Frontiers in network physiology最新文献

{"title":"Investigating cardiorespiratory fitness, cerebral blood flow, and brain metabolism in epilepsy.","authors":"Yun Lien, Brandon S Mitchell, Jerzy P Szaflarski, Lawrence Ver Hoef, Thomas W Buford, Adam M Goodman, William R Willoughby, Charity J Morgan, Anna Moyana, Jennifer Pilkington, Amy R August, Joshua T Bennett, Jane B Allendorfer","doi":"10.3389/fnetp.2026.1894335","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1894335","url":null,"abstract":"<p><strong>Introduction: </strong>Idiopathic generalized epilepsies (IGEs) are characterized by seizures that propagate through widespread thalamocortical networks including the anterior cingulate cortex (ACC). Poor cardiorespiratory fitness may exacerbate neurovascular and metabolic vulnerability including heightened susceptibility to sudden unexpected death in epilepsy. We aimed to examine cardiorespiratory fitness, regional cerebral blood flow (CBF), and metabolite concentrations in patients with IGEs (PwIGEs) and to determine the effect of seizure control status on these physiological and neurochemical measures.</p><p><strong>Methods: </strong>Forty-six participants (31 PwIGEs, 15 healthy controls) underwent a graded exercise test to assess maximal oxygen uptake (VO2peak) as a measure of cardiorespiratory fitness and completed 3T MRI including multi-delayed pseudo-continuous arterial spin labeling (pCASL) to assess CBF and single-voxel spectroscopy (SVS) to assess ratios of N-acetylaspartate and glutamate/glutamine complex to total creatine (NAA/tCr and Glx/tCr, respectively) in the ACC and thalamus. Group differences and seizure control effects in PwIGEs were examined using analysis of covariance (ANCOVA).</p><p><strong>Results: </strong>VO2peak, thalamic CBF, ACC NAA/tCr, and ACC Glx/tCr did not significantly differ between groups. PwIGEs exhibited higher ACC CBF (p = 0.039) and lower thalamic NAA/tCr (p = 0.012) than healthy controls. PwIGEs with active seizures showed significantly lower thalamic Glx/tCr compared to those who were seizure-free (p = 0.003).</p><p><strong>Discussion: </strong>These findings suggest poor cardiorespiratory fitness is not epilepsy-specific and likely attributable to lifestyle and that region-specific alterations in perfusion and metabolic milieu in PwIGEs characterized by higher ACC CBF and lower thalamic NAA/tCr and Glx/tCr in those with active seizures. The multimodal neuroimaging approach provides convergent evidence of thalamocortical network dysregulation underlying IGE pathophysiology.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1894335"},"PeriodicalIF":3.1,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13727442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149328142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating polyspikes and excitability markers for epileptic network identification.","authors":"James E Niemeyer, Benjamin L Barnes, Nitish Seenarine, Meritxell Sainz Barrionuevo, Theodore H Schwartz","doi":"10.3389/fnetp.2026.1966953","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1966953","url":null,"abstract":"<p><p>Epilepsy is increasingly recognized as a disorder of distributed brain networks rather than a disease arising from a single seizure focus. Although clinical practice remains centered on localization of the seizure onset zone (SOZ), persistent seizures following apparently successful resection suggest that epileptogenic activity is often supported by broader networks of interconnected regions. A major challenge for both surgical and neuromodulatory treatment is identifying not only where seizures occur, but also which connected brain structures are components of a network that may underlie the generation of seizures. Here, we propose network excitability mapping as a translational framework for characterizing epileptic networks. In this view, epileptic networks can be described along two complementary dimensions: 1) local excitability and 2) network recruitment. We highlight evidence that the aperiodic (1/f) slope of field-potential recordings provides a mechanistically grounded measure of local excitability, while polyspike structure can reflect the degree to which epileptiform activity recruits distributed network nodes. Recent studies, and preliminary data presented here, combining electrophysiology, calcium imaging, and computational modeling suggest that these measures capture distinct but related aspects of epileptic network function. Together, these approaches support a shift from SOZ-based paradigms toward functional mapping of epileptic networks. We argue that combining measures of excitability and recruitment may enable construction of individualized excitability maps capable of informing surgical planning, optimizing neurostimulation, and improving seizure control. Establishing translational biomarkers of network engagement will be critical for advancing precision therapies in epilepsy.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1966953"},"PeriodicalIF":3.