By Sarah Vizel Genco

I. A dream ended in a single landing

I trained 33 hours a week as a teenage competitive gymnast. Two practices a day, six days a week, year-round (summer “break” meant only 25 hours a week), no more than two consecutive days without workouts - ever. Almost everyone I trained with decades ago carries the consequences of that unrelenting training in their body today.

The evidence of the toll that poorly-programmed training takes on gymnasts’ bodies was apparent in the 2024 U.S. Olympic Trials. Skye Blakely ruptured her Achilles tendon during podium training two days before competition even began. Kayla DiCello ruptured her Achilles on the very first routine of competition, a double-twisting Yurchenko vault she had successfully performed thousands of times. Shilese Jones (one of my personal favorites), a world champion in 2022 and 2023, injured her knee warming up on vault on Day 1.

The moment their bodies chose to give out was the worst possible one, but the damage that caused it had been accumulating for years.

Those injuries were not a result of one-off falls. They were the predictable end result of connective tissue that had been loaded past its recovery capacity, over and over, without enough time between training sessions to rebuild. Their tendons and joints did not fail suddenly; they had been failing slowly for a very long time.

We treat these injuries as the price we paid to compete. That price is too high, and it likely isn’t even a necessary cost to pay for excellence in the sport.

This is a programming problem, and it has a solution.

II. How common is this?

About 70% of injuries in competitive gymnastics happen during landings and dismounts. Overuse injuries, meaning injuries caused not by a single event but by repetitive stress that accumulates over time, make up a large share of the total. These include Achilles tendinopathy, patellar tendinopathy (jumper’s knee), wrist growth plate inflammation (gymnast’s wrist), spinal stress fractures, and cartilage degeneration in the knee and ankle.

The long-term picture is worse. Former elite gymnasts have significantly higher rates of joint pain, osteoarthritis, and limited function in adulthood than non-gymnasts of the same age. Many describe daily pain in multiple joints as something they simply accepted as part of the sport. We built a training system that reliably produces chronic pain in the people who go through it, and then we called that “normal”.

It is not normal. It is a consequence of specific choices about how training is structured. Those choices can be changed.

III. What happens inside the tissue

Tendons, ligaments, and cartilage are not inert cables and cushions. They are living tissue that remodels in response to load. But they remodel slowly, and only within a specific range of stress.

Below about 4% strain, a tendon stretches under load and returns to its original length when the load is removed. No lasting damage. Between 4% and 6% strain, the tissue starts losing stiffness and the collagen fibers begin sliding past each other. Above 6%, structural collagen damage is detectable. Above 8-10%, the tendon tears.

Walking loads the Achilles tendon to about 2% strain. Running reaches 4.6-7.0%. Jumping pushes past that, and gymnastics landings have been measured producing forces at the ankle of up to 23 times body weight. Floor tumbling, vault, and beam dismounts routinely operate at or above the threshold where structural collagen damage begins. Gymnasts hit that range repeatedly, every practice, for years.

This does not automatically cause injury. The body can handle it. But only if there is enough time between sessions for the tissue to repair.

Here is what actually happens during that repair window: cells in the tendon called tenocytes detect the mechanical stress through receptors embedded in the tissue. They activate gene expression programs that synthesize new collagen and rebuild the matrix. The tissue degrades slightly under load, then rebuilds stronger during rest. That is the adaptation cycle. It is why training works at all.

The window for this cycle to complete is roughly 48-72 hours. Muscle recovers faster because it has a rich blood supply. Tendons and ligaments have poor blood supply. Cartilage has none at all. When the 48-72 hour window is not respected, collagen fibers cannot fully reconstitute their cross-links before the next loading session. Damage accumulates faster than the tissue can repair it. Over months and years, the collagen architecture becomes disorganized, stiffness drops, and the tissue enters a degenerative state that is very difficult to reverse.

The gymnasts at the 2024 Olympic Trials were not unlucky. Their tissues had accumulated a debt that could not be paid back. A single landing called it in.

IV. What the traditional training model actually does to the body

The traditional training schedule was designed around skill acquisition and competitive calendars, not tissue biology. Under the model I grew up in, and that many elite gymnasts still train under, the longest recovery window is one and a half days over the weekend. Every other gap between high-impact sessions is about 14 hours or less.

Fourteen hours is not enough time for connective tissue to complete its repair cycle. Not even close. So gymnasts do vault approaches, tumbling runs, and beam dismounts on tissue that is still in the middle of rebuilding from the session before. The muscles feel fine. The athlete feels ready. But the tendons, operating on a slower biological clock with far less blood flow, are not ready.

The body does not signal this with pain. Subclinical tendon damage is silent. Pain arrives late, often only after the tissue has already degenerated significantly. By the time a gymnast notices Achilles pain, the structural damage has usually been building for months, if not years. Many injuries seem to come out of nowhere. They did not.

