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The Case, In Order

1. Displays of the Neural Network: Acuña Jr at Point B — Jul 2025

2. Acuña Jr. Poll Results + Answer — Aug 2025

3. Ronald Acuña Jr’s Season Shows the Link Between ACL and Hamstring Injuries — Jul 2026

4. The ACL-Hamstring Feedback Loop — Aug 2026

Acuña Jr. turns in the right field corner and throws a bullet to third with no bounce. There may not be another right fielder in Major League Baseball who makes that throw. That film types him instantly: he is at Neurological Point B—his neural network is scaled, it compresses, it gives you everything you want.

And the same athlete carries two ACL reconstructions and two hamstring strains in the same season, same leg. That history, not his neurology, is his number one limiting constraint.

This is the case that shows why Neurological Point B and a reactive strength deficit can live in the same athlete at the same time—and why the network is the reason nobody sees the deficit. A trained neural network pushes force straight through a disorganized biology and produces a highlight. It can do that repeatedly, until the accommodation-stagnation cycle catches up. We don’t know the date. We know there’s a date.

Programming is the only way out: using the top-down element he already has to build the bottom-up element he doesn’t.

Learning how to read that asymmetry and program against it is exactly what The Art & Science of Programming teaches.

The programming—the measurement error, the reflexive arc, the exact in-season input and its sequencing—is below for paid subscribers.

Point B Hamsting vs. Usable Biology

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Louie used to talk about them in the Dead Room. I’d have my hands in his tissue—conjugating between palpation and treatment, and he’d be talking—about Dyachkov, about the manuals he had bought through Bud Charniga, about the fact that the Soviets had people whose entire job was the science of sport. Not coaches who read. Not doctors who lifted. Scientists, employed by the state, studying the athlete as a system. That was how the Soviets built Exercise Science, he’d say. They paid people to figure it out.

He talked about them the way you talk about a species that lives on another continent. Real, documented, and not here.

In the fifteen years since, we have educated performance staffs across professional sport. You hear it constantly. We have a sport scientist. We have a whole department. You hear it, you nod, and you go work with the strength staff and the medical staff and the athletes, and the sport scientist is a name on an org chart you never meet.

Until August, at Elite Athletes Center, in the Dominican Republic. Where one of them signed up for our Baseball as a Special Strength course.

What a Soviet sport scientist actually did

It is worth being specific about what the Soviets actually built, because the word has drifted—but that is our lineage. It is the heartbeat of our conjugate strategy, and it is alive.

The best account of it in English is still James Riordan’s Sport in Soviet Society, published in 1977—the first serious academic study of the subject, written by an Englishman who had actually worked inside the Soviet system and had access to primary sources no other Westerner could get to. What Riordan documents is not a training philosophy. It is an institution: physical culture written into state policy, sport tied to labour and defence, a national apparatus with budgets, ranks, research institutes and a career ladder.

That is the part that gets lost when American coaches say the Soviets. There was no Soviet secret. There was a Soviet payroll.

By 1935 the USSR had a Unified Sports Classification System that ranked not only athletes but coaches—expertise itself was given a rank, a standard, and a ladder. That is a strange thing to do unless you believe that knowing how to develop an athlete is a technical discipline with correct and incorrect answers. By the late 1970s there were thousands of researchers working inside that apparatus, publishing across dozens of periodicals in circulations that would embarrass most of what passes for sport science literature today.

So when Louie said the Soviets had sport scientists, he was not describing a job title. He was describing a state that had decided the development of an athlete was a research problem, and then funded it like one for seventy years.

And the lens was primarily physics—but only as far as Newtonian physics goes.

Zatsiorsky is the clearest case. Open Science and Practice of Strength Training anywhere and you are reading force, velocity, work, and the relationships between them, described precisely. That is the measurement language, and it is Newtonian.

What it is not is a model of the athlete.

Soviet physiology spent the better part of a century dismantling the idea that an organism answers an input the way a beam answers a load. Neurophysiologist Nikolai Bernstein took apart the reflex arc and showed that movement is continual correction rather than execution—the same intention never produces the same command twice, because the body it is issued into has already changed. Pyotr Anokhin replaced the arc with a functional system: a loop that carries an anticipated result forward and checks the actual result against it.

Verkhoshansky and Zatsiorsky inherit that directly. The training effect depends on the state of the athlete receiving the load—not on the load. You have to know the organism before you can know what the input will do to it.

Which is Point A, stated in Russian, fifty years early.

Training max is the proof. Zatsiorsky drew that distinction not to describe a resistance ceiling but a psychophysiological one—a competition max carries the full stress response with it, the heart rate spike before the bar leaves the floor, the arousal that lets a lifter produce a number he cannot produce on a Tuesday and cannot produce again for weeks. A training max is what the system will give you without that response. Identical bar. Identical physics. Completely different organism.

That is the whole reason the concept exists—and it is why maximal effort can be run at frequency instead of burning the athlete down. It is a psychophysiological observation wearing a number.

So: the tools were Newtonian and the subject never was. The Soviets used physics to measure an organism they explicitly refused to treat as a mechanism, and that refusal is the thing worth inheriting.

Then 1991, and the apparatus dissolves...

Except it didn’t disappear. It re-emerged here, in America, in a different building. It went upstairs. It stopped being physics and became probability; regression instead of mechanics, outcome distributions instead of force curves, a laptop instead of a lab. Same job, different math.

Which is exactly why I had never met one. I was looking in the weight room.

Why Baseball as a Special Strength — and Why in the Dominican Republic

Two days at Elite Athletes Center. The education was the one we always run—The Hidden Layer of Programming: Point A, then Biological Point B—joint function and reactive strength—then Neurological Point B—absolute strength and speed-strength—and then the conjugation, where all four elements collide into baseball as a special strength.

The purpose was never to hand anyone exercises. Exercises are the cheapest thing in this field. The purpose was so that an organization could program treatment, training, and practice as one strategy in conjugation, rather than three departments that share a hallway, a budget, and nothing else. Treatment and training operates at the Level of Adaptation. Practice operates at the Level of Competition. Conjugate is what makes them one thing—the effects are multiplicative, not additive.

And we went to the Dominican Republic because that is where the baseball athlete is actually physically developed. Not signed. Not developed later, in an organization hierarchy disguised as a system, after somebody else has already made the decisions that matter. Developed—from adolescence, in academies, at the one point in a career when the connective tissue architecture can actually keep pace with a scaling neural network of absolute strength. Regenerative capacity is at its highest. Turnover is fast. The tissue will answer almost anything you ask of it. That window is not a limiting constraint. It is the single best opportunity anyone will ever have to build an athlete who is symmetrical from the start.

