Episode Transcript
[00:00:00] Welcome friends, to the Heart Rate Variability Podcast this week in Heart Rate Variability Edition. Each week we explore the latest research and news in hrv. Please consider the information in this podcast for informational purposes only and not as medical advice. Always consult your healthcare provider before applying any strategies we discuss. This week we have a vibrant lineup that spans the spectrum of autonomic health, from the chronic systemic impact of metabolic disease to acute interventions that chemically alter the firing patterns of the nervous system. We also delve into the genetic underpinnings of autonomic dysfunction and connective tissue disorders and look ahead to the premier gathering of our community in 2026. We begin with a comprehensive systematic review published in CURIS that cements the link between metabolic syndrome and autonomic dysregulation, offering a potential explanation for the high cardiovascular risk in this population. We then examine a physiological experiment published in Autonomic Neuroscience in which researchers used ultrasound guided nerve blocks to selectively silence the sympathetic nervous system, providing a clear demonstration of how HRV reflects neural tone. Next, we review a study from QRIUS that shows how Ehlers Danlos syndrome disrupts the intrinsic coupling of the autonomic nervous system, supporting the lived experience of dysautonomia in these patients. Finally, we look ahead to the 2026 Annual Conference of the association for Applied Psychophysiology and Biofeedback, a critical event for anyone dedicated to the science of self regulation. Let's begin this week with a deep dive into the metabolic drivers of autonomic health. The study is a systematic review titled Autonomic Nervous System Dysregulation in Metabolic Syndrome, an association with Hypertension and Cardiovascular Risk, published in the journal CureUS in 2025. The authorship team includes Sumra Mukhtar, Asif, Khalid, Nareen, Kamar, and Haider. This paper tackles one of the most pervasive health challenges of our metabolic syndrome.
[00:01:47] For context, this syndrome isn't a single disease but a cluster of conditions, specifically abdominal fat, insulin resistance, hypertension and dyslipidemia that occur together, increasing the risk of heart dise, stroke and type 2 diabetes. While we often view these issues through a biochemical lens focusing on glucose and cholesterol, this review asks a more fundamental physiological how does this metabolic cluster impact the autonomic nervous system, the body's master regulator? The researchers conducted a rigorous systematic search across major medical databases including PubMed, Embase and Scopus, focusing on literature published between January 2015 and September 2025. Their goal was to synthesize human studies that measured autonomic function in patients with metabolic syndrome using valid biomarkers such as heart rate variability, hrv, muscle sympathetic nerve activity, msna, and baroreflex sensitivity. The headline result from their synthesis of 16 robust studies is stark. There is a consistent, measurable association between metabolic syndrome and autonomic failure. Specifically, the review found that individuals with METS exhibit a distinct autonomic signature characterized by chronic sympathetic overactivation and parasympathetic withdrawal. Regarding hrv, the data were nearly unanimous. Across the reviewed studies, patients with metabolic syndrome showed significantly reduced time domain measures such as SDNN and rmssd. As we know, a lower SDNN indicates reduced overall adaptability in the system, while a depressed RMSSD specifically indicates reduced vagal tone, the break that calms the heart. In the frequency domain, these patients consistently displayed a shift toward higher low frequency LF power relative to high frequency HF power, a ratio often interpreted as a tilt towards sympathetic dominance. But the review went deeper than just hrv. It validated these findings with direct evidence from microneurography. Studies measuring muscle sympathetic nerve activity, where a microelectrode records the actual firing rates of sympathetic nerves, confirmed that patients with metabolic syndrome have significantly higher bursts of sympathetic activity even when completely at rest. This is a critical finding because it moves beyond the indirect proxy of HRV to directly show neural activity. These individuals are physiologically revving their engines constantly, even while sitting still. Furthermore, the review highlighted a degradation in baroreflex sensitivity. The baroreflex is the body's rapid response mechanism for stabilizing blood pressure. When it is blunted, the cardiovascular system loses its ability to buffer against stress. The authors note that this combination high sympathetic drive, low