[I dedicate this post to my mentors, Kate Wagner, MS and US BRMT Distributor, and Dave Boyland, DPT, and to the greater BRMT community. I look forward to your thoughts, feedback and deeper conversations on this fascinating topic.]
This is the thirteenth post in a series on primitive reflexes and Blomberg Rhythmic Movement Training (BRMT). If you’re new here, start with the Field Guide to Primitive Reflexes for the big picture. The previous post, From Pain to Pattern, established what retained reflexes do to the body over time. This post asks how rhythmic movement (BRMT) may resolve it.
Throughout this series, we’ve established a detailed picture of what retained primitive reflexes do. They hold the body in chronic tension patterns. They keep the autonomic nervous system locked in survival mode. They drive postural asymmetry, joint degeneration, sensory overwhelm, emotional dysregulation, and chronic pain. We’ve mapped many of the foundational reflexes to their specific territory in the body and traced the cascade from brainstem to bone. And, most importantly, I hope this series of posts, so far, has helped drive home the fact that all of these responses are NOT failures that need fixing or blocking, but rather, they’re natural responses of a system that is working the way it was designed to work, in response to the inputs it’s received.
That said, we haven’t yet answered the question that matters most: why does it work?
Why do gentle, rhythmic movements (rocking on the floor for one to two minutes a day) resolve patterns that years of massage, stretching, chiropractic adjustment, and medication couldn’t fully reach? What is the mechanism by which something so simple addresses something so deep?
This post proposes an answer. It’s a hypothesis; a framework drawn from converging lines of research in fascial science, mitochondrial biology, and brainstem neurophysiology. It’s grounded in established science, but the synthesis itself is original. I’m not claiming proof. I’m proposing a mechanism that fits the evidence, that explains what practitioners observe clinically, and that invites further investigation.
The mechanism involves three systems that are rarely considered together. Until recently. Fascia, mitochondria, and the brainstem. I call it the fascia-mitochondria-brain axis, and it may explain why rhythm heals.
Three Systems, One Axis
To understand the proposed mechanism, we need to see each system clearly before we can see how they connect.
System 1: Fascia - The Body’s Signaling Network
Throughout most of the history of medicine, fascia was treated as packing material, the cling wrap between the real structures. It was dissected away in anatomy labs to reveal the muscles, bones, and organs underneath. It was, in the most literal sense, what you threw away to see “what mattered”. As a former gross anatomy assistant professor at the local medical school, I’m very guilty of this behavior!
That picture has changed dramatically in the last two decades. The research of Helene Langevin, Donald Ingber, Robert Schleip, Thomas Myers, James Oschman, Joanne Avison, and others has established that fascia is not inert wrapping. It’s a continuous, body-wide, three-dimensional network of connective tissue that touches every muscle, every organ, every nerve, every blood vessel, and every cell in the body. It is, by volume and surface area, the largest organ system in the human body (Langevin, 2006; Schleip et al., 2012).
But what makes fascia relevant to our question isn’t its size. It’s what it does.
The groundwork for understanding fascia as an electrical system was laid decades before the current wave of fascial research, by Robert O. Becker, MD, an orthopedic surgeon and electrophysiology researcher who spent his career demonstrating that the body runs on a semiconducting direct-current (DC) electrical system. Becker did this work at Upstate Medical University in Syracuse, New York (the same institution where, years later, I would teach gross anatomy and neuroanatomy to medical students, walking the same halls where his research quietly rewrote the rules). Working from a suggestion by Albert Szent-Györgyi (the Nobel laureate who discovered Vitamin C), Becker investigated whether the molecular structure of living tissue could support semiconduction, and found that it could. His research identified a body-wide DC signaling network carried through perineural cells and connective tissue, showed that electrical polarity at wound sites determines whether the body regenerates or scars, and demonstrated that bone functions as a piezoelectric transducer, converting mechanical stress into electrical signals that guide remodeling (Becker & Selden, 1985; Becker, 1990). Becker's work established what the current generation of fascia researchers has confirmed at higher resolution: the body's connective tissue is not inert wrapping. It's a living electrical system.