Consider what the UCL epidemic actually looks like from the inside. The athletes who reach the major leagues are, disproportionately, the ones whose tissue happened to stay synced with their neurology through adolescence—whose architecture kept up, not because anyone programmed specific treatment and training for it, but because the regenerative capacity was there and the volume was tolerable and they got lucky. That is the Absolute thesis on what the pipeline is selecting for. Not talent alone. Survivorship.

Then the rope frays, tissue senescence dominates culminating in repetitive breakdown and regeneration leaving a twenty-five-year-old with an elbow considerably older than he is. Regeneration slows. And the neural network does not slow with it. The network is still enormous, still producing force it took a decade to build, and the architecture underneath it has quietly stopped being able to transmit it.

That is the neurological-biological asymmetry, and it is why these reactive strength deficits and injuries arrive when they do. Not at the start of a career, when the tissue could still answer. Years in, after the biology has stopped keeping up and nobody noticed because the output looked fine right up until it didn’t. This is not just isolated to the UCL.

Whatever asymmetry an athlete carries into professional baseball, most of it was laid down—or prevented—before anyone in a major league front office ever saw him throw.

That is why the intervention has to happen there. If you introduce a programming strategy at the developmental level—one that strategically simulates the neurological and biological ecologies in conjugation while the tissue still answers freely—you are not fixing an athlete. You are changing the state of every athlete who comes out of that pipeline, and you are doing it in the window where the biology is cheap.

Because the alternative is what the game currently has. A development environment that scales neurology relentlessly, programs the treatment and training of the bottom-up element of reactive strength—connective tissue architecture—almost not at all, and then selects for the ones who survived the omission. That is a systemic reactive strength deficit, and it does not stay a deficit. It becomes a UCL, an Achilles, an oblique, a hamstring—usually years later, in a uniform somebody paid a great deal of money for—Juan Soto is current case in point. And the injury is not just a limiting constraint on the athlete, or on the organization that bought him. At the volume baseball is currently producing them, it is a limiting constraint on the entire major league.

That’s the course. That’s why we flew to the DR as those working in baseball refer to it.

The Paul Skenes case study

Day two, live case study: Paul Skenes.

The slide before it was the one the whole course had been building toward—biological accommodation and neurological stagnation, the two failure states, and the specific order in which they emerge. That slide is the reason we were discussing Skenes at all. We’ll come back to it at the end, because it is the piece of this we actually want in your programming neural networks.

What Skenes gave us was the live version: what those two states look like when they finally surface at the Level of Competition, in public, in a box score.

Take a look at these two slides:

June 2025—this is what Point B looks like: four-seam averaging 98 to 100, 102 on the ninety-eighth pitch of a game, six to eight distinct pitches, a twenty-mile-per-hour gap between the fastball and the curveball. All four elements of Point B expressing live, a nervous system in total control of its biology. We wrote that piece over a year ago, and the line at the bottom of it was: assess him now, before stagnation sets in.

Then August 2026—this is what stagnation looks like. Velocity trending down across the season. Ground-ball rate 51% as a rookie, under 40% now. Innings per start down. Thirteen home runs, more than either full season before it. Not one glaring failure. Several small declines reinforcing one another, which is precisely how stagnation presents.

I was at the front of the room presenting it, and I could see him go on his phone. Not scrolling. Working. Pulling the objective evidence and checking my slide against it in real time.

We broke. He came straight up.

This part is incorrect. This part doesn’t matter.

What he was right about

He came at two bullets.

The spin. I had “spin down roughly 70 rpm—less spin-based movement” on the board. He told me it didn’t matter, and cited Alan Nathan, professor emeritus of physics at Illinois and the person most responsible for what baseball actually understands about the flight of a ball.

He was right, and here is why. Raw spin doesn’t move a baseball. Only the component of spin perpendicular to the ball’s direction of travel—the transverse or active component—generates the Magnus force that produces movement. The component running parallel to the direction of travel, gyro spin, spins the ball like a bullet and contributes nothing. A pitcher can lose spin and lose no movement whatsoever, or hold spin and lose all of it, depending entirely on what the axis did. The number on its own has no meaning.

And spin scales with velocity. If the fastball comes down two miles per hour, spin comes down with it and the ratio is unchanged. Seventy rpm off a fastball in that range, tracking a velocity decline, is not a finding. It is the same pitch, thrown slower.

Then the measurement itself. Nathan has been explicit that there is enough noise in the inferred spin values that you can’t attach much significance to a single pitch. Seventy rpm sits inside the error bars.

The standard deviation. I had Stuff+ at 110 last season and 98 this season, described as a fall from a standard deviation above average to average. He doubted the standard deviation claim. He was right to. Stuff+ is a model output scaled to a mean of 100—whether a twelve-point drop is one standard deviation depends on the population and the sample, and the number carries its own error before it carries any meaning. I had stated a modeled estimate as though it were a measurement.

So: two bullets off the board.

And nothing happened to the case. Velocity down. Ground-ball rate collapsed. Innings per start down. Home runs up, past both prior full seasons. Zone rate down, walk rate at a career worst. Those are outputs of the organism, not artifacts of the instrument, and they still say the same thing they said before he walked up.

He didn’t correct the model. He cleaned the data the model was reading. He made it harder to argue with.

And the model he left standing is the one on that earlier slide: accommodation first, stagnation after. Hold that order. It is the whole argument.

Because the model was never the spin number. The model is inside-out special strength—the claim that baseball is a special strength expressed by an internal state, that the internal state is four elements (Point B), and that when the output at the Level of Competition flattens the way Skenes’ has, you can name which internal state produced it. That is what lets us stand in front of a room and say this is biological accommodation in conjugation with neurological stagnation, and mean something operational by it rather than something rhetorical.

He didn’t touch that. He couldn’t have—it isn’t measured by anything on his side of the wall. What he did was strip two numbers out of the evidence that were describing a tracking device rather than a pitcher, and hand the argument back to us with less to attack.

Which is when it registered what was actually happening in that room. If you want to program treatment, training and practice for baseball as one strategy, you have to understand baseball as a special strength—and to do that you need both halves: a measurement layer honest enough to say which numbers are real, and an internal model capable of saying what the real ones mean. We had spent two days teaching the second half to a room that included a man who does the first for a living, and the two halves fit.

We weren’t defending a framework. We were building something with someone.

This is the part of the Soviet system that never got exported. America imported the manuals. What it never imported was the room—physiologists and biomechanists and physicians and coaches on the same payroll, pointed at the same athlete, each one in a position to check the others’ work. Riordan’s whole book is a description of that arrangement. Louie was buying the outputs of it secondhand, through translators, forty years late.

The arrangement was never the secret. It was just expensive, and nobody here was willing to pay for it. Which is the part we want to be precise about, because we were not there by accident. We were hired. Somebody wrote a budget line for two days of programming education at a developmental academy, and that budget line is what put a sport scientist with programming strategists and a room full of coaches in front of the same pitcher’s data at the same time.

