Why NBA Players Keep Tearing Their Achilles — A Physical Therapist’s Perspective
By Dr. Danh Ngo, PT, DPT, OCS, SCS | ReVITALize Rehab Club, Long Beach, CA
The 2024–25 NBA season was one of the most injury-riddled in league history. Seven Achilles tendon ruptures. Jayson Tatum. Damian Lillard. Tyrese Haliburton. All gone in a single season — with the year before recording zero.
Fans are asking why. The NBA convened an expert panel. Sports journalists called orthopedic surgeons.
Everyone is pointing at the same answers: overuse, low-cut shoes, too many games, not enough rest.
Those answers are not wrong. But they are incomplete.
After 20 years as a physical therapist and working with athletes of all levels, I see a bigger picture that nobody in the mainstream sports conversation is talking about. And it directly applies to why your injuries may not be healing the way they should either.
How Much Force Does the Achilles Tendon Actually Handle?
Before we talk about why it’s failing, let’s talk about what it’s up against.
Research shows the Achilles tendon absorbs between 6 and 12.5 times your body weight during running and jumping. For a 230-pound NBA player, that’s over 2,500 pounds of force on a single tendon — repeatedly — across an 82-game season plus playoffs.
The Achilles is built for this. It is the strongest tendon in the human body. It stores energy like a spring and releases it on demand. It doesn’t just randomly snap.
When it ruptures, something in the system that supports it has already broken down. The tear is the last event in a long chain of failures — not the first.
The Modern NBA Game Changed the Loading Pattern
Here’s something I haven’t heard anyone say yet.
The NBA today is a fundamentally different sport biomechanically than it was 20 years ago. Scoring has jumped from roughly 101 points per game in the 1990s to over 115 today. The game is faster, more explosive, and almost entirely offense-driven.
The move that defines the modern era — the Euro-step — is also, biomechanically, one of the most Achilles-loading movements in sport. A player builds momentum going one direction, plants hard, decelerates violently, and explodes the other way. Watch Luka Doncic operate and you’re watching exactly that pattern on every possession.
A published biomechanics study analyzing video of NBA Achilles ruptures found that in every single case, the injured athlete performed a false-step mechanism — planting behind their center of mass before driving forward — with the ankle in a deeply loaded position at the exact moment of rupture. That is the Euro-step plant. The signature move of the modern NBA and the most common Achilles injury mechanism are biomechanically identical.
Meanwhile the defensive side of basketball — lateral shuffling, controlled positioning, lower-velocity contact — has been reduced by rule changes and analytics-driven strategy. What’s been lost is the variety of movement that used to distribute stress across the whole lower body. Today’s game is relentless, one-directional, explosive offense. The Achilles gets hit the same way, at peak force, possession after possession.
That’s not just overuse. That’s a movement monoculture. Tendons that only experience one type of loading — especially at the extreme end of the force range — are tendons being quietly set up to fail.
Why the Achilles Is the Most Vulnerable Spot on the Body
The Achilles sits at the furthest point in the body from the heart and lungs.
That matters more than most people realize.
Blood and lymphatic fluid — the systems that deliver oxygen, clear waste, and repair tissue — have to travel the maximum possible distance against gravity to reach the Achilles and return. The lower leg, from the knee down, has dense fascia, complex anatomy, and multiple points where fluid naturally slows and pools. It is the hardest place in the body to maintain healthy circulation.
This is why lower leg swelling is always the first sign of circulatory problems as people age. The lower leg is where the system shows its cracks first.
In a healthy, rested athlete, fluid still moves. Tissue repairs overnight. The tendon recovers between games.
But in an NBA player deep in a playoff run — traveling across time zones, managing chronic stress, sleeping inconsistently, running on cortisol — that fluid environment starts to break down. The Achilles is being asked to perform at its peak while living in increasingly hostile tissue conditions.
Here’s the critical detail: every one of the three major 2025 playoff Achilles tears was preceded by a documented calf issue. Tatum, Lillard, Haliburton — all had calf tightness before they ruptured.
That calf tightness wasn’t a training problem. It was a warning signal. The tissue was telling the medical staff that the environment was compromised. The signal got managed instead of heard.
The Problem With How Teams Are Managing These Bodies
Professional athletes are managing enormous physical and psychological loads with a pharmacological toolkit that, used chronically, quietly undermines the body’s ability to repair itself.