Fascia is mechanosensitive: it detects and responds to mechanical force. When you press, pull, stretch, compress, or rhythmically load fascial tissue, the fibroblasts embedded within it change shape, alter their gene expression, and modify the mechanical properties of the surrounding matrix. These responses propagate across the tissue through a process called mechanotransduction: the conversion of mechanical signals into biochemical ones (Langevin, 2006; Ingber, 2008).
Fascia’s primary structural protein, collagen, has semiconductive and piezoelectric properties. This means it can conduct electrical charge (collagen fibers have been shown to support electron transport across measurable distances (Kolay et al., 2019)), and it generates electrical signals in response to mechanical stress, a property first demonstrated in bone by Fukada and Yasuda (1957), extended by Becker’s work showing that bone’s piezoelectric properties guide its own remodeling in response to load (Becker & Selden, 1985), and since confirmed across connective tissues throughout the body (Kamel, 2022; Oschman, 2016). These are measurable, reproducible biophysical properties. The fascial network is, in a very real sense, a body-wide bioelectrical communication system, a living matrix that transmits signals at speeds and across distances that purely chemical signaling cannot achieve (Oschman, 2016). Intracellular electric fields have been directly mapped using nanosized voltmeter probes, confirming that cells maintain and respond to electrical gradients that are generated, in part, by the mechanical and piezoelectric activity of the surrounding matrix (Tyner et al., 2007).
When fascia is healthy (hydrated, elastic, and well-loaded), this signaling network functions fluidly. Energy and information move through the connective tissue matrix with ease. Cells receive coordinated signals about load, position, and the state of the tissue around them. The body’s capacity to coordinate repair, regulate inflammation, and maintain structural integrity depends in part on this fascial communication network (Avison, 2021; Schleip et al., 2012).
When fascia is unhealthy (dehydrated, thickened, adhered under chronic tension), its conductivity degrades. The tissue becomes denser, less elastic, less responsive. Signals that should propagate fluidly across the body get restricted, fragmented, blocked. The fascial network stops acting as a conductor and begins acting as an insulator, resulting in a disruption of precisely the semiconducting system that Becker identified as fundamental to healing, regeneration, and biological self-regulation (Becker & Selden, 1985; Becker, 1990). This is what chronic, reflex-driven tension does to the connective tissue over time: it doesn’t just tighten muscles. It degrades the body’s capacity to communicate with itself (Oschman, 2016; Myers, 2014).
System 2: Mitochondria - The Cell’s Environmental Sensors
Mitochondria are known as the cell’s powerhouses, the organelles that produce ATP, the molecule the body uses as energy currency. This is true but incomplete. Mitochondria are also environmental sensors. They don’t just generate energy, they decide what the energy is used for based on signals from the cellular environment.
Robert Naviaux’s Cell Danger Response (CDR) research has fundamentally reframed how we understand mitochondrial function. Naviaux describes a metabolic state in which mitochondria, upon detecting danger signals (chronic stress, inflammation, infection, toxins, unresolved threat), shift from their normal function (energy production, tissue repair, cellular regeneration) to a defensive posture. In CDR mode, mitochondria prioritize survival: they reduce ATP production, increase reactive oxygen species, release extracellular nucleotides that signal danger to neighboring cells, and suppress the metabolic pathways that would otherwise be driving healing (Naviaux, 2014; Naviaux, 2019a, 2020). Mitochondria are not isolated powerhouses, they form coordinated networks, communicating across cells through regulated membrane junctions and even transferring between cells entirely, rewiring the redox signaling and metabolic capacity of their new hosts (Picard et al., 2015; Wang et al., 2026). They are, increasingly, understood as a nexus point where psychological experience, environmental signals, and cellular metabolism converge (Kelly et al., 2024).
The CDR is adaptive in the short term. It’s the cellular equivalent of the body’s stress reflexes: when danger is present, the system shifts from growth and repair to protection and defense. The problem, as with retained reflexes, is when the shift doesn’t reverse. When the danger signal persists, or when the all-clear is never received, the CDR becomes chronic. The mitochondria stay in defense mode. The healing cycle stalls. Tissue repair slows. Inflammation becomes self-perpetuating. The body ages, degenerates, and accumulates damage not because it can’t heal, but because the cellular machinery responsible for healing has been diverted to defense (Naviaux, 2019a, 2023).
