Testing the Glutes
/How are your glute evaluation skills? Check out this quick video to give you a few more tools for your clinical toolbox!
More on weak muscles. Just WHY are they weak? Know before you activate!
Dr Allen’s post last week on chronic ankle instability (click here for post) served as an inspiration for many of us. It brings to mind the many reasons muscles can become “weak”.
So why does a muscle become weak? We like to categorize the causes as follows:
- local
- segmental
- long loop/cortical
Local causes include muscle injury and muscle pathologies, like muscular dystrophy and neuromuscular endplate disorders like myasthenia gravis. Segmental causes are largely due to reflexes which occur at the spinal cord level. Long loop and cortical causes ae due to an increased inhibition or lack of drive from higher centers, such as the motor cortex and cerebellum.
Lets examine local causes in more detail. To understand causes we must understand what makes a muscle contract.
Muscles are composed of many proteins, 2 of which are actin and myosin (see above). Actin has 2 forms, F (filamental) and G (globular) actin. Imagine 2 grapefruits side by side (G actin) held together in the middle by small filaments (F actin). Now imagine these another set immediately below, in a repeating pattern. These groups of 2 are held together at the sides by an additional protein called tropomyosin. This whole complex looks a little like train tracks. Along the strands of tropomyosin, at regular intervals is yet another protein called troponin. We like to think of troponin as a triangular shaped protein and each part of the triangle has a particular binding site: one for tropomyosin, one for actin and another for calcium ions.
Myosin is another component of muscle, that looks similar to a bunch of golf clubs. The head of the club will, under the right circumstances, interact with actin, the body (tail) of the club interacts with other myosin bodies.
Globular actin and myosin heads are like 2 teenagers and like to interact with one another. Normally, in a resting state, troponin protein covers the active site of myosin binding on G actin. In the presence of calcium, there is a change in shape of the troponin molecule, moving it off of the active site of actin, allowing myosin to bind there. When this happens, the head ratchets and muscle contraction occurs. In the presence of adequate fuel (ie ATP) the myosin head detaches from actin and “recocks”, ready for another contraction cycle (see 2nd picture above).
So where does the calcium come from? It is stored in areas of the muscle called the terminal cisterns. It is released when an action potential fires the peripheral nerve to the neuromuscular endplate of a muscle.
Can calcium be released any other way? Sure it can. How about if the terminal cisterns are damaged, from an injury to the muscle? How about if they are damaged from a disease process?
So, when calcium is released, no matter how it is released, muscles contract. If calcium is not released, then muscles do not contract.
From a local cause, If a muscle is weak, one of the following are usually causing the weakness:
- there is physical damage to the muscle causing fewer of the working units of the muscle (called sarcomeres) contract
this is by far the most common, due to overuse or trauma
- there is a problem with the connection of the nerve to the muscle
Disruption of nerve to muscle connections can be also be due to trauma or disease. Weakness that is becoming progressive and worsening, needs to be evaluated further and may be the signal for a progressive muscular or neurological disorder (muscular dystrophy, myasthenia gravis, Gullian Barre, etc)
- there is insufficient neurotransmitter at the neuromuscular end plate to fire the muscle
this is usually due to a disease process
- Insufficient calcium could theoretically hamper a muscles contraction, but since calcium is involved with nerve transmission as well, tetany (ie sustained contraction and spasm) would most likely occur due to other reasons that we will not explore at this juncture.
OK, so that sums up local causes. Look for a follow up post about segmental causes next…
We are: The Gait Guys
Just because a muscle tests weak doesnt mean it needs activated.
/To Activate or Not Activate: That is the question…
Just because a muscle tests weak does not mean it can, should or needs to be activated.
Muscles become inhibited for many reasons. Perhaps it is being forced into a substitution or compensation pattern because the primary motor pattern is not accessible. Perhaps it is because there is a local inflammatory response (ie injury) near by or within the muscle. Perhaps the muscle is lacking in one or several of its primary tenants, S.E.S. (Skill, Endurance, or Strength). Perhaps the joint(s) that muscle crosses are arthritic, inflamed, damaged, remember that an inflamed joint does not like compression/loading. When a muscle contracts it will increase compression across the joint surfaces. Maybe it is being reciprocally inhibited by it’s antagonist, or does not have appropriate sensory feedback from its mechanoreceptors and is neurologically inhibited. The nervous system is wired with many “faults”, which shut things down. Often times, you need to explore the reason why.
So…What happens if you decide to “activate” the muscle regardless of any of the above, which should have been clearly determined by a clinical examination ?
You very well could be forcing that muscle back on the grid encouraging the muscle to perform in an unsafe or undesirable environment. You may be forcing compressive loading across a joint that is inflamed. You could be forcing compression and shear across a damaged cartilage interface, an osteochondral defect, a ligamentous tear or a combination of the above. You will also be over riding the nervous systems inherent neuro-protective mechanism and by forcing the muscle to once again activate and work in a faulty movement pattern. You very likely are reprogramming an unsafe and potentially damaging motor pattern.
Remember, when you “mess around” and over ride neuro-protective inhibition of a motor pattern you reteach a potentially dangerous sensory response telling the joint that the nervous system has been mistaken, that it is actually safe to place load and shear across the joint when in fact it is dangerous. Protective reflexes are there for a reason, to protect you!
We have seen the results of well intentioned or sometimes untrained individuals implementing activation into their clinical practices, coaching, or training. Without a sound clinical examination to determine the reason for muscle inhibition one is taking a whole pile of warning signs and throwing them to the wind. Remember, if you force a muscle back into activation despite all of the warning signs and reasons for inhibition, you will get a temporarily stronger muscle. This is not necessarily success.
In fact, what you have done, is enabled your client the ability to once again impart load and shear across a joint(s) and motor chain that was getting clear central nervous system signals to avoid the loading response. You are essentially forcing a compensation pattern and we all know where that leads to.
As clinicians, we take an oath that states: “Primo Non Nocere”, which means “first, do not injure”. Know what you are doing. If you don’t, then get the training or don’t do it.
The Gait Guys. Were are here to help. We are watching. Do us proud and do the right thing.
