SKELETAL MUSCLE ADAPTATION IN A MODEL OF MASSIVE ROTATOR CUFF TEAR
- Author(s): Sato, Eugene Julius;
- Advisor(s): Ward, Samuel R;
- Engler, Adam J
- et al.
Rotator cuff (RC) tears are a degenerative condition that affects ~30% of people over the age of 60, resulting in pain and loss of function in the shoulder. Chronically torn muscles are prone to atrophy, fatty infiltration, and an increase in tissue stiffness. These changes are insensitive to rehabilitation and are associated with poor patient and surgical outcomes.
Although human clinical studies of RC tears are common, they are limited by a lack of experimental control and logistical difficulties. Thus, animal models have been utilized to study this injury. However, data describing the muscle architecture and mechanics in these models are limited. Therefore, in chapter 2, we characterized muscle architectural adaptations in a rat model of RC injury. We discovered that tenotomy alone leads to mild changes in muscle architecture, while adding a secondary chemical nerve injury causes extensive muscle changes.
Various studies have demonstrated increased passive stiffness of the whole muscle after RC tear, but the mechanisms causing this phenomenon were unknown. Therefore, in Chapter 3, we measured stiffness at the individual fiber and fiber bundle levels. Fiber bundles stiffness increased after a combined tendon and nerve injury, but was unchanged after tenotomy alone. These results suggest that stiffness changes are due to adaptations in the extracellular matrix.
Recent studies have reported functional deficits in tenotomized RC muscles that are not predicted by architectural adaptations. A potential explanation for this could be that muscle strain to sarcomere strain transmission is altered after injury. In chapter 4, we investigated this discrepancy and found that strain transmission was not altered due to tenotomy at low strains. However, sarcomere lengths were significantly shorter in tenotomized muscles at high strains. These results fail to predict the presence of functional deficits in tenomized muscles and do not reconcile the reported deficits.
Overall, these data suggest that this model of RC injury exhibits mild changes that are not representative of the human injury. Future research may need to pursue alternative models (aged animals, alternative species, etc.) of RC tear that result in muscle adaptations that are comparable to what is observed in human patients.