............Experience with my own running injuries is not dissimilar from
that of Sheehan. During a 42-km marathon, a few months after my first Comrades
Marathon in 1973, I developed a persistent injury that resisted all the
conventional medical advice and put me out of running for a year. Only when I
attended the 1976 New York Academy of Science Conference on the Marathon (Milvy
1977) and heard the presentations by George Sheehan (1977), Richard Schuster
(1977), and Steven Subotnick (1977) did I begin to appreciate that attention to
my running shoes and the use of an orthotic might cure my injury. These measures
worked. After 18 months of intense frustration in which I was able to run only
once or twice a week, I was again able to run without pain. The injury was
desperately uncommon-an inflammation of the (pes anserinus) bursa on the inner
side of the knee. However, it was only some years after the injury had been
cured that I finally made the correct diagnosis.
TEN LAWS OF RUNNING INJURIES
This
experience, together with knowledge gained from treating those injured runners
kind enough to risk my advice, has led me to formulate what I call the 10 Laws
of Running Injuries.
Law I: Injuries Are Not an Act of God
Injuries
that occur in sport fall into one of two groups: they are caused by either
extrinsic or intrinsic forces. Extrinsic injuries result when an external force
acts on the body (for example, in contact sports, such as rugby, ice hockey, and
boxing). The first sports medicine specialists were probably the doctors who
looked after the Roman gladiators. In modern times, the orthopedic surgeons who
first cared for athletes in major contact sports were the first exponents of
sports medicine. The result of all this is that textbooks of orthopedics and
sports medicine have until very recently restricted their focus to extrinsic
injuries and have ignored injuries occurring in non-contact sports. Fortunately,
this has now changed, and the first medical textbook specific to the medical
problems of runners was published in 2001 (O'Connor et al. 2001).
Intrinsic injuries, on the other hand, result from factors inherent in the
body itself and have nothing to do with external trauma. They result from the
interaction of at least three identifiable factors-the athlete's genetic build;
the environment in which training is performed, including the shoes that are
worn; and the athlete's training methods. Only the genetic factor remains
constant; environmental factors, especially the type of shoes worn, and training
methods change constantly.
Hereditary influences that may predispose to running injuries relate to
lower limb structure, which largely determines how our hips, knees, and ankles
and their supporting structures-muscles, tendons, and ligaments-function during
running. Because of differences in genetic structure, virtually no two runners
function identically. More important, perfect mechanical function is exceedingly
rare and is restricted to the handful of runners who run as far as they like in
whatever shoes they might choose without ever being injured. The rest of us run
despite varying grades of biomechanical disaster. Take any ten of us and you
will probably find every possible biomechanical running abnormality ever
described (and a few that defy description).
The fundamental teaching in the biomechanics of running injuries is that the
ankle joint functions most effectively when the talar bone is correctly aligned
in the ankle joint, in the so-called neutral position. Figure 14.1A shows the
typical foot of a runner with a flat foot, in which the talar bone has descended
as the subtalar joint has pronated so that the foot can comfortably reach the
ground. When the subtalar joint is returned to its neutral position (figure
14.1B), the arch of the foot is reformed, showing that flat feet are caused by a
misalignment of the ankle joint.
One theory is that this apparent abnormality occurs because the foot position shown in figure 14.1A is better adapted to gripping a vertical structure, like a tree, than to either walking or running on a flat surface. Hence, it is concluded that this abnormality is a throwback to the human's origins from a tree-dwelling ancestor. It is currently believed that this biomechanical abnormality contributes substantially to many different running injuries and that shoes or orthotics that compensate for this abnormality by holding the foot in the more neutral position (figure 14.1B) are important for effective treatment that will produce a long-term cure.

There are several common anatomical afflictions that may potentially
predispose athletes to running injuries, including:. reduced ankle range of
motion:
leg-length asymmetry (short leg syndrome);
anteversion of the femoral neck;
increased quadriceps (Q) angle;
genu varum (bow legs);
genu valgum (knock knees);
forefoot or rearfoot malalignment (figure 14.2)-or, in its worst form, the malicious or miserable malalignment syndrome, comprising twisting (internal rotation) of the femur, squinting (kissing) patellae, knock knees, rnally rotated tibia, and flat feet (excessive foot pronation; see fig. 4.3); and
high-arched (pes cavus) or flat (pes planus) feet (Cowan et al. 1996; Krivickas 1997; Neely 1998a; 1998b).
These biomechanical abnormalities are likely to predispose the athlete to lower limb injuries.

To this
daunting list must be added another set of predisposing factors: female gender,
age greater than 24 years, a high body mass index or high percentage body fat
(documented in military populations), low levels of physical fitness at the
commencement of the training program, and a previous history of injury (Neely
1998a; 1998b).