Naviaux identifies three sequential stages of the CDR (CDR1, CDR2, CDR3), each governed by different metabolic pathways, and describes the transition out of the CDR, into what he calls salugenesis, the healing cycle, as requiring a specific sequence of metabolic shifts. The system doesn’t just “turn off” defense mode. It transitions through a series of stages, each requiring specific inputs, to arrive at restored function (Naviaux, 2019b, 2023).
Here’s what’s critical for our axis: mitochondria are not walled off from the body’s mechanical environment. They respond directly to what’s happening in the extracellular matrix, the fascial world outside the cell. A 2024 study published in Cell by Zhang et al. provided striking evidence for this connection. The researchers demonstrated that degradation of hyaluronan, a key component of the extracellular matrix, directly triggered mitochondrial remodeling, activated mitochondrial stress responses, and augmented immune signaling. In other words, changes in the matrix surrounding the cell were communicated to the mitochondria, which responded by reorganizing their function. The extracellular matrix doesn’t just surround cells passively, it integrates mitochondrial homeostasis (Zhang et al., 2024).
This finding is essential to our axis. It establishes a direct, experimentally demonstrated link between the state of the connective tissue matrix and the functional state of the mitochondria. When the matrix is healthy and intact, mitochondrial function is maintained. When the matrix is degraded or disrupted, as it is under chronic reflex-driven tension, mitochondria respond with stress signaling and functional reorganization.
Additional research has shown that external mechanical forces applied to cells promote changes in mitochondrial dynamics (fission, fusion, and morphological reorganization). Fluid flow and rhythmic loading stimulate mitochondrial ATP production. The cytoskeleton transmits mechanical forces directly to the mitochondria, independent of chemical signaling cascades (Guo et al., 2022; Yamamoto et al., 2018). Mechanical input doesn’t just move the body. It reaches the mitochondria. And what kind of mechanical input the mitochondria receive (chaotic vs. rhythmic, excessive vs. gentle, threatening vs. safe) may influence whether they stay in defense mode or begin the transition to healing.
System 3: The Brainstem - The Regulatory Hub
The brainstem is the oldest, deepest structure of the brain. It controls the functions that keep you alive without your conscious involvement: heart rate, breathing, blood pressure, muscle tone, arousal, and the autonomic nervous system. It’s the level of the brain where primitive reflexes originate and where they’re regulated.
The brainstem is also the primary relay station for vestibular (i.e. balance) information. When the otolith organs and semicircular canals in the inner ear detect head movement (tilt, rotation, acceleration, the pull of gravity), they send signals via the vestibulocochlear nerve directly to the vestibular nuclei in the brainstem. These nuclei are one of the most densely connected regions in the entire brain. They project to the spinal cord (regulating posture and muscle tone via the vestibulospinal tracts), to the eyes (stabilizing vision via the vestibulo-ocular reflex), to the cerebellum (coordinating movement and timing), and, most importantly, to the autonomic centers of the brainstem, including the dorsal motor nucleus of the vagus nerve and the nucleus of the solitary tract (Purves et al., 2001). Think PARASYMPATHETIC outflow…
This last connection is the one that matters most for our axis. The vestibular nuclei have direct neural projections to the autonomic regulatory centers that control the vagus nerve. This means that vestibular input (i.e. information about how the head is moving, how the body is oriented, what kind of motion is happening) directly modulates autonomic state. It influences whether the nervous system is in sympathetic (fight-or-flight) or parasympathetic (rest-repair-digest) mode.
Research has demonstrated that vestibular stimulation modulates sympathetic and parasympathetic activity through descending projections from the vestibular nuclei to the vagal motor nucleus and ascending projections to the parabrachial complex. Gentle, predictable, rhythmic vestibular input supports parasympathetic activation; it tells the autonomic nervous system that the environment is safe, that the body is moving in a predictable way, that there is no threat requiring mobilization (Yates et al., 2014). This is why rocking calms a baby. It’s why swaying eases anxiety. It’s why rhythmic movement feels soothing in a way that’s prior to thought. The brainstem is receiving vestibular information that says safe, rhythmic, predictable, and it responds by shifting the autonomic needle toward parasympathetic, toward vagal tone, toward regulation.
