How We Heal: Tendon Injuries

By: Nick Soleyn, Editor in Chief, PBC

“The idea of the building, the intention of it, its design, are all immutable and are the essence of the building. The intention of the original builders is what survives. The wood of which the design is constructed decays and is replaced when necessary. To be overly concerned with the original materials, which are merely sentimental souvenirs of the past, is to fail to see the living building itself.” Douglas Adams, “Last Chance to See.”

Like Adam’s description of the Golden Pavilion Temple above, our bodies are living structures whose individual parts are continually changing. We grow. Cells die. Age and experience leave their marks, often in the form of scars and scar tissues. No part of our bodies remains the same from birth to adulthood. We comprise living tissues that help carry out our intent, maintain homeostasis, and when they must, heal.

One of the challenges of being an active person is the near-inevitability of injuries, forcing us to figure out how to continue being active while suffering a broken bone, a tweaked back, a muscle strain, or a torn ligament or tendon. While we all want to get back to our regular training and other activities as soon as possible, many people make the mistake of treating all soft tissue injuries alike. Treating a tendon injury the same way you treat a muscle injury or other type of injury will mostly likely prolong your pain, delay a return to full strength, and may cause more damage.

In this article, we discuss how tendons heal and how we should think about tendon injuries from the perspective of the non-medical professional, as lifters and coaches trying to manage pain and help restore functionality.

Read more:

• https://barbell-logic.com/adductor-tendonitis-treatment/
• https://barbell-logic.com/elbow-pain-while-lifting-weights/
• https://barbell-logic.com/325-thursday-qa-49-elbow-tendonitis-breathing-in-the-deadlift-lower-back-pain-more/

Blood Supply

In general, the more vascularized a tissue is, the more quickly it will heal: muscles heal relatively quickly, tendons (having less blood flow) heal less quickly, and ligaments have less than most tendons. Cartilage is a non-vascular connective tissue and has limited repair capabilities.

Different tendons have different blood supplies as well. The flexors of the wrist, for example, are poorly vascularized (even for tendons). Their synovial sheath limits where blood vessels may enter. Serious injuries to those tendons will often require surgery because their natural healing is quite limited. Round and flat tendons, such as the Achilles and the rotator cuff (respectively), have different vascular supplies (Fenwick, Hazleman, and Riley 2002). And some tendons have areas of decreased blood flow, “including the supraspinatus, biceps tendon, Achilles tendon, patella tendon, and posterior tibial tendon. These avascular zones are commonly associated with degeneration and rupture, although there is no direct evidence to suggest that hypovascularity is a primary cause of tendon rupture” (Id.).

Tendons will look more like a muscle where it connects to muscle—at the myotendinous junction—and they will look more like bone where it connects to the bone—at the osteotendinous junction. Injuries at these junctions will heal differently from each other. So, as with real estate, the first step in understanding a tendon injury is location, location, location. The general healing process stays the same, but the nature of the injury will cause the time for healing to vary and the timing for exercise intervention to vary with it.

What are Tendons?

Tendons are tough fibrous tissues that connect muscles to bones, transmit force, and stabilize joints. More like springs than ropes, tendons store and release energy, making them dynamic structures. But, unlike any material you’d find at a hardware store, tendons change according to the needs of the body. They have viscoelastic properties, meaning they act a little bit like liquids (deforming to do their jobs) and a little bit like rubber bands (storing and returning energy). As they deform under increasing stress, their ability to transmit force changes. These properties start with the mechanical makeup of the tendon.

Tendons are a bundle of bundles. The smallest unit is the collagen molecule, arranged into collagen fibrils and bundled together into collagen fibers. Collagen fibers run in the direction of force: “Where tension is exerted in all directions, the fiber bundles are interwoven without regular orientation, and the tissues are irregularly arranged. If tension is in only one direction, the fibers have an orderly parallel arrangement, i.e., are regularly arranged”(O’Brien 2005). Most tendons’ fibers are uniform, being specialized at transmitting tensile forces along only one axis. Collagen fibers are thricely bundled together and encased in an endotenon, which encompasses the fibers, blood vessels, lymphatics, and nerves. This bundle of bundles forms the tendon unit, which is all wrapped together in an epitenon, allowing smooth movement against other bodily structures.

