The review, led by Marc-Olivier Mainville and Philippe Fournier at Université Laval in Québec City, along with colleagues in Canada and France, set out to map every study that had examined heart rate variability biofeedback in veteran-only populations for these three chronic conditions. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews, the team searched PubMed, Embase, and CINAHL in August 2024, with an updated search in February 2025. Of 69 records identified, only five studies met the inclusion criteria, encompassing a total of just 108 participants. Four of the studies were pilot studies with control groups, and sample sizes ranged from a mere 12 to 35 participants each.

The scientific rationale behind heart rate variability biofeedback is rooted in the autonomic nervous system, the branch of physiology that governs involuntary bodily functions such as heart rate, digestion, and stress responses. Heart rate variability — the natural variation in the time intervals between successive heartbeats — serves as a non-invasive window into autonomic regulation, particularly the balance between the sympathetic system, which drives the fight-or-flight response, and the parasympathetic system, which promotes calm and recovery. In a typical biofeedback session, individuals breathe at their so-called resonance frequency, usually around six breaths per minute, with exhalations slightly longer than inhalations, roughly 5.5 seconds out and 4.5 seconds in. This paced breathing stimulates the baroreflex, a key blood-pressure regulatory mechanism, and enhances vagal activity, which is reflected in increased heart rate variability. Proponents argue that repeated practice can improve emotional regulation, stress resilience, and physiological flexibility.

The connection to veterans’ chronic conditions is more than speculative. Post-traumatic stress disorder has been repeatedly associated with reduced parasympathetic, or vagal, activity, and meta-analytic evidence confirms autonomic dysfunction indexed by heart rate variability in PTSD. Chronic pain shows a similar pattern, with a meta-analysis of studies in pain patients finding decreased heart rate variability that implicates parasympathetic dysregulation. Chronic pain-related activation of the body’s stress response has been linked to reduced heart rate variability power and lower resilience and self-regulatory capacity. Tinnitus, by contrast, presents a murkier picture: evidence linking the phantom sound perception to autonomic nervous system dysfunction remains limited and inconsistent, though some studies have reported associations between autonomic imbalance and tinnitus-related distress.

What did the five studies actually find? Four examined heart rate variability biofeedback in relation to PTSD symptoms, with mixed results. Two reported improvements in overall PTSD symptoms, and one of these found that the benefits persisted 16 weeks after the end of training. One study reported reductions limited to intrusion symptoms — the intrusive memories, dreams, and flashbacks that characterize one cluster of PTSD — while another found that biofeedback was not significantly more effective than standard care. The sole study to measure depressive symptoms alongside PTSD reported meaningful decreases in depression. A single pilot study, conducted at a U.S. Department of Veterans Affairs medical center, examined chronic pain and reported significant reductions in perceived pain, perceived stress, negative emotions, and physical activity limitations following four weeks of weekly biofeedback sessions. All four studies that measured heart rate variability reported that the intervention increased it at rest.

Yet the researchers urge strong caution in interpreting these findings. The studies were small, methodologically heterogeneous, and used wildly different approaches to measuring heart rate variability. Some relied on electrocardiography, others on photoplethysmography or blood volume pulse sensors attached to the finger, wrist, or forearm. The metrics used to quantify variability differed across studies, including the coherence ratio, the root mean square of successive differences between normal heartbeats, the standard deviation of inter-beat intervals, and high- and low-frequency power. Non-ECG methods are more susceptible to peak-detection errors and may artificially inflate or attenuate variability estimates, while lower sampling rates can obscure the high-frequency, vagally mediated components of the signal. In some cases, it was unclear whether changes in treatment groups actually differed significantly from changes in control groups, because the statistical analyses were not fully presented.

There is a deeper physiological puzzle as well. The review highlights that reported increases in heart rate variability may reflect transient responses during paced breathing — reductions in heart rate and short-term shifts in parasympathetic activity — rather than sustained changes in autonomic regulation. Because vagal modulation of the heart’s pacemaker operates rapidly, increases in beat-to-beat variability are more pronounced at lower heart rates and may simply occur as individuals enter a more relaxed state, rather than representing a specific therapeutic mechanism. Notably, none of the five studies examined the statistical relationship between changes in heart rate variability metrics and improvements in clinical symptoms, leaving open the question of whether the physiological changes are a mechanism of action or merely a non-specific correlate of feeling calmer.