vagal tone, and a sluggish baroreflex creates a vicious cycle. Metabolic derangements such as elevated insulin and inflammation likely stimulate the sympathetic nervous system, which in turn increases blood pressure and vascular resistance, further worsening the metabolic state. What is the implication of this? The authors argue that autonomic dysregulation is not just a bystander in metabolic syndrome. It is a key pathogenic mechanism linking being overweight and insulin resistance to the development of hypertension and cardiovascular mortality. The autonomic imbalance may actually precede and drive the progression of the disease. The clinical takeaway here is profound. It suggests that risk stratification for metabolic syndrome is incomplete. If we rely only on blood pressure and lipid panels, we are missing the neural risk. The authors propose that autonomic markers, specifically HRV and baroreflex sensitivity, should be integrated into the clinical assessment of these patients. If a patient with metabolic syndrome shows severe autonomic rigidity, very low hrv, they may be at a significantly higher risk for a cardiac event than a patient with the same metabolic profile but a resilient nervous system. This review reclassifies metabolic syndrome as not just a metabolic disorder but a neurometabolic one. Next, we review a study that provides precise experimental validation of the effects of the sympathetic nervous system on HRV metrics. Published in Autonomic NeuroScience in late 2025, the paper is titled Selective Sympathetic Action on Heart Rate Variability after Ultrasound Guided Stellate Ganglion Block by Kim Raum, Feldman Klein Buhl, and Ben Rath. While the previous study was observational, this one is interventional and mechanistic. The researchers used a stellate ganglion block.
[00:05:36] The stellate ganglion is a nerve cluster in the neck that serves as a major relay station for sympathetic signals heading to the head, neck, arms, and, crucially, the heart. By injecting a local anesthetic around this ganglion, clinicians can temporarily switch off the sympathetic drive from that specific pathway. This procedure is commonly used for chronic pain conditions and increasingly for treating ptsd, as it can reset a hyperactive fight or flight system. However, Kame and his colleagues saw it as a unique opportunity to study HRV physiology and by selectively blocking sympathetic outflow, they could observe exactly how the heart rhythm changes when the fight or flight voice is silenced, leaving the parasympathetic vagal voice to speak uninterrupted. The methodology was high precision. They used ultrasound guidance to ensure the anesthetic was delivered precisely to the target nerves, minimizing error. They then recorded HRV before and after the blockade to capture the acute shift in autonomic dynamics. The results were a beautiful confirmation of autonomic theory. Following the stella ganglion block, the researchers observed a significant selective shift in HRV parameters. Most notably, they saw a marked increase in high frequency HF power. Remember, HF power is the spectral signature of the vagus nerve. It reflects the fluctuation of heart rate with breathing, respiratory, sinus arrhythmia. Under normal conditions, sympathetic activity can dampen this respiratory fluctuation. When the researchers blocked the stellate ganglion, they effectively removed the dampening influence, allowing the vagal tone to express itself fully. Simultaneously, they observed a decrease in the low frequency LF components and the LF HF ratio. This provides compelling evidence for the sympathetic contribution to the low frequency band. By blocking the sympathetic nerve, the balance ratio drops significantly, indicating a shift toward parasympathetic dominance. Why does this matter? First, it provides robust validation of HRV as a biomarker. We often say that HRV measures the nervous system's balance. This study demonstrates it by physically perturbing one side of that balance and observing the metrics respond as predicted. Second, the clinical implications are exciting. The authors conclude that HRV can serve as a reliable, non invasive monitor to verify the success of some pathetic interventions. If a clinician performs a nerve block, they don't have to guess whether it worked. The HRV signature will reveal an immediate drop in sympathetic tone. It highlights the potential of using HRV not only for long term health tracking, but also for real time procedural monitoring and interventional medicine. This episode of this week in HRV is brought to you by Optimal hrv. Optimal HRV provides the tools and training to help you measure what matters for health your heart rate variability. Whether you are a clinician looking to integrate objective stress monitoring into your practice or an individual dedicated to