The majority of collagen fibers are type I fibers. Type I collagen is the A-team of connective tissue and is also found in bones and skin. It is strong and suited to the tendon’s work. Type I collagen makes up 60% of the dry mass of the tendon and 95% of its total collagen (See, Wang 2006):

• 20% of the tendon is the cellular component: mostly tenocytes, which are specialized cells that secrete and build up the extracellular matrix (ECM). Very important for healing.
• The other 80% of the tendon is the ECM, which is made of the following:
  • 70% is water.
  • 95% of the remaining 30% is Type I collagen. The rest is mostly types III and V collagens, proteoglycans, and glycoproteins.

At rest, the type I collagen fibers are not completely taught. They have some give or crimp to them—like a too-long rope stretched across a room. This crimping is important in the tendon’s function under tension.

Stress-Strain Curve

The amount of force and the length of time that force is applied to a tendon both affect if and how it may be damaged. Most discussions of tendon injuries look at a stress-strain curve, which plots the typical tolerance of a tendon to a certain amount of force (stress) and the resultant deformation of that tendon (strain).

As an aside, the stress-strain curve illustrates what makes tendons so incredibly useful. Tendons change their structural and mechanical properties in response to mechanical forces (Id.). Not only does this mean that tendons change in response to physical training, but they also change shape under load as the demands for force transfer change.

Two things affect how tendons change under load. The first is their fiber pattern—the crimp to the collagen fibers. When a force first stretches out the tendon, the tendon changes shape easily, without much of the force being transferred to its attached bone. Think of our too-long rope across a room: if you open a door and pull on the rope, at first there is no tension along its length, only a straightening of the rope itself. The tensile force is lost to the shape of the rope. When the crimp is being pulled straight, this will usually be labeled as the “toe region” of the stress-strain curve.

The second important characteristic is the tendon’s viscoelastic properties. After the toe region, the tendon will respond linearly for a little while, showing proportional changes in stress and strain. As the strain rate increases, the tendon becomes less deformable. Becoming stiffer, it is more effective at moving loads but increasingly prone to microscopic failures—small tears. If the strain continues, the tendon will stop transferring force. The force will again be lost in the tendon—this time causing failure, first with macroscopic tears and eventually a rupture.

Damaged Tendons

Tendons are load-bearing tissues, so one might consider that the primary injury concern is when a tendon can no longer handle a load. The collagen matrix stores energy and handles the load, and when something disrupts that matrix, causing it to be disorganized, then, structurally, there is a tendon pathology (tendinopathy). To help explain the stages of tendinopathy based on the structural changes of a tendon, professor Jill Cook proposed a continuum model of tendinopathy in 2009 (Cook and Purdam 2009). “The continuum model proposed a model for staging tendinopathy based on the changes and distribution of disorganization within the tendon” (Cook et al. 2016).

There are three stages to the continuum model: reactive tendinopathy, tendon disrepair, and degenerative tendinopathy. Reactive tendinopathy is an early-stage tendinopathy typically following a sudden increase in load or force that the person experiences in an elastic/release cycle of the tendon, such as jumping for the Achilles tendon in a young athlete. It may also occur from a moderate increase in load for those who are used to continuous low-level, repetitive movements (Cook and Purdam 2009), perhaps what we may think of as an overuse injury. Reactive stage tendinopathy is often but not always painful, and if there is imaging done will show a swollen tendon due to increases in cell activity (not, Cook argues, inflammation) (Cook et al. 2016). Essentially, the reactive stage is a short-term adaptive response. If one removes the offending load, usually an elastic stretch and explosive movement or a compressive load, the early-stage reactive tendon will typically get better quickly, within one to three days.

The second stage of the continuum is tendon disrepair (also tendon dysrepair). “Tendon dysrepair describes the attempt at tendon healing, similar to reactive tendinopathy but with greater matrix breakdown” (Cook and Purdam 2009). At this stage, the tendon experiences separation of the collagen and disorganization of the matrix. Since it is this matrix that handles loads, this stage may also show more dysfunction than the reactive stage. Tendon disrepair is more common in chronically overloaded athletes or older persons with constant and continuous lower loads that move the tendon along the stress-strain curve. At this stage, the damage is reversible with load management (as in the reactive stage) and appropriate exercise. Exercises that do not require storing elastic energy are most appropriate (Cook et al. 2016).

Tendons in the reactive or disrepair states are reversible and can return to normal function with load management and appropriate exercise.

The final stage of the continuum is degenerative tendinopathy. This stage describes irreversible damage, “Areas of cell death due to apoptosis, trauma or tenocyte exhaustion are apparent” (Cook and Purdam 2009). A person may have a combination of stages, including reactive portions of the tendon and degenerative portions in the same tendon. Degenerative portions or ruptures will go through a healing process and are unlikely to return to normal function. The degenerative tendon will go through inflammatory, repair, and remodeling stages.

