## 1 Introduction  
Approximately 15% of the adult population will experience orofacial pain over the course of a year [1]. The prevalence of orofacial pain is greater in individuals between 20 and 40 years old, and it is more common in women [1]. Orofacial pain is usually associated with temporomandibular disorders (TMDs), which are the second most common musculoskeletal disorder causing pain and disability [2, 3]. The classification of TMDs has been described by the Diagnostic Criteria for TMD (DC/TMD) Axis I [4], and states that patients can be divided into Group I (those with muscle disorders including myofascal pain with and without mouth opening limitations); Group II (those with disc displacement and with or without reduction and mouth opening limitations); Group III (those with arthralgia, arthritis, and arthrosis). Common signs and symptoms include a limited and/or abnormal range of motion, clicking, popping or crepits in function with or without the locking of the jaw, temporomandibular joint pain, jaw opening pain, muscular orofacial pain, otalgia, tinnitus, or headache [5]. The most common TMD is of muscular origin and accounts for 42% of diagnosed TMD cases [1]. Myogenic TMD tends to become chronic, resulting in pain sensitization (PS) [6, 7], which is defined by the International Association for the Study of Pain as an increased response from nociceptive neurons above the usual pain threshold [8]. TMD patients may present overlapping symptoms with other chronic pain conditions, including headache, fibromyalgia, and neurological conditions, probably through the phenomenon of central sensitization (mainly allodynia and hyperalgesia) [9]. Widespread PS can involve both central and peripheral sensitization [8]. As central sensitization cannot be clinically assessed, it is difficult to confirm its presence and differentiate it from peripheral sensitization. Tools such as quantitative sensory testing (QST), the pressure pain threshold (PPT), temperature stimulus or temporal summation, and central sensitization index (CSI) have been used to assess central sensitization symptoms and hypothesize their involvement in chronic pain [10; 11; 12]. Patients with myogenic TMD tend to present a decreased PPT in local and remote areas without an alteration of temperature perception and a high CSI score [6]. The usual treatment for myogenic TMD consists of education, manual therapy, and the therapeutic exercise of the jaw and cervical areas [13; 14]. Additionally, new treatment strategies such as radial extracorporeal shock wave therapy have been proposed [15]. These strategies have been shown to reduce the pain intensity, and improve function and the quality of life [13; 14; 15]. However, given the growing evidence of the presence of PS in remote areas in many of these subjects, local treatment may not be enough. Therefore, in addition to usual physical therapy (PT), the treatment for myogenic TMD should include care strategies for the treatment of widespread PS [16; 17]. It has been shown that therapeutic exercises such as aerobic exercise (AE), strength, flexibility, and core or balance training programs have hypoalgesic effects as they reduce pain intensity [18; 19]. Specifically, AE has been proposed as a therapeutic tool for the treatment of widespread PS, and myofascal pain could be modulated thanks to an increased blood supply in the trigger point areas. This increased blood supply allows for the reorganization of fibers, which causes a decrease in PS [10]. In the same way, in the short and long term, AE has been shown to increase the PPT, reduce pain perception, and improve the quality of life for patients with myofascal pain and chronic musculoskeletal pain due to its hypoalgesic effects [17; 20]. Indeed, AE, especially when performed at a high intensity, can also trigger descending inhibition and have an effect on pain modulation by liberating endogenous opioids [21; 22].