The Big Takeaway

The reverse hyper isn’t a single exercise. In our programming, it’s a six-exercise conjugate sequence, and the pendulum swing everyone associates with the machine is exercise five, not exercise one. People who skip ahead bring an unresolved deficit straight to the most demanding version of the movement, and when it goes wrong, they blame the machine.

What We Cover in This Episode

• The Six-Exercise Conjugate Sequence: The reverse hyper program gates progression through Soviet sporting mastery principles—you don’t drop exercise one when you master exercise two, you run them in conjugation. This is true conjugate sequencing, not linear periodization.

• Why Exercise Five Looks Like “The” Reverse Hyper: The pendulum swing most people picture when they think of the reverse hyper is the fifth exercise in the sequence. Starting there means skipping four prerequisite stages—which is why some people try it, get nothing, and conclude the machine doesn’t work for them.

• A Real Case: When the Sciatic Nerve Is the Rate Limiter: A passive straight leg hip flexion assessment revealed restriction in the popliteal space and calf—not the hamstring. That finding identifies nervous tissue, not connective tissue, as what’s stopping the movement, with direct implications for whether this person is ready for pendulum-based loading.

• Why the Pelvis-Hip Uncoupling Has to Happen Passively First: The whole point of the reverse hyper is uncoupling the pelvis and thigh. If that uncoupling can’t happen on the table in a passive assessment, it won’t happen under load on the pendulum — and the structures absorbing that failed uncoupling (facet joints, lumbar spine) take the hit instead.

• How Louie Simmons’ Own History Shaped Exercise One: Louie’s original 1970s sacral drive motion—the one that led to him to rehabilitate this own back injury—was refined into segmental flexion and extension with a four-second HIMA hold at the top. That’s not a simplified warm-up. It’s a deliberately engineered entry point built from the lineage of the exercise itself.

The full case breakdown — including exactly how this finding changes the onboarding path — is below for paid subscribers.

Pendulum Prerequisites: A Real Case for Why You Don’t Start There

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We’ve built Point A around four pillars: Health History, Joint Assessment1, Treatment & Training History, Performance History.

Each one answers a version of the same question: where is this athlete right now, and how did they get here?

The Health History pillar—which we cover in depth in The Art & Science of Programming—captures energy patterns, sleep quality, body composition changes, stress load, and medications. All of it points toward the same underlying system that most coaches and clinicians never actually measure: the endocrine system.

It’s already in your Point A. But without objective data, it stays hidden—and historically, getting that data has been the barrier. Blood panels, salivary cortisol, urinalysis—these weren’t practical in most clinical or performance settings. So the endocrine picture remained a gap in the Point A profile.

It’s 2026. These are solvable problems.

And once we have that data, the question becomes the same one we ask everywhere else in the framework: is the endocrine system synced with the neurology, or has the neural network scaled past what the endocrine system can support? Because that gap—neurology outpacing endocrine function—is just as consequential as neurology outpacing connective tissue. It just takes longer to see, and it’s easier to miss without the lab work to prove it.

The Problem With Ignoring Hormones

Picture the athlete we see most often in this situation. Three to five years into a serious training program. Neural network developed to Point B. Strong, fast, reactive—on paper. Training hard, recovering poorly. Body composition shifting despite no change in nutrition. Sleep degrading. Performance outputs inconsistent in ways that don’t match the programming. And somewhere in the last six to twelve months, a soft tissue injury that didn’t make sense given the load they were under.

This is the athlete whose neurology got there first. The connective tissue couldn’t keep pace. And underneath both of those—quietly decoupling from the entire system—the endocrine environment that was supposed to be funding the adaptation.

The coaches and clinicians working with this athlete are usually looking at only the training log. But they need to also look at the lab work to get a complete Point A.

Here’s what we already know: the nervous system can outpace connective tissue. That gap—neurology ahead of biology—is where reactive strength injuries live. Achilles ruptures, hamstring tears, UCL blowups. The tissue can’t keep up with and express the force the neural network of absolute strength is generating.

What we haven’t talked about yet is that the nervous system can simultaneously outpace the endocrine system.

And when that happens, programming alone isn’t enough.

You can conjugate all four Point B elements perfectly. You can run the Bulgarian strategy for connective tissue at 21 sessions a week. You can have the most sophisticated training strategy. And if the athlete’s endocrine system is already in failure mode, you’re pushing against a wall.

The Cascade

Phase 1 — Acute HPA Activation: A training stimulus hits. Cortisol rises. Sympathetic tone increases. Anabolic hormones—testosterone, growth hormone—follow in cascade. This is normal. This is adaptation.

Phase 2 — Chronic HPA Overload: The stimulus doesn’t stop, or the athlete doesn’t recover. Sustained cortisol suppresses the hypothalamus. GNRH drops, which tanks testosterone. Chronic HPA axis activation suppresses thyroid function through at least three converging pathways: central suppression of the HPT axis via cortisol and inflammatory cytokines reducing TRH/TSH output; direct inhibition of thyroid hormone synthesis; and—critically—downregulation of deiodinase enzyme activity that shifts peripheral conversion away from active T3 toward metabolically inert rT3. Cortisol is high. Testosterone is low. The athlete is catabolic at baseline—even when they feel fine.

Phase 3 — HPA Insufficiency: Cortisol production itself begins to fail. Nervous system function deteriorates. The athlete becomes non-functional—and often, no one knows why.

This isn’t theoretical. We’ve seen it in the lab work. Testosterone at the floor. CRP inflammatory markers 300% above normal. Adrenal profiles showing excessive cortisol output alongside complete anabolic collapse. Athletes who look like they’re training hard but whose tissue is breaking down faster than it’s being developed.

The tissue degradation timeline matches the endocrine failure timeline. That’s not a coincidence.

This is where it connects directly to the injury pattern we’ve been building the framework around. Achilles ruptures, hamstring tears, UCL blowups—we’ve framed all of these as reactive strength injuries. Neurology outpacing connective tissue. The neural network generating force that the bottom-up biological architecture can’t transmit.

What the endocrine picture adds is this: if cortisol is chronically elevated and testosterone is suppressed, tissue repair is already compromised at rest. The athlete isn’t just undertrained biologically—they’re actively breaking down faster than they’re rebuilding. Every training session added into that catabolic environment pushes the gap wider. The connective tissue was already behind the neurology. Now it’s falling further behind with every session, even when the programming looks right on paper.

The endocrine failure doesn’t cause the injury. It accelerates the timeline to it.

What Point A Endocrinology Looks Like

We’re not talking about full endocrinology practice. We’re talking about three targeted assessment pillars that give us actionable programming data.

1. HPA Axis (Adrenal Function) The most complex of the three. A single blood cortisol draw tells you almost nothing—cortisol fluctuates hourly. What you need is the full picture: cortisol awakening response, diurnal rhythm, total output, free cortisol, stored cortisone, clearance rates. The Dutch Plus test (combined urinalysis and salivary cortisol) is the current gold standard for this.

2. Gonadal Function (HPG Axis) Testosterone, estrogen, and the full hypothalamic-pituitary-gonadal loop. The mistake most practitioners make is looking only at testosterone. Low testosterone with low LH tells you something completely different than low testosterone with high LH—the first is a pituitary problem, the second is a testicular problem. You need the axis, not just the output.

3. Thyroid Function (HPT Axis) Thyroid drives mitochondrial biogenesis and cellular metabolism. Under chronic stress, the body downregulates thyroid output as a survival mechanism. Checking TSH alone misses this entirely — you need the full HPT axis evaluation.

Growth hormone and IGF-1 round out the picture, but are lower priority given the broad normal ranges, especially in developing athletes.

The Subjective Layer

Lab work doesn’t exist in isolation. Before we can interpret an endocrine profile, we need to know how the athlete got there. Several health history data points flag endocrine dysfunction before a single test is ordered:

• Energy patterns in the first 60 minutes after waking

• Night waking between 2–4 AM (a specific cortisol dysregulation signal)

• Resting heart rate trends despite maintained training volume

• Body composition changes — particularly muscle loss with concurrent fat gain

• Subjective symptom timeline in the 1–3 months prior to injury

That last one matters for a reason that isn’t obvious: the first time you assess an athlete may not represent their baseline. If they’ve already been injured or overtrained by the time you see them, the lab values you’re looking at are downstream of a dysfunction that started weeks or months earlier. The health history is what lets you reconstruct the trajectory.

