Over 50% (Yu el al 2017) of injuries in sport are due to soft tissues (that being muscle or connective tissues). The old adage is that you just REST ICE COMPRESS & ELEVATE the injury. However, this may not be the best avenue to combat this injury and in fact, may delay recovery for a long time!
Sitting on the bench, icing in the training room while your team is practicing, or not being able to enjoy playing with your kids / grandkids due to a soft tissue issue is no fun. I wanted to shed some light on this and help you understand that no matter your age, there are steps you can take to maximize tissue health and tools to help build a more healthy, robust you!
Our best avenue is obviously not get injured! As we have all found out, life happens, and injuries in physical activity, sports, or just sometimes bad luck are going to happen. I believe that, depending on your endeavor, we can build a more robust you to keep on with your life / passion!
Soft tissue issues can come around from hard physical labor, static postures for long periods of time (sitting at a desk or staring at your phone too long), lack of physical activity / movement, or an acute injury.
My goal is to help people reach their goals with the minimal effective dose to elicit a response and then COACH them with recovery strategies that assist in aiding them to becoming better.
With soft tissue, as the athlete gets older, their tissues lose some of their elasticity. Kids have a good amount of mobility and tissues heal more quickly than those of us that are older. I accuse these kids daily of having the healing powers of Wolverine or Deadpool….I unfortunately have the healing power of Aunt May. I want to ensure that my clients & athletes understand the importance of their tissues and that they can have more fun and potential playing time when being closer to 100% and the tank is full.
Our body has an amazing ability to produce force through our muscular system. As the muscles contract, they pull through their entirety onto the tendon that attaches to the bone. The integration of this process is much more complex but lets keep it relatively simple for our purposes.
Most people believe that all the force produces in the sequential shortening of sarcomeres goes longitudinally down the muscle. However, more than 80% of the force development is transmitted laterally to the intracellular connective tissue (Ramaswamy et al 2011). Knowing and understanding this is important for now we know that this serves 2 purposes;
- Transfer force outside of the working muscle fiber so it can continue to shorten
- Bind adjacent fibers together to protect from injury.
These two functions make lateral transmission essential to performance since this determines the strength / power of a muscle as well as the likelihood of an injury (Ogasawra et al. 2014). This force transmission is carried out via the intramuscular connective tissue.
The most abundant protein in connective tissue is collagen and specifically type I collagen. Collagen forms the mechanical backbone of the intramuscular connective tissue and of the tendons and ligaments within our bodies. The strength and stiffness of our connective tissues and tendons is therefore determined in part by the amount of collagen they contain. However, long thin collagen molecules would not be able to transfer force without the chemical crosslinks that bind them together (Marturano et al., 2014).
Once the force is transmitted outside the muscle, it is passed down the “connective tissue” super highway. This is made up of mostly collagen and water (along with other proteins and enzymatic crosslinks). As the muscle nears the bone for attachment, there is what we call a myotendinous junction (MTJ). This junction is not a smooth transition, but one that helps transmit the force AND protect from injury. These areas are analogous with velcro. The more robust the area is (more loops & hooks), the stronger it can oppose shear forces. The MTJ is also a complex structure in that at one end, it should be more compliant to stress and the other more stiff where it attaches to the bone (Arruda et al 2006). Think of a frayed rope. It still has the same amount of fibers in the rope, but because they are in no order, the individual fibers have less ability to hold stress. An unframed rope has all the parts working together to maximize stiffness. In the tendon, the more cross linking we have, the more force transmission it can accomplish.
HOW DOES FORCE PRODUCED IN THE MUSCLE GET TO WHERE IT NEEDS TO GO?
When working properly, muscles and tendons form a single unit that transfers the force produced in the muscle to the target bone with minimal injury. To function properly, it requires the integration of the contractile proteins of the muscle, the intramuscular force transfer apparatus, the intramuscular connective tissue, and the tendon. This complex systematic approach to movement happens when we walk, run, cut, pick up….everything we do with movement. These systems are vital in the development of force and power, whether it be making a tackle or picking up your grandkid.
Muscles produce force when myosin & actin (contractile proteins) cycle in an energy dependent manner. Other major players involved aid in helping the structures maintain shape, positioning the contractile proteins in the correct position, and ensure forces produced are transmitted along muscle to given tendonious junction. Proteins such as titin, nebulin α-actinin, desmin, MLP, and MARP all serve to make sure that the contractile proteins are positioned properly. These proteins increase with weight trining which allows better force transfer (Barash et al, 2002, Woolstenhulme et al, 2006).
Important things to take away are so far….