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute cardiovascular responses to slow and deep breathing in normotensive non-pregnant and pregnant women.","authors":"Malika Felton, Stephanie Grigsby, Vanora A Hundley","doi":"10.3389/fnetp.2026.1913383","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1913383","url":null,"abstract":"<p><strong>Objective: </strong>To compare the acute cardiovascular responses of non-pregnant and pregnant women to slow and deep breathing (SDB) at a range of breathing frequencies. Participants: Forty-one women (23 non-pregnant and 18 pregnant).</p><p><strong>Methods: </strong>Participants completed five different breathing conditions in a randomised order (5-min duration); spontaneous breathing (S<i>f</i> _<i>r</i> ), dynamic SDB breathing frequency (D<i>f</i> _<i>r</i> ), and three fixed breathing frequencies of 4 breaths^. min^-1 (4F<i>f</i> _<i>r</i> ), 6 breaths. min^-1 (6F<i>f</i> _<i>r</i> ), and 8 breaths. min^-1 (8F<i>f</i> _<i>r</i> ). Main Outcome Measures: Non-invasive beat-to-beat arterial blood pressure, heart rate and respired airflow were monitored continuously.</p><p><strong>Results: </strong>The maximum amplitude of respiratory sinus arrhythmia (RSA) during SDB was 2.1 times higher than during spontaneous breathing (S<i>f</i> _<i>r</i> ) for both groups, maximising at 6 breaths^. min^-1 (0.25s ± 0.1 non-pregnant, 0.15s ± 0.1 pregnant). Although absolute RSA was significantly lower in pregnant women during spontaneous breathing (S<i>f</i> _<i>r</i> ; 0.07s vs. 0.12s non-pregnant), SDB increased RSA to the same level as non-pregnant women's spontaneous breathing levels. In both groups, the amplitude of blood pressure oscillations (both systolic and diastolic blood pressure) increased as breathing frequency declined, reaching a peak at 4 breaths^. min^-1 (4F<i>f</i> _<i>r</i> ), which was up to 4.5 times higher (14.3%, 10 mmHg) than during spontaneous breathing (S<i>f</i> _<i>r</i> ).</p><p><strong>Conclusion: </strong>Cardiovascular responses maximised at ≤6 breaths^. min^-1 and acute haemodynamic responses to SDB are similar in pregnant and non-pregnant women, despite absolute differences under spontaneous breathing conditions. If blood pressure oscillations underpin the anti-hypertensive effect of SDB, the data indicate that these can be amplified in pregnant women at frequencies between 4 and 6 breaths^. min^-1.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1913383"},"PeriodicalIF":3.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corticospinal function does not predict stride-to-stride gait dynamics in older adults.","authors":"J S Gomes, J H Oliveira, P Bauer, L Sousa, A Sel, N Cortes, J R Vaz","doi":"10.3389/fnetp.2026.1946459","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1946459","url":null,"abstract":"<p><strong>Introduction: </strong>Ageing is associated with impaired gait adaptability, which leads to an increased fall risk in older adults. The study of the temporal structure of stride-to-stride fluctuations may help mitigate these inherent risks, as it has been proposed as a marker of locomotor functionality and motor control. However, the underlying mechanisms responsible for the progressive deterioration of stride-to-stride fluctuations in older adults are yet to be fully unravelled. Recent research suggests several central and peripheral factors can influence the walking adaptation process with the corticospinal tract playing a key role in motor control during gait. Thus, the purpose of this study was to investigate whether lower-leg corticospinal drive significantly explains the temporal structure of gait stride-to-stride fluctuations.</p><p><strong>Methods: </strong>Thirty-four older adults underwent transcranial magnetic stimulation (TMS) assessments of the tibialis anterior in one experimental session, where corticospinal excitability (CSE), silent period duration (SP), and short-interval intracortical inhibition (SICI) were quantified. Immediately after the TMS intervention, they also performed a 12-min treadmill walking trial at preferred walking speed, during which inter-stride intervals were extracted and analysed using detrended fluctuation analysis to obtain the fractal scaling exponent (αISIs). Multiple linear regression analysis was used to examine whether CSE, SP and SICI predicted αISIs.</p><p><strong>Results: </strong>The results of the linear regression model indicated that none of the corticospinal measures significantly predicted gait's temporal dynamics (F(3,28) = 0.20, <i>p</i> = 0.896, <i>R</i> ² = 0.021).</p><p><strong>Discussion: </strong>These findings suggest that gait adaptability does not seem to be explained by corticospinal function, likely emerging from distributed, multilevel neural control processes involving spinal, supraspinal, and peripheral mechanisms rather than corticospinal contributions alone.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1946459"},"PeriodicalIF":3.