The Intervention Layer

The intervention layer for this is already in development. If you’ve been following the Founders Meetings, you’ve heard us talk about peptides—specifically BPC-157 and TB-500—in the context of connective tissue repair. What that conversation didn’t cover explicitly is the endocrine dimension. BPC-157’s neuroprotective properties and TB-500’s role in extracellular matrix organization aren’t just tissue repair tools. In a chronically catabolic athlete high cortisol, suppressed testosterone, tissue breaking down faster than it’s rebuilding—they’re part of the anabolic cascade that makes adaptation possible again.

We work directly with performance staffs across professional sport, so it's worth noting: both TB-500 and BPC-157 are currently banned under WADA guidelines—and enforced across the major leagues (MLB, NFL, and NBA). We'll let you draw your own conclusions about what it means when governing bodies move to ban recovery compounds. Our read is that the biology doesn't lie—and neither do the results.

This is why we don’t treat peptides as a standalone recovery intervention. In the context of the Absolute Conjugate Strategy, they sit inside the reactive strength programming layer—specifically on the biological side. You’re running the Bulgarian strategy for connective tissue at 21 sessions a week. You’re progressing through the isometric continuum. You’re building bottom-up CT architecture. The complete reactive strength peptide stack is what ensures the endocrine environment isn’t working against every one of those sessions. It’s not a shortcut. It’s the biological infrastructure that makes the programming actually land.

Point B

Which brings us back to the question we ask about every element of the system: what does Point B look like here?

For the endocrine system, Point B is simple to define and hard to achieve. It’s the state in which the endocrine cascade is synced with neurological output—testosterone, growth hormone, and cortisol operating in a pattern that supports the tissue repair cycle, not works against it. The neural network is scaling. The connective tissue architecture is being built. And the endocrine environment is providing the biological infrastructure that makes both of those adaptations stick.

When the endocrine system decouples from the neurology—cortisol chronically elevated, testosterone suppressed, thyroid downregulated—you don’t have a training problem. You have a system problem. And no amount of programming sophistication closes that gap without first identifying it in your Point A.

That’s what this series is about.

What’s Coming

This is the framework. The first layer.

Over the next several articles, we’re going to go deeper into each axis—how the HPA cascade actually unfolds, what gonadal dysfunction looks like across different athlete profiles, how thyroid function interacts with the tissue repair cycle, and how all of it connects back to the Point A → Point B roadmap.

If you’re a clinician or coach working with athletes who are training hard but not recovering, not adapting, or getting hurt at a rate that doesn’t match the programming—the endocrine layer is worth looking at.

This is the framework we’re building inside The Art & Science of Programming. If you’re not in the course yet, that’s where to start.

More to come.

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This is the single most-asked question we get on specialty equipment: not should I do the reverse hyper, but how are you actually programming it. So we finally answered it directly.

This isn’t competing with Louie Simmons’s original reverse hyper work—eleven-plus years treating Louie and working hands-on with the reverse …

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Reactive Strength is volatile by nature. It’s fast, elastic, and entirely dependent on an athlete’s ability to absorb and dampen force and redirect it without losing time or tissue integrity in the output. That volatility and tissue violence isn’t a flaw—it’s where the performance emerges from.

But every coach and clinician managing a high-performance athlete is holding a position inside that volatility, whether they’d call it that or not.

We made this case in full previously in Understanding Training Risk (Part 1) and Part 2. The Level of Competition (sporting environment) behaves like the market easily exposed to tail risk. Injuries are Black Swans—not random, yet not normally distributed, but predictable once you understand where the fat tails sit. Typically, we have been told that this risk is managed with diversification—however, diversification alone never truly protects you from risk, as Mark Spitznagel puts it, “diversification is a dilution of risk, not a solution to it”. This is where hedging comes into play. To an investor, hedging is a strategy to offset potential losses in a portfolio as a result of market volatility by taking opposite positions in related investments. The investor must balance a know fixed cost (the hedge) that is entirely controllable with an unknown, potentially massive cost that digs into returns and is always uncontrollable. The programmer is faced with a similar situation. How to control the controllables in the management of athletes in high performance so that the market doesn’t control them. To a programmer, this involves adding inputs into the program that offset the potential for catastrophic events (injuries).

The fix we named in Internal Training as a Hedge is simple: internal training and treatment—simultaneous work that stimulates capacity in the biological structures themselves, is what lets an athlete take on higher-risk, higher-return external training, practice and play sessions, allowing them to cultivate deeper gains within the portfolio of performance.

This Conjugate Edge is about the single best internal hedge available for Reactive Strength.

Where the Volatility Actually Comes From

We’ve written before about why this volatility exists in the first place. Reactive Strength depends on the matching of tissue resonance—how connective tissue oscillates under resistance (biology)—to the regulation of that oscillation by the neuromuscular system (neurology). When the neurology and biology are tuned to each other—synced, energy is stored and transmitted efficiently. When they’re not, energy is dissipated, reflected, or absorbed catastrophically. That’s the mechanism we broke down in The Damping Effect: A Programmable Quality of Biological Point B Reactive Strength. If you haven’t read that piece, read it before this one—it names the variable this piece is going to show you how to program directly.

Name the real source of the volatility plainly: a neurological-biological asymmetry. The nervous system—specifically the neural network of absolute strength and the connective tissues are two systems adapting on different timelines, by different rules, and the gap between them is where the risk lives. Understanding Reactive Strength as special strength exposes that gap. But understanding doesn’t close the gap. Taking specific programming action—both clinically and in the weight room, closes that gap.

The Belief: The Asymmetry Has to Be Programmed For

Absolute’s position, plainly: the neurological-biological asymmetry underneath Reactive Strength has to be directly programmed for—synced, not managed. It doesn’t resolve as a byproduct of more reactive work, more plyometrics, more volume, or simply resting. You close the gap by stimulating the neurology and biology in conjugation, in the same input or exercise. Anything short of that leaves the neurological-biological gap in place—or widens it…

Rest Is Not Synchronization—The NBA Proved It Last June

You don’t have to look far to see what happens when you manage this asymmetry instead of syncing it. The CNS recovers in 24 to 72 hours; connective tissue doesn’t—it detrains without mechanical loading over that same window. Rest a player and both systems deload together, but only one comes back: neurology on schedule, biology still degrading. That’s a wider asymmetry, not a smaller one—more volatility, not less.

We watched it play out at the highest stakes the sport has in NBA’s Load Mismanagement & Reactive Strength Problem: rest managed the asymmetry instead of syncing it, and it spiked into a tail event in Game 7 of last year’s Finals.

Isometrics have historically come in two flavors—Holding (HIMA) and Pushing (PIMA). Neither creates the vibrational stimulus connective tissue actually responds to. Jim Seitzer and Westside Barbell had been sitting on a piece of that puzzle for nearly twenty years, in the “shaky bar” experiments that became BandBell—but as Seitzer himself put it introducing Oscillatory Isometric Muscle Actions: A New Class of Isometrics, the actual relationship between tissue and band resonance driving those results “was brought to light by Absolute Sport Science,” which is where OIMA, as its own class of isometric, comes from.

The Hedge: What an OIMA Actually Does

This isn’t another isometric variation competing for a slot next to a the box squat. It’s the sync the NBA case above never got: rest recovers one half of the asymmetry and lets the other degrade, but an OIMA stimulates, loads both the top down and bottom up element concurrently, at once, in the same rep, and constrains them to answer together—in conjugation. That’s not a metaphor—it’s the literal demand of an OIMA. The adaptation isn’t “get stronger” in the static-hold sense; it’s teaching the athlete to output force where damping is expressed, the same quality that separates controlled resonance from the catastrophic oscillation of a tendon injury.

This is why the OIMA should be the number-one programmed isometric in a high-performance setting—not because other isometrics are wrong, but because none of them force neurology and biology to solve the same real-time problem together. That makes it internal training/treatment in the strictest sense: a static, clinical-weight room input/exercise that develops capacity in the biological structures itself, so the athlete can take the higher-risk, higher-return work—the sprinting, cutting, jumping—without the tail event. It’s the internal hedge.

Where This Shows Up in the Spine

The same asymmetry shows up in the spine, with its own damping problem: pendulum damping across the entire posterior chain, not just a single joint. This is exactly the gap our Reverse Hyper Program was built to close—built on how Louie Simmons started with the reverse hyper, not where the special exercise ended up in most gyms as a lower-back accessory machine. Check out the program here.

