| Despite increased awareness of ergonomic risk factors at work, incidence and costs of WMSDs are high. The incidence of tendinopathies increases with exposure to forceful repetitive motion. Substance P, CGRP, and NMDAr1 have been observed in tendons of patients with chronic tendinopathies. 65 female Sprague-Dawley rats were used. Eighteen rats performed a high repetition-high force task (HRHF; >60% maximum grip) in which grasping a lever occurred at a target rate of 8 reaches/minute, 2 hours/day, 3 days/week for up to 12 weeks. Nine rats performed a low repetition-low force task (LRLF; <15% maximum grip) in which they retrieved a 45mg food pellet at a target rate of 4 reaches/min. The remaining rats were controls. Behavior tests included reach performance (duration and reach rate), grip strength, and function (Forehead Sticker Removal). They were examined at the same time points as the neurochemical analysis. Following euthanasia, forelimb tissues were collected, fixed in paraformaldehyde and frozen-sectioned. Immunohistochemistry was performed using anti-Substance P, anti-NMDAr1, or anti-CGRP and quantified bilaterally in the endotenon, epitenon, and paratenon of forelimb tendons. Results show that continued performance of a HRHF task resulted in a neurochemical response in the flexor forelimb tendons, primarily in the peritendon with the greatest increase in HRHF rats. In the peritendon, there were significant increases in Substance P in week 12, NMDAr1 in week 6, and CGRP in weeks 3 and 12 with HRHF task performance. NMDAr1 increased in endotenon in week 6 with the HRHF task. Increased CGRP was observed in peritendon in the LRLF rats transiently in week 3. Decreases in task duration, grip strength, and FHSR score were observed at the same time points as the increased neurochemical response.;Substance P and NMDAr1 increase in tendon regions as a result of performing repetitive and forceful tasks. The response is exposure (HRHF>LRLF) and tissue (peritendon>endotenon) dependent. The results of this study demonstrate that the presence and timing of Substance P and NMDAr1 may contribute to inflammation, cell proliferation, and mechanical allodynia in acute tendinopathies. Pain mediation from these neurochemicals contributes to decreased motor performance, grip strength, and function in HRHF rats. |
