**1. Introduction**

Chronic Achilles tendinopathy (AT) is one of the most common conditions of the ankle and foot, characterized by the combination of pain, swelling and a deficit of functionality in the lower limb [1]. The reported incidence rate was estimated at about 2.35–2.16 per 1000 adults [2]. Recent studies revealed that the presence of disorganization and degeneration in collagen fibers, especially associated with obesity and diabetes disorders, as well as changes in vascularity were risk factors for AT [3]. In addition, changes in tendon thickness and cross-sectional area (CSA) in response to load adaptations were related in patients with AT [4]. Currently, two types of AT were described according to the following locations: Non-insertional (2 to 6 cm from the calcaneus insertion of the tendon) and insertional (at the calcaneus insertion of the tendon).

The Achilles tendon complex may be considered the largest tendon in the body. Its architecture is designed to support tensile loads during its contraction or elongation, and it is susceptible to

overuse injuries [5]. In addition, its location makes it a fundamental structure for ankle mobility and locomotion [6]. The Achilles tendon works in a coordinated manner with the gastrocnemius and soleus muscles [7], and the extrinsic and intrinsic foot muscles [8]. The mechanism of AT remains unclear; Galloway et al. [9] reported that changes in the architecture of the tendon and surrounding structures in response to the mechanical load were related in patients with AT. Those adaptations were associated with changes in plantar fascia (PF) morphology, such as the thickness.

The PF is a soft tissue structure across the plantar foot and provides an important role in ankle and foot biomechanics, being a structure capable of working with greater loads by modifying its thickness and stiffness [10]. For example, Huang et al. [11] reported changes in the thickness of the PF in individuals with pes planus, related to mechanical load changes.

Several authors have studied PF and CPF thickness in different conditions and populations by ultrasound imaging (USI) [12–14]. However, there is a lack of evidence about PF thickness in individuals with AT in comparison with healthy subjects.

Ultrasound imaging (USI) has been employed to assess the thickness and CSA of diverse muscles associated with fascial and musculoskeletal conditions. Regarding the lower limb, Lobo et al. [15] showed a reduction in the thickness and CSA of the flexor hallucis brevis and abductor hallucis in subjects with hallux valgus. The peroneus longus muscle CSA was examined by USI and a reduction was observed in the CSA in individuals with ankle sprains [16]. Angin et al. [10] reported a greater CSA and thickness in PF in subjects with pes planus. In addition, Taniguchi et al. [17] showed a reduced vastus medialis thickness in individuals with knee osteoarthritis. Considering other locations, USI has been useful to evaluate the temporalis, sternocleidomastoid and masseter muscles, showing changes in patients with temporomandibular disorders [18]. CSA of the intrinsic hand muscles has been evaluated by Mohseny et al. [19] with USI in subjects with nerve injuries. In the cervical region, the morphology of the deep cervical muscles were observed by USI while they developed an exercise program in subjects with neck pain [20]. Considering the trunk region, Whittaker et al. [21] related the architecture of the abdominal wall muscles with lumbopelvic pain. Several authors argued that USI is a non-invasive, safe and valid method to examine soft tissues and musculoskeletal disorders [22,23].

For the Achilles tendon complex, prior studies were focused on the tendon thickness and CSA in subjects with AT [13]. However, limited evidence of the surrounding soft tissues has been observed, such as PF and calcaneal fat pad (CFP) by USI [24].

The goal of the present study was to assess, using USI, the thickness of the PF at the insertion of the calcaneus, mid and forefoot fascial locations, and the CFP in patients with AT. We hypothesized that these selected soft tissue structures would demonstrate changes in individuals with AT.