Free readers have the full case now: why the asymmetry exists, why it has to be synced instead of managed, and why the OIMA is the internal hedge that does it. Paid subscribers get the specifics on when and how confidently to reach for it.

Indication: Why OIMAs Is Almost Always the Right Programming Call

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The Big Takeaway

Malik Nabers has never been at reactive strength Point B since high school — and the reason isn’t a lack of talent or effort, it’s a neurological-biological asymmetry that’s never been correctly framed or programmed for. His nervous system was already capable of voluntarily injuring tissue before he ever got to LSU. The turf toe everyone treats as a minor, recurring nuisance is actually the visible symptom of a top-down output that has permanently outpaced the bottom-up tissue capacity to support it. How an injury gets framed determines how it gets programmed—and this one has been framed wrong for years.

What We Cover in This Episode

• Why Turf Toe Isn’t Small: At the level of force production an NFL receiver generates through the medial foot—sprinting, cutting, changing direction—first MTP dysfunction has massive carryover effects up the entire kinetic chain, not just locally.

• The Neurological-Biological Asymmetry, Applied: Nabers’ nervous system was already outputting at a level that could voluntarily injure tissue back in high school—before LSU, before the NFL. That tells you exactly where his neurology was relative to his biology at a formative age.

• Compensation as the Hidden Cost: An athlete operating at elite output with an unresolved bottom-up deficit doesn’t stop performing—he compensates. The cost of that compensation compounds over years and shows up everywhere except where everyone’s looking.

• Framing Determines Programming: If the injury gets labeled as a recurring minor issue rather than a reactive strength deficit rooted in neurological-biological asymmetry, the treatment and training will never be specific enough to resolve it—no matter how good the facility or the surrounding care.

• The Olin Kreutz Programming Model: How a former player without the same evaluative biases approaches programming around a limiting constraint—going Bulgarian on the biological side while keeping the neurological side at a retaining intensity, rather than continuing to work around the actual problem.

The full breakdown—including the Michael Thomas comparison, the Louie Simmons parallel, and what this means for anyone managing a similar case—is below for paid subscribers.

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Welcome to the monthly roundup for Absolute Sport Science! If you’ve been busy programming treatment and training, analyzing Point A → Point B data, or just busy with the pace of life in 2026, this is your one-stop to catch up on everything we covered in June. We’ve got summaries and links to all our Tuesday written posts and Sunday video deep-dives (exclusive to paid subscribers). This is your monthly highlights—straight to your inbox.

Whether you’re a free subscriber or a paid member, these recaps are designed to keep you informed and inspired—to keep you getting better at becoming a programming strategist!

Tuesday Posts: Programming Insights

Tuesdays are all about actionable, evidence-based articles to level up your programming knowledge. June was a reactive strength month—three professional athletes (Lindor, Griffin, Nabers) whose injuries the mainstream read as bad luck, but who actually show the same underlying pattern: a neurology that's outpaced the biology meant to transmit it. Here's what we explored:

• June 2, 2026: Francisco Lindor’s Calf Injury Isn’t a Calf Problem

  • Lindor’s been on the IL since April 22nd with a calf strain—his second in his career, this time on the opposite side. The mainstream read is bad luck. Ours: a bottom-up reactive strength deficit. A high-output explosive athlete with bilateral calf history is a pattern, not randomness—it’s a signal that neurology has outpaced biology.

  • The fix isn’t more calf raises. The posterior leg has three distinct muscular layers, each with its own fiber orientation and mechanical role. Most return-to-sport protocols train the output and ignore the architecture—which is exactly where Absolute’s tissue-specific, fiber-direction-by-fiber-direction strategy begins.

• June 9, 2026: Konnor Griffin’s Flexor Mass Strain: Detailing the Anatomy & Implications

  • The Pirates’ Konnor Griffin is out longer than expected with a forearm flexor mass strain. We break down all three layers of the flexor mass and why, in a throwing athlete, the Flexor Carpi Ulnaris is the tissue that matters most—it has a direct anatomical connection to the UCL and is a key bottom-up reactive strength stabilizer against valgus stress during arm acceleration.

  • Our working hypothesis: the injury sits in the FCU specifically, given its load-bearing relationship to the medial elbow in throwing mechanics.

• June 16, 2026: Nabers Has Never Been at Reactive Strength Point B Since High School

  • Malik Nabers’ chronic left turf toe followed him from LSU through two Giants seasons before his right knee gave way—non-contact—on a jump. From a reactive strength paradigm, that’s not bad luck either: it’s a compensation chain that’s been building since high school, as the nervous system shielded around an unresolved bottom-up deficit until the other side finally failed.

  • We walk Point A—Health History, Treatment & Training History, Level of Competition, Functional Range—through the public record, and use Michael Thomas’s toe dislocation as a reference point for just how much force an elite receiver’s neurology puts through the foot and ankle.

• June 23, 2026: The Conjugate Edge #09: Defining a Conjugate Programming Sequence

  • Concurrent and sequenced aren’t the same thing. Conjugate Edge #08 established that running methods together isconjugation; #09 is about the order those inputs run in—order you can’t know on day one, only discover by iterating with a week of Point A feedback.

  • Featuring Olin Kreutz’s real-world sequencing logic with NFL linemen: scan film for fragility, overlay it with objective reactive strength and joint function data, resolve the biological limiter first, then scale the neural network of absolute strength. New standing definition: Conjugate Programming Sequence—the specific order in which concurrently-run treatment and training inputs are executed inside a recurring feedback loop, arrived at by iterating that loop until the order itself stops changing.

If these four breakdowns made sense, you're already thinking like a programmer—The Art & Science of Programming is where Point A, Point B, and the reactive strength framework get put into your hands as a system. Enroll now →

Sunday Paid Subscriber Video Posts

Sundays are reserved for our premium video content—in-depth breakdowns, Q&A sessions, and practical demos that bring the art and science to life. June's run built out the full isometric triad—PIMAs, HIMAs, and OIMAs—as the toolkit for diagnosing and resolving reactive strength deficits, then closed with a live spine case. If you're not a paid subscriber yet, these are a great reason to upgrade!

• Single-Leg Oscillatory Drops: The Most Powerful Reactive Strength Exercise You’re Not Using June 7, 2026

  • Dave Scholz’s single-leg drop from a 24” box with ~20 lbs of band tension forces the nervous system to rapidly search for, stiffen, and transmit force through the trunk and posterior hip in real time. We break down the damping effect in action, the top-down/bottom-up bridge it exposes, and progression ideas—shorter bands, bare feet, lumbar oscillation via belt—for ACL resilience and spinal control.

• OIMAs: The Missing Middle of Reactive Strength Programming June 14, 2026

  • Oscillating Isometric Muscle Actions (OIMAs) sit between PIMAs (top-down) and HIMAs (bottom-up) in the reactive strength triad. They don’t build tissue or drive neural adaptation directly—they reveal exactly where damping deficits exist, turning the isometric into a diagnostic feedback loop rather than just another exercise.

• OIMAs as a Decision Fork: How to Choose Between HIMAs, PIMAs, and External Load June 21, 2026

  • Once an OIMA reveals a damping deficit, the next question is why: stress-shielded from the bottom up, or neurologically shielded from the top down? We map both paths—HIMA-based tissue loading through the linear loading progression on one side, high-effort PIMAs scaling into external load on the other—and why effort level is non-negotiable in fast-twitch tissue like the hamstring.

• Finding the Open Door: Programming the Spine with Disc Pathology June 28, 2026

  • Disc pathology doesn’t cookie-cutter. The nervous system—not the disc—is the gatekeeper, and the job is finding the spine position where it lets you back in rather than forcing through a symptomatic range. Includes a live case: an extension-intolerant disc with hamstring/glute involvement, resolved using the Reverse Hyper Program and PIMAs on the handles to lock in thoracic and cervical extension.

Founders Meeting: Adrian Guardado

Adrian Guardado Founders Meeting (Recording) June 26, 2026

This Founders Meeting featured Adrian Guardado, Director of Return to Play at UCLA Football. Adrian’s background is in strength and conditioning, and over the last two years he’s transitioned into hands-on table work—bridging the gap between the weight room and the training room in a way most programs haven’t figured out yet. Full recording is available to our Founding Member subscribers.