This is not a criticism of team medical staffs. These are the logical tools for the demands of the job. But the downstream effects are real.
Anti-inflammatories (NSAIDs) suppress the inflammatory cascade that initiates tissue repair — not just the part that causes pain. Chronic use means the repair crew never fully gets called to the job site.
Antibiotics — particularly the fluoroquinolone class like ciprofloxacin — have a well-documented effect on collagen synthesis. Research published in 2025 confirms they impair the cellular machinery responsible for building and remodeling tendon tissue. The Achilles tendon is made of collagen. Connect those dots.
Acid blockers impair absorption of magnesium and zinc — both essential for collagen production and tendon integrity.
Adrenal stress from travel, performance pressure, identity anxiety, and the relentless demands of being elite suppresses immune function, impairs lymphatic circulation, and degrades collagen synthesis at the hormonal level.
The pattern is the same across all of it: the body’s distress signals get quieted. The athlete keeps playing. The tendon keeps silently degrading. Until it doesn’t.
Why “Train Harder” Is the Wrong Answer Right Now
The NBA’s current response to the Achilles crisis is more calf strengthening, more eccentric loading, more precise neuromuscular training. Get the lower leg stronger and better adapted.
For a healthy, rested athlete with good systemic recovery — that is exactly right. I prescribe this. The research supports it. Progressive tendon loading is one of the most powerful tools in rehabilitation.
But here is the problem.
We are not talking about healthy, rested athletes.
We are talking about players in month nine of a season, carrying accumulated stress, disrupted sleep, hormonal depletion, compromised fluid dynamics, and a pharmacological load that has been suppressing their body’s repair signals for months.
Research on overtraining is clear: when tendons are repeatedly loaded without adequate systemic recovery, collagen breaks down, repair capacity is exhausted, and the tissue becomes more vulnerable — not stronger. The same loading protocol that builds a healthy tendon destroys a compromised one.
Loading a depleted system harder does not make it stronger. It accelerates the failure.
Think of it like this: you can give someone who hasn’t slept in three days the best workout program ever written. Their body won’t adapt. It will break down faster. The training stimulus requires a system capable of responding to it.
Less is more when the athlete is already depleted. That is not a recovery slogan. It is the biological reality of how tendon tissue heals — or fails to.
What This Means for You
If you’ve ever been told to push through an injury, work harder, or just strengthen the area around the pain — and it didn’t work — this is why.
The injury is rarely the whole problem. It’s usually the last visible sign of a system that’s been under stress for a long time. The tissue was sending signals. The signals got suppressed or ignored. Eventually the body runs out of ways to compensate.
The question that has to come before “how do we load this tissue better” is: is this body currently capable of adapting to load at all?
That means looking at the whole system — circulation, lymphatic clearance, hormonal status, inflammatory burden, sleep, gut function, stress load. It means asking why instead of just treating where.
That’s what I’ve been doing for 20 years. And it’s what the NBA — and your body — is asking for right now.
The Bottom Line
Seven NBA Achilles tears in one season is not bad luck. It is a system-wide signal.
The tendon is not the problem. The tendon is where the problem finally became visible.
Until elite sports medicine starts looking upstream — at fluid dynamics, systemic recovery capacity, hormonal health, and the real biological cost of suppressing the body’s warning signals — we will keep seeing the same injuries in the same athletes at the same point in the season.
And until your own care starts asking why your body keeps breaking down instead of just where it hurts, you may keep getting the same results too.
Want to understand why your injury isn’t healing the way it should? Schedule a free consultation with Dr. Ngo at ReVITALize Rehab Club in Long Beach.
For a deeper clinical analysis of the systemic mechanisms behind this pattern — including fluid dynamics, osteopathic fascia theory, and the role of peptides in modern athletic recovery — read the full thought leadership piece here.
Dr. Danh Ngo is a Doctor of Physical Therapy and Board-Certified Specialist in Orthopedic (OCS) and Sports Medicine (SCS) — credentials held by fewer than 20 physical therapists in California. He is a Kresser Institute ADAPT Level 1 Practitioner, Titleist Performance Institute Medical Professional Level 2, and OnBase University Pitching and Hitting Specialist. He has practiced in Long Beach, CA since 2005. revitalizerehabclub.com