Inflammatory Stage: Starts Immediately (Days 0 to 7)

“A classic inflammatory response in the tendon is seen when a tendon (and its blood supply) is ruptured or lacerated. The tissue response to such an insult is profound—a large immune cell and tenocyte response increases protein production and tendon size. While inflammatory cells have been observed in pathological tendons, the response does not seem to be a traditional inflammatory response.”(Cook et al. 2016)

When the tendon is damaged, blood vessels in the tendon rupture. The bleeding leads the healing process, followed by fibrous clotting. The secretion of cytokines causes swelling and pain, which will inhibit movement. Two of the cytokines (PDGF and TGF-Beta) activate tenocytes (specialized cells that secrete collagen proteins) which will rebuild the extracellular matrix.

As we will see, movement and exercise can help during the repair phase, but they will not help much with the inflammatory phase. The inflammatory phase needs to run its course. Things like the R.I.C.E. method and NSAIDs may help alleviate pain and make the person more comfortable by treating the symptoms of inflammation. There is some evidence that NSAIDs slow down the healing at this stage of tendon injury. While the reduction in pain from NSAIDs may be appropriate for the reactive tendon, they may have a negative effect on tendon repair (Cook and Purdam 2009).

Repair Stage: Overlaps with the Inflammatory Stage (Days 3 to 60)

The repair stage has two parts to it: extrinsic and intrinsic. Each refers to where the tenocytes (the rebuilding blocks) come from.

During the extrinsic phase, tenocytes from outside of the tendon create type III collagen. Recall that we want type I collagen arranged in relatively uniform rows parallel to the axis of force that will cross the tendon. This type III collagen comes from quick-responding, less-mature tenocytes and acts as a buffer until type I collagen can fill the gaps. Type III collagen is not as strong as type I and is not arranged uniformly.

During the intrinsic phase, mature tenocytes from inside the endotenon begin synthesizing type I collagen. The A-team is back, and it follows the lines of mechanical stress along the tendon. New type I collagen synthesis sees the degradation of the early type III collagen. Even though we now have type I collagen, the repaired tissue will never reach its pre-injury strength, as we will see in the remodeling stage.

Remodeling Stage: Overlaps with the Repair Stage (Days 20 to 180)

The most variable stage in terms of time, process, and results. How well the tendon functions after this stage will depend on a person’s age, the tendon itself, the type of injury, activity level, and the pre-injury status of the tendon.

During the remodeling phase, the rate of new tissue synthesis decreases, and the repaired tissue undergoes some changes. The collagen fibers will form crosslinks and become stronger. The result is stiffer, more fibrous tissue with a higher tensile strength than during the repair phase or early in the remodeling phase. Eventually, the repaired tissue becomes more fibrous and then more scar-like. By the end of the remodeling stage, the metabolism of tenocytes has decreased, as has the tendon vascularity in the injured region (Wang 2006). This scar tissue prevents the tendon from healing to its pre-injury strength, and it will not heal as well if a future injury occurs.

A popular field of study right now is scarless healing of tendons, which would allow surgical fixes that may result in tendons being as strong as they were pre-injury.

How Strength Training Fits

If the structure of the tendon was our only concern, dealing with tendon injuries would be simple. We could target the measures we take to the specific structural issue, as the continuum suggests. The actual presentation of tendon problems, however, provides some wrinkles. Whereas the continuum describes tendinopathies based on tendons’ structure, the presentation of a tendon injury is pain and dysfunction, which may be independent of structural pathology. So, the structural stuff described in the continuum model is more of a risk factor for what we would think of as a tendon injury (pain and dysfunction).

This relationship between structure, pain, and function is what makes dealing with a tendon challenging as a strength coach or lifter. A tendon may be structurally in the reactive or disrepair stages while the lifter experiences more or less pain and more or less function than typical for a tendon injury. Still, “Tendon pain is partly related to function, with tendinopathy decreasing muscle strength and motor control, which in turn reduces function” and “changes in function also occur in the presence of structural pathology, independent of pain” (Cook et al. 2016).

Much of how we deal with tendon injuries in lifting is preventive. Basic strength training does not involve the typical movements that cause most tendon issues—energy storage and release and compressive loads. We also practice gradual loading, cycling of high volume, high repetition training, and an awareness of the effects of high-intensity loading for long periods of time, and we build training histories. When abnormal pain occurs, this allows the lifter or strength coach to take a wait-and-see approach to determine whether there is a possible underlying structural issue or whether the pain needs to be treated. If so, the earliest stage of the presentation will typically be the reactive stage. In these cases, simply reducing or removing the offending load or movement should return the lifter back to baseline in short order—usually one to three days.