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13714503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Open wavefront ablation terminates rotor-driven atrial fibrillation.","authors":"Arthur S Bezerra, Robin Van Den Abeele, Bram Van Landeghem, Bjorn Verstraeten, Sebastiaan Lootens, Viktor Van Nieuwenhuize, Sander Hendrickx, Vincent F M Segers, Mattias Duytschaever, Nele Vandersickel","doi":"10.3389/fnetp.2026.1940428","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1940428","url":null,"abstract":"<p><strong>Introduction: </strong>Atrial arrhythmias, notably atrial fibrillation (AF), exhibit complex spatiotemporal patterns that remain incompletely characterized. Based on topological constraints requiring counter-rotating reentries in two-dimensional manifolds, we present a framework classifying all atrial wavefronts into two fundamental archetypes: open and closed waves. Open waves are line-like structures bounded by endpoints that tend to self-perpetuate; closed waves are ring-like structures lacking endpoints that tend toward self-termination.</p><p><strong>Methods and results: </strong>We demonstrate that complex wavefront interactions reduce to five elementary processes: (1) Open wave creation, (2) Open wave annihilation, (3) Closed wave creation, (4) Closed wave annihilation and (5) Open wave collision. Validation within a cohort of 600 patient-specific AF simulations showed that all observed events adhered to these constructed topological rules, suggesting that complexity of fibrillatory conduction within the studied computational framework arises from simple underlying principles. Furthermore, closing all open waves, achieved a 100% success rate when electrical silence was used as the primary criteria for efficacy.</p><p><strong>Discussion: </strong>This unified framework reconciles existing electrophysiological theories, including the multiple wavelet hypothesis, the mother rotor hypothesis, meandering rotors, and focal sources, while providing a foundation for optimizing clinical interventions.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1940428"},"PeriodicalIF":3.1,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13686894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149278056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complexity of plantar flexor torque and gait covaries in older adults: a network physiology approach to neuromuscular aging.","authors":"Philipp Bauer, João S Gomes, Tiago Marques, Sandrina Lourenço, João H Oliveira, Jamie Tallent, Nelson Cortes, João R Vaz","doi":"10.3389/fnetp.2026.1947848","DOIUrl":"10.3389/fnetp.2026.1947848","url":null,"abstract":"<p><strong>Introduction: </strong>Falls are a leading cause of injury, disability, and loss of independence in older adults, and are closely linked to age-related declines in neuromuscular function. Underlying these declines is a loss of physiological complexity, reflected in more predictable and repetitive temporal structures (i.e., decreased entropy) of motor output. Within a network physiology framework, this loss of complexity may manifest as reduced network dimensionality. It may also be consistent with an increased co-variation between motor outputs in different tasks. Therefore, the present study examined the relationship between the complexity of plantar flexor torque and gait in young and older adults.</p><p><strong>Methods: </strong>Thirty-eight healthy older adults and forty-six healthy young adults participated in a single laboratory session. Plantar flexor torque and gait were assessed in separate tasks: submaximal isometric contractions and continuous treadmill walking, respectively. Complexity was inferred from sample entropy, which quantifies the temporal structure of both signals.</p><p><strong>Results: </strong>A positive Bayesian correlation between torque and gait complexity was observed in older adults (τ = 0.245, BF₁₀ = 3.985). In contrast, an absence of such correlation was found in young adults (τ = -0.079, BF₁₀ = 0.257). The Bayesian comparison of the two correlations revealed a stronger association between gait and torque in older adults compared to young adults (Δτ = 0.324, BF₁₀ = 3.456).</p><p><strong>Discussion: </strong>These findings are consistent with, but do not directly demonstrate, an age-related loss of dimensionality in the neuromuscular network, in which motor outputs that vary independently in young adults co-vary in older adults. By identifying plantar-flexor torque complexity as a potential modifiable factor that is associated with gait complexity in older adults, these results motivate longitudinal work testing whether interventions that target torque control, such as resistance training, can elicit corresponding improvements in gait and thereby reduce fall risk.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1947848"},"PeriodicalIF":3.