Next Founders Meeting

We’ll focus on the programming variable of load with a focus on resistance:

• We will go over how the Soviets graded out resistance in the sport of Olympic Weightlifting

• Show how that graded resistance was utilized by Louie Simmons in his Westside Barbell Conjugate System

• Advance the grading out of resistance for today in 2026 and what that means in programming resistance optimally for not just the athlete but also the special strength that is desired for treatment or training

If you have any other topics worth discussing at a Founders Meeting, leave them in the comments below.

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The Big Takeaway

Disc pathology doesn't follow a script. Extension doesn't always hurt, flexion doesn't always help, and cookie-cutter approaches consistently fail because the nervous system—not the disc—is the gatekeeper. The clinical strategy here is to stop forcing outputs the nervous system won't allow, and instead systematically change spine position, cue, and loading parameters until you find the opening. Once that door is open, that position becomes your new baseline—and you build from there.

What We Cover in This Episode

• Why Disc Cases Don’t Cookie-Cutter: Disc pathology presents differently than it’s described in textbooks—sometimes extension is the problem, sometimes flexion, sometimes both. The symptom pattern is the starting point for a search, not a prescription.

• The Gatekeeper Concept: With discogenic pathology, the nervous system closes the door on certain outputs. The job of the clinician isn’t to force through it—it’s to find the position and conditions where the nervous system allows access to the tissue that needs loading.

• Spine Position as the First Variable to Change: When an input creates symptoms, the first adjustment is spine position. Shift out of the symptomatic range—change the degree of freedom at the source—until the output becomes available without driving symptoms.

• Establishing a New Baseline: Once the door opens and you get the output you want, that position and those parameters become the new Point A. From there you can scale load and reps within that window, and adjust again when the door starts to close.

• Real Case: Extension-Intolerant Disc with Hamstring and Glute Involvement: A live case using the Reverse Hyper Program—extension intolerant at Point A, hamstring curl driving symptoms initially, resolved by finding the right spine position and using PIMAs on the handles to lock in thoracic and cervical extension. Loading into the hamstring tendinopathy followed from there.

The full breakdown—including the decision-making process and how this played out in a real case—is below for paid subscribers.

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Adrian Guardado is the Director of Return to Play at UCLA Football. His background is strength and conditioning, but over the last two years he’s transitioned into table work, bridging the gap between the weight room and the training room in a way most programs haven’t figured out yet.

In this Founders Meeting, Adrian wal…

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Founders Meeting Announcement

Mark your calendars and join us for the next Founders Meeting!

Date: Friday, June 26, 2026
Time: 12:00 PM Eastern Time (US and Canada)

We’re excited to have a conversation with Adrian Guardado.

Topic: Adrian will be joining us to discuss:

• His unique role at UCLA Football

• How he moves from the gym to the treatment table

• How he’s using Oscillating Isometric Muscle Actions (OIMAs) to reduce return to performance timelines

This will be an open discussion with all founding members, so please come prepared to participate.

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Zoom Meeting Information

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In Conjugate Edge #08, we made the case that concurrent is conjugate—programming methods together inside one training week is what conjugation means. That piece was about structure: which methods, run together.

This piece is Conjugate Edge is about order.

What It Means to Sequence

Concurrent and sequenced are not the same thing. Concurrent means multiple treatment and training inputs—thermodynamic cycles of propagating work—running together. That work is programmed at a retaining or stimulatory intensity; never at a detraining one.

Sequenced means you’ve organized the order those inputs run in. You can’t sequence something that isn’t concurrent—but running things concurrently doesn’t mean you’ve sequenced them. This is why the Soviets termed it a Conjugate Sequencing System. They were signaling something specific: sequence is what makes the difference.

Uncertainty to Order to a Conjugate Sequence

We’ve told you there is uncertainty in programming—here’s the case in point. As a programmer, you don’t know the right order on day one. A single day only shows you what the inputs do in real time and how the individual responds to them. You need a handful of sessions across a week to select which inputs you need, based on what your Point A findings are telling you.

Once you have that information flow—how the trainee is responding to each input—you decide which ones stay in, which Point B capacities need more attention than the others, and from there you sequence the inputs and iterate on that sequence using those same inputs.

At Absolute, this is what we mean by conjugating inputs.

Conjugating—definition (Absolute Sport Science): Liking multiple inputs that are each propagating work toward Point B, and sequencing them together on purpose so they produce a cumulative, multifaceted effect—rather than the isolated effect each would produce on its own.

We like all the inputs we have in. They’re all propagating work, each moving the athlete toward Point B. The question becomes how we sequence them to create that cumulative, multiplicative effect. You’ve got the inputs—now you iterate with them to actualize that effect. Push it to the edge. Stack stimulatory onto stimulatory onto stimulatory, and find where the edge is.

Understand: To get more, you’ve got to move that edge.

An NFL Lineman Programming Other NFL Linemen’s Training Work

Here’s what that looks like in real life, in 2026. Olin Kreutz programs the first training work that constrains and uses the nervous system to maximally output its neural network of absolute strength into a joint. He does this to prime the joints he’s identified, on film, as being a limiting constraint on the emergence of a special strength of blocking. His best Point A feedback loop is scanning the film for fragility in the lineman’s ability to get violent at the Level of Competition.

He overlays that film read with an up-to-date, objective physical assessment of reactive strength and joint function—the biological capacities for Point B. Integrating those two feedback loops tells him exactly which joints and tissues need propagating training work.

After the scan, he observes what’s missing on the field from either a joint or a tissue perspective. Does the athlete have a dysfunctional joint that needs to be normalized? Is the joint functioning normally but the tissue is abnormal, resulting in a reactive strength deficit?

It’s normally both to some degree (see, more uncertainty)—an untrained, dysfunctional joint paired with a reactive strength deficit. He knows this firsthand, not just from the film and the assessment data, but from fourteen-plus seasons in the NFL: that biological limiter, if not removed, can prematurely end a playing career where the neurology is still there but the biology isn’t.

Once the neural network has voluntarily and maximally output into the joints, he transitions directly into building toward a training max on a box squat or press. So: stimulatory work for the joint and reactive strength first, then stimulatory work to scale up the neural network of absolute strength. That’s exactly what’s happening, and understand: it’s not an accident—he sequenced it that way by intent. He wants to find the limiting joint function and reactive strength deficiencies the football field exposes, and resolve those before adding more nodes into the neural network. Joint function and reactive strength get added to that network first.

This is strategy, this is discipline. Scan for trainable weaknesses from the Level of Competition and leverage the programming strategy to acquire the capacities that fill those weaknesses. Be aggressive with programming. Find the edge—push the edge until you get what you want, then drop back and hold. Integrate. Be patient when you want to get aggressive, and use that aggression to acquire a capacity you don’t have yet—one that changes the game. This type of programming work rewards in non-linear ways. Once again, he knows this via skin in the game.

The sequence doesn’t stop there. It keeps going—into special practice, into the punch, into the biological tissue work that comes right after it—and that’s where Olin’s cascade actually finishes multiplying and compounding.

If you stop reading here, you get the setup. You don’t get the sequence.

Paid subscribers get the rest of Olin’s cascade—how he sequences practice, the punch, and biological tissue work on top of everything above, the full Conjugate Programming Sequence definition earned through his example, his weekly structure, and a live walkthrough of his logic applied to Malik Nabers.

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The Big Takeaway

Once an oscillating isometric muscle action reveals a damping deficit, you face a critical decision: is the tissue being stress-shielded from the bottom up, or neurologically shielded from the top down? These two findings point in completely different programming directions—one toward HIMA-based tissue loading and the linear loading progression, the other toward high-effort PIMAs and eventually external load to scale the neural network. The OIMA doesn't just expose the problem. It gives you the information you need to solve it correctly.

What We Cover in This Episode

• Stress Shielding vs. Neurological Shielding: How to distinguish between a bottom-up connective tissue deficit and a top-down neural output deficit using the damping feedback from an OIMA — and why getting this distinction right determines your entire programming direction.

• The Bottom-Up Path: When the OIMA reveals stress shielding, the prescription is HIMA-based tissue loading at length, progressing through the linear loading progression — loading to length, loading through length, eccentrically — to build the connective tissue architecture that’s missing.

• The Top-Down Path: When the OIMA reveals neurological shielding, the nervous system is driving output to one area and routing around another. The prescription is PIMAs at high effort levels — 7s, 8s, 9s, 10s — to recruit the higher-threshold portions of the neural network and restore output across the full tissue.