The Axis: How the Three Systems Connect
Now we can see the proposed mechanism.
When a person lies on the floor and performs the gentle, rhythmic, rocking movements of BRMT, three things happen simultaneously:
Pathway 1: Rhythm → Brainstem → Autonomic Shift
The rhythmic movement stimulates the vestibular organs in the inner ear. The otoliths detect the slow, predictable rocking. This information travels via the eighth cranial nerve to the vestibular nuclei in the brainstem. The vestibular nuclei project to the vagal motor nucleus and the nucleus of the solitary tract. The autonomic needle shifts toward parasympathetic. Vagal tone increases. Heart rate settles. Breathing deepens. Cortisol production decreases. The brainstem (the same level of the brain where the primitive reflexes live) receives the signal: safe. Rhythmic. Predictable. No threat.
This is the “all-clear” that the retained reflex has been preventing the brainstem from sending. The rhythm bypasses the cortex entirely. It speaks directly to the brainstem, in the brainstem’s own language.
Pathway 2: Rhythm → Fascia → Mechanotransduction → Mitochondria
Simultaneously, the rocking movement is loading the fascial network. The body’s weight shifts rhythmically against the floor. The connective tissue experiences gentle, cyclical compression and release. This mechanical input is transduced by the fibroblasts in the fascia through integrins, the transmembrane receptors that connect the extracellular matrix to the cell’s internal cytoskeleton, into biochemical signals inside the cell (Ingber, 2008; Langevin, 2006).
The piezoelectric properties of the collagen in the fascia generate electrical signals in response to the rhythmic loading. The semiconductive properties of the fascial matrix conduct those signals across the tissue. The fascia that has been thickened and adhered under years of reflex-driven chronic tension begins to receive the specific kind of input that it needs to restore its elasticity and conductivity: gentle, rhythmic, sustained, non-threatening mechanical loading.
And those mechanical signals reach the mitochondria through multiple converging routes. As Zhang et al. (2024) demonstrated, the extracellular matrix directly integrates mitochondrial homeostasis; changes in the matrix are communicated to the mitochondria, which respond by reorganizing their function. But how, specifically, does a rocking movement on the floor translate into changes at the mitochondrial membrane?
Direct mechanical transmission. The integrins that detect fascial loading don’t just generate chemical signals. They physically transmit force through the cytoskeleton (the internal scaffolding of actin filaments and microtubules that gives the cell its structure). Mitochondria are physically tethered to this cytoskeletal network. When the cytoskeleton transmits mechanical force, the mitochondria experience it directly, their membranes deform, their morphology shifts, and their dynamics change (Guo et al., 2022; Ingber, 2008). This is a direct, physical, mechanical pathway from the floor through the fascia through the cell membrane through the cytoskeleton to the mitochondrial membrane. No chemical intermediary required.
Calcium signaling. Mechanical loading also opens mechanosensitive ion channels in the cell membrane, particularly the Piezo1 and Piezo2 channels. When these channels open, calcium ions flow into the cell. Calcium is one of the primary regulators of mitochondrial ATP production: it activates key dehydrogenases in the Krebs cycle (pyruvate dehydrogenase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase), increasing NADH production, feeding more electrons into the electron transport chain, driving more protons across the inner mitochondrial membrane, spinning ATP synthase faster, and producing more ATP. Yamamoto et al. (2018) demonstrated this directly: fluid flow and shear stress across cell surfaces augmented mitochondrial ATP generation through this mechanosensitive calcium pathway. Rhythmic loading creates gentle waves of interstitial fluid flow through the fascial matrix; the tissue isn’t solid, it’s a fluid-filled network. And those waves activate calcium signaling in the cells embedded within it.