The tinnitus gap is perhaps the most striking finding of the review. Despite tinnitus being the most prevalent service-connected disability among U.S. veterans, and despite its frequent co-occurrence with PTSD — one study found that 34 percent of the first 300 patients enrolled in the Veterans Affairs Medical Center Tinnitus Clinic also had a PTSD diagnosis — no studies have ever investigated heart rate variability biofeedback in relation to tinnitus in veterans. Large-scale cohort data involving more than 570,000 Iraq and Afghanistan veterans receiving care through the U.S. Department of Veterans Affairs found that PTSD alone was significantly associated with hearing loss and tinnitus, with veterans in this group having greater odds of tinnitus than those without PTSD, depression, or traumatic brain injury. Several pain-related conditions, including headache, neck pain, and jaw pain, were also associated with tinnitus. In the general population, only a single publication, covering three case studies, reported a potential effect of the technique on tinnitus handicap — and only in one of the three tested patients.

The rationale for exploring the technique in veterans is strengthened by clinical guidelines. The Veterans Affairs/Department of Defense guidelines for managing chronic conditions emphasize the underutilization of non-pharmacological interventions, which may provide symptom relief while reducing the risks associated with polypharmacy — a significant concern in veteran populations, where high rates of multimorbidity and medication use are common. The review also points to evidence that evidence-based PTSD psychotherapies produce measurable changes in psychophysiological responses, including reduced trauma-potentiated startle and altered heart rate reactivity, providing additional rationale for investigating interventions that target physiological processes directly.

Despite the limitations, the review highlights the feasibility of studying heart rate variability biofeedback in veterans with chronic conditions. The intervention is non-invasive, requires minimal equipment, and has not been associated with any adverse effects — none of the reviewed studies reported negative side effects. Several studies reported some level of improvement in the targeted chronic condition, and it is plausible that additional, unmeasured benefits may have occurred, although this remains to be validated. The authors conclude that the current evidence does not allow conclusions regarding the technique’s efficacy as a standalone intervention for PTSD or chronic pain, although it may have potential as an adjunctive or supportive approach. They call for rigorously designed, adequately powered studies to evaluate the feasibility, safety, and potential relevance of the technique in well-characterized veteran populations, including those with tinnitus and co-occurring conditions — and they stress that future research should avoid assuming shared underlying mechanisms across conditions, instead adopting designs that account for clinical heterogeneity, individual differences, and tinnitus subtypes.

Subject of Research: Heart rate variability biofeedback for tinnitus, PTSD, and chronic pain in veterans

Article Title: Heart rate variability biofeedback and implications for tinnitus, PTSD and chronic pain in veterans: a scoping review

Article References: Mainville, M.-O., Lacasse-Rioux, É., Noreña, A. J., Vallet, G. T., & Fournier, P. (2026). Heart rate variability biofeedback and implications for tinnitus, PTSD and chronic pain in veterans: a scoping review. Frontiers in Audiology and Otology, 4, Article 1917408. https://doi.org/10.3389/fauot.2026.1917408

Image Credits: AI Generated

DOI: 10.3389/fauot.2026.1917408

Keywords: heart rate variability biofeedback, veterans, PTSD, tinnitus, chronic pain, autonomic nervous system, vagal activity, non-pharmacological intervention, scoping review, paced breathing, baroreflex, polypharmacy

The research team, led by Nikolay Syrov of Ruhr University Bochum together with colleagues from the Skolkovo Institute of Science and Technology and Lomonosov Moscow State University, set out to fill a conspicuous gap in neuroscience. Over the past two decades, scientists have meticulously mapped how cortical excitability fluctuates across the heartbeat, revealing that the brain’s response to transcranial magnetic stimulation varies with cardiac phase. Yet the spinal cord, the critical relay between brain and body, had remained largely unexplored in this respect. Because the spinal cord hosts the final common pathway for all voluntary movement, understanding how its excitability is modulated by the heart carries direct implications for rehabilitation medicine and neurostimulation therapies.

To probe this relationship, the researchers recruited twenty healthy volunteers and employed trans-spinal magnetic stimulation, or TSMS, a technique in which a magnetic coil placed over the cervical spine induces electric currents that activate spinal motor neurons and their incoming pathways. The key methodological innovation was real-time adaptation: the stimulation system continuously monitored the electrocardiogram and triggered each single pulse at a defined fraction of the individual’s RR interval, the time between two consecutive R-wave peaks of the ECG. Pulses were delivered at five cardiac phases, corresponding to 0, 15, 30, 60, and 85 percent of the RR interval, a range that spans both systole, the contraction phase, and diastole, the relaxation phase.

