What creates muscle tone, anyway?

Not for the timid, here is an excellent , free, full text article on spasticity. More importantly, it is an excellent review on what creates muscle tone and how it is maintained, starting and the spindle and moving centrally.  Think about this the next time you have a patient with mm spasm and you can se things in a whole new light

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478/

More thoughts on stretching

   We get a lot of interest in our posts on stretching. Seems like this is a pretty hot subject and there is a lot of debate as to whether it is injury preventative or not. Are you trying to physically lengthen the muscle or are you trying to merely bring it to its physiological limit?  There’s a big difference in what you need to do to accomplish each of these goals. Lets take a look at each, but 1st we need to understand a little about muscles and muscle physiology.

 Muscles are composed of small individual units called sarcomeres. Inside of these “sarcomeres” there are interdigitating fibers of actin and myosin (proteins) which interact with one another like a ratchet when a muscle contracts.  Sarcomeres can be of various lengths, depending on the muscle, and are linked and together from one end of the muscle to the other. When a muscle contracts concentrically (the muscle shortening while contracting) the ends of the sarcomere (called Z lines or Z discs) are drawn together, shortening the muscle fiber over all (see the picture above).
 
 Signals are sent from the brain (actually the precentral gyrus of the cerebral cortex areas 4, 4s and 6) down the corticospinal tract to the spinal cord to synapse on motor neurons there.  These motor neurons (alpha motor neurons) then travel through peripheral nerves to the muscles to cause them to contract (see picture above).

   The resting length of the muscle is dependent upon two factors:
The physical length of the muscle
2. The “tone” of the muscle in question.

The physical length of the muscle is determined by the length of the sarcomeres and the number of them in the muscle.   The “tone” of the muscle determined by an interplay of neurological factors and the feedback loops between the sensory (afferent) receptors in the muscle (Ia afferents, muscle spindles, Golgi tendon organs etc.), relays in the cerebellum and basal ganglia as well as input from the cerebral cortex.

 If you’re trying to “physically lengthen” a muscle, then you will need to actually add sarcomeres to the muscle. Research shows that in order to do this with static stretching it must be done 20 to 30 minutes per day per muscle.

 If you were trying to “bring a muscle to its physiological limit” there are many stretching methods to accomplish this.  Pick your favorite whether it be a static stretch, contract/ relax, post isometric relaxation etc. and you’ll probably be able to find a paper to support your position.

  Remember with both not to ignore neurological reflexes (see above). Muscle spindle loops are designed to provide feedback to the central nervous system about muscle length and tension. Generally speaking, slow stretch activates the Ia afferent loop which causes causes physiological contraction of the muscle (this is one of the reasons you do not want to do slow, steady stretch on a muscle in spasm). This “contraction” can be fatigued overtime, causing the muscle to be lengthened to it’s physiological limit.  Do this for an extended period of time (20-30 mins per day) and you will physically add sarcomeres to the muscle.

 Next time you are stretching, or you were having a client/patient stretch, think about what it is that you’re actually trying to accomplish  because there is a difference.

We are and remain The Gait Guys.  Bald, good-looking, and above-average intelligence. Spreading gait literacy with each post we publish.

thanks to scienceblogs.com for the corticospinal tract image

Why does it feel so good to stretch? 

We are sure you have read many articles, some written by us, about the good the bad and the ugly about stretching.  Regardless of how you slice the cake, we think we can all agree that stretching “feels” good. The question of course is “Why?”

Like it or not, it all boils down to neurology. Our good old friends, the Ia afferents are at least partially responsible, along with the tactile receptors, like Pacinian corpuscles, Merkel’s discs, Golgi tendon organs, probably all the joint mechanoreceptors and well as a few free nerve endings. We have some reviews we have written of these found here, and here and here.

What do all of these have in common? Besides being peripheral receptors. They all pass through the thalamus at some point (all sensation EXCEPT smell, pass through the thalamus) and the information all ends up somewhere in the cortex (parietal lobe to tell you where you are stretching, frontal lobe to help you to move things, insular lobe to tell you if it feels good, maybe the temporal lobe so you remember it, and hear all those great pops and noises and possibly the occipital lobe, so you can see what you are stretching.