• Why Effort Level Matters for PIMAs: In a predominantly fast-twitch muscle like the hamstring, low-effort PIMAs are unlikely to recruit the portions of the network responsible for shielding. You need to go to the higher end of the continuum — and then move to external load to push above the internal ceiling and add nodes to the network.

• External Load as the Next Step: When internal PIMAs at maximal effort aren’t sufficient to restore neural output, external loading becomes necessary. The neural network is highly responsive to external load — it’s the most potent stimulus for adding new nodes to the network and signaling regions that internal effort alone can’t reach.

The full breakdown—including how to run through this decision sequence in practice—is below for paid subscribers.

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When a high-output athlete presents with a chronic soft tissue issue that won’t resolve—one that persists through daily treatment + training, and the full resources of a professional sports organization—the reactive strength paradigm asks a specific question:

Is the neurology outputting more than the biology can currently transmit?

Because if the answer is yes, the resolution is specific: you have to use the neurology to stimulate the biology. Deliberately conjugate specific treatment and training from a shared framework so that the neurological output becomes the stimulatory mechanism driving biological adaptation at the site of the deficit. Without that framework, the deficit doesn’t stay static. It deepens. What begins as a manageable soft tissue issue becomes chronic. What is chronic accumulates pathological change. And what accumulates pathological change eventually expresses itself as something that can no longer be managed—a structural failure at the point the system could no longer compensate through.

Malik Nabers has had a chronic left foot turf toe since before his college days at LSU. It followed him through two NFL seasons with the New York Giants. He called it “a mosquito he couldn’t kill”. The staffs around him worked on it continuously.

The mosquito never went away.

On September 28, 2025, Nabers jumped for a deep ball against the Los Angeles Chargers. His right knee gave way on the takeoff—not the landing. Torn ACL + torn meniscus. Season over.

That distinction matters. The tissue didn’t fail under the load of landing like Odell Beckham Jr.’s ACL rupture with the Cleveland Browns. It failed under the neurological output of the jump itself—the precise moment the nervous system fired maximally to generate force, and the biology couldn’t transmit it. That is not a contact injury or a landing mechanics problem. That is a reactive strength failure in its clearest form.

From a reactive strength paradigm, what happened to Nabers is entirely legible—and it was observable long before that moment. His injury record is a coherent clinical picture of what happens when elite neurological output runs ahead of its biological infrastructure for long enough, without a programming strategy in place to close the gap.

Naber’s Has Never Been at Biological Point B

When Nabers tore his ACL, sources noted that for the first time since high school, he would have a chance to be fully healthy.

At Absolute Sport Science, Point B describes an athlete’s full neurological and biological expression of all four physical capacities—operating concurrently and without inhibition. Absolute Strength is the maximal force the neuromuscular system can voluntarily produce. Speed Strength is the ability to express that force rapidly—at the highest attainable speed. Reactive Strength is the capacity to absorb, store, release, and dampen elastic connective tissue energy in conjugation with the neural network of absolute strength. And Joint Function is the range and neurological control available at each articulation to support all three. When all four are expressed simultaneously, the athlete is at Point B. Nabers has never occupied it.

From a reactive strength paradigm, this tells us his neurological output was already exceeding his biological tissue’s transmission capacity in his teenage years. That is not a weakness—it is the signature of an exceptional athlete. But it is also a programmable signal. A leading indicator visible early enough that a specific intervention strategy could have been built around it. That neurological output, channeled through a conjugated treatment and training framework, was the exact stimulus needed to drive biological adaptation at the site of the deficit.

Instead it ran unchecked. And the biology has been falling further behind ever since.

Reading Naber’s Through Point A

At Absolute Sport Science, every athlete assessment begins at Point A—the current state of the athlete across four domains: Health History, Treatment and Training History, History at Level of Competition, and Functional Range Assessment. Point A is what tells you where the neurology-biology relationship actually stands before you build a single rep of programming around it.

We don’t have access to Nabers’ full Point A. But the public record gives us enough to construct a partial picture—and that partial picture is, on its own, deeply informative.

Health History (available) Chronic left first MTP turf toe present since high school. Reported as never fully healthy since before LSU. Right knee ACL and full meniscus repair October 2025. Arthroscopic debridement of scar tissue, right knee, spring 2026. Two surgical procedures on the same joint within eight months.

Treatment and Training History (inferrable, not confirmed) Continuous daily treatment across LSU athletic training staff and two years with the New York Giants medical and performance staff. Pre-hab protocol implemented prior to October surgery. Elite training environment throughout. Specifics of modalities, loading strategy, and programming philosophy are not publicly available—but the outcome of those years of work is clear: the turf toe never resolved. From a reactive strength paradigm, that outcome tells us the strategy—however well executed in isolation—was not conjugated around a shared model with a mechanism for resolving a reactive strength deficit at its root. Treatment addressed the biology. Training built around it. But neither, operating on separate tracks, had a framework for using the neurological output to drive biological change at the site.

History at Level of Competition (strong) LSU starter. NFL rookie record 109 receptions. Pro Bowl Year 1. Elite route precision and first-step quickness documented extensively at every level. Missed OTAs and training camp reps across both NFL seasons due to the left foot. Exited four games into his sophomore year with the ACL injury. Performance at full expression has never been sustained across a full season of professional football.

Functional Range Assessment—Joint-by-Joint Movement Capacity (unavailable) The FRA quantifies the joint function component of Point B—distinguishing between passive range, active range, and the degree of neurological control the athlete can express within that range at each individual articulation. That distinction identifies whether the deficit at a given joint is biological, neurological, or both, and therefore which system is the rate limiter. In addition, the CARs analysis from FRA helps us quantify the amount of movement that occurs externally at each articulation to allow for the observation of areas of movement that may be deficient or inadequate. An FRA of the left first MTP, left ankle, and right knee would have provided the joint-by-joint map the reactive strength assessment overlay sits on top of. Without it, the work was being done without a map.

The Mosquito Was the Signal

Turf toe is, at its core, a reactive strength injury. The first MTP joint is the final transmission point in the lower extremity force output propulsion chain—every route, every cut, every takeoff passes through it. When it is compromised, the nervous system doesn’t reduce its output. It neurologically shields around it, shifts load, and reorganizes movement to protect the site.

For Nabers, that shielding has been active since high school—on the left side. Every rep executing with a neuromuscular system already protecting the left forefoot by asking more of the right lower extremity. Every season, the left-right asymmetry deepened. Every season, the probability climbed that the right side would encounter a demand it could not meet.

The right knee ACL was not random. It was the endpoint of a compensation chain building, compounding, since before he was recruited to go to LSU, let alone drafted in the NFL.

The resolution was always available. That same neurological output driving the compensation was the stimulus that could have built the biological foundation the left foot needed—through a conjugated treatment and training strategy designed to use it that way. That is what treating reactive strength means. And it is what years of managing pain and symptoms of the toe, without that special strength capacity framework, could not provide.

Michael Thomas: What Elite WR Output Actually Looks Like

To understand the magnitude of force the neural network of an elite wide receiver generates—and what the reactive strength of the foot and ankle must be capable of transmitting—consider what happened to Michael Thomas.

Thomas is not just any receiver. In 2019 he was named NFL Offensive Player of the Year—the best offensive player in the entire league, not just at his position—after catching 149 passes in a single season, the NFL single-season reception record. That designation is Point A information. It tells us the neurological output Thomas was operating at—the force his nervous system was generating through every route, every cut, every plant and release—was at the absolute ceiling of what the human performance system produces at the professional level.

In Week 1 of 2020, a defender was thrown onto his left ankle, tearing the deltoid ligament and surrounding structures. Two years of recovery followed. When he returned in 2022, three games in, he left the field against the Panthers with a toe injury. No contact recorded.

The diagnosis: a dislocated second toe on his right foot.

Not a sprain. A dislocation—the joint forced entirely out of position by his own neuromuscular output. Nothing external caused it. The neural network fired at the level it always fires at elite output. The foot and ankle, which must have sufficient reactive strength to receive and transmit that force, could not. The joint gave way.

This is the reference point for what the reactive strength of the foot and ankle is required to handle at the elite wide receiver level. The force being generated is so significant that when the biological capacity to transmit it is compromised—through injury, asymmetry, or accumulated deficit—the tissue doesn’t just strain. It blows up and dislocates the joint.

The neurology outputs violence onto the tissues at these levels of elite output.

Now consider that Nabers was showing connective tissue issues at the foot since high school—before the professional workload, before NFL-level speeds, at a lower cumulative load and with less provocation. His neurology is operating at that same elite output ceiling. The reactive strength demand on his left first MTP has always been at that level. And the biology has never been built to fully meet it.