The development in the early 1970s of a hypothesis proposing how these
structural abnormalities interfere with the normal functioning of the foot and
lower limb during running and how they interact with running surfaces, shoes,
and training methods to cause injury led to the single most important practical
advance in sports medicine in the 1980s. That the theory now appears to be an
oversimplification (Ilahi and Kohl 1998; Razeghi and Batt 2000; Nigg 2001) is
less important than is the fact that it produced methods of treatment that have
proved relatively effective. Of course, when we better understand the real
biomechanical cause of these injuries, our treatments will improve. But in the
meantime, and until we know better, we must stick with the explanation that has
proved to be practically helpful for the past 25 years. This explanation
proposes a common pathway by which these common biomechanical abnormalities
cause running injuries by altering the biomechanics of the running stride.
The running stride (figure 14.4) is divided into two major phases, the short
support (stance) phase and the longer swing (recovery) phase. One running cycle
is from heel strike to the next heel strike of the same foot. During each
running stride, the leg rotates in the following sequence: during the longer
swing phase of the cycle (figure 14.4, A through F, right leg), the leg rotates
inward (internal rotation), and this continues during the first part of the
support phase (figure 14.4B, left leg). By midsupport (figure 14.4C, left leg),
the direction of rotation reverses to one of outward (external) rotation, which
continues at toe-off (figure 14.4, E and F, left leg).
As soon as the foot is planted on the ground (figure 14.4B, left leg), the
frictional forces between the sole and the surface prevent the foot from
passively following the internal/external rotation sequence occurring in the
lower limb. Therefore, a mechanism has to be present to allow the rotation
sequence of the upper limb to continue without involving actual movement of the
foot in relation to the ground. To achieve this, the subtalar component of the
ankle joint acts as a universal joint, transmitting the internal rotation of the
lower limb (in the transverse plane) into an inward rolling or pronatory
movement at the ankle (in the frontal or horizontal plane; see figure 14.5). As
the ankle joint pronates, it unlocks the joints of the midfoot, allowing these
also to roll inward. The importance of this movement is that it absorbs and
distributes the shock of landing and allows the foot to adapt to an uneven
running surface.


In the athlete with normal running mechanics, after 55% to 60% of the stance
phase has been completed, the upper limb begins to rotate externally, and the
ankle rotation reverses itself and rotates outward (supination) until, just
before toe-off, the ankle and midfoot joints lock in a fully supinated position.
This results in the lower limb becoming a rigid lever, allowing for a powerful
toe-off. Thus, in the ideal running gait there is an early, limited degree of
pronation, followed sometime near the middle of the stance phase of the running
stride by supination of the subtalar joint.
The original theory, proposed in the mid-1970s, holds that very few runners
have a sufficiently normal biomechanical structure to allow this normal sequence
of events. Despite the lack of any firm scientific grounds for this theory, the
design of running shoes and the treatment of injured runners are still to a
large extent based on it (Ilahi and Kohl 1998; Nigg 2001). We are taught that
most of us are saddled with feet that either do too much rolling-the hypermobile
foot-or else roll too little-the so-called rigid, or clunk, foot. And when these
feet are attached to minor mal alignments in the lower limbs, the theory holds
that it is remarkable that any runner can escape injury.
It is theorized that athletes with hypermobile feet pronate excessively
during the stance phase of the running cycle so that, instead of reversing ankle
pronation in mid-support (figure 14.4D, left leg), pronation continues. As a
result, the foot leaves the ground in a pronated and not in the normally
supinated position shown in figure 14.5. It is then argued that this excessive
ankle pronation during the latter stages of the stance phase of running is the
specific biomechanical abnormality that causes certain running injuries, not
only in the foot and ankle but also higher in the lower limb. The latter effect
results from abnormal internal rotation of the tibia (shin) bone, a consequence
of excessive ankle pronation (Hintermann and Nigg 1998).

In contrast, it is argued that the rigid foot fails to pronate sufficiently,
and this causes another set of injuries, as the lower limb is unable to pronate
enough to absorb the shock of landing.
It is on the basis of this theory that shoes are designed and marketed
according to their ability either to resist over-pronation (anti-pronation
shoes) or to absorb shock (neutral or cushioned shoes). Perhaps surprisingly,
the facts we now have do not convincingly support the theory, even though shoes
designed according to that theory seem to be relatively effective in preventing
injury.
Therefore, the major weakness of the theory is that despite more than 20
years of intensive and highly sophisticated research, no one has yet been able
to show that running shoes either reduce the risk of new injuries or cure
established injuries specifically by preventing excessive pronation in those
with hypermobile feet or by increasing shock absorption in those with rigid feet
(Razeghi and Batt 2000; Nigg 2001).
Benno Nigg, a biomechanist from the University of Calgary in Canada, who has
studied and helped in the design of running shoes for more than 20 years, has
identified the following paradoxes (Hintermann and Nigg 1998; Nigg 2001):
Over-pronation probably causes a maximum of about 10% of all running injuries (Walther et al. 1989; Nigg 2001).
Approximately 70% of runners with lower limb injuries improve when they use orthotic devices (James et al. 1978; Bates et al. 1979; McKenzie et al. 1985; Gross et al. 1991), which should act by controlling their excessive pronation.