Piezoelectric charge. The collagen under rhythmic loading generates rhythmic electrical pulses (Fukada & Yasuda, 1957; Kolay et al., 2019). Mitochondria produce ATP through a proton gradient across their inner membrane, what we know as a membrane potential. External electrical fields, including those generated by piezoelectric collagen, can influence that membrane potential, either directly or through modulation of voltage-sensitive ion channels in the cell. Rhythmic loading generates an oscillating electrical signal; static loading generates a monotone.
The quality of the signal matters as much as its presence. The mitochondria have been in defense mode, holding the CDR, waiting for conditions that signal safety. The rhythmic mechanical input (arriving through a fascial network that is beginning to soften and restore conductivity, generating cyclical calcium pulses and oscillating electrical fields) is precisely the kind of patterned, non-threatening input that accumulates the conditions for transition.
Pathway 3: The Convergence - From Defense to Healing
The two pathways converge. The brainstem receives the vestibular signal and shifts the autonomic state toward parasympathetic. The fascia receives the mechanical signal and begins restoring its signaling capacity. The mitochondria receive both the autonomic shift (via the vagus nerve’s influence on cellular metabolism) and the mechanical signal (via mechanotransduction through the cytoskeleton). The conditions for exiting the Cell Danger Response begin to accumulate:
The brainstem sends the all-clear from above.
The fascia sends the all-clear from below.
The mitochondria, sitting at the intersection, receiving signals from both directions, begin the transition from CDR to salugenesis.
From defense to repair. From inflammation to resolution. From holding to healing.
Why Rhythm? Why Gentle? Why So Little?
The overarching motto in BRMT is “less is more” - To quote Daniel Wilke, DC: “The pause is as important as the push”.
I have just laid out a proposed mechanism for how it could be that rhythmic movement training (BRMT) may be working: not a single pathway but a convergent axis; three systems that normally operate in isolation coming into alignment through one specific kind of input: gentle, rhythmic, whole-body movement.
The specificity of BRMT (one to two minutes per day, gentle, rhythmic, with rest periods between sessions) makes more sense in light of this axis.
Why rhythm? Because all three signaling pathways respond differently to rhythmic vs. static vs. chaotic mechanical input; and the difference matters.
Rhythmic loading creates cyclical calcium pulses, cyclical piezoelectric charge, and cyclical interstitial fluid flow. The mitochondria can entrain to a rhythm; they can synchronize their dynamics to the oscillating signal. Picard et al. (2015) showed that mitochondria coordinate across cells at regulated membrane junctions, meaning they’re already organized to respond to patterned, coordinated signals.
Static loading (the kind produced by chronic reflex-driven muscle tension) generates a flat, unchanging signal (i.e. the monotone referenced above). The mechanosensitive ion channels adapt and stop responding. The calcium signal plateaus. The piezoelectric charge is constant rather than oscillating. The mitochondria don’t receive the cyclical input they need; they receive a monotone. This is precisely the mechanical environment that a retained reflex creates: sustained, unvarying contraction, day after day, year after year. The fascia under chronic tension isn’t being rhythmically loaded. It’s being held. And this is a beautiful response from a system under threat of falling apart! It comes in handy at certain times, and under certain circumstances. But when it’s not allowed to complete, to resolve, then the system runs into an existence in a monotone state.
Chaotic or excessive loading (intense exercise, forceful manipulation, trauma) pushes calcium influx past the stimulatory window into the inhibitory window, following the biphasic dose response (Huang et al., 2009). Too much calcium is cytotoxic. Too much force activates the CDR rather than resolving it.
Gentle, rhythmic, brief loading sits precisely in the sweet spot: enough to open the channels and generate the signals, patterned enough for the mitochondria to entrain, brief enough to stay in the stimulatory window, and followed by a pause that allows processing. BRMT replaces the monotone of chronic tension with a pulse, and the mitochondria respond to the pulse because that’s what they’re designed to respond to. Rhythm is the language of biological systems, from heartbeat to breath to circadian cycle.
The vestibular system confirms this from the other direction: it is specifically tuned to detect rhythmic, oscillatory motion. It evolved for this. And the fascial system responds to cyclical loading in ways it doesn’t respond to static stretching or abrupt, forceful input. Rhythm is the common language that all three systems understand.
