Exercise- and diabetes-related adaptations in medial collateral ligament (MCL) geometry, MCL tibial insertion histomorphometry, and femur-MCL-tibia (FMT) unit biomechanics were studied in immature female Sprague-Dawley rats. The first study examined the effects of 10-wk strenuous treadmill exercise on normal rats. Results showed no differences in MCL geometry between the two groups. Structurally, the average tensile stiffness, proportional load, and maximum load of exercised FMT units were significantly greater. Cell densities increased significantly at the MCL tibial insertion and in the cortex under the insertion. The MCL insertional length increased, suggesting that more ligament fibers entered the bone rather than the periosteum. The exercised MCL tibial insertion had significant structural adaptations that may have contributed to the enhanced mechanical properties of FMT units.

In a second experiment, the influences of a HFS diet versus a low-fat complex-carbohydrate diet on FMT unit were studied. The results showed no differences in MCL geometry between the two groups. Structurally, the maximum and failure loads of FMT units were significantly less in the HFS group, and the cell density, longitudinal area, and insertional length of insertion also decreased significantly. Thus, after a 10-wk HFS diet, the FMT units were mechanically weaker and showed altered insertion histomorphometry.

Bone-ligament properties were then examined in diabetes (DM), insulin-treated diabetes (DI), and control rats. The DM group had significantly less ligament length, width, thickness, and cross-sectional area of MCL compared with control or DI groups. The maximum and failure loads of DM FMT units were significantly lower than control. The stiffness/body mass ratio of DM was significantly greater than DI. The insertion cell density, longitudinal insertional area, and insertional length were significantly less in DM. After 10 wk of diabetes, the FMT units had significant changes in MCL geometry and distal insertion, and, subsequently, FMT units were mechanically weaker. Insulin treatment partially mitigated the adverse effects of diabetes.

Finally, effects of exercise and diabetes on the FMT properties were studied comparing:​ untreated diabetes (DM, n = 16), exercised diabetes (DME, n = 18), exercised insulin-treated diabetes (DIE, n = 7), and control (n = 22) rats. DM and DME rats had significantly shorter MCL, femur, and tibia, and less body mass. MCL geometry was normal in the DIE rats. The mechanical strength of DM FMT units was significantly less than control, but exercise maintained the FMT unit strength at a normal level in DME and DIE. The cell density in tibial insertion, longitudinal insertional area, and insertional length decreased significantly in DM. Exercise reduced the severity of the microscopic changes in both DME and DIE. Exercise, combined with insulin treatments, mitigated the adverse diabetic effects on rat body growth and FMT units.