Push-off intensity is largely governed by the interaction between the triceps surae muscles (i.e., gastrocnemius and soleus) and the architecturally complex Achilles tendon (AT). Recent evidence suggests that the gastrocnemius and soleus muscles transmit their forces through bundles of tendon fascicles (i.e., “subtendons”) that form the AT. Using ultrasound imaging, we and others have revealed non-uniform displacement patterns within the AT – evidence for sliding between adjacent subtendons that may facilitate independent muscle actuation. This dissertation contends that independent muscle actuation is biomechanically important;​ despite sharing a common tendon, the triceps surae muscles undergo different fascicle kinematics during walking and contribute differently to powering walking. However, in older adults, we have observed more uniform AT tissue displacement with the potential to disrupt independent muscle actuation. This dissertation aims to fill two major gaps. First, to our knowledge, no empirical studies have characterized the origins of sliding between human Achilles subtendons. Second, more uniform AT tissue displacements correlates with reduced push-off intensity, alluding to unfavorable shifts in muscle fascicle behavior during walking – a finding that is unsubstantiated but has wide-reaching translational implications.

In study 1, we introduced a dual-probe imaging approach and presented evidence that triceps surae muscle dynamics precipitate non-uniform AT displacement patterns. In study 2, we revealed that older adults have more uniform AT tissue displacements that are accompanied by potentially unfavorable changes in muscle contractile behavior during isolated contractions. In study 3, we combined electromyography, ultrasound imaging, and musculoskeletal modeling and revealed the gastrocnemius muscles play a more significant role than the soleus in governing changes in forward propulsion during walking. In study 4, again during walking, we suggest that the capacity for sliding between subtendons facilitates independent muscle actuation in young adults but restricts actuation in older adults, likely contributing to reduced push-off intensity. In study 5, using electrical stimulation, we reveal evidence that localized AT displacements respond in anatomically consistent ways to different patterns of muscle activation. Together, these studies accelerate our understanding of musculoskeletal mechanisms underlying age-related mobility impairment and could accelerate the development of engineered tissues and orthopaedic surgical intervention.