Background The heel fat pad is an important structure of the foot as it functions as a cushion to absorb shock and distribute plantar force during ambulation. Clinical practice guidelines or decision support platforms emphasize that heel fat pad syndrome (HFPS) is a distinct pathology contributing to plantar heel pain. We aimed to identify and synthesize the prevalence, etiology and diagnostic criteria, and conservative management of HFPS. Methods A comprehensive search was conducted in May 2021 and updated in April 2022, using MEDLINE, Scopus, Cinahl, EMBASE, Cochrane Library, SPORTDiscus, and PEDro and ClinicalTrials.gov and the World Health Organization's International Clinical Trials Registry Platform (ICTRP) for pertinent registrations. We included all study types and designs describing the prevalence; etiology and diagnostic criteria; and non-pharmacological, non-surgical interventions for HFPS. Results We found a small body of original research for HFPS (n = 7). Many excluded full-text articles were expert-opinion articles or studies of heel fat pad in participants with plantar fasciitis/fasciopathy or unspecified heel pain. HFPS may be the second leading cause of plantar heel pain, based on two studies. A number of differentiating pain characteristics and behaviors may aid in diagnosing HFPS vs. plantar fasciopathy. Thinning heel fat pad confirmed by ultrasonography may provide imaging corroboration. Randomized controlled trials assessing the efficacy of viscoelastic heel cups or arch taping for managing HFPS do not exist. Conclusions The research literature for HFPS is sparse and sometimes lacking scientific rigor. We have identified a substantial knowledge gap for this condition, frequent inattention to distinguishing HFPS from plantar fasciopathy when describing plantar heel pain, and an absence of robust clinical trials to support the commonly recommended conservative management of HFPS.

Objectives Exercise-induced hypoalgesia (EIH) is characterized by an increase in pain threshold following acute exercise. EIH is reduced in some individuals with chronic musculoskeletal pain, although the mechanisms are unknown. It has been hypothesized that this may relate to whether exercises are performed in painful or non-painful body regions. The primary aim of this randomized experimental crossover study was to investigate whether the presence of pain per se in the exercising muscles reduced the local EIH response. The secondary aim was to investigate if EIH responses were also reduced in non-exercising remote muscles. Methods Pain-free women (n=34) participated in three separate sessions. In session 1, the maximal voluntary contraction (MVC) for a single legged isometric knee extension exercise was determined. In sessions 2 and 3, pressure pain thresholds (PPT) were assessed at the thigh and shoulder muscles before and after a 3-min exercise at 30 % of MVC. Exercises were performed with or without thigh muscle pain, which was induced by either a painful injection (hypertonic saline, 5.8 %) or a non-painful injection (isotonic saline, 0.9 %) into the thigh muscle. Muscle pain intensity was assessed with an 11-point numerical rating scale (NRS) at baseline, after injections, during and after exercises. Results PPTs increased at thigh and shoulder muscles after exercise with painful (14.0–24.9 %) and non-painful (14.3–19.5 %) injections and no significant between-injection EIH differences were observed (p>0.30). Muscle pain intensity was significantly higher following the painful injection compared to the non-painful injection (p<0.001). Conclusions Exercising painful muscles did not reduce the local or remote hypoalgesic responses, suggesting that the pain-relieving effects of isometric exercises are not reduced by exercising painful body regions. Ethical committee number S-20210184. Trial registration number NCT05299268.