When faced with the question of how long you need to stretch a muscle on a daily basis to prevent the development of a contracture, orthotists will give you an interesting collection of responses. Most of these attempt to address the question without actually providing an answer. “As much as possible” and “How long has your doctor recommended?” are two common favorites. However, in my experience, a few venturesome therapists and practitioners have committed to times ranging from six to ten hours. So, where does that magic number come from?
A good deal of what we know about muscle contracture comes from
the dedicated work of a French physician, Catherine Tardieu, and
his colleagues. To study the topic, we will peruse our way through
some preliminary studies in which a number of guinea pigs and house
cats gave their all.
The first study was published in 1972 and involved the
evaluation of soleus muscle bellies harvested from several groups
of cats after several weeks in serial casts1. Cats were
assigned to one of five experimental groups. The first acted as a
control group with no intervention. The second group had one of
their hind limbs immobilized in complete dorsiflexion, such that
the soleus muscle was kept in its maximally lengthened position.
The hind limbs of a third group were immobilized in complete
plantarflexion, with the soleus in its most shortened position.
After four weeks of immobilization, the muscle bellies of the
second and third groups were examined both physiologically and
histologically.
The fourth and fifth groups also were immobilized in full
plantarflexion for four weeks. However, upon the removal of the
casts, those in the fourth group were allowed four weeks to recover
without further interventions, and those in the fifth group were
recast in an intermediate range of motion for an additional four
weeks. At the conclusions of the second four-week periods, these
muscle bellies also were examined.
For those who have a working knowledge of glutaraldehyde fixative and nitric acid baths, the details of the authors’ methodology are available in the original publication. For most of us, it’s the outcomes that we’re interested in. What
Tardieu’s group found was that striated muscle is very adaptable tissue. More specifically, muscle is able to adjust its length by producing or removing sarcomeres. While lengthened, the dorsiflexed limbs produced 19 percent more sarcomeres in series. In contrast, the plantarflexed or shortened, muscle fibers lost 40 percent of the sarcomeres in series. The significance from a physiologic standpoint was the realization that muscle can ensure maximum functional overlap of actin and myosin filaments at varying lengths. More relevant to our practices was the fact that these significant physiologic changes occurred in a relatively short space of time.
Fortunately, the research found that muscle also was able to
adjust its properties back to those of its original length
relatively quickly. In the latter two groups, the sarcomere number
returned to normal within four weeks of cast removal.
There was one more rather interesting finding. Researchers found
a greater abundance of connective tissue when dissecting out the
fibers in the muscles that were immobilized in their shortened
position. This increase in connective tissue correlated with a
reduced extensibility in the same group. The authors speculated
that this might be a type of defense mechanism to ensure that a
shortened muscle cannot be overstretched to the point that there is
no interdigitation of the actin and myosin filaments.
Quantifying Muscle Behavior
Fast-forward nine years to 1981. Having examined the cellular
and molecular behavior of muscle when passively shortened, the same
research team set out to observe what happens to muscle in the
presence of prolonged active shortening (think neurologically
induced muscle imbalance). This time around, the authors used
guinea pigs to quantify the muscle behavior.2
To do so, they divided the animal subjects into three groups.
All three underwent “stimulation” of the sciatic nerve for 12 hours
to simulate a neurologic muscle imbalance. This was accomplished
through a low-voltage electrical current to the distal sciatic
nerve sufficient to obtain a clinically observable, sustained
contraction of the soleus. The first group was passively maintained
in plantarflexion during the stimulation period. The second group
was identical to the first with the addition of a 36- to 48-hour
recovery period. The final group also underwent a 12-hour
stimulation period. However, in these animals the soleus was held
in dorsiflexion throughout the stimulation, maintaining the soleus
in a lengthened position.
Following the stimulation period the soleus muscles of groups
one and three were analyzed and compared against those of the
contralateral leg. Following their recovery period, the same
procedures were carried out on the animals in group two. Again, for
those who would like to know more about the delivery of square wave
pulses of 0.3-msec duration and 20 Hz frequency through the Sachs
Electrode, that information is outlined in detail in the original
publication. For the rest of us, it is the results that are of
interest.
Surprises Found
Clinically, the researchers observed that among those animals in
group one, the majority developed significant equinus contractures.
Remember, this is after only 12 hours of stimulated muscle
contraction! A similar phenomenon was observed among the animals in
group two immediately after the nerve stimulation. However, after
the 36- to 48-hour recovery period, no significant differences were
found between the stimulated and contralateral muscle groups. Of
great clinical significance, in the third group, in which the
animals were cast in dorsifexion throughout the stimulation of the
soleus, there was no noticeable difference in ankle angle between
the two sides. In other words, the structural changes in the muscle
required both a stimulated contraction and an extreme shortening of
the muscle. Furthermore, in the absence of the induced contraction,
the muscle could stretch itself back out to its normal range.
