Beyond the Hit: Muscle and Vascular Tissue Responses to Contact Exposure in Collision Sports-A Narrative Review

Abstract

Contact events in rugby codes such as tackling, running into contact, scrums, rucks, and contact with the playing surface may expose athletes to muscle damage known as impact-induced muscle damage. These repetitive impacts to muscle tissue have the potential to diminish muscle force production and delay recovery following contact-focused training and match-play. Repetitive exposure to contacts may also affect the surrounding vascular and neuronal tissues, an area that has received little attention in the collision sports. Depending on the severity and duration of tissue damage, repetitive contact exposure without sufficient recovery or noticeable adaptation may predispose collision sport athletes to impaired performance and long-term health complications. The aim of this narrative review is to provide a conceptual framework for understanding the physiological implications of contact exposure in collision sports. We examine the current understanding of impact-induced muscle damage (IIMD), how it differs from exercise-induced muscle damage (EIMD), and its relationship with contact exposure in collision sports. Drawing on both experimental animal models of contusion injury and limited human observational research, we explore the effects of repeated contact exposure on the microvasculature and its implications for both athletic performance and player welfare. To account for all tissues that may be affected by impacts, including muscle, nerve, vascular, connective tissue, skin, other organs and bones, we recommend impact-induced tissue damage (IITD) as the preferred descriptor rather than IIMD. Finally, we discuss the concept of contact adaptation and provide recommendations for future research on IITD in collision sports.

Fig. 1

Illustration of the flow of primary and secondary tissue damage following impact-induced tissue damage (IITD). Grey dashed lines represent pathways that may contribute to excessive tissue damage under conditions of high levels of IITD without adequate recovery. TNF-α tumour necrosis factor-alpha, IL-1 interleukin-1, NO nitric oxide, Ca²⁺ calcium. Created in BioRender. Bolger, C. (2025) https://BioRender.com/i99q395

Fig. 2

Proposed mechanism for endothelial glycocalyx (eGC) degradation following excessive impact-induced tissue damage (IITD): The structural integrity of the eGC relies on a balance between enzymatic degradation and de novo biosynthesis of its components, as well as the adsorption of circulating molecules from the blood. Several enzymes responsible for eGC degradation are activated by pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1), along with reactive oxygen species (ROS), which promote the damage and shedding of key glycocalyx components. This process leads to the release of components like heparan sulfate, hyaluronan, and syndecan into the circulation. As the eGC degrades, its structural integrity diminishes, leading to a thinner layer that increases leukocyte adhesion to the endothelial surface. This promotes excessive neutrophil infiltration into surrounding tissues, further exacerbating injury in previously unaffected areas. Conditions characterized by excessive loss of the eGC may also exhibit reduced endothelial nitric oxide (NO) production, which enhances neutrophil adhesion and perpetuates vascular dysfunction and inflammation. Created in BioRender. Bolger, C. (2025) https://BioRender.com/y99y354

Fig. 3

Proposed mechanism for vascular (endothelial) dysfunction following excessive impact-induced tissue damage (IITD): Upregulated arginase-1 reduces l-arginine availability for endothelial nitric oxide synthase (eNOS), resulting in decreased nitric oxide (NO) production and increased superoxide (O₂⁻) generation in the vascular endothelium. The excess O₂⁻ from uncoupled eNOS reacts with NO, forming peroxynitrite (ONOO⁻), which further amplifies arginase activity [159]. TNF-⍺ contributes to this process by upregulating arginase expression, shifting arginine metabolism from eNOS to arginase pathways [177, 178]. Increased arginase activity consumes more l-arginine, leading to further eNOS uncoupling and greater O₂⁻ production. This cascade of events leads to reduced NO bioavailability, impaired vasodilation and amplified oxidative stress, contributing to overall vascular dysfunction. Grey dashed lines represent pathways that may contribute to excessive tissue damage under conditions of high levels of IITD without adequate recovery. Created in BioRender. Bolger, C. (2025) https://BioRender.com/y99y354