1) stiffer tendons are better for performance but increase the risk of injury,
2) lateral transmission of force protects individual muscle fibers from injury by linking them to their neighbors, and
3) the compliant region of the tendon (finger – like structures FIGURE 2) acts as a shock absorber and protects the whole muscle from injury.
The next important question is, how is the compliant region of the tendon generated?
Around 60% of the mass of a tendon is water which has important mechanical effects on this tissue. Crosslinked collagen and water mechanically make tendons viscoelastic; they act as both a liquid and an elastic solid. It means that the faster you load the tissue, the stiffer it acts and the more energy it can store. To help understand this, lets use a swimming pool and you are getting in it. If you lower yourself slowly into the water, you barely notice the transition into the water. Moving slowly, the water acts more like individual water molecules & are easy to move through. If you jump off the diving board and do a belly buster, the water acts more like a sheet of connected molecules (or bricks lol) and as a result seems much stiffer. You will definitely notice the transition from air to water when going at high speeds! So, when velocities are slow, tendons act more like individual collagen fibrils, and at high speeds, act more like a single unit.
At the MTJ, the crosslinking of collagen fibers change from the muscle side to the bony attachment (Figure 2). Ideally, we want the collagen of the tendon on the muscle side to interdigitate (fingerlike almost grabbing of the muscle tissue). Which serves 2 purposes.
1). Increases the surface area of connection at MTJ
2). Interdigitate loads in shear (velcro) and not tension.
Speed of contraction also plays a major role in the architecture of the collagen in our tissues. We know that the MTJ has fibers are in more or less in the shape of fingers gripping onto the muscle and as they get nearer the insertion, line up more uniformed. Moving a heavy weight slowly causes more shear force in the tissues, it breaks the crosslinks between adjacent collagen molecules and results in a LESS STIFF TENDON. In contrast to slow speeds, fast movements cause the collagen fibers to act more like a single unit. The result is a stiffer tendon, it stretches less, and generates less shear force to break the crosslinks. For athletes, self myofascial release (SMR) and massage are good alternatives to help manage some of the passive stiffness felt from these activities (Huang et al 2010).
IN CONCLUSION, REMEMBER THAT:
1). There is a gradient and that tendons are more elastic (like muscle) at the MTJ
2). As the tendon migrates towards the bone, collagen fibers line up more and tissue becomes more stiff.
3). The force production AND speed of contraction, or lack thereof, determines architecture of these tissues and therefore must be understood as part of a quality training program.
Having a connective tissue issue is something most athletes will deal with in their career. Understanding the mechanics of how they work and the architecture of these amazing structures gives us the tools to help keep our athletes more robust and playing their sport, whether it be a court or field sport, or the game of life! In the next blog entry, lets look at a case study with a high school athlete and how we progressed him pain free!
REFERENCES
Arruda, E.M., S. Calve, R,G, Dennis, K. Mundy, and K. Baar (2006). Regional variation of tibialis anterior tendon mechanics is lost following denervation. J. Appl. Physiol. 101:1113-1117.
Barash, I.A., D. Peters, J. Friden, G.J. Lutz, and R.L. Lieber (2002). Desmin cytoskeletal modifications after a bout of eccentric exercise in the rat. Am. J. Physiol. 283:R958-R963.
Baar, Keith (2017) Podcast; Science of Ultra w/ Shawn Beardon. Tendons and Sinews with Keith Baar, PhD.
Marturano, J.E., J.F. Xylas, and G.V. Sridharan, I. Georgakoudi, and C.K. Kuo (2014). Lysyl oxidase-mediated collagen crosslinks may be assessed as markers of functional properties of tendon tissue formation. Acta Biomater. 10:1370-1379.
Ogasawara, R., K. Nakazato, K. Sato, M.D. Boppart, and S. Fujita (2014). Resistance exercise increases active MMP and beta1-integrin protein expression in skeletal muscle. Physiol. Rep. 2:e12212.
Ramaswamy, K.S., M.L. Palmer, J.H. van der Meulen, A. Renoux, T.Y. Kostrominova, D.E. Michele, and J.A. Faulkner (2011). Lateral transmission of force is impaired in skeletal muscles of dystrophic mice and very old rats. J. Physiol. 589:1195-1208.
Woolstenhulme, M.T., R.K. Conlee, M.J. Drummond, A.W. Stites, and A.C. Parcell (2006). Temporal response of desmin and dystrophin proteins to progressive resistance exercise in human skeletal muscle. J Appl. Physiol. 100:1876-1882.
Yu, B., L. Hui, W.E. Garrett (2017). Mechanism of hamstring strain injury in sprinting. J. Sport Health Sci. 6(2): 130 – 132.