Exercise training induces physiological adaptations that have traditionally been interpreted mainly through changes in skeletal muscle, cardiovascular, metabolic, immune, and endocrine systems. Recent evidence from Kindel and colleagues shows that ventromedial hypothalamic steroidogenic factor-1 neurons are activated by exercise and are required for endurance gains. Here, we highlight complementary evidence from the autonomic nervous system. Our recent stereological study of rat stellate ganglia showed side-specific structural remodelling after treadmill training, including right-left asymmetry in neuronal number and divergent changes in neuronal soma size. Together, these observations suggest that exercise-associated adaptation may involve neural plasticity across central and peripheral autonomic circuits. This perspective raises testable questions about whether central hypothalamic and autonomic ganglionic adaptations act independently, sequentially, or as part of a coordinated body-brain-autonomic feedback system relevant to cardiac sympathetic regulation.

There is a growing body of literature evaluating both postural orthostatic tachycardia syndrome (POTS) and Ehlers-Danlos syndrome (EDS). We conducted a systematic review to evaluate what is currently known about the co-existence of both conditions. A search of MEDLINE and EMBASE was performed in December 2025 and data were collected in tables and pooled to determine the prevalence of POTS in EDS and EDS in POTS. A total of 30 studies were included with 8421 patients with EDS and 12,983 patients with POTS. The average age across 16 studies that reported mean age was 33.3 years. POTS in patients with EDS ranges from 17.5% to 92.7% depending on the population. EDS in patients with POTS ranges from 17.9% to 50.0% depending on the population. One study suggested that patients with EDS and POTS had greater medication use, pain medications and greater number of clinic visits compared to POTS alone while another suggests that these patients have greater gastrointestinal symptoms and the odds were greatest for postprandial distress syndrome, chronic nausea and vomiting syndrome, vomiting and post-prandial fullness. We conclude that EDS and POTS frequently co-occur, and proportions of patients with POTS and EDS depends on the population evaluated. Overall, more research is needed to better understand how to effectively manage patients living with both EDS and POTS.

Urodynamics remain the gold standard for objectively evaluating bothersome lower urinary tract symptoms (LUTS) and offer indirect insight into the autonomic innervation of the lower urinary tract (LUT). Disruptions to the autonomic nervous system (ANS), particularly sympathetic and parasympathetic denervation, are frequently encountered in urological and neurological practice due to their common manifestation as LUTS. This narrative review synthesises current evidence on urodynamic features observed during bladder filling and voiding and their relationship to autonomic innervation in health and disease, drawing on established principles of LUT neural physiology. It contrasts normal urodynamic patterns with characteristic findings reported in neurological disorders associated with ANS disruption, such as multiple system atrophy, Parkinson's disease, diabetic and amyloid neuropathies, and spinal cord injury, to infer autonomic pathway integrity. These findings include changes in cystometric capacity, bladder compliance, filling sensations, and bladder neck appearance, the presence of detrusor overactivity or incontinence, and voiding phase abnormalities, including detrusor underactivity and bladder outflow obstruction. Together, these findings may provide insight into autonomic regulation across both health and disease. Urodynamics do not directly measure neural activity, and interpretation may be influenced by overlapping somatic effects, variable diagnostic thresholds, and non-neurogenic or co-existing pathology, but they remain an indispensable clinical tool for understanding LUT function and ANS involvement.

This systematic review aims to assess the current use of heart rate variability (HRV) analysis in clinical research, focusing on the diseases studied, the common indices used, and the physiological insights gained. A search was conducted in PubMed, articles published in recent years (2019-2025) in English or Spanish involving humans and pathophysiological interpretations were reviewed. After screening and verifying quality criteria, 99 articles were included in the review. HRV was most frequently applied in mental, behavioral, or neurodevelopmental disorders; diseases of the nervous system, and diseases of the circulatory system. Across studies, interpretations clustered around Treatment/Stimulus effects and Etiology/Mechanisms, with comparatively fewer works focused on Diagnostic/Screening or Severity/Staging. Approximately 58% of articles justified a targeted selection of HRV indices aligned with their clinical hypotheses, whereas the rest relied on batteries of indices. This review highlights the diverse use and interpretation of HRV across clinical contexts, pointing to a lack of standardized protocols. The heterogeneity of recording durations, maneuver use, and spectral units provided, together with under-reporting of nonlinear prerequisites, all limit cross-study comparability and clinical translation. We outline a tentative roadmap for clinically oriented HRV work that emphasizes, where appropriate, measurement standardization, analytic rigor and transparency, and clinical translation, ideally supported by preregistration, harmonized reporting, and open, validated resources. Future research should focus on developing standardized and updated guidelines for HRV analysis to improve its clinical utility and to encourage interdisciplinary collaboration in selecting and interpreting HRV indices based on research objectives and clinical hypotheses.