The outcome measure was the amplitude of the motor-evoked potential, or MEP, recorded from hand muscles with electromyography. When a magnetic pulse excites spinal circuitry, a small electrical volley travels down the peripheral nerves and produces a measurable twitch-related potential in the target muscle. Larger MEPs indicate a more excitable spinal cord at the moment of stimulation. By comparing MEP amplitudes across the five cardiac phases, the team could reconstruct a fine-grained temporal profile of cardiac influence on spinal motor excitability.

The results were unambiguous. MEP amplitudes varied significantly across the cardiac cycle, with maximal facilitation occurring at 60 percent of the RR interval, deep in mid-diastole. This temporal profile stands in sharp contrast to the pattern previously documented for the cerebral cortex, where excitability tends to be facilitated during systole, when arterial pressure surges and baroreceptors in the great vessels fire most vigorously. The dissociation is scientifically tantalizing: it suggests that the heart’s grip on the spinal cord is governed by different timing and possibly different mechanisms than its grip on the cortex, even though both structures are exposed to the same rhythmic cardiovascular signals.

To analyze the data rigorously, the authors turned to linear mixed-effects models, a statistical framework well suited to repeated-measures designs in which multiple observations are nested within each participant. Crucially, the models controlled for two potential confounds: the duration of the preceding RR interval, which reflects moment-to-moment heart rate variability, and the respiratory phase, since breathing is known to modulate neural excitability in its own right. The analysis confirmed the cardiac-phase effect on spinal excitability and added an intriguing secondary finding: the length of the preceding RR interval was itself significantly associated with spinal excitability, whereas respiratory phase was not. In other words, the recent history of the heartbeat, not the breath, carried the predictive weight for how responsive the spinal cord would be.

What mechanism could explain a diastolic peak in spinal excitability? The authors advance two non-exclusive hypotheses. The first is physiological and centers on the baroreflex, the homeostatic loop through which pressure sensors in the carotid arteries and aortic arch relay information to the nucleus tractus solitarius in the brainstem. Baroreceptor firing peaks during systole, and the downstream autonomic adjustments ripple through the nervous system with characteristic delays. A delayed, reflex-mediated modulation of spinal motor circuits could plausibly produce facilitation in diastole, after the systolic pressure wave has been sensed and processed. The second hypothesis is strikingly mechanical: the spinal cord does not sit motionless in the vertebral canal but is bathed in cerebrospinal fluid and subjected to pressure pulses synchronized with the heartbeat. With each cardiac cycle, the cord may undergo small displacements within the spinal canal, altering the geometric relationship between the stimulation coil, the induced electric field, and the excitable neural tissue. If the cord drifts closer to the coil or into a more favorable orientation during certain phases, the effective stimulation strength would fluctuate, masquerading as genuine neurophysiological modulation.

The authors are careful to note that these mechanisms are not mutually exclusive, and that disentangling them is a priority for future work. The distinction matters enormously for translational science. If baroreflex-related physiology drives the effect, then cardiac-timed spinal stimulation could be harnessed to deliver neuromodulation when spinal circuits are naturally most receptive, potentially amplifying the efficacy of rehabilitation protocols for spinal cord injury, stroke, and other motor disorders. If mechanical displacement is the dominant factor, then apparent phase-dependent effects must be corrected for in experimental designs, lest researchers mistake coil-to-cord geometry for neural plasticity. Either way, the study delivers a clear methodological warning: experiments and clinical protocols involving spinal stimulation should record and account for the cardiac phase of each pulse, just as the field has learned to control for respiratory phase and cortical state.

The work also enriches the broader and rapidly growing field of heart-brain interaction research. Cardiac-phase effects have now been documented in perception, cognition, and cortical physiology, feeding into theories that frame the heartbeat as a fundamental rhythm shaping information processing in the nervous system. Extending this framework to the spinal cord closes the loop in a satisfying way: the structure that ultimately commands every movement is itself modulated by the organ that powers it. The finding that spinal excitability peaks in mid-diastole, a window when the heart is at rest, hints at an elegant temporal architecture in which the motor machinery of the body is primed during the cardiovascular system’s quietest moment.