optimizing your own resilience, our platform makes the complex science of HRV accessible and actionable. And here's something new. Optimal HRV now offers E gift cards. Perfect for colleagues, clients or loved ones on a journey to better nervous system health. These digital gift cards can be applied toward APP subscriptions, clinician dashboards or or HRV training programs. It's a thoughtful way to support someone's wellness or clinical practice. With science backed resources, you can learn more about gift cards and our full range of offerings at Optimal hrv. Now back to the show. Next, we examine a study that illuminates the autonomic landscape of a complex genetic disorder. Published in Cureus in 2025, the paper is titled Heart Rate Variability and Intrinsic Autonomic Coupling in Ehlers Danlos Syndrome by Alauddin Radke, Janardana Singh, Sharma, Arora, Prajesh Sri and Shaikh Ehlers Danlos syndrome is a group of hereditary connective tissue disorders characterized by joint hypermobility, skin extensibility and tissue fragility. However, patients and clinicians have long noted that the symptoms often extend far beyond the joints. Fatigue, dizziness, palpitations and gastrointestinal distress are rampant in this population, pointing to a systemic issue with the autonomic nervous system. This condition is often referred to broadly as dysautonomia. This study sought to move beyond anecdotal reports and quantify the specific autonomic profile of EDS patients compared to healthy controls. They recruited 30 patients with diagnosed EDS and matched them with 30 healthy individuals. The assessment included resting HRV analysis and standardized autonomic testing, including the head up tilt test. To assess orthostatic tolerance, the researchers introduced a concept they called intrinsic autonomic coupling. This refers to the physiological relationship between resting heart rate and heart rate variability in a healthy, well regulated system. These two are tightly coupled. As heart rate declines, variability, specifically vagal tone increases. This inverse relationship is a hallmark of a responsive, efficient nervous system. The study results were striking and confirmed the significant burden of dysautonomia in eds. First, the baseline comparison showed that EDS patients had a significantly higher resting heart rate, 87 beats per minute versus 75 beats per minute in controls and significantly lower HRV. Their time domain indices, SDNN and RMSSD, were markedly lower than those of the healthy group. Specifically, the RMSSD, our primary marker for vagal tone, was about 33% lower in the EDS group. This indicates a chronically stressed nervous system. Even when lying supine, the EDS patients were in a state of sympathetic predominance, high heart rate, low variability and vagal withdrawal. However, the most significant finding came from tilt table testing. The researchers found that more than 53% of EDS patients demonstrated objective orthostatic intolerance, eg, postural orthostatic tachycardia syndrome, or POTS, compared with only 10% of healthy controls. This means that for more than half of these patients, simply standing up is a significant physiological stressor that their autonomic nervous system struggles to manage. Regarding intrinsic autonomic coupling, the study found that this relationship was altered in eds. While there was still a correlation higher HR linked to lower hrv, the strength and slope of this coupling suggested a system that is struggling to maintain homeostasis. The authors found a strong positive correlation between resting heart rate and the LF over HF ratio in EDS patients, suggesting that the tachycardia observed in these patients is directly driven by sympathetic overdrive that the vagal break cannot counteract. The implications of this paper are vital for patient care. It confirms that dysautonomia is not all in the head of EDS patients. It is a measurable physiological reality. The authors conclude that HRV profiling should be a standard part of the clinical workup for eds. By identifying this autonomic dysfunction, early clinicians can offer targeted interventions such as fluid loading, salt supplementation, compression garments, or specific exercise protocols to help manage the sympathetic burden. It turns HRV into a tool for validation and management in the context of a complex chronic illness. Finally, we shift our focus from the present research to the future of our field. We are excited to highlight an upcoming event that promises to be a landmark for the biofeedback and HRV community.
[00:12:00] The 2026 Annual Scientific Meeting of the association for Applied Psychophysiology and Biofeedback AAPB scheduled for May 13, 2026 in Baltimore, Maryland at the historic Lord Baltimore Hotel. This conference represents the 56th annual gathering of this prestigious organization.