Communication between the gastrointestinal tract and the central nervous system, known as the gut-brain axis, is fundamental to physiology and is implicated in a range of pathological conditions. A critical component of this axis is the sensory information conveyed from the gut to the brain through spinal afferent pathways. Understanding the location and types of spinal afferents present in the GI tract and their mechanisms of activation is essential to advance our knowledge of gut-brain communication in health and disease. Though generally trailing knowledge of gut vagal afferents, major advances have been made in understanding spinal sensory pathways through recent critical adaptations of neuroanatomical tracing, neurogenetics and molecular profiling techniques, revealing an unforeseen diversity in the morphology of their endings in the gut wall and novel classifications based on molecular identity. Moreover, spinal afferents have been implicated in multiple physiological functions besides their well-known role in nociception, including potential roles in nutrient sensing and regulating gut motility. Among spinal afferent endings in the gut mucosal layer, much has been learnt about how enterochromaffin (EC) cells communicate with spinal (and vagal) afferents. Evidence now suggests that EC cells release substances (like serotonin), which activate the terminals of spinal (and vagal) afferent endings via a paracrine, not synaptic, transmission. Here, we review the latest findings regarding spinal afferent endings and point to outstanding questions and future directions for research into this complex and clinically relevant area of neuroscience.

Sixty-two children (18 with inflammatory bowel disease [IBD], 28 with irritable bowel syndrome [IBS], 18 healthy controls) underwent pre- and postprandial electrogastrography and autonomic assessment with the Composite Autonomic Symptom Score-31 (COMPASS-31) and Composite Autonomic Severity Scale (CASS). No between-group differences in EGG parameters were observed. Children with IBS showed increased postprandial normogastria. Higher autonomic symptom burden correlated with lower postprandial power dominant frequency, and symptomatic dysautonomia was associated with reduced postprandial power dominant frequency. These exploratory findings suggest a link between autonomic symptoms and postprandial gastric activity and warrant confirmation in larger cohorts.

Chronic kidney disease (CKD) impairs cardiac baroreflex sensitivity (cBRS), contributing to poor blood pressure (BP) control and heightened cardiovascular risk. Emerging evidence indicates that isometric handgrip (IHG) exercise may enhance cBRS in healthy individuals; however, its effects in CKD remain unclear. Therefore, this study tested the hypothesis that a single IHG session increases cBRS and reduces beat-to-beat BP variability (BPV) in CKD patients. In 21 patients (61 ± 12 yr; stages III-IV), beat-to-beat BP (finger photoplethysmography), heart rate (HR, electrocardiography), and respiration were continuously measured before and 10-, 20-, and 30-min post IHG vs. sham exercise in a crossover design. cBRS was assessed via the sequence technique and cardiac autonomic modulation via time- and frequency-domain HR variability (HRV). BPV was quantified using time domain indexes. cBRS increased following IHG exercise (10-min: Δ20 ± 4%; 20-min: Δ23 ± 5%; 30-min: Δ17 ± 5%; all P < 0.004 vs rest). This increase was significantly different from sham at 10-min and 20-min (all P < 0.006 vs sham), but not at 30-min post-IHG (P = 0.074). HR decreased throughout recovery (all P = 0.001 vs rest). Systolic BP decreased 30-min following IHG exercise (Δ-5 ± 2 mmHg; P = 0.047 vs. rest). Time-domain HRV increased during recovery (P = 0.005) whereas BPV remained unchanged following IHG exercise. After sham, all variables remained similar to rest, except systolic BP was significantly higher 20-min after sham. A single IHG session increased cBRS and vagal modulation, with a modest reduction in systolic BP and no change in BPV, in CKD patients. Overall, these findings suggest that IHG may serve as a non-pharmacological intervention for cardiovascular regulation in CKD.