The basic (VERY basic) pathways are:Peripheral receptor-peripheral nerve-spinal cord-brainstem-thalamus-cortex; we will call this the “conscious” pathway:  and peripheral receptor-peripheral nerve-spinal cord-brainstem-cerebellum- cortex; we will call this the “unconscious” pathway.

Of course, the two BASIC pathways cross paths and communicate with one another, so not only can you “feel” the stretch with the conscious pathway but also know “how much” you are stretching through the unconscious pathway. The emotional component is related through the insular lobe (with relays from the conscious and unconscious pathways along with collaterals from the temporal lobe to compare it with past stretching experiences) to the cingulate gyrus and limbic cortex,  where stretching is “truly appreciated”. 

As we can see, there is an interplay between the different pathways and having “all systems go” for us to truly appreciate stretching from all perspectives; dysfunction in one system (due to a problem, compensation, injury, etc) can ruin the “stretching experience”. 

Hopefully we have stretched your appreciation (and knowledge base) to understand more about the kinesthetic aspect of stretching. We are not telling you to stretch, or not to stretch, merely offering a reason as to why we seem to like it.

The Gait Guys

On the subject of manual muscle work…There is more to it than meets the eye….

Following with our last few posts, here is an article that may seem verbose, but has interesting implications for practitioners who do manual muscle work with their clients. We would invite you to work your way through the entire article, a little at a time, to fully grasp it’s implications.

Plowing through the neurophysiology, here is a synopsis for you:

Tactile and muscle afferent (or sensory) information travels into the dorsal (or posterior) part of the spinal cord called the “dorsal horn”. This “dorsal horn” is divided into 4 layers; 2 superficial and 2 deep. The superficial layers get their info from the A delta and C fibers (cold, warm, light touch and pain) and the deeper layers get their info from the A alpha and A beta fibers (ie: joint, skin and muscle mechanoreceptors).

So what you may say.

The superficial layers are involved with pain and tissue damage modulation, both at the spinal cord level and from descending inhibition from the brain. The deeper layers are involved with apprising the central nervous system about information relating directly to movement (of the skin, joints and muscles).

Information in this deeper layer is much more specific that that entering the more superficial layers. This happens because of 3 reasons:

  1. there are more one to one connections of neurons (30% as opposed to 10%) with the information distributed to many pathways in the CNS, instead of just a dedicated few in the more superficial layers
  2. the connections in the deeper layers are largely unidirectional and 69% are inhibitory connections (ie they modulate output, rather than input)
  3. the connections in the deeper layers use both GABA and Glycine as neurotransmitters (Glycine is a more specific neurotransmitter).

Ok, this is getting long and complex, tell me something useful...

This supports that much of what we do when we do manual therapy on a patient or client is we stimulate inhibitory neurons or interneurons which can either (directly or indirectly)

  1. inhibit a muscle
  2. excite a muscle because we inhibited the inhibitory neuron or interneuron acting on it (you see, 2 negatives can be positive)

So, much of what we do is inhibit muscle function, even though the muscle may be testing stronger. Are we inhibiting the antagonist and thus strengthening the agonist? Are we removing the inhibition of the agonist by inhibiting the inhibitory action on it? Whichever it may be, keep in mind we are probably modulating inhibition, rather than creating excitation.

Semantics? Maybe…But we constantly talk about being specific for a fix, not just cover up the compensation. Is it easier to keep filling up the tire (facilitating) or patching the hole (inhibiting). It’s your call

The Gait Guys. Telling it like it is and shedding light on complex ideas, so you can be all you can be.

link: http://jn.physiology.org/content/99/3/1051

On the subject of manual muscle work…There is more to it than meets the eye….

Following with our last few posts, here is an article that may seem verbose, but has interesting implications for practitioners who do manual muscle work with their clients. We would invite you to work your way through the entire article, a little at a time, to fully grasp it’s implications.

Plowing through the neurophysiology, here is a synopsis for you:

Tactile and muscle afferent (or sensory) information travels into the dorsal (or posterior) part of the spinal cord called the “dorsal horn”. This “dorsal horn” is divided into 4 layers; 2 superficial and 2 deep. The superficial layers get their info from the A delta and C fibers (cold, warm, light touch and pain) and the deeper layers get their info from the A alpha and A beta fibers (ie: joint, skin and muscle mechanoreceptors).