The Soviets needed a state to build that room. It now costs a seminar. That is the whole finding.

He wasn’t arguing with the framework. He was auditing Point A.

Here is what made this collaboration worth writing about.

Go read Have We Been Assessing Hitters Backwards?—his (Jack Cecil) 2020 piece at Pitcher List, built on multiple regression against per-pitch plate discipline data to produce expected walk and strikeout rates. The argument is that hitting analysis has always lagged behind pitching analysis for a structural reason: a pitcher decides what to throw, where, and how—that’s an input. The hitter reacts to all of it—that’s an output. And when you evaluate an output, you are evaluating something that could have been produced four or five different ways. A 22% strikeout rate could be three called strikes, three whiffs, or a ten-pitch battle lost to an umpire’s zone. The number is identical. The athlete is not.

So he goes underneath it. He decomposes the outcome into the per-pitch decisions that generated it, and only then does he tell you what he thinks a hitter actually is.

That is our discipline in a different currency.

A performance drop is not something we ignore—it is Point A. The Level of Competition is the ultimate feedback loop, the place where the internal state finally declares itself in public and generates data we cannot generate any other way. A complaint, a symptom, a velocity decline, a bat speed that fell off in August: all of it is Point A, and all of it is why we assess at all.

What it is not is a programming instruction. Those are outputs, and any given output can be produced by more than one internal state. A hamstring that won’t optimally output could be a hamstring, or a hip, or a neural net that has never been trained, and the presentation reads identically from the outside. The output tells you that something is true. It does not tell you what. Point A exists to take the output apart until you know which internal state produced it—and only then are you permitted to program.

Which is why the quality of the data going into Point A determines the quality of everything downstream of it. Bad inputs don’t produce a bad answer. They produce a confident one.

And the internal states we are decomposing toward are not infinite. There are two failure modes available to a trained athlete, they arrive in a fixed sequence, and almost everyone in this field has the sequence backwards. That is the slide.

He found two numbers in our Point A that were properties of the tracking apparatus rather than properties of the athlete. That is precisely the error he spends his career finding in hitters. Same move, different domain.

The discipline is identical. The refusal is identical. I will not assess this thing on a number I cannot take apart.

Five tools, four elements

He had already done something else for us, earlier in the course, that mattered more than the correction. He gave us the five tools.

This is a man who has ranked an entire farm system prospect by prospect, and who has worked inside the Angels, the Athletics, Baseball Info Solutions and TrackMan. When he tells you what the game is actually buying, you write it down.

Hit for contact, hit for power, run, field, throw. The scouting language—and it landed instantly, because it is the external target our internal model has to resolve into. We do not come from baseball. We knew we didn’t know what baseball actually wants from a body, and a real strength of Absolute is that we know what we do not know, specifically and without embarrassment. What we do know—better than anyone working today—is programming and conjugate.

So he handed us the currency of the Level of Competition, and we handed him the currency of the Level of Adaptation.

Five tools are how the game prices an athlete. Four elements are how the athlete is built. The scouts defined baseball’s Point B decades before anyone had a force plate, and they defined it well—they just defined it externally, in terms of what comes out. Absolute strength, speed-strength, joint function and reactive strength are the same target described from the inside, in terms of what has to exist for any of those five to be expressed at all.

Inside-out special strength is exactly the translation between those two vocabularies. It is not a competing model. It is the layer underneath the one baseball already has.

Why baseball is on the edge

This is the thing I flew home with.

Baseball has built the most sophisticated Level of Competition measurement apparatus in the history of sport. Every pitch decomposed. Spin axis, active spin ratio, per-pitch swing decisions, bat speed, arm angle to the degree. Physicists publishing openly on the mechanics of the ball. An entire public research culture layered on top of a private one. Nothing else in professional sport is close.

And at the Level of Adaptation, it has almost nothing.

Jack can tell you, to the decimal and with error bars, that Skenes’ output is flattening. He can tell you which parts of that flattening are real and which are instrument noise, and he will do it standing at the front of a classroom to a guy who flew in to teach. What he cannot tell you—what nobody in that building can currently tell you—is why. Whether the neural network has stagnated. Whether the connective tissue architecture has failed to keep pace with a nervous system that scaled faster than the tissue could follow. Whether this is a top-down problem or a bottom-up one.

That is not a criticism of him. It is not his layer. Nobody has been assigned that layer.

The measurement apparatus at the Level of Competition is world class and the model of the athlete at the Level of Adaptation is subjective opinion. That gap is the entire reason both of us were standing in that room in the Dominican Republic. It is also, I’d argue, the reason baseball currently leads professional sport in the injuries that come from exactly this asymmetry— bottom-up reactive strength deficits—a game full of enormous neural networks and no institutional model of the tissue underneath them.

What closes it

Inside-out special strength is that layer. Not a competing measurement—a translation.

The five tools are the outside. They describe what the game buys. The four elements are the inside. They describe what has to exist for any of the five to be expressed, and—this is the part that matters—they are trainable and treatable, which the five tools are not. Nobody can program hit for power. You can program the absolute strength, speed-strength, joint function and reactive strength that make hitting for power available to a body, and then let the tool emerge.

Which is the answer to the question Jack couldn’t reach from his side of the data. He can establish, with error bars, that the output is flattening. The inside-out model asks the next question in a form that has an action attached to it: which of the four elements moved, in which direction, and is this a neurological constraint or a biological one? Those two answers produce completely different Mondays. One says compress the network. The other says the network is fine and the architecture underneath it is failing to transmit what the network is producing.

That fork—which of the two failure states you are actually looking at, and which one came first—is the slide I keep pointing at.

And that translation is exactly what happened in the room, in real time, in both directions.

He took two numbers out of our Point A that were describing his instrument rather than our athlete. We gave him a decomposition of the remaining numbers that his framework has no way to generate—not how much Skenes has declined, but what internal state produces a decline shaped like that one. Neither of us could have done the other’s half. Both halves were required, and it took about fifteen minutes on a break.

That is not a metaphor for how the two layers close. That is the two layers closing.

Baseball is one layer away from high performance. It has the external half already built.

Neither lens closes the loop

He is in the Dominican Republic looking for the next billion-dollar talent. We are looking at what it will take to keep that talent intact once he finds it.

Same athlete. Two Point A’s. His is measured at the Level of Competition and it is enormously more precise than ours. Ours is measured at the Level of Adaptation and it is the only one that tells you what to do on Monday.

I spent a decade hearing about sport scientists from the man who's responsible for bringing Soviet training methods to the West in a chalk-covered room in Columbus, Ohio who was buying Soviet manuals to get at what they knew. It took until this August to sit across from one—and to find out that the first thing he’d do is take two of my bullets off the board.