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13683066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network analysis reveals that total hip arthroplasty restores shared segmental motion before segmental differentiation.","authors":"Madhur Mangalam, Brian Schlattmann, Christopher Deans, Elizabeth Wellsandt","doi":"10.3389/fnetp.2026.1916345","DOIUrl":"10.3389/fnetp.2026.1916345","url":null,"abstract":"<p><p>Unilateral hip osteoarthritis (HOA) reshapes whole-body movement, and total hip arthroplasty (THA) restores function only partially-but conventional kinematic analyses fall short of characterizing how the body's distributed coordination reorganizes. Network analyses of inter-segment kinematic coupling offer a systems-level alternative, but they conventionally collapse the sign of coupling, treating two mechanically distinct relationships as equivalent: segments whose displacement amplitudes covary, rising and falling together, and segments whose amplitudes trade off, one displacing little while the other displaces a great deal. Here, we introduce a signed partial-correlation decomposition of marker-displacement coordination into parallel covarying <math><mrow><mo>(</mo> <mrow> <msup><mrow><mi>W</mi></mrow> <mrow><mo>+</mo></mrow> </msup> </mrow> <mo>)</mo></mrow> </math> and trading-off <math><mrow><mo>(</mo> <mrow> <msup><mrow><mi>W</mi></mrow> <mrow><mo>-</mo></mrow> </msup> </mrow> <mo>)</mo></mrow> </math> networks, applied to gait from 80 healthy adults and 106 HOA patients assessed before and 6 months after THA (ClinicalTrials.gov Identifier: NCT01907503). HOA reorganizes the two networks in opposite directions: covarying coordination loses modular structure and small-worldness, while trading-off coordination becomes more locally clustered and more small-world; global efficiency falls in both. This is consistent with pain-driven splinting that consolidates a few fixed trading-off configurations. Surgery acts predominantly on covarying coordination, partially restoring its topology, while the trading-off network's reorganization persists across the six-month post-surgical window-and on one measure, i.e., how broadly each segment spreads its trading-off partners, a deficit emerges during recovery that was absent before surgery. A node-level sign-balance metric shows that the proportion of each segment's coordination carried by covarying relationships returns to healthy values by 6 months, even though the underlying networks remain structurally altered. Standard post-surgical care thus restores the gross balance of coordination within 6 months, while the underlying architecture remains reorganized at that mid-recovery time-point-and, on at least one measure, consolidates further. Whether this reorganization reflects protective motor strategies, and whether training targeted at segmental differentiation would reverse it, are hypotheses that the present observational data raise but cannot test.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1916345"},"PeriodicalIF":3.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13683197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytes at the interface of peri-ictal breathing dysfunction and SUDEP.","authors":"Isato Fukushi, Isamu Ozaki, Mieczyslaw Pokorski, Yasumasa Okada","doi":"10.3389/fnetp.2026.1955271","DOIUrl":"10.3389/fnetp.2026.1955271","url":null,"abstract":"<p><p>Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related mortality and is typically characterized by a terminal cascade of respiratory failure, cardiac arrhythmia, and cerebral suppression. Although epilepsy has long been regarded as a neuron-proprietary disorder, accumulating evidence indicates that glial cells, particularly astrocytes, play pivotal roles in both epileptogenesis and the progression to SUDEP. Astrocytes maintain neuronal homeostasis by regulating extracellular potassium through the inwardly rectifying potassium channel Kir4.1 and by clearing extracellular glutamate. Impairment of these homeostatic functions, together with reactive astrogliosis and the release of pro-inflammatory cytokines, including interleukin-1β and tumor necrosis factor-α, promotes neuronal hypersynchrony and lowers the seizure threshold. Severe hypoxia, a critical consequence in respiratory disturbance, sequentially activates microglia and astrocytes, thereby facilitating seizure generation and further depression of respiratory output. Furthermore, seizure propagation or spreading depolarization into brainstem respiratory centers, including the pre-Bötzinger complex and the nucleus tractus solitarius, may induce fatal central apnea or upper airway obstruction. Neuropathological evidence of neuronal and astrocytic loss in the ventrolateral medulla further suggests that chronic brainstem dysfunction increases susceptibility to respiratory failure. Experimental studies demonstrate that pharmacological inhibition of astrocytic activation delays hypoxia-induced seizures and respiratory arrest, highlighting astrocytes as a potential therapeutic target. A deeper understanding of neuron-glia interactions within the active neural milieu will facilitate the development of novel preventive strategies for SUDEP.