So what you may say.

The superficial layers are involved with pain and tissue damage modulation, both at the spinal cord level and from descending inhibition from the brain. The deeper layers are involved with apprising the central nervous system about information relating directly to movement (of the skin, joints and muscles).

Information in this deeper layer is much more specific that that entering the more superficial layers. This happens because of 3 reasons:

  1. there are more one to one connections of neurons (30% as opposed to 10%) with the information distributed to many pathways in the CNS, instead of just a dedicated few in the more superficial layers
  2. the connections in the deeper layers are largely unidirectional and 69% are inhibitory connections (ie they modulate output, rather than input)
  3. the connections in the deeper layers use both GABA and Glycine as neurotransmitters (Glycine is a more specific neurotransmitter).

Ok, this is getting long and complex, tell me something useful...

This supports that much of what we do when we do manual therapy on a patient or client is we stimulate inhibitory neurons or interneurons which can either (directly or indirectly)

  1. inhibit a muscle
  2. excite a muscle because we inhibited the inhibitory neuron or interneuron acting on it (you see, 2 negatives can be positive)

So, much of what we do is inhibit muscle function, even though the muscle may be testing stronger. Are we inhibiting the antagonist and thus strengthening the agonist? Are we removing the inhibition of the agonist by inhibiting the inhibitory action on it? Whichever it may be, keep in mind we are probably modulating inhibition, rather than creating excitation.

Semantics? Maybe…But we constantly talk about being specific for a fix, not just cover up the compensation. Is it easier to keep filling up the tire (facilitating) or patching the hole (inhibiting). It’s your call

The Gait Guys. Telling it like it is and shedding light on complex ideas, so you can be all you can be.

link: http://jn.physiology.org/content/99/3/1051

Ah yes, the Ia and type II afferents.

One of our favorites! Acting as a sentinel from the muscle spindle, concentrated in the antigravity and extensor musculature, Ia and type II afferents live in the belly of the muscle and send information regarding length and rate of change of length to the CNS via the spino cerebellar and inferior olivary pathways. In more simpler terms, think of muscle spindles as small computer chips embedded in the muscle and using la and type II afferents the team act as volume controls helping to set the tone of the muscle and it responsiveness to stretch. If they are active, they make a muscle more sensitive to stretch.

So what does that mean? Muscle spindles turn up the volume or sensitivity of the muscles response to stretch. Remember when we stretch a muscle, it’s response is to contract. Think about when a doctor tests your reflexes. What makes them more or less reactive? You guessed it, the muscle spindle; which is a reflection of what is going on in the higher centers of the brain. The muscle spindles level of excitation is based on the sum total of all information acting on the gamma motor neuron (ie the neuron going to the muscle spindle) in the spinal cord. That includes all the afferent (ie. sensory) information coming in (things like pain can make it more or less active) as well as information descending from higher centers (like the brain, brainstem and cerebellum) which will again influence it at the spinal cord level.

So we found this cool study that looks at spindles and supports their actions:

_____________________________________________________________________

http://www.ncbi.nlm.nih.gov/pubmed/19451207

J Physiol. 2009 Jul 1;587(Pt 13):3375-82. Epub 2009 May 18.

Mechanical and neural stretch responses of the human soleus muscle at different walking speeds.

Cronin NJ, Ishikawa M, Grey MJ, af Klint R, Komi PV, Avela J, Sinkjaer T, Voigt M.

At increased speeds of walking, the muscles themselves (particularly the soleus in this study) become stiffer due to changes in spindle responsiveness. The decline in amplitude and velocity of stretch of the soleus muscle fasicles with increasing walking speeds was NOT accompanied by a change in muscle spindle amplitude, as was hypothesized.

Clinically, this means that the spindles were STILL RESPONSIVE to stretch, even though the characteristics of the muscle changed with greater speeds of action. This may be one of the reasons you may injure yourself when moving or running quickly; the muscle becomes stiffer and the spindle action remains constant (the volume is UP).

Thankfully, we have another system that can intervene (sometimes) when the system is overloaded, and take the stress of the muscle. This is due to the golgi tendon organ; but that is a post for another day…

Geeking out and exploring the subtleties of the neurology as it relates to the system, we remain…The Gait Guys