That’s the collaboration. That’s what it’s supposed to feel like when the loop closes.

Further reading

• James Riordan, Sport in Soviet Society: Development of Sport and Physical Education in Russia and the USSR—Cambridge University Press, 1977.

• Jack Cecil, Have We Been Assessing Hitters Backwards?—Pitcher List. The input/output distinction that runs underneath everything above.

• Jack Cecil, Oakland Athletics 2021 Preseason Top 50 Prospects—Pitcher List. What evaluation looks like at scale.

• Alan Nathan, The Physics of Baseball—University of Illinois. The active-spin work behind the correction.

• Absolute Sport Science, Paul Skenes: Not Just Arm Talent—This Is What Point B Looks Like (June 2025).

The slide

Everything above is the story. This is the bit of programming information of it worth keeping.

This is the slide put up on day two, before Skenes—the one the entire course is organized around, and the one I’ve been pointing back at throughout. It is our account of the two failure states available to a trained athlete, and the order in which they arrive.

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The Big Takeaway

“Conjugate” hasn’t moved since Louie Simmons—everyone’s just repeating what he said, a decade or more after he said it. Louie built an effective system, but a system and a strategy aren’t the same thing: a system says “this is how we do things,” a strategy asks “given this Point A, how do we get to Point B.”

The Conjugate Edge exists to make that shift—turning bits of information from conjugate systems, including the Soviets Conjugate Sequencing System into a real-time strategy that works in the clinical setting too, not just on the weight room. That’s the difference between plugging in someone else’s 1970s or 1990s template and actually sequencing (programming) treatment and training for the athlete in front of you today.

Learning how to build that strategy instead of borrowing someone else’s system is exactly what The Art & Science of Programming teaches.

What We Cover in This Episode

• Why “Edge”: Conjugate hasn’t moved since Louie—everyone’s repeating what he said 10+ years after he said it.

• System vs. Strategy: A system says this is how we do things. A strategy asks given this Point A, how do we get to Point B.

• Conjugate Predates Louie: A conjugate sequencing system emerged out of the Soviet Union as Tom Malinsky’s PhD thesis enabled us to know, well before Louie ever touched it—his programming for powerlifting success hijacked the word.

• Breaking the Silo Between Treatment and Training: Conjugate strategy syncs the therapist and the strength coach so they run in parallel, not in sequence.

• A Live Point A Feedback Loop: A real example of holding off on a finding because of an upcoming training max.

• Bits of Information, Not a Whole New System: The goal isn’t claiming Louie was wrong—it’s giving programmers usable pieces to run in their own setting.

System vs. Strategy, in One Example

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Friday was a private session with the Pittsburgh Pirates performance staff at their academy. Saturday and Sunday were an open seminar at Elite Athlete Center. Three days, one reframe.

The Reframe: Baseball as a Special Strength

Baseball is understood as a skill, and that understanding is useful—it is what makes skill coaching possible. But the skill lens returns coachable findings: self-organizing, things the athlete solves, things a skill coach can practice, cue and rep. It does not return treatable and trainable findings. And you cannot program a coachable finding.

So if you want to know how to program treatment and training work for specific to the sport of baseball and individual to the athlete, you have to observe and understand baseball as a special strength—strength expressed under the exact neurological and biological conditions the sport imposes. Every throw, every hit, every time a ball gets fielded qualifies as a special strength. The scout grades five tools—hitting for contact, hitting for power, fielding, running, and throwing; every one of them has top-down neurological components and a bottom-up biological components.

A tool is what gets graded and coached. The neurological and biological prerequisites of those tools are what get programmed.

Friday. With the Pirates staff we built the model from the ground up—Absolute’s inside-out mental model of special strength, the neural network of absolute strength, Point A → Point B, the Neurological–Biological Asymmetry, and the conjugate strategy that answers it.

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Saturday—bottom-up biology. This was Biological Point B. Joint function and reactive strength. Joint function is macro range externally and micro motion internally, governed by capsular space—and space is dynamic. It can be acquired and it can be lost. Reactive strength is emergent: the CNS outputs, the connective tissue reacts. The damping effect sits at the center of it, tissue stiff enough to self organize to transmit force rapidly and compliant enough to dissipate what would otherwise damage tissue.

Then main focus of the day was centered on framing connective tissue injuries are reactive strength injuries. Calf, hamstring, forearm, UCL, Achilles—different tissues, one mechanism, a bottom-up capacity that never scaled with top-down output. We worked through published case studies of Konnor Griffen, the Phillies, Francis Lindor and then spent the afternoon on the Internal Isometric Continuum and the three classifications—HIMAs, PIMAs and OIMAs—including the oscillatory work we have spent the last year refining.

Sunday—top-down neurology. This was Neurological Point B. Absolute strength and speed strength, and the neural network of absolute strength that produces both. We programmed and did a practical for how to take a training max. Discussed the distinction most people never make is intensity: at a stimulating intensity you are adding nodes to the network, at a retaining intensity you are turning the existing ones on.

Everything we taught is published here. If you want the mechanics rather than the lens, The Art & Science of Programming is the module that lives in the hidden layer.

Which sets up the most practical idea of the weekend—conjugating training and practice for the baseball athlete. Turn the nodes of the network on, then go use it—a training max at a retaining intensity, then straight into the cage with neural intent on the tool the Level of Competition says the athlete needs. Training converges; practice diverges. Practice can only draw on what training has made available. Use programming to get the baseball athlete to neurological Point B and practice now becomes the special strength of baseball emerging.

We closed on neurological stagnation—the accommodation–stagnation loop, and programming as strategy that gets the most out of treatment and training. The absolute conjugate strategy for baseball is to acquire the neurological and biological prerequisites of the five tools—getting the athlete from Point A to Point B.

We are already scheduling the next Baseball as a Special Strength seminar for this offseason. Make sure to subscribe and you will hear about it first.

Thank you to the Pittsburgh Pirates performance staff—specifically Orlando Crance, Ariel Mercedes, Jack Cecil and to Elite Athlete Center for hosting, and to everyone who traveled and asked hard questions for two days.

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Want to run this inside your program?

Friday we did exactly this with the Pittsburgh Pirates’ performance staff at their academy — the full model, built from the ground up, in their facility with their people.

We run in-house seminars for professional and collegiate programs. Tell us about your program and we’ll set up a call.

In-house seminar

The Big Takeaway

The Soviets found a neurological strength deficit decades ago and programmed their training trying to close it. We found a biological reactive strength deficit, and closing it is the wrong move entirely. This one you fill—by taking the neurology an athlete already has and funneling it to stimulate the actualization of biology that’s missing.

