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 c…

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/

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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. T…

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

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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

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A Scientific Look at High Heels

http://well.blogs.nytimes.com/2012/01/25/scientists-look-at-the-dangers-of-high-heels/

PROCEED WITH CAUTION! INFO DENSE POST AHEAD!

Can you think of a better way to start the week than with a discussion of high heels? We all like high heels… Well, at least guys do (and we know quite a few women who do as well…some of you may be reading this post). NO, WE DO NOT LIKE TO WEAR THEM, but we can admire the way they make the calves look so great and the increased lumbar lordosis and accentuation of the greatest gait muscles ever created!

Were they based off “chopines” from the 15th century; an elevated shoe (7-30 inches high!) which kept the peoples feet literally “out of the muck” (they didn’t have modern plumbing back then) or are they older? Or was the heel invented out of necessity to keep horse riders literally “in the saddle” ? Chinese and Turkish history says maybe they were to keep women (particularly concubines) from escaping. For the intents of discussion, we will stick with this last premise, as it fits nicely with the findings of this article (based on the study published here)

Remember the neuromechanics posts on muscle spindles or golgi tendon organs (GTO’s) ? If not, click the links and check them out; suffice it to say that the take home message is: Spindles respond to length and GTO’s respond to tension.

We also remember that GTO;’s modulate the muscles function that they come from. In other words, they literally “turn off” the muscle they come from (it is a disynaptic, post synaptic pathway for you neuro geeks out there). In light of that, lets look at some quotes form the article:

“the scientists found that heel wearers moved with shorter, more forceful strides than the control group, their feet perpetually in a flexed, toes-pointed position. This movement pattern continued even when the women kicked off their heels and walked barefoot. ”

No surprises here. Go up on your toes and take a few strides (more difficult for guys, since the biggest heel we may have is about 12mm in our running shoes). Which muscles are engaging? See how difficult it is to take a full stride? Try to engage your glutes. Not so easy, eh? Now put your foot flat on the floor, extend your toes and NOW engage your glutes. Easier? Presyanptic loading of the motor neuron pool pays big dividends!

They go on to say: “As a result, the fibers in their calf muscles had shortened and they put much greater mechanical strain on their calf muscles than the control group did.”

Hmmm… shortened muscles put under greater tension. Sounds like a job for the golgi’s, and what do they do? Inhibit the muscle from contracting. No wonder is was harder.

“In the control group, the women who rarely wore heels, walking primarily involved stretching and stressing their tendons, especially the Achilles tendon. But in the heel wearers, the walking mostly engaged their muscles.”

Wow, here is evidence They changed their motor programming!  Did you ever think that high heels could change the way our brain works? Maybe it’s a secret plot to take over the world….or maybe not…

The Gait Guys…Lovers of high heels as long as you don’t walk in them….

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More on Gait and Vision:  Along the lines of Binocular Parallax….

Yesterdays post talked about vision and parallax. Today’s explores some adaptations we have to poor visual quality. (Note 3 pictures today, toggle amongst them.)

In the attached study, we see people with poorer vision quality had 3 particular gait parameters (although probably had many more parameters) which changed with vision quality:

1. shorter step length

2. less trunk flexion

3. earlier heel contact with the ground (which goes along with shorter step length.)

If we think about what we know about the nervous system, this all makes sense. There are 3 systems that keep us upright in the gravitational plane: vision, the vestibular system and the proprioceptive system. If we remove one of the systems, the other 2 become enhanced (or better said, they had better become enhanced).

In this study they took away (or impaired) vision. This left the vestibular and proprioceptive systems to take over. The vestibular system affects position of the HEAD ONLY and measures linear and angular acceleration.  It makes sense to say that a more upright posture would do wonders for the stability of the system. The semicircular canals found in the inner ear measure angular motion, or rotation. Placing the body upright shifts the position of the semicircular canals in a different posture (particularly the LATERAL semicircular canal, which sits at 30 degrees to the horizontal; ) and places the utricle and saccule (which measure tilt and linear acceleration) in a better position to appreciate these. Translation, correct upright posture and neutral head positioning are critical for their contribution to detecting and maintaining balance and spacial stability.

The study also suggests that earlier heel contact in gait creates an “exploration” of the ground. This is quite important because the foot has so much cortical representation (see bottom picture) and is important for proprioception owing to its 31 articulations LOADED with joint mechanoreceptors, not to mention 4 LAYERS of muscles, LOADED with spindles and Golgi Tendon Organs.  The foot is a highly dense sensory receptor, the problem is we have had it hibernating in shoes for far too long. Imagine the advantage to balance, gait and posture we might have if we hadn’t dampened the mechano-sensory receptors for the better part of our lives. 

So, bringing this all full circle with the study; If you have poor vision, you had better make up for it with good upright posture and a sensory system that is unimpaired.  Most of us could have better posture and could use some retraining of foot function and sensory reception. Blind people generally have good postural and environmental awareness. They are not slouched over leading their gait head first while wearing oven mits on their hands and rigid steel-toed work boots. They take advantage of these systems and optimize them.