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1955271"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149217519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioenergetic impedance: a network physiology framework for stress adaptation, maladaptation, and recovery.","authors":"Torsak Tippairote, Pruettithada Hoonkaew","doi":"10.3389/fnetp.2026.1967461","DOIUrl":"https://doi.org/10.3389/fnetp.2026.1967461","url":null,"abstract":"<p><p>Stress adaptation depends not only on challenge magnitude but on the capacity of physiological systems to conduct, transform, buffer, and recover energetic demands. We propose <i>bioenergetic impedance</i> as a Network Physiology construct describing the time-dependent constraint on energetic throughput and recovery that arises when energetic pressure exceeds available biological capacity. Resistance, delay, congestion, and buffering burden may reflect mechanisms or manifestations of this mismatch, whereas compensatory rerouting may represent an adaptive response to constrained throughput. At the cellular level, substrate congestion and redox backpressure provide plausible mechanistic anchors, while metabolic rerouting and mitochondrial stress signaling may represent compensatory or signaling responses through which local energetic constraints may be accommodated or communicated. Their physiological consequence depends critically on reversibility. In <i>adaptive impedance cycling</i>, challenges that transiently exceed available capacity produce impedance followed by recovery, restoration or adaptive recalibration of flexible cross-system organization, and potentially expanded reserve. In <i>impedance lock-in</i>, repeated or unresolved challenge produces incomplete recovery, persistent residual constraint, compensatory allocation, reduced network flexibility, and constrained adaptive reserve. The framework therefore places recovery dynamics at the center of resilience and generates a testable prediction: adaptive states should show temporary, context-appropriate reconfiguration of cross-system interactions followed by restoration of flexible network organization, whereas maladaptive states should show incomplete recovery and persistent or functionally inappropriate network reconfiguration. Bioenergetic impedance thus provides a systems-level framework linking cellular energetic constraints with stress adaptation, maladaptation, and recovery across physiological networks.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1967461"},"PeriodicalIF":3.1,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain-heart coupling in tourette syndrome: a precision functional mapping study of discordant siblings.","authors":"Sana A Ali, Damion V Demeter, Abigail R Baim, Jonathan Ahern, J H Ben Ahn, Sarah E Chang, Emily M Koithan, Sujin Park, Benjamin L Smarr, Deanna J Greene","doi":"10.3389/fnetp.2026.1881914","DOIUrl":"10.3389/fnetp.2026.1881914","url":null,"abstract":"<p><p>Tourette syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics that are modulated by internal physiological state and interoceptive state, including premonitory urges and associated changes in short-timescale parasympathetic variability. Since tic expression is thought to be linked to fluctuations in autonomic state, understanding how brain networks integrate physiological signals may provide insight into the neural mechanisms contributing to tic generation and suppression. In recent years, there has been increasing interest in understanding interactions between the brain and autonomic physiology, given their shared central role in shaping cognition, emotion, and behavior. Methodological advances have enabled the study of brain-heart coupling, yet much of this work has focused on static or region-based approaches, limiting insight into how autonomic fluctuations are integrated within dynamic, large-scale brain networks. Here, we examined time-resolved brain-heart interactions using densely sampled resting-state fMRI data and concurrent pulse oximetry in two sibling pairs (n = 4) discordant for Tourette syndrome (TS). Using two targeted network analyses organized around interoceptive/urge awareness and inhibitory control/action regulation processes, we quantified coupling between pulse-derived RMSSD and between-network functional connectivity using sliding-window analyses and Bayesian linear mixed-effects models. We observed marked individual variability in functional network organization and autonomic measures. The most consistent observation was a pattern of opposing coupling directions between individuals with and without TS: those with TS showed positive associations between pulse-derived RMSSD with connectivity between internal-state and attentional networks, as well as among action-related systems, while unaffected siblings showed positive associations along broader integrative pathways linking internal-state and action-control networks. These preliminary findings generate hypotheses regarding individualized patterns of brain-heart coupling in TS and illustrate the potential value of integrating individualized network mapping with time-resolved physiological measures in clinical populations.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":"6 ","pages":"1881914"},"PeriodicalIF":3.1,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}