What We Cover in This Episode

• The Soviets’ Muscular Strength Deficit, Defined: the gap between voluntary maximal strength and absolute strength (measured via electrical stimulation)—and why that gap is purely neurological.

• Why the Best Athlete on the Team Gets Hurt Most: the highest neural nets carry the highest neurological-biological asymmetry, and that asymmetry is the bottom-up deficit.

• Don’t Close It. Fill It.: why funneling existing neurological output into the biology is the opposite move from the Soviets’ close-the-deficit approach.

• The Connor Griffin Case: why Point A means an FRA across every extremity, not just the injured joint, and how a joint function deficit elsewhere explains an overloaded UCL.

• Conjugating the Programming: using PIMAs, HIMAs, and OIMAs together—and why teaching the nervous system to dampen matters more here than adding more output.

• Any Input Can Be an Assessment: how slow eccentrics, faster eccentrics, over-speed eccentrics, and oscillatory isometrics pinpoint exactly where reactive strength breaks down.

• Where OIMAs Actually Came From: the clinical problem—tissue the athlete can’t feel—that oscillatory isometrics were built to solve.

Same Word, Different Deficit

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In our last substack on Ronald Acuña Jr., we highlighted his injury timeline—two ACL reconstructions, followed by two hamstring strains in the same 2026 season—both reactive strength injuries, on baseball specific efforts (base running + sprinting after a fly ball) at the Level of Competition. It is our belief that this is case study on link between the ACL and hamstrings—specifically not a strength deficit per se but an information flow feedback deficit.

Since we do not work with him directly, we are assuming that he can pass basic strength testing of the hamstrings—whatever the Braves are utilizing. Most likely they have force plate testing of the hamstrings that is showing that the magnitude of force output is there and is symmetrical between limbs. With him being at Neurological Point B—that is possessing a large neural network of absolute strength, we assume that he passed that in flying colors, but what that type of testing/assessment does not show is whether the loop between the ACL and the hamstrings—the one that lets the neurological network of absolute strength react to chaotic loading on the baseball field—has been reestablished and is intact.

If that feedback loop is what’s missing—or even lagging, general hamstring strengthening won’t rebuild it. It needs a specific input that trains the ACL and the hamstrings in conjugation, in the same rep, under the same reactive strength loading that injured his hamstrings in the first place. That’s exercise 3 in Absolute’s Reverse Hyper Program.

The Exercise that Reestablishes the ACL-Hamstrings Feedback Loop

Exercise 3 is three dynamic effort repetitions of an open chain hamstring curl on the reverse hyper, followed by a pendulum catch + damping.

The athlete uses their neural network of absolute strength to generate dynamic efforts with their hamstrings to curl into knee flexion. As the pendulum gains energy from the hamstrings curls and swings faster and faster, on the eccentric phase of is repetition, the training intent switches to use the hamstrings to catch the pendulum and damp it.

That means the hamstrings have to eccentrically absorb and stress-stiffen against real, moving energy, not static load/resistance. The knee is doing genuine deceleration work through that catch, which means the ACL isn’t a passive bystander in this exercise—it’s an active participant in stabilizing the joint while the hamstrings + ACL and other connective tissue structures of the knee joint like the capsule, do the work of killing the pendulum’s momentum.

That’s the loop, trained directly. The hamstrings can’t stress-stiffen effectively without accurate real-time information from the joint about where it is and how much tension it’s under. And the joint’s signal is only useful if the hamstrings can act on it fast enough to catch a moving load. Exercise 3 constrains the hamstrings and ACL to conjugate together and as result the ACL-hamstrings feedback loop gets stimulated and reestablished.

Conjugating Joint Function with Reactive Strength to Reestablish the ACL-Hamstrings Information Feedback Loop

Pre-exercise 3, knee joint CARs. This stimulates the articular receptors of the knee before the pendulum work starts, so the joint is already feeding accurate signal into the neural network of absolute strength before the reflexive loop gets asked to output. Post-CARs, exercise 3 locks that signal in—it’s the loop having to operate under real, moving load right after the receptors have been primed.

Two sets is the floor to make sure the loop is actually getting stimulated. And this isn’t a once-a-week input—it’s daily. For Acuña specifically, given where he sits in return-to-play, multiple sessions per day is warranted to get the loop reestablished at the rate his case demands.

The research behind why this specific movement targets the loop, and how it should be programmed into Acuña’s specific case, is available to paid subscribers.

How Exercise 3 Stimulates the ACL-Hamstrings Feedback, Loop

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The Big Takeaway

The headline reads "hamstring." But Acuña's Point A history reads ACL, then ACL, then hamstring, then hamstring—same leg, every time. That's not five unrelated injuries in our opinion. It's one reflexive arc between the ACL and the CNS that never got fully reestablished, and a hamstring that's been running without its network support ever since.

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Ronald Acuña Jr's Season Shows the Link Between ACL and Hamstring Injuries

Recently it was reported that Ronald Acuña Jr was getting closer to his return to the Atlanta Braves lineup after finishing his second game on his current rehabilitation stint in the minor leagues for his second hamstring strain this season…

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a month ago · 7 likes · 1 comment · Dr. Michael Chivers and John Quint

What We Cover in This Episode

• The Reflexive Arc, Discovered: Scott Dye’s arthroscopy research—probing an exposed ACL and watching that mechanical stimulus fire electrical output straight into the hamstring.

• Why the Arc Goes Quiet: how incomplete rehab or an overly conservative knee can both leave the hamstring “unprotected,” just through opposite mechanisms.

• His Network Isn’t the Problem: Acuña came back an MVP-caliber player after ACL tear #1—proof his neural output was never the constraint.

• The Real Point B Targets: why knee flexion, extension, and internal rotation are the specific joint function elements that have to reestablished first.

• Top-Down Disguised as Bottom-Up: how a joint function gap gets misread as a hamstring, reactive strength problem.

• The Programming Call: why his Health History overrides the injury report when you’re actually building Point A.

The Reflexive Arc, Explained

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A note before we start: the reporting on Caleb Downs’ knee is unconfirmed. We have no relationship with Downs or his medical team. We’re using the public reporting as a hypothetical to illustrate a finding we see constantly in our own practice—because the case, if true, is a textbook example of something most performance staffs never assess for.

Here’s the report, via USA Today: a partially torn meniscus, and a potentially degenerative ACL. No confirmation, just a denial from Downs. A lot of questions that swirled around him and his knee joint ahead of the 2026 NFL draft—and a slide out of the top 10, despite being the consensus best defender in the class, that ended with Dallas trading up to take him at 11.

The meniscus tear, if real, isn’t confusing. Downs is dynamic, explosive, violent in how he closes space. Any clinician in high performance hears “meniscus” on a player like that and nods. Makes sense.