Neither specifically designed running shoes (Reinschmidt et al. 1997; Stacoff et al. 2001) nor orthotics (Nigg et al. 1998; Nigg 2001) measurably alter the degree to which the ankle pronates during the stance phase of running. Indeed, those studies found that differences in lower limb biomechanics when running barefoot, with shoes, or with shoes and orthotics were negligible, at least in the parameters that those researchers measured. Thus, Nigg (2001) has concluded that "These experimental results do not provide any evidence for the claim that shoes, inserts or orthotics align the skeleton. . . . One may even challenge the idea that a major function of shoes, shoe inserts or orthotics consists in aligning the skeleton." Of course, the possibility remains that these researchers were not measuring the really important biomechanical changes that are produced by these shoes. But the point is that they were unable to show that running shoes produce those biomechanical changes to the running stride that we have always believed in.
Specific anatomical abnormalities are not predictably related to specific running injuries (Wen et al. 1997; Razeghi and Batt 2000; Nigg 2001).
To this list of paradoxes must be added the findings of a study of two groups of New Zealand runners. One group included runners who had never suffered running injuries, and the other, runners who had suffered injuries at or below the knee.
The study
found that uninjured runners had greater hamstring flexibility and a running
gait that produced lower levels of impact loading but higher rates of ankle
pronation. This is paradoxical since, according to the conventional theory, high
rates of ankle pronation should increase injury risk. No other anatomical or
biomechanical factors differed between the groups. Hence, the authors concluded
that reduced impact loading seems to be important in reducing injury risk in
runners, a finding that mirrors my personal experience treating my own running
injuries but that conflicts with the finding of another study, which found that
subjects with higher impact loadings had fewer running injuries (Nigg 2001).
Attempts to alter impact loading by changes in the hardness of the mid-sole
material in the running shoes are largely ineffective (Nigg 2001). Furthermore,
running on hard surfaces does not increase the risk of running injuries compared
to running on soft surfaces (Van Mechelen 1992). Nigg (2001) acknowledged that
as we are unable to conclude that impact forces are an important factor in the
development of chronic or acute running-related injuries, or both, the paradigm
of cushioning to reduce the frequency or type of running injuries needs to be
reconsidered.
To explain these anomalies, Nigg (2001) has proposed a novel model of how
the shoes, shoe inserts, and orthotics alter muscle function both before (muscle
pre-activation) and during the stance phase of the running cycle to produce
preferred joint movement patterns in the lower limb.
Nigg (2001) proposes that the impact forces when the foot strikes the ground
serve as an input signal to the body. This signal produces a response-muscle
tuning-in the body in time for the next foot strike. The function of muscle
tuning is to minimize vibrations in the tendons and muscles and to support a
preferred movement pattern.
The input signal to the body is filtered first by the shoe sole and second
by the shoe insert or orthotic, before being sensed by the plantar surface
(sole) of the foot. This sensory information passes to the brain, which then
produces the necessary muscle pre-activation and related movement patterns to
optimize performance and comfort with that specific combination of shoes,
orthotics, running surfaces, and degree of muscle fatigue. As a result, the
ideal combination of shoe and shoe insert or orthotic reduces muscle activation,
improves running comfort and economy, and (presumably) reduces the risk of
injury.
In this way, shoes, shoe inserts, or orthotics do not act by altering the
preferred joint movement patterns. Rather, they alter lower limb muscle function
during the stance phase of running, thereby influencing comfort, the development
of fatigue, and hence running performance.
As I
survey the proliferation of running shoes and the complexity of their design
compared to what was popular and seemingly very effective during the 1980s, I
begin to wonder whether Nigg might not be on the right track. Indeed, Nigg's
proposal is that the "needs of a large segment of the population can be served
with four or five specific groups (of running shoe/orthotic combinations)"
(2001, p. 8). Perhaps it is time that we began to design and prescribe shoes not
solely on whether they are anti pronation or cushioning shoes. The finding that
shoes do not alter pronation indicates that a thorough testing of the new ideas
proposed by Nigg is long overdue.
Law 2: Each Injury Progresses Through Four Grades
Unlike extrinsic injuries, in which the onset is almost always sudden and dramatic for example, in the case of a rugby player caught in a ferocious tackle-the onset of intrinsic running-related injury is almost always gradual. Running injuries become gradually and progressively more debilitating, typically passing through four stages or grades.
Grade 1: An injury that causes pain after exercise and is often only felt some hours after exercise has ceased.
Grade 2: An injury that causes discomfort, not yet pain, during exercise, but that is insufficiently severe to reduce the athlete's training or racing performance.
Grade 3: An injury that causes more severe discomfort, now recognized as pain that limits the athlete's training and interferes with racing performance.
Grade 4: An injury so severe that it prevents any attempts at running.
Appreciating the distinction in the severity of running injuries allows a more
rational approach to treatment. An athlete with a grade 1 injury requires less
active treatment than does the athlete with a grade 4 injury. Similarly, the
athlete with a grade 1 injury does not have to be excessively concerned about
the injury as long as it does not progress to being a grade 2 injury. Should the
injury progress, the athlete needs to pay more attention to it.
