Simon and Colleagues:
Simon wrote:
<< Orthoses are also thought to limit ROM, thus we may create immobilization:
If orthoses act through selective immobilization then we should see
predictable and moreover, measurable changes in the muscles: Muscle becoming
increasingly disorganised with significant loss of fibre mass and concurrent
loss of tension generating ability in response to immobilization. Thus, in
your example we should expect orthoses to have an immobilizing effect on the
muscles providing pronatory moment. However, the work of Lieber R.L.,
Bodine-Fowler, S.C.: Skeletal muscle mechanics, implications for
rehabilitation. Physical Therapy. 1993; 73: 844-856, suggests that the
muscles most susceptible to immobilization are single joint antigravity
muscles with a high proportion of slow twitch fibres e.g. soleus. Two-joint
antigravity muscles with a high proportion of slow twitch fibres are next
likely to be effected, e.g. gastrocnemius. Finally, phasic muscles are
affected to a lesser degree e.g. Tib. anterior. What is also key is whether
the muscles are immobilized in a lengthened or shortened position- shortened
results in reduction in sarcomeres, while lengthened results in an increase.
But in either case the length and overall mechanical properties of the
muscle will be altered.>>
Kevin replies:
I don't know if foot orthoses have predictable effects on all individuals in
regard to muscle function or long term effects on strength. As I have
mentioned in previous discussions, the orthosis may diminish the overall
contractile activity of a specific muscle by altering the moments acting
about the joint which the muscle acts across and thus tend to make it weaker
over time. However, if the patient becomes less symptomatic over time with
the use of orthoses, then exercises more than they would have (or could have)
, then the same muscle may tend to become stronger over time. Another factor
is that the absolute strength of muscle is determined not only by
cross-sectional area of the muscle, but the length of the muscle and also by
muscle internal structure (unipennate, multipennate).
In addition, and something I have written on in the literature a few times
(Kirby, Kevin A.: "Rotational Equilibrium Across the Subtalar Joint Axis",
J. American Podiatric Medical Assoc., 79: 1-14, January 1989.; Kirby, Kevin
A., and Donald R. Green: "Evaluation and Nonoperative Management of Pes
Valgus", pp. 295-327, in DeValentine, S.(ed), Foot and Ankle Disorders in
Children. Churchill-Livingstone, New York, 1992.), is how altering the
position of the insertion of the muscle in relation to the joint axis which
the muscle is acting across has a huge effect on the magnitude of rotational
force (i.e. moment) which the muscle can produce with its contraction.
Take for example the posterior tibial (PT) muscle. In a foot which has a
normal subtalar joint (STJ) axis position which is standing close to the STJ
neutral position, the posterior tibial muscle has a moment arm to the STJ
axis of about 30 mm (very gross estimate). If the same foot now pronates
maximally in relaxed bipedal stance and has a large range of eversion range
of motion, the STJ axis may move (medially translate and internally rotate)
in relation to the medial navicular (i.e. the insertion of the PT tendon) by
25 mm (for example). Now, if the maximum tension which the PT can develop
during isometric contraction is 100 N (for example), then the maximum STJ
supination moment which can be developed in the foot close to neutral by PT
contraction is 3.0 Nm (30 mm x 100 N) and the maximum STJ supination moment
which can be developed in the foot in the STJ maximally pronated position is
only 0.50 Nm (5 mm x 100 N). Therefore, a 25 mm medial shift in STJ axis in
relation to the insertion of the PT tendon creates a 25 mm reduction in STJ
supination moment arm and an 83% reduction in the STJ supination moment which
the PT muscle can generate! In fact, if the STJ axis moves another 3 mm
medially from the maximally pronated STJ position so the moment arm is 2 mm
(e.g. by plastic deformation of the spring ligament complex of the
talo-navicular joint, for example), the supination moment which the PT muscle
can generate is reduced to 0.20 Nm (2 mm x 100 N) which is a whopping 93%
reduction in STJ supination moment.!!! Another way of putting it is that if
the STJ supination moment arm reduces from 30 mm to 2 mm, the PT
tendon/muscle, in order to produce equivalent STJ supination moments, would
have to increase its tensile force on the navicular tuberosity from 100 N to
1,500 N (a 15 fold increase in PT tendon tension)!! This greatly increased
demand on PT muscular contractile force in a maximally pronated foot with
relative medial STJ axis deviation which is needed to produce adequate STJ
supination moment to resist overwhelming STJ pronation moments is the most
likely etiology of the tendon injury seen in PT dysfunction.
Therefore, muscle strength is a complex issue, affected by multiple factors,
many of which are difficult to measure in human subjects.
Simon continues:
<< Orthoses are also said to decelerate motion, taking some of the eccentric
work off muscles- what effect will this have on muscle morphology and
function?
But perhaps, as Eric suggests- muscles are more active in the presence of an
orthosis; we should be able to measure this with EMG. But how do orthoses
increase activity and what changes should we expect to see in the
morphology?>>
Kevin replies:
In the clinical setting, I worry less about absolute muscle power than about
muscle function (or dysfunction) during weightbearing activities. I am sure
that there are many effects which foot orthoses have on muscle function,
neuro-muscular coordination, joint and soft tissue afferent inputs, etc.
which we can only guess at this point in our knowledge. Much more research
is needed just to have enough knowledge to know how best to design
experimental protocol which measures some of these critical factors which
determine how foot orthoses affect the human locomotor system.
Cheers,
Kevin
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Kevin A. Kirby, DPM
Assistant Professor of Biomechanics
California College of Podiatric Medicine
Private office:
2626 "N" Street
Sacramento, CA 95816 USA
Voice: (916) 456-4768 Fax: (916) 451-6014
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