The degenerative ACL (if true) is the part that doesn’t make sense. Until it does. Once you see special strength from the inside-out—you just a cannot unsee it.

If you want to program for reactive strength you need a mental model not a definition.

Most college football programs treat reactive strength as a number—RSI on a force plate, if they even have any feedback loop at all to monitor this special strength. RSI stands for Reactive Strength Index, and it’s a measurement, not a model.1 RSI isn’t wrong—it’s incomplete. It is a measurement and not a model.

When we take that measurement and funnel it through our inside out mental model of reactive strength, it obvious that it primarily captures the behavior of the top-down element: how well the nervous system organizes and expresses force in that moment. That is great, but understand—it entirely misses the nuances of bottom-up element—programable connective tissue bits of information.

Put simply, just like an MRI does not tell a manual practitioner how to program treatment in real time, information from the RSI does not enable the programming strategist the ability to know how to program reactive strength in real time. This is why as programming strategist that work in the clinical space, do we ever ask before treating and athlete with a reactive strength deficit do we ask: what is the RSI?

Neurological Point B Arrives First, Maybe Biological Point B Catches Up

Our programming model is Point A to Point B: the distance between where an athlete operates now and the optimal physical state they need to reach to perform at the Level of Competition, repeatedly—without injury.

Point B has two versions, and they rarely arrive together.

Neurological Point B is the neural network’s capacity to organize a magnitude of and express that output at speed. For us, it’s a real time conjugation of absolute strength with speed strength. Neurological Point B is trainable, and it adapts in real time fast. If you know what to look for you see the neutral network learn in real time.

Biological Point B is the biological capacity of the joints + connective tissue transmitting the energy the neural network is outputting into force—at the highest attainable speeds. That’s reactive strength, in the narrow sense.

In the college football athlete, the neurology can get to Point B years ahead of what the biology can optimally express at the Level of Competition. Don’t take our word for it—see Malik Naber’s having a reactive strength deficit in high school, that is still present to this day.

Biological Point B is the bottom half of our inside-out special strength mental model almost no college football program in the country, outside the couple we work with directly, ever assesses, regardless if the athlete is hurt or healthy and is the blind spot this substack is about.

The Neurological-Biological Asymmetry

We’ve never worked with Downs—but we have and currently work directly with this athlete population, extensively. Our experience allows us to not need to have to work directly with these athletes to recognize the pattern of bottom up reactive strength deficits—because we see it in every college football athlete who comes through our practice. These athletes are on some of the best rosters in the country and getting paid millions: operating at Neurological Point B, nowhere near Biological Point B, and a Point A performance history built entirely on that gap that has never been filled.

Programming the treatment and training strategy of these specific athletes is how the concept of the neurological-biological asymmetry emerged from Absolute. Not theory, this is our direct work with this specific athlete type. As programming strategist responsible for their physical development, safety and well-being, we have to immediately label them as possessing this asymmetry and having to take the appropriate programming action. It’s the same asymmetry we laid out with Malik Nabers—a nervous system years ahead of the tissue underneath it, compensating in ways that look like talent until the exact moment they don’t.

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College football is the perfect ecosystem for developing neurology and never assessing the biology.

Every program has force plates. Every program has GPS tracking. Most have 1080s. What almost none have is a staff member whose job is monitoring the bottom-up, tissue-level side of reactive strength—the biology that enables the output the wearables are celebrating.

College football will show you all the neurological output you want. These programs have the resources—they pay players millions, they can pay to acquire—literally buy, the best neurology in the country. What they can’t show you is the biology. Nobody’s monitoring the bottom-up side of reactive strength, because the top-down side is what the football coaches want and that is who the performance staffs work for.

In investing terms, these programs are over-leveraged with zero hedge. The neurological system is the leverage—it’s producing returns (speed, explosiveness, violence) far beyond what the underlying asset (the joint/tissue) has been shown to support without degradation. Nobody’s hedging the position, because nobody’s tracking the asset. It’s remarkable to watch play out in real time across a sport this well-resourced.

Physicist Richard Feynman put it best: “The first principle is that you must not fool yourself—and you are the easiest person to fool.”

Sport scientists monitoring reactive strength with zero biological data aren’t lying. They’re just fooling themselves—mistaking a complete-looking dashboard for a complete picture. That gap is exactly how you get athletes like Nabers and Downs scaling up to the next Level of Competition into the NFL already carrying a reactive strength deficit nobody measured—and the gap is likely widening.

This reactive strength deficit is something we identified first at Absolute, and one we’ll be covering all college football season. That's the case we made in The Conjugate Edge #10: OIMAs (the hedge)—our argument for why OIMAs should be the number one isometric programmed for this specific athlete demographic.

Everything above is the pattern. Everything below is the mechanism: how a nervous system actually shields a joint, why we think that’s exactly what happened with Downs, and a live example from a major program’s ACL protocol showing how invisible this is—even to one of the best staffs in all of college football. For paid subscribers.

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The Big Takeaway

“Conjugate” hasn’t moved since Louie Simmons—everyone’s just repeating what he said, a decade or more after he said it. Louie built an effective system, but a system and a strategy aren’t the same thing: a system says “this is how we do things,” a strategy asks “given this Point A, how do we get to Point B.”

The Conjugate Edge exists to make that shift—turning bits of information from conjugate systems, including the Soviets Conjugate Sequencing System into a real-time strategy that works in the clinical setting too, not just on the weight room. That’s the difference between plugging in someone else’s 1970s or 1990s template and actually sequencing (programming) treatment and training for the athlete in front of you today.

Learning how to build that strategy instead of borrowing someone else’s system is exactly what The Art & Science of Programming teaches.

What We Cover in This Episode

• Why “Edge”: Conjugate hasn’t moved since Louie—everyone’s repeating what he said 10+ years after he said it.

• System vs. Strategy: A system says “this is how we do things.” A strategy asks “given this Point A, how do we get to Point B.”

• Conjugate Predates Louie: A “conjugate sequencing system” existed in Tom Malinsky’s PhD thesis before Louie ever touched it—his powerlifting success just hijacked the word.

• Breaking the Silo Between Treatment and Training: Conjugate strategy syncs the therapist and the strength coach so they run in parallel, not in sequence.

• A Live Point A Feedback Loop: A real example of holding off on a finding because of an upcoming training max.

• Bits of Information, Not a Whole New System: The goal isn’t claiming Louie was wrong—it’s giving programmers usable pieces to run in their own setting.

What continues below for paid subscribers: the specific real-time example of holding off on a neurological shielding finding because of an upcoming training max, and how that same sequencing logic exposes exactly what keeps going wrong if you programmed for Malik Nabers today.

Conjugate Isn’t a System. It’s a Strategy.