Why gentle? Because any input the nervous system reads as threatening reactivates the very protective patterns you’re trying to help resolve. Forceful manipulation, intense exercise, aggressive stretching, these can trigger the Moro, activate the Tendon Guard, and reinforce the CDR. Gentle input signals safety. It tells the brainstem, the fascia, and the mitochondria that this is not an emergency. That the body can afford to soften.
Why so little? Because the transition from CDR to salugenesis is not instantaneous. Naviaux describes it as a staged process, with each phase requiring time and specific metabolic conditions. Flooding the system with input doesn’t accelerate the transition; it can overwhelm it. This is consistent with the biphasic dose response documented across biological systems: low-dose stimulation promotes healing and repair, while high-dose stimulation inhibits it (Huang et al., 2009). One to two minutes provides the signal. The rest period, the hours and days between sessions, provides the processing time. The body integrates at its own pace, in its own sequence, layer by layer. The pause is not empty space. It’s where the integration happens.
What This Framework Explains
If this axis is correct, if rhythmic movement simultaneously reaches the brainstem (via vestibular input), the fascia (via mechanotransduction), and the mitochondria (via both pathways converging), then several observations that are otherwise difficult to explain begin to make sense.
Why reflex integration works when downstream interventions don’t hold. Massage, chiropractic, and stretching address the musculoskeletal consequences of the reflex but don’t reach the brainstem where the reflex originates, or the mitochondria where the healing cycle is stalled. BRMT addresses all three levels simultaneously.
Why the movements are done on the floor. The floor (or a comparable, relatively firm surface, such as a massage table) provides the surface against which the body’s weight creates the fascial loading. It also supports the body fully, which reduces the vestibular complexity and allows the brainstem to focus on the rhythmic signal rather than on managing balance. The floor is the simplest, safest mechanical environment available.
Why results are gradual and cumulative. Each session sends the signal. Each rest period allows the system to process it. The CDR transition happens in stages. The fascial remodeling takes time. The reflex integration progresses layer by layer. What practitioners observe (tension easing, then posture shifting, then pain diminishing, then deeper patterns emerging) mirrors what a staged biological transition would look like.
Why emotional content surfaces during physical work. If the fascia is a signaling network, and if chronic tension has been restricting that network’s conductivity, then restoring conductivity may release signals that have been stored or suppressed in the tissue. The emotions, dreams, and memories that often surface during BRMT aren’t psychological artifacts, they may be the informational content of a fascial network that is coming back online.
Why the same simple movements help such a wide range of conditions. Chronic pain, anxiety, ADHD, autism-spectrum presentations, emotional dysregulation, postural dysfunction, vision problems, learning difficulties, these look like completely different conditions. But if they all share a common substrate, i.e. retained reflexes driving chronic CDR, fascial restriction, and autonomic dysregulation, then an intervention that addresses the substrate would be expected to influence all of them. Not because it treats each condition specifically, but because it addresses the foundational disruption they all share.
Beneath the Mechanism - The Importance of the In-Between
There’s a temptation, at this point, to stop. We’ve described the axis. We’ve traced the pathways. We’ve explained why rhythm, why gentle, why so little. We have a mechanism.
But I want to resist that stop because stopping at “mechanism” is exactly the habit of mind that made this axis invisible for over a century. The last hundred years of biomedical science have been built on a mechanistic, reductionist frame: isolate the part, describe the pathway, name the molecule. And that frame has produced extraordinary knowledge. But it has also produced a blind spot: it sees the parts and misses what connects them. It sees the chemistry and misses the physics. It sees the molecule and misses the field.
As Iain McGilchrist has argued, the Western intellectual tradition has increasingly privileged the left hemisphere’s way of knowing, the mode that isolates, categorizes, and grasps at fixed things at the expense of the right hemisphere’s capacity to perceive wholes, relationships, and the living connections between things (McGilchrist, 2009). In biology, this shows up as the habit of naming the parts while ignoring the between, the field, the wave, the relationship that gives the parts their meaning. But there are no particles without the wave that connects them. There is no mitochondrion without the matrix it’s embedded in, no brainstem without the body it regulates, no fascia without the rhythm that keeps it alive. The axis proposed in this post is not three things connected by pathways. It’s one relational field, seen from three vantage points.
