Osteoarthritis (OA) is one of the leading causes of disability in the US. Quadriceps weakness, one of the most common symptoms of knee OA, has been correlated with difficulty performing activities like walking. However, the underlying mechanism relating the function of the quadriceps to gait impairments is unknown. Dynamic computer simulations are powerful tools for investigating the role of muscles during gait, but to date they have not been utilized to study the role of the quadriceps in OA gait. Furthermore, the influence of subject-specific quadriceps muscle parameters on model predictions of muscle function in simulations of OA gait has not been evaluated.

We created muscle-driven simulations of gait investigating the effect of two sources of simulated quadriceps weakness, atrophy and activation failure, on the muscle compensation strategies needed to maintain healthy gait kinematics at a self-selected speed. We found that the gluteus maximus and soleus muscles displayed the greatest ability to compensate for simulated quadriceps weakness. Our findings also suggested different compensation strategies by the lower extremity musculature in response to the different types of weakness.

To gain a better understanding of the factors that limit walking speed in individuals with weakened quadriceps, we expanded our first study to investigate the muscle compensation strategies needed to maintain healthy gait kinematics over a range of speeds in response to simulated quadriceps weakness. As with the first study, we found that the gluteus maximus and soleus muscles displayed the greatest ability to compensate for simulated weakened quadriceps at all gait speeds;​ however, soleus force output decreased at faster speeds. All simulations were able to track gait kinematics at all speeds, suggesting that it is physiologically feasible for persons with quadriceps weakness to walk at fast speeds, and that other factors not simulated in our models (e.g. pain or instability) likely contribute to reduced walking speeds.

Lastly, we performed the first study incorporating subject-specific quadriceps muscle properties into simulations of OA gait. We developed models with various implementations of subject-specific quadriceps properties measured in an individual with knee OA, resulting in six different simulations:​ 1) generic quadriceps muscle properties (“Generic”), 2) peak isometric quadriceps forces calculated from a maximum voluntary contraction (MVC) in a dynamometer (“MVC”), 3) peak isometric quadriceps forces calculated using the burst superimposition test (“Burst”), 4) peak isometric quadriceps forces and maximum activation constraints calculated using the burst superimposition test and CAR value (“Burst+CAR”), 5) peak isometric quadriceps forces calculated using muscle volumes from magnetic resonance images (“MRI”), and 6) peak isometric quadriceps forces calculated using muscle volumes from MRI and maximum activation constraints from the burst superimposition test and CAR value (“MRI+CAR”). Gait simulations using the different models revealed large changes in quadriceps function in response to different model complexities, but small changes in other muscles. We then performed a virtual gait re-training simulation in which we estimated the changes in muscle function needed for the model with the highest degree of subject-specificity to track healthy gait kinematics. Our findings revealed that changing kinematics had a much greater effect on muscle function than differences in model complexity, suggesting that subject-specificity of quadriceps properties in muscle-driven simulations may be secondary to kinematic changes for some individuals with knee OA.

This dissertation advances our understanding of the relationship between quadriceps weakness and gait impairment, and represents an important step towards the design of more comprehensive rehabilitation strategies. The methodology presented in these studies lays the groundwork for future research that will continue to add to our understanding of pathological gait and, more importantly, improve the function and quality of life of individuals with movement disorders.