This is the real cost of the traditional model: not dramatic acute injuries, but the quiet, relentless degradation imposed on every gymnast who trains through it. The system does not hurt athletes occasionally. It degrades them systematically.

V. What a better training structure looks like

Alternating high- and low-impact days

The fix is not to train less. It is to train smarter by alternating high-impact days with low-impact days, with at least 48 hours between sessions that heavily load the same joints.

In women’s artistic gymnastics, vault, floor, and beam are the high-impact events. Uneven bars is comparatively low impact. There are few landings (mainly the dismount), and the forces on the hips, knees, and ankles are minimal. A practical weekly structure could look like this: high-impact days (vault, floor, beam tumbling) on Monday and Thursday; low-impact days (bars, strength conditioning) on Tuesday and Friday; active recovery on Wednesday and Saturday (dance, flexibility training); complete rest on Sunday. Total training hours stay roughly the same. The load pattern on connective tissue changes completely.

Strength training on off days

Controlled strength work on low-impact days does two things. It builds the muscle that absorbs force before it reaches the tendon, which is a direct injury buffer. A 2020 meta-analysis found that strength training reduced sports-related overuse injuries by 33-50%. And slow, heavy eccentric exercises, meaning exercises that emphasize the lowering phase of a movement, directly stimulate tendon collagen synthesis, as long as there is enough recovery between sessions.

Strength training at moderate loads, roughly 60% of one-rep max, loads tendons with sustained tension rather than rapid high-magnitude impact. Tenocytes get a positive adaptive signal without the cumulative micro-damage that comes from landing mechanics. It is an investment in tissue quality.

Where plyometrics fit

Plyometrics are closer to tumbling skills training than to strength training in terms of tendon strain. Rapid ground contact, spring-loading mechanics, high force peaks. They do not belong on recovery days. They work best at the start of a high-impact session, when the athlete is fresh, or as their own dedicated block. Stacking them onto an already-loaded skills session is how you drive tissue into the damage zone without realizing it.

Sleep and nutrition matter more than most coaches think

Recovery is not just the absence of training. The biological repair processes need active support.

Sleep is probably the most underrated variable. Growth hormone is released in pulses during deep sleep, and it is one of the main drivers of collagen synthesis in tendons and ligaments. Gymnasts who are also students and sleeping six hours a night are not recovering the way their training assumes they are.

Nutrition timing for connective tissue is counterintuitive. Tendons cannot absorb nutrients from the bloodstream the way muscles can, because they have such poor vascular supply. Instead, they rely on synovial fluid being mechanically pumped through the tissue during loading. This means that consuming gelatin or hydrolyzed collagen peptides, plus vitamin C (which the body needs to cross-link collagen), about 30-60 minutes before practice, rather than after, gets those amino acids into circulation exactly when mechanical loading can drive them into the tissue. Studies have shown this timing produces meaningfully higher collagen synthesis than post-exercise supplementation.

Standard whey protein is not sufficient for connective tissue repair. Collagen synthesis requires glycine, proline, and hydroxyproline, amino acids that are scarce in whey. A gymnast can be hitting her total protein targets and still be underfueling her tendons.

Light movement on recovery days, bar work at low intensity, cycling, swimming, helps too. Gentle joint loading compresses and releases synovial fluid, delivering nutrients to tendons and cartilage without adding significant stress. This is active recovery in a literal sense, not just a psychological one.

VI. The objections

“Reducing volume will hurt skill development.” This assumes the current volume is actually producing the intended adaptation. A gymnast with progressively degenerating tendons is not benefiting from her repetitions the way that assumption requires. She is borrowing capacity from her future body. The goal is not necessarily fewer total repetitions over a career. It is spacing sessions so that they can get in the reps and also have sufficient recovery time.

“Other elite sports train just as hard.” Yes, and they are also dealing with serious overuse injury crises. Basketball and soccer have ACL epidemics. Distance running has stress fracture problems. The serious programs in those sports are actively building load management protocols in response. Gymnastics has been slow to follow. The fact that other sports also have this problem is not an argument for keeping it.

“This is just how elite gymnastics works.” This is the one that needs the most pushback, because it is the most entrenched. Chronic pain is not a biological feature of gymnastics. It is a consequence of how gymnastics is programmed. The sport has changed its scoring systems, its equipment standards, and its athlete welfare policies many times. Programming is not exempt from scrutiny just because it has always been done this way.

VII. What research would actually help

This piece makes a case, not a proof. The underlying physiology is solid. The programming implications follow logically. But translating them into practice requires research that does not fully exist yet.

The most useful first step would be biomechanical studies that calculate tendon and ligament strain for specific gymnastics skills, not just generic jumping tasks, but actual elite-level skills. How much Achilles tendon strain does a Yurchenko double pike landing produce? How does a bar dismount compare? Or a take-off after a backhandspring into a full-in? Those numbers would let coaches assign real load values to specific training activities instead of guessing.