Runners need not fear that a grade 1 injury that has existed for some time
will suddenly deteriorate into a grade 4 injury. (The only exceptions are stress
fractures and the iliotibial band [IT band] friction syndrome, both of which can
become severe and incapacitating very rapidly.)
The grade of the injury helps the doctor define each athlete's pain or
anxiety threshold. The athlete who seeks attention for an injury only when it
reaches grade 4 clearly has a different anxiety threshold from that of the
athlete who seeks urgent attention for a grade 1 injury. Obviously, the advice
given for each type will also differ greatly: a runner with a grade 1 injury
requires substantial psychological support; a runner with a grade 4 injury
requires a psychological analysis of why running is so important that the
athlete will only stop when forced to do so.
Law 3: Each Injury Indicates a Breakdown
This law can be viewed as a corollary to the first law, which holds that
there is a reason running injuries occur. This law simply emphasizes that once
an injury has occurred, it is time to analyze why the injury happened. Often the
injury is due to the fact that the athlete has reached the breakdown point,
usually because a higher level of training has been sustained for longer than
one to which the body can adapt. Occasionally, it is the result of a more sudden
change in training routine. The athlete may be training harder, farther, or on a
different terrain or in different or worn-out running shoes, all of which can
precipitate a physical breakdown.
Every athlete has a potential breakdown point-a training intensity and a
racing frequency at which breakdown becomes inevitable-whether this point is a
weekly total of 30 km or 300 km in training or a racing frequency of 1 or 50
races a year. Indeed, the more races you run, the longer your longest training
run; and the faster you run, the greater your risk of injury (Van Mechelen 1992,
p. 61). The key to preventing and treating injuries is to understand that just
as most of us will never win a big race because of certain genetic limitations,
so our genes limit our choice of shoes, influence the surfaces that we can
safely train on, and ultimately determine what training methods our bodies can
handle. Only when we learn this perspective will we have sufficient wisdom to be
injury-resistant. The corollary, of course, is that athletes who are frequently
injured do not yet appreciate their bodies' thresholds. When a running injury
occurs, the factors that the wise runner needs to consider are training
surfaces, training shoes, and training methods.
Training Surfaces
Running surfaces are often too hard or too cambered and accordingly, in
terms of the Nigg model (2001), require increased muscle activity to produce the
preferred lower limb movement patterns. The ideal running surface is a soft,
level surface, such as a gravel road, which is more forgiving and requires less
muscle pre-activation to ensure optimum shock absorption. Unfortunately, we are
usually forced to run on tarred roads or concrete pavements. Furthermore, roads
are usually cambered, and this forces the foot on the higher part of the slope
to rotate inward (pronate) excessively, while the range of movement of the foot
on the lower part of the slope is reduced. In addition, the leg on the lower
side of the camber is artificially shortened and therefore acts as a short leg.
Running on a concrete surface increased the risk of injury in women but not in
men (Macera et al. 1989).
Grass surfaces, although soft, can be uneven, while the sand on beaches is
either too soft (above the high-water mark) or too cambered (below the
high-water mark). Athletic tracks are of varying hardnesses and introduce the
problem of running continuously in one direction around a curve. This causes
specific stresses on the outer leg, which must overstride to bring the athlete
around each corner.
Similarly, uphill running puts the Achilles tendon and calf muscles on the
stretch and tilts the pelvis forward, while downhill running accentuates the
impact shock of landing and pulls the pelvis backward, thereby extending the
back. Downhill running also causes the muscles to contract eccentrically,
thereby increasing muscle damage (Schwane et al. 1983). Over-striding, more
common when running downhill, also increases the loading on the anterior calf
muscles.
A running injury may first occur shortly after the runner has changed to
uphill or downhill running, or to running on the beach or on a Tartan or cinder
track, or to running continuously on an unfavorable road camber. The best plan
of action is to vary the terrain on which you run, to run in both directions
around a track, and to avoid running on the beach, except for an occasional
session.
Training
Shoes
Injury may follow a recent change in shoes, either simply from one pair of
shoes to another, or from a training shoe to racing flats or spikes or, more
commonly, from one model to another. Other significant potential factors in
injury include running in worn-out shoes, either with worn-off heels, with heel
cup and midsole having molded to your genetic foot faults (usually collapsing
inward), or with mid-soles that have flattened out or become hard (figure 14.6).

Surprisingly, one study found that runners who used the more expensive shoes
(Marti, Vader, et al. 1988) or who owned two pairs of shoes (Walther et al.
1989) had more injuries. This probably reflects selection bias: only runners who
run greater distances in training or who have been injured previously are likely
to buy expensive running shoes or to own more than one pair of shoes.
Training Methods
High training volumes and previous injury are two of the most important
predictors of injury (Powell et al. 1986; Marti, Vader, et al. 1988; Brill and
Macera 1995; Van Mechelen 1992). But injury may also follow a sudden increase in
training distance or speed (training too much, too fast, too soon, too
frequently; Van Mechelen 1992; Brill and Macera 1995; Almeida et al. 1999) or
may occur when undertaking too many races or long runs.