The more difficult question is how to adjust in-the-gym work when presented with an injury that occurred outside the gym. If the injury is minor enough that it hasn’t been referred out, requiring a medical diagnosis or professional treatment, the lifter or coach is going to want to reduce pain and restore function. “Addressing pain is critical; however, interventions directed solely at pain have a minimal effect on the associated kinetic chain deficits or tissue capacity and may result in the recurrence of pain” (Cook et al. 2016). While the strength coach is not responsible for either diagnosing tendinopathy or fixing it, lifters and coaches can recognize that exercise is a component of healthy recovery, and strength training is particularly effective when done correctly (Id.).

The types of loading and exercises that help tendons heal and help restore function will vary depending on the location and root cause of the issue. As a general rule, however, in the early stages, one should avoid loading the tendon with movements that will require storing and releasing energy—jumping, throwing, and dynamic movements. The early-stage presentation is most likely to respond to isometric holds with a reduction in pain (See, e.g., Rio et al. 2015)). The lifter should avoid eccentric loading in these early stages as that may aggravate the issue.

As pain reduces and function is restored, efforts shift to “treating the doughnut, not the hole,” meaning the in-the-gym efforts will use progressive loading to strengthen the function of the tendon and surrounding tissues without worrying too much about potential areas of degenerative pathology or dysfunction. The only way to help protect against reinjury is by improving “the load capacity of the ‘doughnut’ through progressive loading rehabilitation” (Cook et al. 2016). Movement and exercise also help minimize adhesions in scar tissue formation, which can improve movement, reduce pain, and improve the function of the tendon long-term (Wang 2006).

The immediate goal should not be to strengthen the tendon as much as possible. Tendons are not hypertrophic the way muscles are and will not heal faster or better with a too-early increased load. The important parts of tendon healing are reducing pain, restoring function, and strengthening function.

Though time and the form of healing will vary greatly from issue to issue, the takeaway here should be to treat your tendons like tendons. If you suffer a tendon injury, you do not fix it with a titrating mechanical load or increased volume of stress to the tissue. In fact, you do not fix it at all. The tendon heals, and you help it out.

References

Cook, J L, and C R Purdam. 2009. “Is Tendon Pathology a Continuum? A Pathology Model to Explain the Clinical Presentation of Load-Induced Tendinopathy.” British Journal of Sports Medicine 43 (6): 409–16. https://doi.org/10.1136/bjsm.2008.051193.

Cook, J L, E Rio, C R Purdam, and S I Docking. 2016. “Revisiting the Continuum Model of Tendon Pathology: What Is Its Merit in Clinical Practice and Research?” British Journal of Sports Medicine 50 (19): 1187–91. https://doi.org/10.1136/bjsports-2015-095422.

Fenwick, Steven A, Brian L Hazleman, and Graham P Riley. 2002. “The Vasculature and Its Role in the Damaged and Healing Tendon.” Arthritis Research 4 (4): 252. https://doi.org/10.1186/ar416.

O’Brien, Moira. 2005. “Anatomy of Tendons.” In Tendon Injuries, edited by Nicola Maffulli, Per Renström, and Wayne B. Leadbetter, 3–13. London: Springer-Verlag. https://doi.org/10.1007/1-84628-050-8_1.

Rio, Ebonie, Dawson Kidgell, Craig Purdam, Jamie Gaida, G Lorimer Moseley, Alan J Pearce, and Jill Cook. 2015. “Isometric Exercise Induces Analgesia and Reduces Inhibition in Patellar Tendinopathy.” British Journal of Sports Medicine 49 (19): 1277–83. https://doi.org/10.1136/bjsports-2014-094386.

Wang, James H.-C. 2006. “Mechanobiology of Tendon.” Journal of Biomechanics 39 (9): 1563–82. https://doi.org/10.1016/j.jbiomech.2005.05.011.

Helpful Videos

Tendon Anatomy (https://www.youtube.com/watch?v=44UbshvyQt4)

Physiology of Tendon Healing (https://www.youtube.com/watch?v=zSwwvit00mg)

Biomechanics: Tendon & Ligament Injury (https://www.youtube.com/watch?v=43I_rGIngFQ&list=PLfNRQ67UEa-HhAqdKAJzfNxU9X6-wRMv7&index=11)