The processes described in this post are not purely mechanical or chemical. They are, at their foundation, quantum processes. And naming that isn’t an exotic addition to the model; it’s a recognition of what the model is actually made of:
Electron transfer in the mitochondrial electron transport chain (ETC) involves quantum tunneling. Electrons don’t hop from carrier to carrier classically, they pass through energy barriers by tunneling, a quantum-mechanical phenomenon that is well-established in biochemistry and increasingly recognized as essential to the efficiency of oxidative phosphorylation (Qaswal, AB et al., 2025). The efficiency of ATP production depends on tunneling rates that are sensitive to the geometry and physical environment of the protein complexes, including mechanical forces transmitted through the cytoskeleton from the fascia.
The electron carriers are chromophores; they interact with light. NADH absorbs UV light at 340 nm and has a quantum yield for electron generation of over 40% upon photoexcitation. FADH₂ absorbs blue light. Cytochrome c oxidase absorbs red and near-infrared, which is the basis for photobiomodulation (Hamblin, 2018). Mitochondria also emit photons (biophotons) as byproducts of electron transfer. The molecules at the heart of energy production are photonically active, absorbing and emitting light as part of their normal function. Light isn’t peripheral to mitochondria. It’s intrinsic to how they work. I would go further and say that light comes first, then, and only if we’re in the presence of the correct light, comes the calcium signaling I referenced above. First light. Then calcium.
Collagen doesn’t just transmit force, it transmits charge. The piezoelectric properties of collagen mean that rhythmic mechanical loading generates rhythmic electrical pulses (Fukada & Yasuda, 1957; Kolay et al., 2019). Moving charge generates a magnetic field. Radical pairs in the ETC (pairs of molecules with quantum-correlated electron spins) are sensitive to magnetic fields, even weak ones (Binhi & Rubin, 2022; Krylov & Osipova, 2023). The quality of the mechanical input (rhythmic vs. static) may influence the spin relationship of the radical pairs and thereby the direction of electron transfer.
The water in fascia is not a passive solvent. Gerald Pollack’s research has demonstrated that water at hydrophilic surfaces (exactly the kinds of surfaces that collagen and proteoglycans provide throughout the fascial matrix) forms a structured, negatively charged, energy-storing fourth phase (exclusion zone, EZ, water) with measurably different properties from bulk water (Pollack, 2013). This EZ water is generated by infrared radiation, which mitochondria produce as metabolic heat (Chai et al., 2009; Sommer, 2020). Mitochondria also produce water directly as the terminal product of oxidative phosphorylation. If this metabolic water emerges already structured, then mitochondria aren’t just energy producers, they’re generating the very medium that maintains the fascial matrix’s electrical conductivity.
For deeper, more comprehensive dives into how these 4 things work and may be contributing to this hypothetical model, head on over HERE.
When chronic, reflex-driven tension compresses the fascia, it degrades this water structuring, reduces conductivity, and impairs signaling. When rhythm restores flow and loading, the structured water rebuilds, the conductivity returns, and the signaling environment that the mitochondria depend on comes back online. This is a feedback loop that operates beneath chemistry, at the level of physics: light, charge, water structure, and spin.
I don’t raise these points to overwhelm the framework with complexity. I raise them because stopping at the mechanistic description (calcium channels, integrins, ATP synthase) recreates the very reductionism that kept the fascial network, the Cell Danger Response, and retained reflexes invisible to mainstream science for decades. The mechanism described in this post is real. But it’s not the bottom of the stack. Underneath the biochemistry, there is biophysics. Underneath the signaling pathways, there are quantum processes. And understanding that, understanding that healing operates at levels deeper than a molecular mechanism, changes not just what we think is happening, but what we think is possible.