Absolute’s Prediction for Naber’s in 2026

The conversation will center on timing. Week 1 or not. Same player or diminished. From a reactive strength paradigm, we can be more specific than that.

Nabers will return in 2026 carrying more biological limitation than he has ever had—on both sides of the lower extremity simultaneously. The right knee is post-surgical twice over, with connective tissue architecture still organizing. The left foot deficit that started this entire cascade remains unresolved. As of mid-June 2026, he is reported to be over 70% through his rehab and targeting Week 1—but from a reactive strength paradigm, a return timeline is not a resolution. His neurological output will return to elite levels faster than his biology can meet it—because that is exactly what it has always done. That gap has been widening since high school. Two procedures on the right knee have added variables to that side that weren’t there before.

What that looks like on the field: flashes of the exceptional neurology that made him a Pro Bowl receiver as a rookie, constrained by a biological system on both sides that cannot yet fully transmit what the nervous system is asking of it. Route precision will return before top-end reactive strength. First-step neurological quickness will return before the ability to sustain it across a full game at full output. The early weeks of his return will look like Nabers—and they will also look like an athlete whose biology is still catching up to his neurology.

This is not a prediction about his character, his work ethic, or his will to compete. Those have never been in question. This is a prediction about the neurology-biology relationship that the reactive strength paradigm makes visible—and what it tells us will happen when an athlete with Nabers’ output profile returns to full-speed football before both sides of his lower extremity have been built to meet that output through a conjugated programming strategy designed to close the gap at the root.

The question for 2026 isn’t whether Nabers comes back.

It’s whether the strategy around him is finally built to close the gap that has been widening since high school.

The remainder of this article—covering our clinical read of the ACL mechanism from the video and injury record, what the second surgical procedure tells us about the post-surgical reactive strength deficit now present on the right side, and the three-component programming strategy the reactive strength paradigm demands for an athlete with Nabers’ profile—is available to paid subscribers.

If the reactive strength paradigm is new to you, the learning module is the right place to start:

The Art & Science of Programming—Absolute Sport Science →

When the ACL Yielded—What Was Happening at the Knee

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The Big Takeaway

Oscillating isometric muscle actions (OIMAs) occupy a distinct and necessary position between PIMAs (top-down, neurological) and HIMAs (bottom-up, biological) in reactive strength programming. Rather than building new connective tissue architecture or driving direct neural adaptation, OIMAs train the self-organizing behavior of pre-existing connective tissue—and in doing so, reveal exactly where damping deficits exist. That diagnostic signal is what makes OIMAs a programming feedback loop, not just another isometric.

What We Cover in This Episode

• The Isometric Triad for Reactive Strength: PIMAs, HIMAs, and OIMAs as three foundational inputs always present in Absolute’s conjugate reactive strength strategy—with their proportions shifting depending on where the athlete is in rehab or performance development.

• What OIMAs Actually Do: OIMAs don’t grow the connective tissue network or directly drive neural adaptation—they improve the self-organizing behavior of the architecture that already exists, allowing it to dampen oscillatory force more effectively.

• OIMAs as a Diagnostic Feedback Loop: By asking a client to dampen oscillation at a specific joint angle, you can identify which regions of a tissue are stress-shielding. The hamstring example shows how OIMAs expose gaps in tissue recruitment that direct where HIMAs need to go.

• The Neural-Biological Decision Fork: If damping is poor, OIMAs help you determine whether the breakdown is top-down (insufficient neural signaling → prescribe PIMAs) or bottom-up (insufficient connective tissue architecture → prescribe HIMAs with linear loading progression).

• Why This Is Compressing Return-to-Performance Timelines: When OIMAs sync the neural network with the connective tissue network, the result is faster integration and more durable reactive capacity across multiple clinical cases.

• Connective Tissue Nodes and the Self-Organization Hypothesis: An emerging framework around functional intersection points in the 3D collagen architecture — sites where, under oscillatory input, self-organizing damping behavior is being trained.

If you want the full breakdown of how to program OIMAs, use them diagnostically, and integrate them into your conjugate strategy—that's below for paid subscribers.

Continue reading for paid subscribers →

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The Pittsburgh Pirates Konnor Griffin is on the DL and for longer than originally anticipated based on the latest outcome of an assessment of his throwing arm.

Griffin initially went on the DL on May 31 with elbow soreness and what was deemed to be a low grade strain of one of his flexors according to the Pirates. During a subsequent road trip, the shortstop visited Dr. Keith Meister who determined the injury required a more specific approach based on its location and the potential impact it may have, if Griffin returned to the lineup too early. As is the case in MLB, the exact muscle tissue affected and the extent to which it is, has not been disclosed. More generally, it has been diagnosed as a flexor mass muscle strain.

This recent information begs the question: what is a flexor mass muscle strain, and what is its relationship to the throwing athlete?

The Flexor Mass

The flexor mass of the arm (more specifically, the forearm flexor mass) refers to the group of muscles on the medial (inner) side of the forearm that primarily flex the wrist and fingers. In throwing athletes (e.g., baseball pitchers, quarterbacks, javelin throwers), this muscle group is critically important for performance, injury prevention, and rehabilitation.

Key Muscles in the Flexor Mass

The muscles of the flexor mass are located proximally from the medial epicondyle of the humerus, as well as the medial elbow joint capsule and thickenings of the capsule referred to as the Ulnar Collateral Ligament. They form a prominent, fleshy mass on the inner forearm.

There are three layers of muscles in the flexor mass.

Layer 1 (Superficial)

• Pronator Teres

• Flexor Carpi Radialis (FCR)

• Palmaris Longus

• Flexor Carpi Ulnaris (FCU)

  

Layer 2 (Intermediate)

• Flexor Digitorum Superficialis (FDS)

Layer 3 (Deep)

• Flexor Digitorum Profundus (FDP)

• Flexor Pollicis Longus (FPL)

Role of Flexors in Throwing Mechanics

Throwing, especially high-velocity throwing, places enormous valgus stress on the elbow especially during the late cocking and acceleration phases. During these phases the flexor mass plays several key roles:

1. Dynamic Stabilization of the Elbow. The flexor-pronator mass acts as a secondary stabilizer against valgus forces that try to open up the inside of the elbow during the arm acceleration phase. This role is highly dependent on the anatomical continuity that exists between the flexors and the elbow capsule and ligamentous system. As a result, there is a dynamic role that occurs to help shield the Ulnar Collateral Ligament (UCL) from bearing excessive forces. As a result, there exists a very important bottom-up reactive strength capacity within these muscles and their associated connective tissues.

2. Wrist Flexion and Grip Strength. Powerful wrist flexion and finger flexion are essential for ball release and imparting velocity/spin (e.g., fastballs, curveballs, sliders). Strong flexors help “snap” the wrist and maintain grip on the ball.

3. Deceleration and Eccentric Control After ball release, the flexor mass along with the posterior arm, works eccentrically to slow down the arm and absorb forces, reducing stress on tendons and ligaments. Again, this highlights the need for reactive strength of the flexor mass, specifically towards the right hand side of the Linear Loading Progression

4. Forearm Pronation Pronator teres and other flexors contribute to pronation, which is a key part of the follow-through phase of throwing and helps reduce elbow stress. More importantly, the ability of the elbow to pronate efficiently comes from the underlying capacity at the elbow joint itself, highlighting the role of joint function in the throwing arm.

The Bulls-Eye

Without the knowledge of the specific details surrounding the case of Konnor Griffin, we at Absolute hypothesize that the specific detail that was found on examination as well as the imaging was located within the Flexor Carpi Ulnaris, which has a large anatomical connection to the UCL.

In this section, paid subscribers will learn: why the FCU is the most likely tissue involved in Griffin's injury, the anatomical evidence linking the FCU directly to the UCL, and what a Reactive Strength-based rehabilitation strategy looks like for the medial elbow stabilizing complex in a throwing athlete.

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The Big Takeaway

Oscillatory isometrics delivered through single-leg drop landings with light band resistance are a powerful, real-world way to train reactive strength and damping. This setup forces the nervous system to rapidly search for, stiffen, and transmit force through the trunk, posterior hip, and lower back—exactly the qualities missing in most programs. Dave Scholz’s input shows how even 20lbs of oscillation on a single leg from a 24-inch box creates visible adaptation in real time. Refining cues, amplitude, and ground contact turns this into a high-transfer tool for ACL resilience, spinal control, and athletic durability.