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Jonathan Davis is an assistant strength coach with Florida Gators Football, functioning as the return-to-play arm of that staff. His background is backwards from most: he was working on tables before he ever got certified as a strength coach, and he brought that table into the weight room on day one.

In this Founders Meet…

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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!

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Tuesday Posts: Programming Insights

Tuesdays are all about actionable, evidence-based articles to level up your programming knowledge. July was an infrastructure month—we made the case for OIMAs and the reverse hyper as the internal hedges that keep neurology and biology in sync, then extended that same asymmetry to a new case study on the Braves' Ronald Acuña Jr. Here's what we explored:

• July 7, 2026: The Conjugate Edge #10: OIMAs—The Hedge at the Edge

  • Reactive strength volatility isn't fixed by rest—the nervous system recovers in days, connective tissue unloads, so resting only widens the neurological-biology gap instead of closing it.

  • The hedge is the OIMA: an isometric that stimulates top-down (neurology) and bottom-up (biologically) simultaneously, forcing both systems to sync/conjugate and solve the same problem together.

  • Same neurological-biological asymmetry shows up when the spine is a limiting constraint.

    • Which is why we program pendulum-damping (OIMAs) across the entire posterior chain—glutes, hamstrings, multifidus, erector spinae, lats, etc. in our Reverse Hyper Program.

• July 14, 2026: The Hidden Layer in Your Point A: Endocrine Function

  • Endocrine system function is already hiding inside Point A’s Health History pillar (energy, sleep, body comp, stress, meds)—it’s just never been named or tested directly, since blood panels and cortisol testing aren’t practical in most settings.

  • For athletes training hard but not recovering or adapting, or getting hurt at a rate the programming doesn’t explain, this is the layer to check.

  • Peptides BPC-157 and TB-500 views as neuroprotective/endocrine lens, not just biological tissue repair.

• July 21, 2026: Ronald Acuña Jr’s Season Shows the Link Between ACL and Hamstring Injuries

  • A prior ACL tear doesn't just heal and disappear—it meaningfully raises re-injury risk on the same leg for years, especially when the graft is hamstring-sourced and never fully recovers its strength. Acuña's 2024 ACL reconstruction, followed by repeated hamstring strains on the same leg, is exactly that pattern playing out in real time. The likely failure: treating the ACL rehab program as a knee problem, then handing him back to general conditioning—an incomplete Point A carried into an incomplete strategy and never getting to Biological Point B.

If the Ronald Acuña breakdown 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 strategy. 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. July's run moved region by region—Nabers' toe, the reverse hyper's onboarding sequence, and the elbow—showing the same neurology-outpacing-biology pattern shows up everywhere, not just the usual hotspots. If you're not a paid subscriber yet, these are a great reason to upgrade!

July 5, 2026: Malik Nabers—The Mosquito He Can't Kill

• Nabers has never been at reactive strength Point B since high school, and it isn't a talent gap—it's a neurological-biological asymmetry that's gone unframed and unprogrammed for years. His nervous system was already capable of outrunning his tissue's capacity before he reached LSU. The turf toe everyone dismisses as a nagging nuisance is actually the visible symptom of that gap—a top-down output that's permanently outpaced the bottom-up tissue meant to support it. First MTP dysfunction at NFL-receiver force levels carries massive effects up the entire kinetic chain, not just locally.

July 12, 2026: An Update From Absolute—The Reverse Hyper Program, New Merch, and Four Years In

• Answers the single most-asked question on how to logically onboard someone onto the reverse hyper. Built on years treating Louie Simmons and working hands-on with the reverse hyper itself, this isn't competing with Louie's original work—it's Absolute's programming layer on top of it which is solving the reactive strength deficit in the spine. Also covers new merch and marks four years of the publication.

July 19, 2026: Pendulum Prerequisites — Why Most People Start the Reverse Hyper 5 Exercises Too Early

• The reverse hyper is a six-exercise conjugate sequence, and the pendulum swing everyone knows is exercise five, not one in our programming. Skip ahead and you bring an unresolved deficit to the hardest version of the movement—then blame the machine when it fails. A real case showed the rate-limiting tissue was the sciatic nerve, not the hamstring, proving why the pelvis-hip uncoupling has to happen passively first, before it's ever loaded.

July 26, 2026: The Reactive Strength Deficit Leading Indicator at the Elbow

• A generic label like "flexor mass strain" is programming noise—you can't write a set until you know which specific tissue is compromised. The UCL isn't one structure either: its anterior, posterior, and middle bundles tension at different elbow angles, so the "safe" position shifts depending on which bundle is stressed. Key finding: palpating the flexor carpi ulnaris, not imaging, is the fastest read on ligament stress, since its insertion interweaves with the UCL bundles. Two patterns show up in pitchers convinced their UCL is torn—shielding vs. disorganization—and each calls for a different same-day program decision.

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Coming Up This Wednesday: Founders Meeting with Jonathan Davis

Mark your calendars—our next Founders Meeting is Wednesday, July 29, at 1:30 PM Eastern. We’ll be sitting down with Jonathan Davis, Florida Football’s Strength & Conditioning and Return to Play lead, for an open discussion with all founding members. Come prepared to participate!

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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This is a follow-up to Konnor Griffin's Flexor Mass Strain: Detailing the Anatomy & Implications, the anatomy piece we wrote back in June.

The Big Takeaway

Flexor mass strain isn’t a programming signal—it’s noise. The program input is what you feel when you palpate: which specific tissue is shielding, whether that shielding is neurological or a sign of tissue disorganization, and what that tells you about a UCL you can’t directly feel. That single read decides whether today’s session removes a shield or loads a tissue—and it’s the difference between a return timeline that drags and one that compresses.

Turning a palpation finding into a same-day program decision like this is exactly what The Art & Science of Programming teaches.

What We Cover in This Episode

• Why Injury Labels Are Programming Noise: “Flexor mass strain” bundles multiple flexors and a pronator into one term. You can’t write a single set until you know which specific tissue is actually compromised.

• The UCL Isn’t One Structure: Anterior, posterior, and middle bundles come under tension at different elbow angles—meaning the “safe” position to load or protect the elbow changes depending on which bundle is stressed.

• Flexor Carpi Ulnaris as the UCL’s Early Warning System: Its broad, U-shaped insertion physically interweaves with the UCL bundles, so palpating FCU—not imaging—is the fastest read on ligament stress.

• Shielding vs. Disorganization: Two different palpation findings that call for two different program decisions—clear the neurological shield first, or load the tissue directly if it’s disorganization instead.

• The Point A Feedback Loop in Real Time: A real case—on a non-throwing day, a shielding finding means going aggressive to clear it so the UCL can be loaded; if the UCL itself is compromised, it can shield the flexor mass right back, closing the door until that’s addressed first.

