Home / News

Rockville, Md. (November 9, 2020)—Tendons, the strong bands of connective tissue that connect muscles to bones, stabilize the structure of the body and facilitate movement. The internal balance (homeostasis) of this dynamic tissue can become disturbed easily, which can lead to tendon disease. Researchers featured in the “Homeostasis and adaptation of tendons to exercise” symposium—presented this week virtually at the American Physiological Society (APS) Integrative Physiology of Exercise conference—will discuss how exercise, inactivity and the body’s internal clock drive structural changes to tendons and their supportive tissues.

Circadian Clock Regulates Body's Collagen Production
“Tendons are a highly dynamic tissue with genetic, biochemical and structural changes occurring day and night regulated by the circadian clock,” Karl Kadler, PhD, of the University of Manchester in the U.K said. The circadian clock is the natural 24-hour cycle that organizes biological processes in the body. Kadler and his research team studied the role of the circadian clock in tendons in regulating the homeostasis of collagen, the most abundant structural protein found in connective tissue. They found that collagen accumulates in tendons during times when the body’s circadian clock is turned off. Excessive collagen leads to fibrosis in the tissues and may even be fatal in some cases. The researchers developed a collagen reporter tool, called DyProQ, that measures the number of collagen molecules being synthesized by a cell and can determine whether circadian clocks are active or disabled. They found that the circadian cycle regulates collagen synthesis by cells in the body.

Intense Training Disturbs Tendon Homeostasis, Leads to Injury
Michael Kjaer, MD, PhD, of Copenhagen University and Bispebjerg Hospital in Denmark, will discuss the effects of exercise and sedentary behavior on tendon loading and collagen turnover. “The collagen turnover in tendon can be up- and down-regulated with exercise or inactivity, respectively, and specific parts of the tendon are responsible for this loading-induced collagen dynamics. Long-term overuse of tendon (e.g., intense training) results in disturbed homeostasis and swelling of the tendon, excess angiogenesis and upregulated formation of collagen,” Kjaer wrote.

Researchers Explore How Exercise Influences Tendon Inflammation
Stephanie Dakin, PhD, BVetMed, from the University of Oxford in the U.K., studied the microscopic characteristics of tendons in people with exercise-related tendinopathy. Tendinopathy is a tendon disorder that causes pain, inflammation and limited function of the affected joint. Her research team found an increased number of blood vessels and cells—suggestive of inflammatory response—in the injured tendon samples when compared with healthy tissue. “Advancing understanding of how exercise influences tendon inflammation at the cellular level during early-stage injury will inform the development of treatment regimens that optimize tissue repair during this critical therapeutic window. This knowledge is important to reduce the formation of scar tissue and likelihood of recurrent injury,” Dakin explained.

The symposium “Homeostasis and adaptation of tendons to exercisewill be held on Thursday, November 12.

NOTE TO JOURNALISTS: The APS Integrative Physiology of Exercise will be held November 9–13 on a virtual platform. To schedule an interview with the conference organizers or presenters, contact the APS Communications Office or call 301.634.7314. Find more research highlights in the APS Newsroom.

Physiology is a broad area of scientific inquiry that focuses on how molecules, cells, tissues and organs function in health and disease. The American Physiological Society connects a global, multidisciplinary community of more than 10,000 biomedical scientists and educators as part of its mission to advance scientific discovery, understand life and improve health. The Society drives collaboration and spotlights scientific discoveries through its 16 scholarly journals and programming that support researchers and educators in their work.

Related Content

Contact Us

For questions, comments or to share your story ideas,  email us or call 301.634.7314.