What We Cover in This Episode

• Dave Scholz’s Oscillatory Isometric Drill: Single-leg drop from a 24-inch box with ~20 lbs of red band resistance. The athlete must absorb the landing and immediately dampen the resulting oscillation.

• Damping Effect in Action: Clear demonstration of the nervous system searching for tissues (primarily trunk and backside of hip) to stop oscillation. Visible foot rotation, heel drop, and postural adjustments reveal how the athlete self-organizes under dynamic input.

• Top-Down vs Bottom-Up Reactive Strength: Damping is primarily a bottom-up connective tissue response (stress stiffening) guided by top-down neural search. This bridges the neuromuscular lag that traditional reactive strength definitions overlook.

• Clinical & Coaching Insights: Links to open-chain ACL injury mechanisms (e.g., Odell Beckham-style non-contact injuries). The drill exposes where force absorption breaks down and provides immediate feedback for cueing and progression.

• Refinement Ideas: Shorten bands for quicker oscillations, remove shoes for better ground feel, cue full-system rigidity from foot upward, or add lumbar oscillation via belt for targeted spinal damping.

Continue reading for paid subscribers →

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The best shortstop in baseball has been on the injured list since April 22nd.

Francisco Lindor—Gold Glove defender, perennial All-Star, the heartbeat of the New York Mets—went down rounding third base against the Twins, limping home as his left calf gave way mid-sprint. An MRI confirmed the strain was more severe than his teammates’ recent calf issues, and manager Carlos Mendoza made clear: “He’s going to be down for quite a bit.”

The coverage has been sympathetic. Bad luck. Freak injury. Wrong place, wrong time.

We’d like to offer a different explanation.

This isn’t bad luck. This is a pattern. A Bottom Up Reactive Strength Deficit.

Lindor is 32 years old. He has played over 150 games in seven of his eleven MLB seasons—one of the most explosive, high-output players in the game. Elite range, elite first-step quickness, elite base-running instincts. Everything about his game demands that his neurology outputs fast and outputs hard.

He strained his right calf in 2019 with Cleveland and missed the start of that season. Now, seven years later, the left calf. Same athlete. Same tissue type. Different side.

When you see a pattern like this—a high-output explosive athlete, bilateral calf history, injury occurring during a high-force dynamic movement—it isn’t randomness. It’s a signal. And the signal is pointing at something the mainstream injury conversation almost never identifies correctly.

His neurology outpaced his biology. Lindor has a bottom-up reactive strength deficit.

What that actually means

At Absolute Sport Science, our framework for both performance and injury management centers on Point B—the optimal internal physical state of the athlete—which conjugates four trainable capacities: Absolute Strength, Speed-Strength, Joint Function, and Reactive Strength.

Reactive Strength is where Lindor’s injury lives.

Our inside-out mental model of Reactive Strength has two components that must develop concurrently:

Top-down: the neurological and CNS drive that generates force. In elite athletes, this is typically well-developed. Years of explosive training, sprint work, and competition have built a neural network of absolute strength that can output enormous forces rapidly.

Bottom-up: the connective tissue architecture of the posterior leg: the inter and intramuscular connective tissues, the Achilles complex, and their collective ability to absorb, transmit, and dampen forces during dynamic movements like sprinting, cutting, and high-speed base running.

Here is the problem no one is naming: when top-down neurological output scales faster than bottom-up connective tissue resilience, you get a volatile system. The CNS can demand more than the tissue can deliver—not in one catastrophic moment, but through repetitive maladaptive loading that accumulates across hundreds of games, thousands of reps, over years.

Until one day, rounding third base, the bill comes due.

This is not a muscle strain. This is a reactive strength deficit. And it is entirely predictable.

Why the posterior leg is uniquely vulnerable

The calf is not a simple structure. Most athletes—and most treatment + training programs—treat it like one. Calf raises. More calf raises. Maybe some eccentric heel drops if you’re being progressive.

This is insufficient. And understanding why requires looking at what the posterior leg actually is.

The posterior leg has three distinct muscular layers, each with its own fiber orientation, its own mechanical role, and its own contribution to the connective tissue architecture that makes reactive strength emergence possible. The direction of those fibers—and how load is applied relative to them—determines whether you are actually building the biological foundation Lindor needs, or simply creating the illusion of preparation.

Most return-to-sport protocols never get to this level of specificity. They train the output. They ignore the architecture.

As of mid-May, manager Carlos Mendoza confirmed Lindor was moving into “the strength part, in the weight room, before he starts his running progression.” Building strength in the tissue is a necessary step. But strength is not architecture. And architecture is what determines whether Lindor returns from this injury and if this injury happens again.

This is where most programs stop. It’s where ours begins.

Paid subscribers: below the fold, we break down the full tissue-specific management strategy through the Absolute lens—layer by layer, fiber direction by fiber direction—and what a Conjugate strategy to Lindor’s return would actually look like at the Level of Adaptation.

The Architecture Problem—What the Posterior Leg Actually Is

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Anti-motion drills. Bracing cues. Hip hinge patterns. None of it develops what the spine actually needs.

The things are missing in almost every Reverse Hyper program:

1. Joint function: each segment moving independently, not the spine as one rigid unit.

2. Reactive strength: the tissue’s ability to absorb force, not just produce it.

3. Strength endurance: the capacity to sustain output across a full game, round, or season.

Louie Simmons figured this out in his garage in the 70s. He built the tool that brought us to where we are today. What he never published was the full progression—the journey from a broken spine to the pendulum. We took what Louie built and went further.

Yesterday we ran a live webinar walking through the origin of the Reverse Hyper and demonstrating Exercise 1 of the complete progression. John Quint—who treated Louie personally as his neuromuscular therapist—brought the original Powerlifting USA article where Louie described exactly what he was doing on that wooden platform before the machine ever existed.

You can watch the full 30-minute webinar above.

The Reverse Hyper Program is now live. Point B for the lumbar spine. The complete programming guide is 29 pages.

Early bird pricing ends tonight at 11:59pm EST. After midnight it goes from $299 to $399.

Get the Program

Welcome to the monthly roundup for Absolute Sport Science! If you’ve been busy programming treatment and training, analyzing Point A → Point B data, or just busy with the pace of life in 2026, this is your one-stop to catch up on everything we covered in May. We’ve got summaries and links to all our Tuesday written posts and Sunday video deep-dives (exclusive to paid subscribers). This is your monthly highlights—straight to your inbox.

Whether you’re a free subscriber or a paid member, these recaps are designed to keep you informed and inspired—to keep you getting better at becoming a programming strategist!

🚨 Reverse Hyper Program Launch + Free Zoom—May 29

Two things happening on May 29th that you don’t want to miss.

First: Join us for a free 30-minute Zoom session—Reverse Hyper: How Louie Actually Used It—at noon EST. We’re covering exact setup, loading, and programming before the program goes public. Save your spot here.

Then: Immediately after the call, the Reverse Hyper Program goes live. Everything we’ve been building toward this month—the history, the asymmetry, the gap in programming—lands in a complete, actionable program. Stay tuned.

Tuesday Posts: Programming Insights

Tuesdays are all about actionable, evidence-based articles to level up your programming knowledge. Here’s what we explored this month:

• May 5, 2026: The Conjugate Edge #08: Concurrent Is Conjugate → The Soviet Edge

  • There are only two programming philosophies: linear and concurrent. When you program concurrently andstructure the four Soviet methods of strength training inside that framework, you’re no longer just training concurrently — you are training conjugately.

  • Louie Simmons took the neurological aggression of the Bulgarians and conjugated it with the systematic method rotation of the Soviets. The result wasn’t a compromise — it was a synthesis. At Absolute, we’ve taken that method-based foundation and translated it into the language of capacities, giving today’s programmers a clearer framework to consciously manage the Multiplication Principle across all four fundamentals of Point B.

  • Programming Shift: Linear programming is additive and predictable — and it has two destinations: neurological stagnation or biological accommodation. Conjugate programming is multiplicative. Absolute Strength × Speed Strength × Reactive Strength × Joint Function = High Performance. Neglect any one variable and the product collapses. Improve all four simultaneously and the gains compound in ways a linear roadmap can never produce.

