The mighty Gluteus Medius, in all its glory!

Perhaps the delayed action of the gluteus medius allows an adductory moment of the pelvis, moving the center of gravity medially. This could conceivably place additional stress on the achilles tendon  (via the lateral gastroc) to create more eversion of the foot from midstance on

“The results of the study demonstrate altered neuromuscular control of the GMED and GMED in runners with Achilles Tendonitis. During running, GMED typically activates before heel strike so as to stabilize the hip and the pelvis. In runners with Achilles Tendonitis, GMED is activated with a delay, which consequently might affect the kinematics of knee and ankle resulting in rear foot inversion. Similarly, GMAX is activated with a delay and for a shorter duration in runners with Achilles Tendonitis. GMAX is the primary hip extensor and via a kinetic chain, a decreased hip extension moment might be compensated by an increased ankle plantarflexion moment which could potentially increase the load on the Achilles tendon.”

Franettovich Smith MM1, Honeywill C, Wyndow N, Crossley KM, Creaby MW. : Neuromotor control of gluteal muscles in runners with achilles tendinopathy.
Med Sci Sports Exerc. 2014 Mar;46(3):594-9.

Foot “core” anyone?

And a good time was had by all. Day 1 of the event in Vancouver. Lots of info and a bonus exercise session. Thanks to all who attended and looking forward to another great day tomorrow!

We spent a great deal of time talking about muscular firing sequences and the reasoning as to why things fire when.

Take a look at the picture and focus on the tib posterior, flexor digitorum longus, and flexor hallucis longus. They fire from loading response and fire through terminal stance. Up to midstance, they act eccentrically to slow pronation and after midstance, they fire concentrically to assist in supination. Note the sequence starts with the tib posterior (more proximal attachments in the foot) and ends with the flexor hallucis longus, more distal attachements (because in “ideal” gait, the hallux is the last to leave the party (or the ground, in this case)). Stability is a priority, so the central or “core” of the foot needs to fire before adding on peripheral (appendicular) muscles. Remember the foot intrinsics fire from midstance to pre swing, further stabilizing the foot “core”

The Gait Guys

This is a nice study looking at lateral gastroc activity and changing firing patterns with speed of movement. It also melds nicely with yesterdays Neuromechanics post…

Those darn Ia afferents….

You remember them, large diameter afferent (sensory) fibers coming from muscle spindles and appraising the nervous system of vital information like length and rate of change of length of muscle fibers, so we can be coordinated. They act like volume controls for muscle sensitivity. Turn them up and the muscle becomes more sensitive to ANY input, especially stretch (so they become touchy…maybe like you get if you are hungry and tired and someone asks you to do something); turn them down and they become less or unresponsive.

Their excitability is governed by the sum total (excitatory and inhibitory) of all neurons (like interneuron’s) acting on them (their cell bodies reside in the anterior horn of the spinal cord).

If we slow things down, the rate of change of length slows as well and excitability decreases, like we see in this study (3-6% slower). We also notice that the length of contraction increases; hmmm, why doesn’t it decrease?

Remember these folks are on a treadmill. The treadmill is constantly moving, opposite the direction of travel. With the foot on the ground, this provides a constant rate of change of length of the gastroc/soleus (ie, it is putting it through a slow stretch); so , once the muscle is activated, it contracts for a longer period of time because of the treadmill putting a slow stretch on the gastroc (and soleus).

This article also talks about people with upper motor neuron lesions. An important set of inhibitory neurons come from higher centers of the brain, in the motor cortex. These tend to attenuate the signals affecting the Ia afferents, and keep us stable. When we have an upper motor neuron lesion (like a brain lesion or stroke), we lose this “attenuation” and the stretch reflexes (and muscle tone) becomes much more active (actually hyperactive), making the muscle more sensitive to stretch. This loss of attenuation, along with differing firing patterns of the gastroc are important to remember in gait rehab.

The soleus and medial gastroc begin firing in the first 10% of the gait cycle (at the beginning of loading response) and fire continuously until pre swing (peaking just after midstance). The lateral head begins firing at midstance; both leads (along with soleus) decelerate the forward momentum of the tibia, flex the knee at midstance, and the medial head assists in adducting the calcaneus to assist in supination.

We remain, inexplicably….The Gait Guys

Effects of treadmill walking speed on lateral gastrocnemius muscle firing.

by Edward A Clancy, Kevin D Cairns, Patrick O Riley, Melvin Meister, D Casey Kerrigan

American journal of physical medicine rehabilitation Association of Academic Physiatrists (2004) Volume: 83, Issue: 7, Pages: 507-51 PubMed: 15213474

Abstract

OBJECTIVE: To study the electromyographic profile-including ON, OFF, and peak timing locations-of the lateral gastrocnemius muscle over a wide range of walking speeds (0.5-2.1 m/sec) in healthy young adults. DESIGN: We studied gastrocnemius muscle-firing patterns using an electromyographic surface electrode in 15 healthy subjects ambulating on a treadmill at their normal walking speed and at three paced walking speeds (0.5, 1.8, and 2.1 m/sec). Initial heel contact was determined from a force-sensitive switch secured to the skin over the calcaneous. RESULTS: For all speeds, the gastrocnemius firing pattern was characterized by a main peak, occurring 40-45% into the gait cycle, that increased in amplitude with walking speed. Speeds of > or =1.3 m/sec produced a common electromyographic timing profile, when the profile is expressed relative to the stride duration. However, at 0.5 m/sec (a speed typical of individuals with upper-motor neuron lesions), the onset of gastrocnemius firing was significantly delayed by 3-6% of the gait cycle and was prolonged by 8-11% of the gait cycle. CONCLUSION: Many patients with upper motor neuron lesions (e.g., stroke and traumatic brain injury) walk at speeds much slower than those commonly described in the literature for normal gait. At the slow walking speed of 0.5 m/sec, we have measured noticeable changes in the electromyographic timing profile of the gastrocnemius muscle. Given the importance of appropriate plantar flexor firing patterns to maximize walking efficiency, understanding the speed-related changes in gastrocnemius firing patterns may be essential to gait restoration.