Sometimes the simple answers are not as simple as we like, but it is nice to know there is a reason.

The Gait Guys….Providing both simple answers to complex problems and complex answers to apparently simple ones.

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Study: Low vision affects dynamic stability of gait

Gait Posture. 2010 Oct;32(4):547-51. Low vision affects dynamic stability of gait. Hallemans A, Ortibus E, Meire F, Aerts P. Source

Research group of Functional Morphology, Department of Biology, University of Antwerp, Belgium. ann.hallemans@ua.ac.be

Abstract

The objective of this study was to demonstrate specific differences in gait patterns between those with and without a visual impairment… .  Adults with a visual impairment walked with a shorter stride length (1.14 ± 0.21m), less trunk flexion (4.55 ± 5.14°) and an earlier plantar foot contact at heel strike (1.83 ± 3.49°) than sighted individuals (1.39 ± 0.08 m; 11.07 ± 4.01°; 5.10 ± 3.53°). When sighted individuals were blindfolded (no vision condition) they showed similar gait adaptations as well as a slower walking speed (0.84 ± 0.28 ms(-1)), a lower cadence (96.88 ± 13.71 steps min(-1)) and limited movements of the hip (38.24 ± 6.27°) and the ankle in the saggital plane (-5.60 ± 5.07°) compared to a full vision condition (1.27 ± 0.13 ms(-1); 110.55 ± 7.09 steps min(-1); 45.32 ± 4.57°; -16.51 ± .59°). Results showed that even in an uncluttered environment vision is important for locomotion control. The differences between those with and without a visual impairment, and between the full vision and no vision conditions, may reflect a more cautious walking strategy and adaptive changes employed to use the foot to probe the ground for haptic exploration.

homunculus photo courtesy of : http://joecicinelli.com/homunculus-training/

Its a great day to be a neuro geek
So if the receptors on the bottom of the foot aren’t involved aren’t involved in 2 joint muscles staying coordinated (like the hamstring and rectus femoris in this study), how do we determine the approp…

Its a great day to be a neuro geek

So if the receptors on the bottom of the foot aren’t involved aren’t involved in 2 joint muscles staying coordinated (like the hamstring and rectus femoris in this study), how do we determine the appropriate muscle length and ratios? How about our built in muscle length receptors? Lets hear it for muscle spindles! Hooray for Ia and type II afferents!

Sifting through the science so you don’t have to. We are The Gait Guys…

Exp Brain Res. 1998 Jun;120(4):479-86.

Coordination of two-joint rectus femoris and hamstrings during the swing phase of human walking and running.

Prilutsky BI, Gregor RJ, Ryan MM.

Source

Department of Health and Performance Sciences, Center for Human Movement Studies, The Georgia Institute of Technology, Atlanta 30332-0110, USA.

Abstract

It has been hypothesized previously that because a strong correlation was found between the difference in electromyographic activity (EMG) of rectus femoris (RF) and hamstrings (HA; EMG(RF)-EMG(HA)) and the difference in the resultant moments at the knee and hip (Mk-Mh) during exertion of external forces on the ground by the leg, input from skin receptors of the foot may play an important role in the control of the distribution of the resultant moments between the knee and hip by modulating activation of the two-joint RF and HA. In the present study, we examined the coordination of RF and HA during the swing phase of walking and running at different speeds, where activity of foot mechanoreceptors is not modulated by an external force. Four subjects walked at speeds of 1.8 m/s and 2.7 m/s and ran at speeds of 2.7 m/s and 3.6 m/s on a motor-driven treadmill. Surface EMG of RF, semimembranosus (SM), and long head of biceps femoris (BF) and coordinates of the four leg joints were recorded. An inverse dynamics analysis was used to calculate the resultant moments at the ankle, knee, and hip during the swing phase. EMG signals were rectified and low-pass filtered to obtain linear envelopes and then shifted in time to account for electromechanical delay between EMG and joint moments. During walking and running at all studied speeds, mean EMG envelope values of RF were statistically (P<0.05) higher in the first half of the swing (or at hip flexion/knee extension combinations of joint moments) than in the second half (or at hip extension/knee flexion combinations of joint moments). Mean EMG values of BF and SM were higher (P<0.05) in the second half of the swing than in the first half. EMG and joint moment peaks were substantially higher (P<0.05) in the swing phase of walking at 2.7 m/s than during the swing phase of running at the same speed. Correlation coefficients calculated between the differences (EMG(RF)-EMG(HA)) and (Mk-Mh), taken every 1% of the swing phase, were higher than 0.90 for all speeds of walking and running. Since the close relationship between EMG and joint moments was obtained in the absence of an external force applied to the foot, it was suggested that the observed coordination of RF and HA can be regulated without a stance-specific modulation of cutaneous afferent input from the foot. The functional role of the observed coordination of RF and HA was suggested to reduce muscle fatigue.

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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:

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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