Novice runners, women in particular, are especially prone to injury if they
run too frequently and too far and are too ambitious during their first three
months of running (Brill and Macera 1995). Risk of injury is also greatest in
those who have not been particularly active or physically fit before beginning
more intensive training (Jones et al. 1993; 1994). Beginning runners who
increase their training according to the rapid improvement in the fitness of
their heart, lungs, and leg muscles may exceed the capacity of their bones
(which adapt more slowly) to cope with the extra load caused by running and may
develop tibial or fibular bone strain (shin splints) or a stress fracture. It is
for this reason that it is advisable to follow the structured training programs
for beginners proposed in chapters 5 and 9.
Different training methods can also promote muscle strength and flexibility
imbalances. Every kilometer that we run increases the strength and inflexibility
of the muscles most active in endurance running-the posterior calf, hamstring,
and back muscles-with a corresponding reduction of strength in their opposing
muscles---the front calf, front thigh, and stomach muscles. This
strength/flexibility imbalance has traditionally been regarded as such an
important risk factor in injury that many authorities (Anderson 1975; Dram 1980;
Beaulieu 1981), but not all (Osler 1978), believe that it is important to
maintain muscle flexibility as you train. For this reason, flexibility
(stretching) exercises are usually prescribed to both prevent and cure injuries.
However, insufficient stretching has not been found to be a risk factor for
injury. In fact, injured runners were those who stretched for longer before
running (Jacobs and Berson 1986; Ijzerman and van Galen 1987). Indeed, a careful
analysis of all the published literature (Shrier 1999; 2000) and a controlled
clinical trial (Pope et al. 2000) all conclude that pre-exercise stretching,
even when combined with adequate cool-down and warm-up sessions (Van Mechelen
1992; 1993; Brill and Macera 1995; Pope et al. 2000) does not influence the
incidence of lower limb injuries. However, a full description of the commonly
prescribed stretching exercises is included in this chapter for those who wish
to follow a regular stretching program.
Table 14.1 provides an analysis of all the factors that have been evaluated
and their postulated relationship to the risk of developing a running injury
(Van Mechelen 1992).

Law 4: Most Injuries Are Curable
Only a small fraction of true running injuries are not entirely
curable by simple techniques, and surgery is only required in very exceptional
cases. For example, in a study of 200 consecutive running injuries seen at our
sports injury clinic, we (Pinshaw et al. 1983) found that within eight weeks of
following the simple advice described in this book, nearly three-quarters of the
injured runners were pain free and running almost the same training distance as
before injury. In addition, most of the runners who were not helped had not
adhered to our treatment protocol.
Armed with this knowledge, the first priority of any caregiver is to
reassure injured runners that they can almost certainly be completely cured. The
only possible exceptions to this rule are the following types of injuries:
Those that occur in runners with very severe biomechanical abnormalities for which conventional measures are unable to compensate adequately. Such runners are always likely to become injured whenever they train sufficiently hard. However, in my experience, only a small number of runners have such severe mechanical abnormalities that they are unable to run without injury.
Those that result in severe degeneration of the internal structure of important tissues, in particular the Achilles tendon. There is now a growing appreciation that most injuries to the Achilles tendon are due to degeneration of the tendon (tendinosis), not inflammation (tendinitis) (Khan et al. 1999). Degenerative conditions tend to heal poorly, requiring more prolonged periods of rest than do inflammatory conditions. In addition, the prospects of a complete cure without recurrence are rather small.
Those that occur in persons who start running on abnormal joints (in particular, hips, knees, and ankles). The typical patient with this problem is the former rugby or football player who has damaged one of these major joints and undergone major surgery. The joint is never again quite the same after major surgery, and by the time such players start to run, usually in their late 30s, their joints have often degenerated to the point at which they cause pain during running.
An
important corollary to this fourth law is that if you are not completely cured
of your running injury by the experts with whom you consult, it is time to look
elsewhere. But treat even the advice of runners with some caution, and do not
accept it unconditionally without seeking a professional assessment from someone
knowledgeable about running and sympathetic to runners.
Law 5: Sophisticated Methods Are Seldom Needed
Most running injuries affect the soft tissue structures (tendons,
ligaments, and muscles), particularly those near the major joints. These
structures do not show up on X rays. You should therefore be wary of the
practitioner whose first reaction to your injury is to order an X ray. Unless
that X ray can be justified, you are probably better off putting the money that
would have been spent on the radiological examination into a good pair of
running shoes.
The diagnosis of most running injuries is made with the hands, so the advice
of any caregiver who does not carefully feel the injured site before making a
diagnosis must be treated with caution. As with any injury, a correct diagnosis
requires a careful, unhurried approach in which the injured athlete is given
sufficient time to explain the situation and describe the training methods used.
The doctor must have the time and the patience to listen carefully and
sympathetically. Seldom is it necessary to use expensive tests to establish the
diagnosis, and the treatment pre- scribed is usually very simple. Indeed, I
believe that 60% of the doctor's success is due to an ability to understand what
the injury means to the patient, the fears that the injury engenders, and how
best to allay those fears. For this, the doctor needs to understand the
patient's psyche and understand why the patient came at that particular time to
have the injury examined (see also chapter 8).