Second, computational models that combine those strain values with tissue recovery timelines to predict cumulative damage under different programming schedules. This approach has worked in intervertebral disc research. It is increasingly being applied to ligament fatigue prediction. A gymnastics-specific version would let coaches and researchers stress-test proposed schedules against biological thresholds before putting them in front of athletes.

Third, prospective studies comparing injury rates and long-term tissue health between gymnasts trained under conventional programming and those trained under alternating-load models. The evidence base for load management in gymnastics is thin. Building it is the only way to move this from a reasonable argument to a practice standard.

Institutions with the right combination of sports medicine, biomechanics, and orthopedic research capacity are natural partners for this work. The research is doable. It just needs to be done.

VIII. The actual cost of doing nothing

A gymnast who ruptures her Achilles at Olympic Trials is not a data point. She is someone who spent a decade or more of her life on this sport, who made it further than almost anyone, and whose body gave out at the worst possible moment. She is not an outlier. She is what the system produces when it is working exactly as designed.

The gymnasts who never rupture anything are not spared. They just carry the damage differently, in the form of knee pain at 35, ankles that ache in cold weather, hips that have been quietly degenerating since their teens. They do not show up in injury statistics. They show up in their own lives, every day, for the rest of them.

None of this is inevitable. The biology is understood. The recovery windows are known. The nutritional interventions exist. A programming model that respects the repair cycle is not a fantasy. It is an engineering problem, and the inputs are already on the table.

What we owe the next generation of gymnasts is not softer training. It is smarter training, built around what we actually know about how connective tissue works. That is not a concession to weakness. It is how you build athletes who are still intact when it counts and can enjoy their lives without chronic pain after elite sport.

Selected bibliography

Arampatzis, A., et al. (2007). Influence of the muscle-tendon unit’s mechanical and morphological properties on running economy. Journal of Experimental Biology, 209(17), 3345-3357.

Bahr, R., & Maehlum, S. (Eds.). (2004). Clinical guide to sports injuries. Human Kinetics.

Bojsen-Moller, J., et al. (2005). Mechanical properties of the patellar and quadriceps tendons in elite volleyball players. Journal of Applied Biomechanics, 21(4), 352-369.

Cook, J. L., & Purdam, C. R. (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43(6), 409-416.

de Vos, R. J., et al. (2012). Patellar tendinopathy: Some aspects of basic science and clinical management. British Journal of Sports Medicine, 41(4), 211-216.

Docking, S. I., & Cook, J. (2019). How do tendons adapt? Going beyond tissue responses to understand positive adaptation and pathology development. Journal of Musculoskeletal and Neuronal Interactions, 19(3), 300-310.

Fahlstrom, M., et al. (2002). Chronic Achilles tendon pain treated with eccentric calf-muscle training. Knee Surgery, Sports Traumatology, Arthroscopy, 11(5), 327-333.

Gymnastics Medicine. (2025). Injury prevention and connective tissue health in competitive gymnastics. gymnasticsmedicine.org.

Heinemeier, K. M., & Kjaer, M. (2011). In vivo investigation of tendon responses to mechanical loading. Journal of Musculoskeletal and Neuronal Interactions, 11(2), 115-123.

Kannus, P. (2000). Structure of the tendon connective tissue. Scandinavian Journal of Medicine & Science in Sports, 10(6), 312-320.

Lai, A., et al. (2018). Tendon elastic strain energy in the human ankle plantar-flexors and its role with increased running speed. Journal of Experimental Biology, 217(17), 3159-3168.

Lichtwark, G. A., & Wilson, A. M. (2006). Interactions between the human gastrocnemius muscle and the Achilles tendon during incline, level and decline locomotion. Journal of Experimental Biology, 209(21), 4379-4388.

Magnusson, S. P., et al. (2010). The pathogenesis of tendinopathy: Balancing the response to loading. Nature Reviews Rheumatology, 6(5), 262-268.

Marshall, S. W., et al. (2007). Descriptive epidemiology of collegiate women’s gymnastics injuries. Journal of Athletic Training, 42(2), 234-240.

Parkinson, A. O., et al. (2023). Analysis of landing performance and ankle injury in elite British artistic gymnastics. Journal of Science and Medicine in Sport, 26(4), 212-218.

Shaw, G., et al. (2017). Vitamin C-enriched gelatin supplementation before intermittent activity augments collagen synthesis. American Journal of Clinical Nutrition, 105(1), 136-143.

Theobald, P., et al. (2006). In vivo measurement of Achilles tendon forces during jumping. Journal of Biomechanics, 39(S1), S612.

van Dijk, C. N., et al. (2011). Achilles tendopathy. Acta Orthopaedica, 82(5), 521-527.

Woo, S. L. Y., et al. (1990). Mechanical properties of tendons and ligaments. Biorheology, 19(3), 385-396.

Zitnay, J. L., et al. (2017). Molecular level detection and localization of mechanical damage in collagen enabled by collagen hybridizing peptides. Nature Communications, 8, 14913.

← Back to the knowledge base