For those who want to explore these threads more deeply (fourth phase water, biophotons, electron spin dynamics, and the quantum biology of mitochondria), this work continues in a dedicated series I’m co-developing with Nikko Kennedy, from Brighter Days, Darker Nights: Mitochondria as Environmental Antennae: The Fascia-Mitochondria-Brain Axis. It lives on this Substack and goes where this post opens the door.
And if you are not subscribed to Nikko’s brilliant Substack, today’s the day!
A Hypothesis, Not a Conclusion
I want to be clear about what this is and what it isn’t.
This is a proposed framework. It synthesizes converging lines of research (from fascial science, mitochondrial biology, vestibular neurophysiology, and clinical observation) into a coherent mechanism that explains what practitioners see. Each individual line of research is well-established. The synthesis is original, and it requires further investigation.
I’m not claiming that this mechanism has been experimentally verified as a unified pathway. What I’m saying is that the research supports each component independently, that the clinical observations are consistent with the proposed mechanism, and that the framework generates testable predictions. If rhythmic movement works through this axis, then we should be able to measure changes in fascial conductivity, mitochondrial function, vagal tone, and CDR markers before and after BRMT sessions. Those measurements would either support or refute the hypothesis.
What I’m also saying is that the absence of a verified mechanism doesn’t mean the clinical effects aren’t real. Practitioners worldwide observe consistent, reproducible changes in clients who do this work. Children whose attention transforms. Adults whose chronic pain resolves. Trauma survivors whose nervous systems finally settle. These observations are data. They deserve a mechanistic explanation. This framework is an attempt to provide one.
The fascia-mitochondria-brain axis says: rhythm reaches the brainstem through the vestibular system and the connective tissue through mechanical loading. The brainstem shifts the autonomic state toward safety. The fascia begins restoring its signaling capacity. The mitochondria transition from defense to repair. And the body, which was never broken, only held in a pattern of protection, begins to heal.
Not because you forced it. Because you gave it the signal it was waiting for.
Like I always say:
If you’re recognizing these patterns and want to explore whether primitive reflex integration might be relevant for you or your child, consider connecting with a certified BRMT practitioner. You can find more information at brmtusa.com. Not in the US? Check out blombergrmt.com.
I am a BRMT consultant and I’d be more than happy to connect with you and answer any questions you may have. Feel free to book a Complimentary Discovery Call so we can chat.
Learn This Work From the Inside Out
If this series has you wanting to move beyond reading and into practice, I’m teaching BRMT Level 1 and BRMT Level 2 this fall. In BRMT Level 1 you’ll learn the foundational reflexes, how to test for them, and the specific rhythmic movements and isometric techniques used to integrate them. In Level 2 you’ll learn the stress reflexes and how to support a system that arrives in full fight-flight or freeze. Taking Level 1 is a pre-requisite for Level 2. Aside from that, come as you are. No additional training needed! Whether you’re a parent, therapist, educator, or someone who simply recognizes these patterns in your own body, these courses give you the tools to work with them directly. No prerequisites. Just curiosity and a willingness to get on the floor.
References
Avison, J. (2021). Yoga, Fascia, Anatomy and Movement. (2nd ed.). Handspring Publishing.
Binhi, V. N., & Rubin, A. B. (2022). Theoretical concepts in magnetobiology after 40 years of research. Cells, 11(2), 274. https://doi.org/10.3390/cells11020274
Becker, R. O., & Selden, G. (1985). The Body Electric: Electromagnetism and the Foundation of Life. William Morrow.
Becker, R. O. (1990). Cross Currents: The Perils of Electropollution, the Promise of Electromedicine. Jeremy P. Tarcher.
Blomberg, H. (2015). The Rhythmic Movement Method: A Revolutionary Approach to Improved Health and Well-Being. CreateSpace Independent Publishing Platform.
Chai, B., Yoo, H., & Pollack, G. H. (2009). Effect of radiant energy on near-surface water. The Journal of Physical Chemistry B, 113(42), 13953–13958. https://doi.org/10.1021/jp908163w
Fields, R. D., & Burnstock, G. (2006). Purinergic signalling in neuron-glia interactions. Nature Reviews Neuroscience, 7(6), 423–436. https://doi.org/10.1038/nrn1928
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