[00:12:17] For those who may not know, the AAPB is the oldest and most respected professional society dedicated to the study and practice of biofeedback and applied psychophysiology. The theme for the 2026 conference is the Science of Self Regulation and Resilience through Biofeedback. This theme could not be more relevant as we saw in the studies we discussed today. From the metabolic strain of modern life to the genetic challenges of eds, the human organism's ability to self regulate and maintain resilience is central to health. The AAPB meeting is unique for bridging the gap between the laboratory and the clinic. It is a place where basic scientists such as those mapping the neural pathways of the stellate ganglion collaborate with clinical psychologists, physical therapists and performance coaches who apply these concepts with patients every day. We want to highlight the opportunities specifically for students and early career professionals. The AAPB has a strong tradition of mentorship. The meeting includes dedicated poster Sessions scheduled for May 15, 2026 and scholarship opportunities such as the FERB Scholarship to support student attendance. It is an unparalleled environment to find mentors, collaborators and inspiration for clinicians. This event is a goldmine of practical knowledge. You move beyond HRV theory to the how to. Registration for the 2026 meeting is now open, with early bird incentives available until January 30, 2026. The organization is offering significant discounts for early commitment, a testament to their confidence in the quality of the upcoming program.
[00:13:40] We've covered a comprehensive range of topics this week, from the systemic risks of metabolic syndrome and the specific physiology of nerve blocks to the genetic nuances of EDS and the upcoming community gathering. Let's turn now to our actionable insights for individuals. The common thread across these studies is the profound connection between metabolic state and the nervous system. If you are managing weight, blood sugar issues or high blood pressure components of metabolic syndrome, your nervous system is likely under significant stress. The review we discussed shows that your body may be stuck in a chronic fight or flight mode. This means that interventions that soothe the nervous system are not just relaxation, they are metabolic medicine. Incorporating daily practices that boost vagal tone can help take your foot off the sympathetic gas pedal. For those with ehlers Danlos syndrome or hypermobility. The research validates your symptoms. If you feel dizzy, tired or have a racing heart, it is real physiology. Knowing that your intrinsic coupling is altered means you need to be patient with your body. Tracking your HRV can be a powerful tool here not to judge yourself, but to understand your energy envelope. For clinicians, this week's studies offer critical guidance on assessment and validation. The metabolic syndrome review strongly suggests that we need to look beyond the blood panel.
[00:14:47] Consider autonomic screening for your metabolic patients. A simple resting HRV measurement or a stand test can reveal hidden risk regarding eds. The message is clear Screen for dysautonomia. The finding that over 50% of EDS patients have orthostatic intolerance means you should perform orthostatic vital signs on every hypermobile patient who reports fatigue or dizziness. Validating their dysautonomia enables effective management strategies for those in interventional pain or psychiatry. The stellate ganglion study is a proof of concept. HRV is your objective verification tool. Using a wearable or ECG to track HRV before and after procedures can provide data driven confirmation of therapeutic success. Moving beyond subjective patient reports, for researchers, the landscape is rich with opportunity. The chicken or egg question in metabolic syndrome remains a massive gap. We need longitudinal studies to determine if autonomic dysfunction precedes insulin resistance. The concept of intrinsic autonomic coupling used in the EDS study is a compelling metric that warrants broader application.
[00:15:41] Researchers should consider applying this analysis to other chronic conditions to see if the uncoupling of heart rate and variability is a shared biomarker. Finally, the AAPB conference announcement is a call to action to share your work. The field grows only through dissemination. In summary, this week reinforces that HRV is a universal translator. It translates the silent strain of metabolic disease into a visible signal. It translates the chemical effect of a nerve block into measurable data. And it translates the complex symptoms of a genetic disorder into a physiological profile. It is the common language of our body's resilience. Thank you for joining us on the Heart Rate Variability podcast this week in Heart Rate Variability Edition. Each week we're reminded that HRV is much more than a number. It's a reflection of our body's capacity for adaptability, balance and recovery. Science is moving fast and it's moving in a hopeful direction. Until next time, keep listening to your heart and we'll see you soon.