• May 12, 2026: Conjugate in the Clinic: Leveraging Point B Neurology to Restore Cervical Function + Reactive Strength

  • A live clinical case featuring elite grappler Dante Leon—who has graciously allowed us to share select elements of his treatment for educational purposes. His extensive training history places him at a high-functioning Neurological Point B, and we’re leveraging that existing neurology to simultaneously improve joint function (segmental control + arthrokinematics) and reactive strength—the two elements of Biological Point B.

  • This is the conjugate clinical approach in action: treating and training concurrently, in real time, with the athlete’s own neurology as the accelerant.

• May 19, 2026: The Asymmetry That Broke Louie Simmons’ Back...Twice

  • Everyone knows Louie broke his back. Everyone knows he built the reverse hyper to rehab himself. What nobody talks about is why his back broke in the first place. This piece makes the case: the neurological-biological asymmetry. His nervous system wrote a check his spine couldn’t cash.

  • The asymmetry is what happens when the neural network of absolute strength scales faster than the connective tissue that has to transmit the force it generates. When the athlete and programmer don’t know it’s there, injury risk trends up—every time.

  • Key distinction: This is where the Absolute Conjugate Strategy diverges from Louie’s Westside system. We value reactive strength over absolute strength and constrain the strategy accordingly. Go Bulgarian on the biology—not the neurology.

Sunday Paid Subscriber Video Posts

Sundays are reserved for our premium video content—in-depth breakdowns, Q&A sessions, and practical demos that bring the art and science to life. If you’re not a paid subscriber yet, these are a great reason to upgrade!

The Gap in Reverse Hyper Programming & Training May 3, 2026 — Dr. Michael Chivers & John Quint

The Reverse Hyper is far more than a back machine. Most people start where Louie finished—heavy pendulum swings—skipping the foundational steps that rebuilt his spine after a career-threatening injury. The gap is reactive strength: the ability to absorb, stiffen, and transmit force through a healthy, segmented spine—and the damping effect that makes it possible. This episode traces the origins of the machine, how Louie actually programmed it, and where Absolute’s approach becomes radically different from anything else you’ve seen on the Reverse Hyper.

Baseball as a Special Strength May 10, 2026 — Dr. Michael Chivers & John Quint

The Inside-Out Special Strength Model flips traditional programming by using real-world competition data—exit velocity, sprint times, on-field performance—as a direct feedback loop into the athlete’s neurological Point B. Exit velocity isn’t just an outcome. It reveals whether the neural network of absolute strength is fully expressed or being shielded by underlying joint dysfunction and a reactive strength deficit. Most coaches chase surface-level skill fixes when the nervous system is already in protection mode. We reference Pittsburgh Pirates Co-Director S&C Coach Alan Burr and apply the model to a Fernando Tatis Jr. case study to show what neurological shielding actually looks like in the data.

Acute Low Back Herniation Case Study: Rapid Relief Using Specific Reverse Hyper Programming May 17, 2026 — Dr. Michael Chivers & John Quint

A former professional athlete. An acute L5-S1 herniation with clear MRI findings, compression, and motor deficits in the foot extensors. Two days of targeted Reverse Hyper work—open-chain, sacral-driven segmental motion and lat isometrics, no external load — and motor function returned with significant symptom reduction. This case study shows exactly how to program the Reverse Hyper in an acute back presentation, and why starting with the pendulum is almost always the wrong call.

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Next Founders Meeting

We’ll focus on the programming variable of load with a focus on resistance:

• We will go over how the Soviets graded out resistance in the sport of Olympic Weightlifting

• Show how that graded resistance was utilized by Louie Simmons in his Westside Barbell Conjugate System

• Advance the grading out of resistance for today in 2026 and what that means in programming resistance optimally for not just the athlete but also the special strength that is desired for treatment or training

If you have any other topics worth discussing at a Founders Meeting, leave them in the comments below.

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The Big Takeaway

Treating reactive strength in the clinic is a game-changer. Most practitioners stop at joint function assessments and basic manual therapy, missing the reactive layer that drives neurological shielding. Absolute’s Inside-Out approach uses specific isometrics and oscillatory damping to engage the neural network, reduce shielding, and then address specific connective tissue issues (reactive strength deficits). This progression dramatically improves clinical outcomes by restoring the nervous system’s confidence in the tissue and allowing true biological Point B restoration.

What We Cover in This Episode

• Why Reactive Strength Must Be Assessed & Treated: Most clients/athletes are not at biological Point B and present with reactive strength deficits. Assessing only joint function is no longer enough—you must specifically test and treat the reactive component.

• Clinical Framework (Top-Down + Bottom-Up): A strategy for prompting the neural network of absolute strength to assess the bottom up connective tissue behaviors and using OIMAs to conjugate the two and stimulate reactive strength development clinically.

• Real-World Case Example: Powerlifter with suspected lat tear during deficit deadlifts. Neurological shielding prevented normal assessment. After specific reactive work, shielding dropped, allowing tissue specific palpation and treatment of the actual issue (epimysial space between teres major and lat). Tissue was intact—rapid resolution.

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The real paradigm shifter—and what almost everyone in the clinic misses—is using the Internal Isometric Continuum and …

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Louie Simmons broke his back—twice.

Most people in the strength world know the story. He told it a lot. But the story everyone tells is about the reverse hyper—the machine he innovated and built (literally) to rehab himself. The story nobody tells is why his back broke in the first place.

Bad luck? Maybe. Technical error in the good morning? He told me himself he lost focus at the bottom of the lift, so possibly—maybe neurological stagnation intra-set?1 But there’s a third explanation, one we’ve been building the language for since the inception of Absolute: the neurological-biological asymmetry.

Operationally the asymmetry is what happens when the nervous system generates more force than the biological matter can express. Neurology and biology are different. Layer the Law of Specificity on top of that difference and the logic is unavoidable—the program must train each one specifically. Concurrently. In conjugation.

When the neural network of absolute strength scales faster than the connective tissue that has to transmit the force it generates, the asymmetry is alive and breathing. If the athlete and the programmer don’t know it’s there, the risk of injury trends up. Every time.

Now think about Louie.

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Point A: Louie’s Training History

When we do case studies, the intent is to learn. Get the Point A. See why the athlete wasn’t at Point B. That gives us bits of information about why the injury occurred, and—more importantly—how we learn how to program our way to Point B and stay there.

Programming is the Hidden Layer that links Point A to Point B. It’s how we leverage treatment and training work. Select, sequence and organize the work in a conjugate strategy.

Louie’s Point A is legendary. He ushered the Soviet training methods into the West—thanks, Louie. Two methods in particular: max effort and dynamic effort. Dr. Zatsiorsky, the former Soviet sports scientist and author of Science and Practice of Strength Training, says explicitly that these methods exist to stimulate the nervous system. Translated into our programming language: they scale the neural network of absolute strength. More nodes get added and interconnected which enables the athlete to generate larger magnitudes of force, expressed at higher speeds, actualized into + through the biology.

Louie’s nervous system ran those methods for decades. His neural network of absolute strength was elite—not opinion, fact. He was an elite powerlifter for decades. And when you’ve got that kind of skin in the game, you get scars in the game. There is a cost. A toll that gets paid when your standard is breaking all-time world records.

All Gas, No Brakes

Here’s the thing about an elite Point B neural network of absolute strength: it generally means you’re running all gas, no brakes. Literally.

It’s a fun ride. But you need to program some brakes while you’re concurrently hitting the gas. See how that itself requires a conjugate strategy?

The Soviet methods scale the nervous system—rapidly, and we emphasize the rapidly. That means the biological tissues lag behind. The biology is constantly playing catch-up. That’s exactly why in our conjugate programming strategy we teach you to go Bulgarian on the biology—not on the neurology. This is a key difference from Louie’s Westside Conjugate System to the Absolute Conjugate Strategy. We value reactive strength over absolute strength and constrain the strategy accordingly.

So what happened to Louie?

His nervous system wrote a check his spine couldn’t cash.

This has been happening to athletes at Neurological Point B since the dawn of the asymmetry. At the time of Louie’s injuries—and every injury like it before him—we just didn’t have a formal name for it.

Now we do.

The rest of this post is for paid subscribers.

Below the paywall:

• Why the reverse hyper isn’t a “back exercise” — and what it actually is

• The inside-out model that makes Louie’s injury almost inevitable in hindsight

• How to stop programming the reverse hyper like an accessory and start programming it like a special exercise

• What all of this means for how you program your next training block

The Reverse Hyper: A Biological Tool (Special Exercise) Born from a Neurological Problem

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