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Chronic hyperglycemia accelerates the accumulation of advanced glycation end-products and collagen cross-linking, which may impair collagen remodeling, alter tissue morphology, and increase muscle-tendon stiffness. These changes may restrict ankle mobility and elevate forefoot plantar loading, increasing susceptibility to skin breakdown and ulcers in individuals with diabetes. Because many muscle-tendon impairments in those with diabetes are attributed to neuropathy, whether these changes are present before clinically detectable neuropathy remains unclear. This study investigated biomechanical alterations of the ankle joint, Achilles tendon, and plantar flexor muscles in individuals with diabetes without neuropathy.

Morphological and mechanical properties of the Achilles tendon, soleus, medial gastrocnemius, and lateral gastrocnemius muscles were evaluated using ultrasound across preset ankle and knee positions. Participants included individuals with diabetes without neuropathy (n = 11, age 53 ± 12 years, 3 males, 8 females, 87 ± 16 kg, HbA1c 7.37 ± 1.80, duration of disease 75 ± 79 months) and non-diabetic controls (n = 12, age 45 ± 16 years, 5 males, 7 females, 75 ± 14 kg). A custom ankle-foot device was used to measure passive ankle joint torque.

Compared to controls, individuals with diabetes demonstrated reduced Achilles tendon cross-section area (p = 0.018). They also demonstrated increased Achilles tendon and lateral gastrocnemius stiffness (p = 0.024, p = 0.035), after adjusting for Achilles tendon/fascicle length.

Significant reductions in Achilles tendon cross-sectional area, and increased Achilles tendon and lateral gastrocnemius stiffness were observed in individuals with diabetes without neuropathy. These findings are consistent with changes in tissue properties that may occur before overt neuropathy and warrant further investigation into their functional and clinical significance.