When the muscles were examined histologically, there were even
more surprises. As might be expected, in the animals in group one,
there was a decrease in the number of sarcomeres in series. The
authors had predicted this based on their earlier work. However,
the rapidity of sarcomere loss was impressive. Within 12 hours the
number of sarcomeres reduced by an average of almost 30 percent!
Remember, the changes they observed in the first study were
observed after four weeks of passive positioning. Thus contracting
muscle is at a much greater risk for shortening than idle muscle.
The clinical significance of this finding should be immediately
apparent when the cerebral palsy population is considered.
So, 27 cats and 37 guinea pigs later, we’ve learned the
following:
- Muscle adapts its molecular build-up in response to changes to
length, both with respect to sarcomere number and connective tissue
content in the case of shortening; - Muscle that is shortened and contracting is at much greater
risk for these changes; - Muscle can restore itself to its previous length in the absence
of abnormal contractions and external restrictions to motions;
and - Passive prevention of muscle shortening can prevent these
structural changes, even in the presence of unopposed
contraction.
Clinical Study
Realizing the clinical implications of these statements, it was
only natural to seek their application in a treatment population.
Seven years later, Tardieu’s team did just that in their attempt to
answer the question, “For how long must the soleus muscle be
stretched each day to prevent contracture?3”
At the time of the publications, several treatment modalities
had been proposed for the prevention of equinus contracture among
children with cerebral palsy. These included serial castings,
bracing, and aggressive stretching. Tardieu’s group was careful to
point out that they were not out to compare the various modalities,
but to determine if there was a time threshold that needed to be
met, regardless of how the stretching occurred.
To do so, the team identified ten children with cerebral palsy
with “clinically observed, persistent, sustained contractions of
the triceps surae.” The first step in the process was to determine
each child’s passive range of motion. It sounds straightforward
enough, but suffice it to say that great pains were encumbered to
standardize how this was done. If the reader has any desire to see
the testing apparatus utilized, he or she is referred to the
original article. For our purposes, let’s just say that Galileo
would have been proud.
Each child was stretched until minimal torque or resistance was
encountered, and this measurement (think R1) was recorded.
Stretching continued until a maximal torque of 5 to 7 Nm was
reached, and this measurement (think R2) also was recorded. The
difference between the two was the range of passive soleus muscle
stretch. This was assessed at the beginning and at the conclusion
of an observation period averaging seven months.
In between these two assessments, a 24-hour period was selected
for each child in which the researchers continuously monitored the
sagittal angle of the ankle. Again, their methods were impressive,
and beyond the scope of this review. However, the authors were
clear to point out that the measurement equipment did not hinder
eversion or inversion, produced “minimal disturbance to the
children,” and allowed them to wear their usual shoes and
participate in their normal day-to-day activities. For each child,
the equipment recorded the range of ankle motion experienced in the
24-hour period and the amount of time spent at each angle. The
amount of time that the soleus was spent “in stretch” could be
determined for each child by summing up the time spent at every
dorsiflexion angle in excess of their respective “angle 1,” or the
angle at which initial resistance was encountered.
Unsurprisingly, over the course of the observation period, some
children retained their available range of motion at the ankle, and
lost range. However, among the four children who did not experience
progressive soleus contracture, the mean soleus stretching time
over the 24 hours was about six hours. In other words, these kids
spend about six hours in relative dorsiflexion over the course of a
given day. Among the six children who lost range in their soleus,
the mean time spent in a dorsiflexion angle exceeding “angle 1” was
just under two hours.
Now, there are a lot of limitations to this study. The
demanding nature of the protocols restricted the number of kids
that could be examined. While the observation period between
measurements was an average of seven months, the children were only
monitored over one 24-hour period which was assumed to be
representative of normal life. Also, this evaluation was restricted
to the soleus muscle only. However, at the present time, it’s the
best answer we have. How many hours do you have to stretch the
soleus to prevent progressive contractures? According to this
study, six hours.
Here’s to you, Monsignor Tardieu.
Phil Stevens is the director of Clinical Education at
SPOT-Specialized Prosthetic and Orthotic Technologies, in Salt Lake
City, Utah. He can be reached at [email protected]
References
- Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiologic and structural changes in the cat’s soleus muscle due to immobilization at different lengths by plaster casts. J Physiol. 1972; 224: 231-244.
- Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiologic and structural changes in the cat’s soleus muscle due to immobilization at different lengths by plaster casts. J Physiol. 1972; 224: 231-244.
- Tabary JC, Tardieu C, Tardieu G, Tabary C. Experimental rapid sarcomere loss with concomitant hypoextensibility. Muscle Nerve. 1981; 4:198-203.
- Tardieu C, Lespargot A, Tabary C, Bret MD. For how long must the soleus muscle be stretched to prevent contracture? Dev Med Child Neurol. 1988; 30:3-10.