For a field racing toward closed-loop neuromodulation, in which stimulation devices read physiological signals and fire only at optimal moments, the study offers a concrete and immediately actionable parameter. Real-time, ECG-triggered stimulation is technically feasible, as this experiment demonstrates, and the identified diastolic window provides a natural target for such algorithms. As the authors emphasize, a more complete understanding of how the heart shapes the nervous system, through both reflex pathways and mechanical forces, will be essential for building the next generation of neurostimulation-based treatments. The heartbeat, it turns out, is not merely background noise for the spinal cord; it is part of the score to which the cord plays.

Subject of Research: Cardiac-cycle modulation of human spinal cord excitability measured with heart-rate-adapted trans-spinal magnetic stimulation

Article Title: Cardiac cycle shapes spinal cord excitability

Article References: Syrov, N., Morozova, P., Popova, A., Melashenko, E., Takhirov, R., Mustafina, A., Benachour, A., Yakovlev, L., Knyshenko, M., & Kaplan, A. (2026). Cardiac cycle shapes spinal cord excitability. BMC Biology. https://doi.org/10.1186/s12915-026-02752-y

Image Credits: AI Generated

DOI: 10.1186/s12915-026-02752-y

Keywords: cardiac cycle, spinal cord excitability, trans-spinal magnetic stimulation, motor evoked potential, heart-brain interaction, baroreflex, diastole, systole, neurostimulation, electrophysiology, RR interval, cerebrospinal fluid

The research, led by Leandro C. Brito and colleagues at Oregon Health & Science University, set out to answer a deceptively simple question: does the baroreflex system itself follow a circadian rhythm, and if so, does that rhythm line up with the circadian rhythm of blood pressure? Previous studies had hinted at a daily pattern in baroreflex function, with sensitivity appearing greatest around three in the morning in both normotensive and hypertensive individuals. But those studies measured people during their normal sleep-wake cycles, meaning the results were hopelessly entangled with behavior. Sleep, posture, meals, and physical activity all influence blood pressure and autonomic function, making it impossible to separate the effect of the internal clock from the effect of simply being asleep.

To untangle this knot, the team turned to one of the most powerful tools in human circadian physiology: the forced desynchrony protocol. In this design, volunteers live on a behavioral schedule that is too short for their internal circadian pacemaker to follow. Because the human circadian clock runs on an intrinsic period of roughly 24.1 hours and cannot entrain to cycles far outside its entrainment range, the internal rhythm is forced to free-run at its own pace while the behavioral cycle marches to a different drummer. When physiological measurements are later plotted against circadian phase rather than clock time, any rhythm that emerges must be driven by the endogenous circadian system rather than by sleep, meals, or activity.

Eleven healthy young adults, aged 20 to 39, completed a 30-hour laboratory stay built around five consecutive six-hour cycles, each containing four hours of wakefulness followed by a two-hour sleep opportunity. Every aspect of their environment was tightly controlled. Wake periods took place in dim light below eight lux, sleep occurred in total darkness, and no time cues were provided. Identical isocaloric meals of roughly 322 kilocalories, composed of about 35 percent fat, 50 percent carbohydrate, and 15 percent protein, were delivered every three hours. Participants remained supine except during meals, scheduled restroom visits, and supervised exercise. Polysomnography confirmed that they slept an average of 114 minutes during each two-hour window, with no significant differences in sleep duration across the protocol. Circadian phase was anchored to the dim light melatonin onset, the gold-standard marker of the biological clock, determined from hourly salivary samples.

During each wake period, the researchers recorded beat-to-beat blood pressure with finger photoplethysmography and cardiac electrical activity with a standard three-lead electrocardiogram. From these continuous signals they extracted two distinct measures of baroreflex function. The first, baroreflex sensitivity, quantifies how strongly the heart rate responds to a given change in systolic pressure, expressed as the slope of the relationship between the two. The second, the baroreflex effectiveness index, counts how often the baroreflex actually intervenes: it is the ratio of validated baroreflex sequences, in which pressure and heart interval change in the appropriate opposing directions across at least three consecutive cardiac cycles, to the total number of spontaneous systolic pressure sequences observed. Sensitivity measures the strength of the reflex when it fires; effectiveness measures how frequently it fires at all.