• Rotational Dysfunction vs. True Medial Stress: Pronator/supinator shielding means the elbow can’t rotate through pitch types. FCU/FCR/FDS shielding means the medial elbow is actually absorbing excess load. Both walk in as “sore elbow”—they are not the same program.

What continues below for paid subscribers: the specific palpation findings that separate a rotational elbow problem from a true UCL problem, and when the case calls for aggressive shield-clearing versus passive, directional-only loading.

The Reactive Strength Deficit Leading Indicator at the Elbow

The Palpation Findings That Separate a Rotational Elbow Problem from a True UCL Problem

Two clean patterns show up in pitchers who come in with elbow soreness convinced their UCL is torn:

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Founders Meeting Announcement

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

Date: Wednesday July 29, 2026
Time: 1:30 PM Eastern Time (US and Canada)

We’re excited to have a conversation with Jonathan Davis.

Topic: Jonathan will be joining us to discuss:

• What he’s changed in his practice over the last 2 years

• How he’s reducing his return-to-play timelines

• Where he sees return-to-play going in the future

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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Recently it was reported that Ronald Acuña Jr was getting closer to his return to the Atlanta Braves lineup after finishing his second game on his current rehabilitation stint in the minor leagues for his second hamstring strain this season.

Acuña Jr who has immense baseball skill has dealt with repetitive injury issues, specifically in his legs in each of the last five years. When healthy, he is a devastating player for opponents as evidenced by his 2023 NL MVP award.

Despite his prowess, since 2021 he has been forced to battle through numerous setbacks that have stolen time and production from his baseball career. Here is a chronological list of his injuries:

Acuna Jr’s Injury Timeline

• July 2021: Acuña tore his right ACL, ending his season mid-way through what was shaping up to be an MVP-caliber year.

• May 2024: Acuña tore his left ACL on a non-contact baserunning play—he planted his left foot trying to redirect back to second base and his knee gave way. He missed the remainder of the 2024 season after an MRI revealed a complete tear, suffered on a non-contact play while running the bases. Surgery was performed by Dr. Neal ElAttrache in Los Angeles, who had also performed the 2021 procedure.

• May 3–18, 2026: First left hamstring strain of the season, also sustained while attempting to run out a grounder.

• June 9–11, 2026: Second left hamstring strain in the same season. He was placed on the 10-day injured list with a Grade 1 left hamstring strain after exiting a loss to the White Sox the day before, having injured himself running out a ground ball. Manager Walt Weiss noted it didn’t appear as severe as the previous strain but would still require time to heal.

Even though his initial setback was on the right leg with the ACL tear, subsequent to the same injury in 2024 on the left side, he has suffered from repeated hamstring strains—reactive strength injuries, exhibiting the exact same mechanism.

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Why the Same Leg Matters

The connection between a prior ACL reconstruction and a subsequent hamstring strain on the same limb isn’t just narrative—it’s a recognized pattern in sports medicine, for a few overlapping reasons:

1. Graft-related muscle deficits (if a hamstring graft was used). One of the most common ACL graft sources is the patient’s own hamstring tendon (typically the semitendinosus, sometimes with the gracilis). Research comparing graft types found that while quad tendon grafts showed a transient quadriceps strength deficit that fully resolved by return to play, hamstring grafts showed both quadriceps and hamstring strength deficits that never fully recovered. If Acuña’s graft was harvested from his own hamstring, that tendon is now structurally different and permanently weaker than it was pre-surgery—a very plausible substrate for recurrent strains (Acuña’s specific graft type hasn’t been publicly reported).

2. Altered biomechanics and compensation patterns. Even when the graft doesn’t come from the hamstring, ACL reconstruction changes how the entire kinetic chain of that leg functions. Rehab focuses heavily on rebuilding quad strength and knee stability, and athletes commonly develop compensatory movement patterns—altering stride length, hip extension, or deceleration mechanics to protect the reconstructed knee. Unfortunately, in some cases the athlete will progress through rehabilitation such that these alterations will not manifest until the athlete has returned to the Level of Competition. Obviously this has the potential to shift load onto the hamstring in ways the muscle isn’t conditioned to absorb under the constraints of sport, especially during high-speed, high-eccentric-load actions like sprinting out of the box or decelerating into a bag.

3. Residual neuromuscular deficits. ACL tears don’t just damage the ligament—they disrupt sensory feedback and neuromuscular control throughout the limb. Studies on ACL-reconstructed athletes consistently show measurable strength and activation asymmetries between limbs that can persist for years, even after athletes are cleared to “full” activity. This is the importance of the neural network of absolute strength. A hamstring operating with imperfect neuromuscular coordination is more vulnerable to a strain during an explosive, uncoordinated moment—like Acuña “beating out a grounder,” which is precisely how both 2026 strains occurred.

4. The general pattern of reduced durability. Beyond the specific hamstring mechanism, there’s a broader and well-documented finding in the sports medicine literature that lower-body soft-tissue injuries cluster and recur—an ACL tear meaningfully raises the risk of subsequent injuries (hamstring, quad, groin, calf) on the same leg for years afterward, even absent a single clean causal link. Acuña’s injury history is “the critical variable” for his hamstring strain specifically, considering he spent much of 2024 rebuilding movement patterns and lower-body mechanics from scratch after the ACL tear and subsequent reconstruction. Considering we wrote about durability as a quality possessed by the athlete individually, that is characterized by ecological efficiency, any injury that creates reverberations through the system has the potential to decrease it.

Point A: The Diagnostic Starting Point

Within the Absolute model of high performance, Point A synthesizes four lenses—Physical Assessment, Health History, Performance History, Training History—before any programming happens. Acuña’s Health History alone is a flashing yellow signal. Given that a prior ACL injury carries roughly 2.2–2.25x greater risk of a future hamstring strain, his Point A profile wasn’t just “athlete recovering from knee surgery”—it was “athlete in a documented high-risk category for subsequent (hamstring) injury on that same leg.”

Absolute has no inside information regarding Acuna Jr or his management through the Braves medical staff or any of his potential private health team. Having said that, if his programming managed the 2024 ACL rehabilitation as solely a knee problem to solve and then handed him back to general baseball conditioning, that’s an incomplete Point A being carried forward into an incomplete strategy—exactly the failure mode the framework warns about.

The remainder of this article—covering which of the four capacities (Joint Function, Absolute Strength, Speed Strength, Reactive Strength) most likely broke down in his return-to-play programming, why a hamstring can pass a strength test while still carrying a CNS-level activation deficit, and what a properly conjugated strategy would look like for an athlete with Acuña’s profile—is available to paid subscribers.

If the Absolute Conjugate Strategy is new to you, the learning module is the right place to start: The Art & Science of Programming—Absolute Sport Science

Point B: Where the Four Capacities Likely Broke Down

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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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