However, if the injury persists, it may be necessary to undergo a more
sophisticated evaluation with a magnetic resonance imaging (MRI) scan. These
scans specifically show the soft tissues in previously unimaginable detail and
will detect those rare and unexpected injuries that defy the more simple and
conventional diagnostic methods described here.
Law 6:Treat the Cause, Not the Effect
Because all running injuries have a cause, it follows that the
injury can never be cured until the causative factors are eliminated. Therefore,
surgery, physiotherapy, cortisone injections, drug therapy, chiropractic
manipulations, and homeopathic remedies are likely to fail if they do not
correct all the genetic, environmental, and training factors causing the
runner's injury. Remember the following axiom: the runner is an innocent victim
of a biomechanical abnormality arising in the lower limb. First treat the
biomechanical abnormality and then, and only then, attend to the injury. Even
though we may not yet fully understand the exact biomechanical abnormalities
that cause specific running injuries (Razeghi and Batt 2000; Nigg 2001), the
overriding belief that biomechanics determines injuries remains intact.
Unfortunately, there are some runners whose injuries exist more in their
heads than in their legs. Runners in this group are characterized by their
failure to respond to those forms of treatment that would normally be expected
to succeed. An approach to the management of these injuries is described in
chapter 8.
Law 7: Complete Rest Is Seldom the Best Treatment
If an injury is caused solely by running, then the logical answer
for those who know no better is to advise avoidance of running (rest) as the
obvious cure. Rest does indeed cure the acute symptoms, but like any therapy
that does not aim to correct the cause of the injury, it must ultimately fail in
the long term, because as soon as the athlete stops resting and again starts
running the lower limbs are exposed to the same stresses as before, and the
injury must inevitably recur. Furthermore, there is no doubt that rest is "the
most unacceptable form of treatment for the serious runner" (James et al. 1978).
Complete rest is unacceptable to most serious runners, because running
involves a type of physical and emotional dependence. An athlete who is forced
to stop running for any length of time will usually develop overt withdrawal
symptoms (Mondin et al. 1996), and either the runner or, not uncommonly, the
runner's spouse will immediately commence the search for anything that will
allow the distraught runner to return to the former running tranquility.
The only injuries that require complete rest are those that make running
impossible. For example, the athlete with a stress fracture simply cannot run,
no matter how strong the desire to do so. Thus, my approach is to advise runners
to continue running, but only to the point at which they experience discomfort.
In other words, they are only allowed to run to the point at which their injury
becomes painful. In addition, supplementary or alternative activities can be
prescribed. Fortunately, most current runners are not the complete specialists
typical of former years, and many also swim, cycle, or exercise in the gym.
These alternative activities, including running in water using a flotation
device, can provide the daily physical stimulus to which most athletes are
accustomed without adversely affecting the healing of the injury. Indeed, there
is a possibility that mild exercise, including water activities, may stimulate
healing.
If these treatments are effective, then the runner's discomfort should
become progressively less during running, making it possible to run
progressively further. On the other hand, if the pain does not improve on
treatment, then either the treatment is ineffective (occasionally because the
runner has a psychological basis for the injury) and an alternative method of
treatment must be tried, or else the diagnosis is wrong.
Furthermore, if the injury does not respond to what should be adequate
treatment within three to five weeks, then the alarm bells should ring very
loudly. The failure of an injury to respond indicates that you may be dealing
with an obscure injury, such as effort thrombosis of the deep veins in the calf,
or an injury unrelated to running (for example, a bone cancer) for which another
form of treatment may be urgently required.
Law 8: Never Accept As Final the Advice of a Non-runner (MD or
Other)
Over the years I have come to the conclusion that all people
consider themselves experts on sport. People who are otherwise extremely wary
about expressing opinions on subjects about which they may actually know
something feel no such restraint when the topic of sport arises. This applies
equally to sport injuries and their management.
How, then, do you know whose advice you can trust? I suggest four simple
criteria:
Your adviser must be a runner. Without the first-hand experience of running, this person will not have sufficient insight to help you. Of course, this does not mean that all the advice you get from runners will be sound-only that there is a greater probability that it will be correct.
Your adviser must be able to discuss in detail the genetic, environmental, and training factors likely to have caused your injury. If the practitioner is unable to do this, together you will go nowhere.
If unable to cure your injury, your adviser should feel as distressed about this failure as you do. The person from whom you seek help must understand the importance of your running to you. It is patently ridiculous to accept advice from someone who is antagonistic to your running in the first place.
Your adviser shouldn't be expensive, as most running injuries can be cured without recourse to expensive treatments.
Other
advice given by Tom Osler (1978) is that you should tell the practitioner that
you will only consider the possibility of treatment after all the choices are
clear and you have had time to reflect on them. After hearing the treatment that
has been suggested, go home and discuss it with other runners. At all times, be
conservative in the advice you accept. Finally, Osler reminds the runner to
remember that "God heals and the doctor sends the bills." Osler's comments are
particularly apt as they were written at a time when so little was known about
these injuries and how they should be treated.