We tested the validity of the Polar H10 chest strap against criterion electrocardiography (ECG) for heart rate variability (HRV) and cardiac autonomic reflex assessment in young adults and examined associations between supine HRV and other cardiovagal markers. Forty-three healthy adults (18-39 years, 44% male) completed an 8-min protocol: 3 min supine rest (HRV assessed in minute 2 after 1-min stabilization), 1 min paced deep breathing (minute 4; 0.1 Hz), 1 min supine washout, and 3 min active standing (30:15 ratio assessed post-transition; HRV assessed in minute 6 after 1-min post-transition stabilization). Simultaneous RR intervals were recorded via ECG and H10. Agreement was evaluated for time-domain HRV (mean RR interval, root-mean square of successive differences [RMSSD], and standard deviation of normal RR intervals) and reflex tests (deep breathing expiratory [E] to inspiratory [I] ratio, E - I difference, heart rate response; orthostatic 30:15 ratio). Excellent agreement was observed between devices for all metrics (concordance correlation ≥0.99; mean absolute percentage error < 1%; and narrow 95% limits of agreement (widest = -1.5 to 1.7 ms). Supine RMSSD shared 39-53% of variance with deep breathing outcomes, 34% with standing RMSSD, and < 1% with the 30:15 ratio. The H10 provides measurements effectively interchangeable with laboratory ECG for time-domain HRV and standard cardiovagal reflex tests in healthy young adults. Supine RMSSD shares approximately half or less of the variance with other cardiovagal markers, reinforcing the importance of incorporating complementary reflex and orthostatic tests for comprehensive cardiac autonomic assessment.

The biliary system consisting of bile ducts and the gall bladder plays a crucial role in digestion and its function is controlled by both humoral and neural mechanisms. Despite the intense pain associated with gall bladder and bile duct pathologies, little is known about the sensory innervation, particularly sensory innervation by the vagus nerve. Here using anterograde viral tracing from either the left or right nodose ganglion, we demonstrate the presence of a dense sensory innervation of the murine gall bladder by vagal afferents. Entering via the cystic duct, bundles of vagal sensory axons travel along blood vessels from the neck towards the fundus of the gall bladder, where individual axons divide copiously to innervate large territories of the gall bladder wall. Reminiscent of the stomach wall, some vagal afferent axons end in intramuscular array-like endings or in laminar endings within gall bladder ganglia or in the tunica fibromuscularis. However, most axons form a variety of non-distinct endings mostly in the muscle layer. The innervation pattern is consistent with the detection of both mechanical and chemical stimuli. This calls for functional studies determining specific sensory modalities, and translational studies exploring their possible involvement in immune regulation, pain sensation, and interoceptive capacity.

Cannabinoid agonists may ameliorate bladder pain associated with interstitial cystitis/bladder pain syndrome. Visceromotor responses (VMRs) to bladder distension were recorded in urethane-anesthetised control and protamine/zymosan-treated guinea pigs. The peripherally restricted preferential CB1 receptor agonist PrNMI and the selective CB2 receptor agonist 4Q3C each reduced cystitis-induced enhancement of VMRs at high intravesical pressures. Co-activation of CB1 and CB2 receptors abolished cystitis-induced bladder hyperalgesia. These findings indicate that simultaneous targeting of peripheral CB1 and CB2 receptors may provide clinically meaningful benefits for the treatment of bladder pain associated with cystitis.

The menstrual cycle is characterized by fluctuations in ovarian hormones that influence the regulation of physiological systems, including homeostatic adjustments in cardiovascular control. The sympathetic nervous system maintains refined control over cardiovascular homeostasis through adjustments in systemic and local hemodynamics, and via neural reflexes and sympathetic neurovascular transduction. However, the extent to which these autonomic pathways are modulated by endogenous hormonal shifts remains a significant knowledge gap. This narrative review consolidates current evidence on autonomic function across the menstrual cycle, with a focus on muscle sympathetic nerve activity, sympathetic neurovascular transduction, sympathetic neural reflexes, and heart rate variability. Additionally, we briefly explore the influence of exogenous hormone use, primarily oral contraceptive pills, on autonomic regulation. A critical and often overlooked distinction in the literature is that while resting sympathetic drive is significantly elevated during the mid-luteal phase, the sensitivity of most neural reflexes remains functionally stable. This stability suggests that the mid-luteal surge in estradiol acts as a vital vascular buffer, enhancing sympatholysis and nitric oxide bioavailability to offset the increase in underlying neural drive. We further examine exceptions to this stability, specifically the peripheral chemoreflex, and explore the impact of exogenous hormones on neurovascular homeostasis. Characterizing these interactions is essential for understanding physiological and pathophysiological changes across the female lifespan.