activity (a 9.2 ± 5.4% increase in resting HR and a 6.5 ± 3.4% decrease in the natural logarithm of rMSSD from baseline values). After the lockdown (weeks 12–20), the training volume was gradually increased before attaining 68.8% and 88.2% of the baseline training volume at weeks 15 and 17, respectively. Resting HR and Ln rMSSD returned to baseline values four weeks after the lockdown. Conclusions: The lockdown period induced a decreased training volume which was associated with a decrease in vagal activity. However, HRV values returned to the baseline 4 weeks after the resumption of swimming training.

Reduced Cell Excitability of Cardiac Postganglionic Parasympathetic Neurons Correlates With Myocardial Infarction-Induced Fatal Ventricular Arrhythmias in Type 2 Diabetes Mellitus

ObjectiveWithdrawal of cardiac vagal activity is considered as one of the important triggers for acute myocardial infarction (MI)-induced ventricular arrhythmias in type 2 diabetes mellitus (T2DM). Our previous study demonstrated that cell excitability of cardiac parasympathetic postganglionic (CPP) neurons was reduced in T2DM rats. This study investigated whether cell excitability of CPP neurons is associated with cardiac vagal activity and MI-induced ventricular arrhythmias in T2DM rats.MethodsRat T2DM was induced by a high-fat diet plus streptozotocin injection. MI-evoked ventricular arrhythmia was achieved by surgical ligation of the left anterior descending coronary artery. Twenty-four-hour, continuous ECG recording was used to quantify ventricular arrhythmic events and heart rate variability (HRV) in conscious rats. The power spectral analysis of HRV was used to evaluate autonomic function. Cell excitability of CPP neurons was measured by the whole-cell patch-clamp technique.ResultsTwenty-four-hour ECG data demonstrated that MI-evoked fatal ventricular arrhythmias are more severe in T2DM rats than that in sham rats. In addition, the Kaplan-Meier analysis demonstrated that the survival rate over 2 weeks after MI is significantly lower in T2DM rats (15% in T2DM+MI) compared to sham rats (75% in sham+MI). The susceptibility to ventricular tachyarrhythmia elicited by programmed electrical stimulation was higher in anesthetized T2DM+MI rats than that in rats with MI or T2DM alone (7.0 ± 0.58 in T2DM+MI group vs. 3.5 ± 0.76 in sham+MI). Moreover, as an index for vagal control of ventricular function, changes of left ventricular systolic pressure (LVSP) and the maximum rate of increase of left ventricular pressure (LV dP/dtmax) in response to vagal efferent nerve stimulation were blunted in T2DM rats. Furthermore, T2DM increased heterogeneity of ventricular electrical activities and reduced cardiac parasympathetic activity and cell excitability of CPP neurons (current threshold-inducing action potentials being 62 ± 3.3 pA in T2DM rats without MI vs. 27 ± 1.9 pA in sham rats without MI). However, MI did not alter vagal control of the ventricular function and CPP neuronal excitability, although it also induced cardiac autonomic dysfunction and enhanced heterogeneity of ventricular electrical activities.ConclusionThe reduction of CPP neuron excitability is involved in decreased cardiac vagal function, including cardiac parasympathetic activity and vagal control of ventricular function, which is associated with MI-induced high mortality and malignant ventricular arrhythmias in T2DM.