Muscle strains are among the most common injuries in sport, striking everyone from weekend joggers to elite professionals, and they carry one of the highest re-injury rates of any athletic condition. When a strained muscle tears away from its tendon or aponeurosis, the hope among athletes and clinicians alike is that time, rest and rehabilitation will restore the tissue to something close to its original state. A new study challenges that assumption in an unexpected way, showing that injured muscles quietly accumulate fat within three months of the injury and that this fatty infiltration persists for at least a year, even in people who have returned to full sports participation.
The research, published in Physiological Reports, followed 50 sports-active men and women who suffered acute strain injuries to either the calf or hamstring muscles. Using a quantitative magnetic resonance imaging technique called DIXON, the team measured the fat fraction of the entire injured muscle volume in the first week after injury, then again at three months and twelve months post-injury. DIXON imaging separates water and fat signals within tissue, generating water-only and fat-only images that allow researchers to calculate precisely how much of a muscle’s volume is occupied by fat rather than contractile tissue.
The findings were striking in their clarity. Acutely after injury, there was no measurable difference in fat content between the injured and uninjured legs. But by three months, the injured muscles showed significantly higher fat fractions than their healthy counterparts, and this elevation remained unchanged at the twelve-month follow-up. The uninjured legs showed no such change across the entire year, confirming that the effect was specific to the damaged tissue. Notably, all participants had returned to full sports participation at a median of 48 days after injury, meaning the persistent fat accumulation occurred despite active loading and rehabilitation of the muscles.
The study also uncovered meaningful relationships between fat accumulation and other measures of injury severity. Muscle volume loss correlated negatively with the rise in fat content between the acute scan and the three-month follow-up, suggesting that the more contractile tissue a muscle loses, the more fat it accumulates in its place. The team additionally found a positive correlation between enlargement of the aponeurosis, the fibrous sheet into which muscle fascicles insert, and the increase in fat fraction at three months. This hints at a deeper story about how the muscle and its connective tissue framework fail to re-establish their normal mechanical coupling after injury.
Previous work had already hinted at lasting structural changes after strain injuries. Tissue biopsies from previously injured muscles have shown fat accumulation both inside and between muscle cells that could not be reversed by three months of rehabilitation training, and electron microscopy of chronic injury sites has revealed a loss of contractile elements. Ultrasound imaging has further suggested that muscle fascicles at the injury site fail to contract normally, instead being passively dragged along by the aponeurosis during movement. The new imaging data extend these observations to the whole-muscle level and establish a clear timeline for when fatty infiltration first appears.
The researchers propose that a fundamental defect at the muscle-aponeurosis interface may drive the process. When muscle fascicles cannot generate proper tension at their insertion points, the biomechanical cues within the tissue change, potentially altering the behavior of resident cells. Fibro/adipogenic progenitors, a heterogeneous population of cells capable of differentiating into either fat or fibrous tissue, have been implicated in fatty infiltration in animal models. Whether these cells are responsible for the fat accumulation seen in human strain injuries remains unknown, but the persistent, seemingly irreversible nature of the change points to a fundamental shift in the local cellular environment rather than a simple consequence of disuse.
The clinical implications are significant. Fatty infiltration is recognized as a major contributor to impaired muscle quality and is a strong predictor of poor recovery and high recurrence rates in rotator cuff tears. If similar processes operate in the hamstring and calf muscles, where re-injury rates are notoriously high, the persistent fat accumulation documented here could help explain why so many athletes suffer repeated strains at the same site. The current findings suggest that rehabilitation protocols may need to address not just strength and flexibility but the underlying structural integrity of the muscle-tendon unit.
One of the study’s key methodological strengths was its measurement of fat across the entire three-dimensional muscle volume rather than in a single representative slice, an approach that other work has shown is more reliable for capturing the true extent of infiltration. The team also took care to exclude the outer edge of the muscle near subcutaneous fat deposits to ensure that only intramuscular fat was quantified. The researchers acknowledge certain limitations, including the resolution limits of the DIXON technique at the low fat fractions observed and the inability to analyse fat distribution at the specific injury site, which could hypothetically show even greater local accumulation.
Looking ahead, the team emphasises that the cellular mechanisms underlying this rapid and persistent fatty infiltration remain poorly understood. Future work will need to determine whether affected muscle fibres retain their nerve supply, whether they can generate contractile force, and how the interplay between mechanical loading, connective tissue structure and progenitor cell behaviour drives the process. For now, the message for athletes and clinicians is sobering: a muscle strain leaves a measurable metabolic and structural fingerprint that persists long after the pain has gone and normal training has resumed, and current rehabilitation approaches may not be sufficient to prevent it.
Subject of Research: Persistent fatty infiltration in skeletal muscle following acute strain injuries in sports-active adults
Article Title: Early and persisting increase in fat content after human muscle strain injuries in adults
Article References: Bayer, M. L., Mertz, K. H., Eriksen, A. S., Kjaer, M., Magnusson, S. P., Linden, F. H., & Svensson, R. B. (2026). Early and persisting increase in fat content after human muscle strain injuries in adults. Physiological Reports, 14(17), Article e71086. https://doi.org/10.14814/phy2.71086
Image Credits: AI Generated
DOI: 10.14814/phy2.71086
Keywords: muscle strain injury, fatty infiltration, DIXON MRI, aponeurosis, hamstring injury, calf injury, sports injury, muscle volume, fat fraction, rehabilitation, reinjury, muscle quality
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Ophelia Keating. (September 12, 2026). Muscle Strains Leave Lasting Fat Deposits That Rehabilitation Cannot Reverse. Scienmag. https://scienmag.com/muscle-strains-leave-lasting-fat-deposits-that-rehabilitation-cannot-reverse/
Ophelia Keating. “Muscle Strains Leave Lasting Fat Deposits That Rehabilitation Cannot Reverse.” Scienmag, 12 September 2026, https://scienmag.com/muscle-strains-leave-lasting-fat-deposits-that-rehabilitation-cannot-reverse/. Accessed 12 September 2026.
Ophelia Keating. “Muscle Strains Leave Lasting Fat Deposits That Rehabilitation Cannot Reverse.” Scienmag. September 12, 2026. https://scienmag.com/muscle-strains-leave-lasting-fat-deposits-that-rehabilitation-cannot-reverse/
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