Law 9: Avoid Surgery
The only true running injuries for which surgery is the first
line of treatment are muscle compartment syndromes and interdigital neuromas.
Surgery may also have a role in the treatment of chronic Achilles tendinosis of
six or more months' duration (Smart et al. 1980; Leppilahti et al. 1994; Testa
et al. 1999), low back pain from a prolapsed disc (Gut en 1981), and the
iliotibial band friction syndrome (Noble 1979; 1980; Firer 1992), but only when
all other forms of non-operative treatment have been allowed a thorough trial.
The obvious danger of surgery is that it is irreversible: what is removed at
surgery cannot be returned. It is a tragedy, as I have seen on more than one
occasion, for a runner to have undergone major knee, ankle, or back surgery for
the wrong diagnosis. Not only will that surgery fail to cure the injury, but it
may seriously affect the unfortunate athlete's future running career.
Surgery should only be considered for a small group of injuries, and only
when such injuries are grade 3 or 4. These concerns do not apply as rigidly to
arthroscopic surgery, in which a small flexible fiber optic cable is placed
inside the joint through a small skin incision. This procedure allows
visualization of the joint surfaces and all the relevant structures within the
knee, enabling a more accurate diagnosis to be made or, alternatively, showing
that the joint is normal. Corrective surgery can also be performed with
miniature instruments, also introduced through small skin incisions. Since the
entire knee is not opened in this procedure, recovery is usually rapid.
Law 10: Recreational Running Does Not Appear to Cause
Osteoarthritis
Osteoarthritis is a degenerative disease in which the articular
cartilage that lines the bony surfaces inside a joint becomes progressively
thinner until the bone beneath the cartilage on both sides of the joint
ultimately becomes exposed. In the advanced stages of osteoarthritis, the
exposed bones rub against one another, causing pain and severely limited joint
movement. The view of some orthopedic surgeons is that this degenerative process
can be initiated and exacerbated by long-distance running (Sonstegard et al.
1978).
However, the more modern evidence shows that if running does indeed increase
the risk of osteoarthritis, this occurs only in those elite athletes who run
many miles in their careers. Recreational joggers are not at any increased risk
of developing osteoarthritis (Panush and Inzinna 1994; Buckwater and Lane 1997).
Nevertheless, it is important that the literature on this topic should be
presented, most especially those studies that show a (moderately) increased risk
for osteoarthritis in elite athletes, including runners.
Puranen and his colleagues (1975) obtained the hip X-rays of 74 former
champion Finnish athletes, who had run for a mean duration of 21 years. Advanced
degenerative osteoarthritic changes were found in three runners (4%) but were
present in more than twice as many (9%) of the control subjects treated at that
hospital for conditions other than hip diseases. In two runners with advanced
radiological changes, their symptoms were insufficiently severe to restrict
their running, even at the ages of 75 and 81. It was reported that despite what
his radiograph showed, the 75-year-old runner would not even consider
interrupting his lifelong obsession with marathon running.
Similarly, in other studies of highly active sports people, including
professional soccer players (Adams 1976), physical education teachers (Bird et
al. 1980; Eastmond et al. 1980) and even sport parachutists (Murray-Leslie et
al. 1977), the incidence of osteoarthritis was no higher than that found in the
non-athletic population. Neither Wally Hayward, when studied in 1981 (Maud et
al. 1981), nor Jackie Mekier had any evidence of osteoarthritis, despite the
prodigious distances they ran. In no large series of people with osteoarthritis
is there a preponderance of athletes (Jorring 1980), as would be expected if
sport were a significant cause of osteoarthritis.
Sohn and Micheli (1984) found that the incidence of osteoarthritis in a
group of runners who competed between 1930 and 1960 at seven universities in the
eastern United States was lower than that of a matched group of swimmers who
competed at the same universities at the same time, whose joints had not been
exposed to the same loading stresses as had those of the runners. A Danish study
(Konradsen et al. 1990) found that the incidence of osteoarthritis in 30 Danish
orienteers during the 1950s, most of whom continued running 20 to 40 km per week
for 30 years, was no different from that in controls. Similarly, runners with a
mean age of 60 who had run an average of 3 hours per week for 12 years did not
have a greater prevalence of osteoarthritis but did have a 40% greater density
in their vertebral bones (panush et al. 1986).
Lane et al. (1986) reported that the incidence of osteoarthritis was not
higher in a group of 41 runners aged 70 to 72 than it was in a matched control
group. A similar finding was reported by Panush et al. (1986). The study of Lane
and her colleagues (1986) also found that the bone mineral content of the
runners, both male and female, was approximately 40% greater than that of the
controls. A subsequent prospective, five-year follow-up study of 35 runners aged
63 at the start of the trial found that at age 68, although X ray evidence of
osteoarthritis had increased in both runners and controls, there was no
difference in the radiographic scores for osteoarthritis in runners who were
still running, in those who had stopped running, or in control subjects who had
never run (Lane et al. 1993). Runners in that group ran an average of 163
minutes a week.