The results were striking in their asymmetry. Systolic blood pressure showed a clear circadian rhythm with a peak-to-trough amplitude of ten millimeters of mercury, bottoming out at a circadian phase corresponding to roughly 1:40 in the morning and peaking near 11:40 in the morning. Diastolic pressure showed no significant rhythm. Baroreflex sensitivity, perhaps surprisingly, also showed no significant circadian variation. But the baroreflex effectiveness index told a different story entirely. It peaked at a circadian phase corresponding to about one in the morning, averaging 34 percent above its overall mean, and fell to its lowest value, 48 percent below the mean, at around nine in the morning. In other words, the reflex was most active precisely when systolic pressure was at its circadian minimum.

Deeper analysis of the directionality of the reflex added an important nuance. When the researchers separated the data into up-up sequences, in which the reflex slows the heart in response to rising pressure, and down-down sequences, in which it accelerates the heart as pressure falls, they found that the nocturnal advantage came almost entirely from the up-up responses. During the circadian night, the baroreflex was 110 percent more effective at correcting increases in blood pressure than during the circadian morning. This asymmetry carries real clinical weight. Prior work has shown that in women with a family history of hypertension, the ability to correct pressure rises is selectively impaired, and in people with established hypertension, a deficient baroreflex response to pressure increases independently predicts death and adverse cardiovascular events.

The study also mapped the circadian rhythms of the vasculature. Brachial artery vascular conductance, an index of skeletal muscle vasodilation, peaked around two in the morning at 27 percent above its mean, immediately preceding the systolic pressure trough, and fell to its lowest point around six in the evening. Vascular endothelial function, measured as flow-mediated dilation of the brachial artery, peaked later, at around ten in the morning, 34 percent above the mean, and was lowest at six in the evening. Notably, this morning peak in endothelial function occurred about five hours earlier than previously reported in middle-aged adults studied with the same technique, raising the possibility that aging shifts the circadian phase of vascular protection. The authors suggest this morning peak may help explain why, paradoxically, adverse cardiovascular events cluster between six in the morning and noon in epidemiological studies.

Why did sensitivity fail to rhythm while effectiveness did? The authors offer several possibilities. Their participants were exceptionally healthy, young, and recreationally active, conditions that may have created a ceiling effect masking a true rhythm in sensitivity. Alternatively, sensitivity and effectiveness may act in counterphase, as earlier work by di Rienzo and colleagues proposed when the effectiveness index was first introduced. It is also possible that the circadian system exerts a stronger influence on the spontaneous engagement of the reflex than on its gain. Importantly, the findings held up when the total number of pressure sequences and validated baroreflex sequences were included as covariates, ruling out the trivial explanation that more opportunities to detect sequences arose at night.

The implications extend well beyond basic physiology. No currently available antihypertensive medication acts directly on the baroreflex, but non-pharmacological interventions, including exercise training, respiratory muscle training, and non-invasive vagal nerve stimulation, are known to improve baroreflex function. If the circadian system genuinely gates baroreflex effectiveness, these therapies might be timed to exploit that rhythm, opening a chronotherapy-based avenue for treating non-dipping blood pressure. The authors are careful to note the limits of their work: the sample was small and predominantly young and healthy, the 30-hour protocol offers only six-hour phase resolution, and the findings must be reproduced in older adults and in people with hypertension before they can inform clinical practice. Still, by rigorously isolating the internal clock from the noise of daily behavior, the study elevates the baroreflex from a passive bystander to a leading suspect in the mystery of nocturnal blood pressure regulation, and it hands researchers a concrete, testable target in the search for why some hearts fail to dip when night falls.

Subject of Research: Circadian variation in cardiac baroreflex effectiveness and its alignment with the nocturnal trough in systolic blood pressure in young healthy adults

Article Title: Nocturnal peak in cardiac baroreflex effectiveness aligns with nocturnal trough in systolic blood pressure in young healthy adults: Possible circadian effects

Article References: Brito, L. C., Jones, M. L., Chaudhary, N., Shea, S. A., & Thosar, S. S. (2026). Nocturnal peak in cardiac baroreflex effectiveness aligns with nocturnal trough in systolic blood pressure in young healthy adults: Possible circadian effects. Physiological Reports, 14(17), Article e71092. https://doi.org/10.14814/phy2.71092

Image Credits: AI Generated

DOI: 10.14814/phy2.71092

Keywords: circadian rhythm, baroreflex, blood pressure, nocturnal dipping, forced desynchrony, autonomic nervous system, vascular function, hypertension, melatonin, flow-mediated dilation, cardiovascular physiology, chronotherapy