The cooperation and relationship within biological systems are important since these systems are energetically open, exchanging information with their immediate environment (internal and external). This exchange of information is a catalyst for change. One such system, the inflammatory response, and the subject of this manuscript in relation to stretching, specifically stretching intensity, conveys information in response to several stimuli (trauma, injury, pathogens). Inflammation can be either acute or chronic, characterised by the mobilisation of inflammatory cells. Unlike chronic inflammation, acute inflammation is self-limiting and resolves with return of tissue homeostasis and integrity. Stretching, defined as an external and/or internal force, and the sensing of force being a fundamental feedback to the environment, suggests that this form of physical activity, specifically the intensity associated with the stretch, may be responsible for provoking an inflammatory response, a response entailing the infiltration of inflammatory cells and their relationship to the extracellular matrix (ECM). With much research on inflammation focused on its inhibition with the use of drugs, the focus on stretching intensity may provide another means of modifying the inflammatory response by specifically referring to stretch intensity.
- Marschall, F. (1999). Wie beinflussen unterschiedliche dehnintensitaten kurzfristig die veranderung der bewegungsreichweite? (Effects of different stretch-intensity on the acute change of range of motion). Deutsche Zeitschrift fur Sportmedizin, 50, 5–9.Google Scholar
- Mecham, R. P. (2001). Overview of extracellular matrix. Current Protocols in Cell Biology, 00.10.1, 10.1.1–10.1.14.Google Scholar
- Merskey, H., & Bogduk, N. (1994). Classification of chronic pain. Seattle, WA: IASP Press.Google Scholar
- Nordenstrom, B. E. W. (1983). Biologically closed electric circuits-clinical, experimental and theoretical evidence for an additional circulatory system. Stockholm, Sweden: Nordic Medical Publications.Google Scholar
- Rubartelli, A., Lotze, M. T., Latz, E., & Manfredi, A. (2013). Mechanisms of sterile inflammation. Frontiers in Immunology, 2013, 1–2.Google Scholar
- Wheater, P. R., & Burkitt, H. G. (1996). Wheater's basic histopathology: A colour atlas and text. New York: Chruchill Livingstone.Google Scholar
- Young, B., Stewart, W., & O’Dowd, G. (2010). Wheater's basic pathology: A text, atlas and review of histopathology. New York: Churchill Livingstone.Google Scholar