In a related study, Lane et al. (1987) showed that runners develop fewer
musculoskeletal disabilities as they age, and develop them at a slower rate,
than do non-runners. Thus, far from making them more infirm and disabled, their
running preserves the functional integrity of their joints and muscles.
Similarly, female former college athletes were not found to be at increased risk
of developing osteoporotic fractures in later life than were non-athletes
(Wyshak et aI. 1987).
Other evidence to support this belief is that experimental osteoarthritis in
rabbits is not made worse by running (Videman 1982); that the absence rather
than the presence of normal weight bearing across a joint leads to degenerative
changes similar to those found in early osteoarthritis (Palmoski et al. 1980);
and that even in patients with the more serious form of arthritis (rheumatoid
arthritis), regular exercise seems to delay rather than to expedite the
progression of the disease (Nordemar et al. 1981).
Many sports people who develop osteoarthritis have had previous joint
surgery. In the study of Murray-Leslie et aI. (1977), 75% of sport parachutists
who developed osteoarthritis had undergone previous surgery for removal of a
torn cartilage (meniscectomy). It was those athletes who exercised on abnormal
joints who ultimately developed osteoarthritis. Another study (Kohatsu and
Schurman 1990) found that obesity, significant knee injury, and heavy daily
physical labor, but not leisure time physical activity, increased the risk of
osteoarthritis.
The type of sport injuries requiring surgery are typical of those that
result from an external blow to the joint, as occurs in contact sports, such as
football or rugby, or from rapid changes in direction that occur in both contact
and non-contact sports that are contested at speed. Thus, those who blame
running as a significant cause of osteoarthritis are blaming the wrong sport.
They should rather focus on contact sports or other sports in which there are
frequent, rapid changes in direction. Nevertheless, we cannot ignore a growing
body of evidence showing that running at a very high level of competition,
sustained for many years, is associated with a measurable, but small, increased
risk of osteoarthritis.
A famous study of a large group of residents of Framingham,
Massachusetts-the Framingham study was the first to show that there are certain
personal risk factors for heart disease, including cigarette smoking, high blood
pressure, and high blood cholesterol concentrations (see chapter 15)-reported
that the most physically active residents were at increased risk of
osteoarthritis, as were those residents who were the most obese (Felson et al.
1988; McAlindon et al. 1999).
But residents who participated in light to moderate physical activity were
not at any increased risk of osteoarthritis. Essentially, the same conclusions
were drawn from a study of elderly women (Lane et al. 1999). As might be
expected, weight loss of 5 kg reduced the risk of osteoarthritis in women in the
Framingham study (Felson et al. 1992).
A 15-year study of 27 long-distance runners revealed that those who were
running the fastest in 1973, when the study began, had the most marked
radiological changes of degenerative hip disease at follow-up. The authors
concluded that past long-term, high-intensity, and high-mileage running cannot
be dismissed as a potential risk factor for premature osteoarthritis of the hip
(Marti et al. 1989).
A Swedish study of 233 men who underwent hip replacement surgery for
advanced osteoarthritis found that men who were exposed to high levels of
sporting activities for more than 29 years had a 3.5- to 4.5-fold increased risk
of developing osteoarthritis (Vingard et al. 1993). For men who were also
involved in high levels of physical work in their occupations, the risk was
increased 8.5-fold. The most hazardous sports were racket sports and track and
field, in which risk was increased 3.3- to 3.7-fold respectively for those with
high exposure for the longest time. Risk was increased 2.1-fold for
long-distance runners in the same category. Sports in which there was less
impact loading on the joints, including golf, swimming, hiking, bowling, and ice
hockey, were not associated with any increased risk.
Two Finnish studies (Kujala et al. 1994a; 1995) have evaluated the
prevalence of osteoarthritis in former elite male Finnish athletes. The first
study (Kujala et al. 1994a) evaluated 2049 male athletes who had represented
Finland in international competition between 1920 and 1965. The study found that
athletes from all types of competitive sports were at slightly increased risk of
seeking medical care for osteoarthritis-1.9-fold increased risk for endurance
athletes and 2.2-fold increased risk for power athletes. Interestingly,
endurance athletes first sought medical care for osteoarthritis at a much older
average mean age (71 years) than did athletes in other sports (58 to 62 years).
The second Finnish study (Kujala et al. 1995) compared the prevalence of
osteoarthritis of the knees in former top-level Finnish athletes participating
in long-distance running, soccer, weightlifting, or shooting. The study found
that previous knee injuries (4.7-fold increased risk), a high body mass index
(1.8-fold increased risk), and playing soccer (5.2-fold increased
risk)----because of the likelihood that soccer would cause a previous knee
injury----were the principal risk factors for knee osteoarthritis. In contrast
to its effects on the hip (Kujala et al. 1994a; Raty et al. 1997), long-distance
running did not increase the risk for premature osteoarthritis of the knee.
A study of former elite British female long-distance runners and tennis
players also found a 2- to 3-fold increased risk for the development of X ray
changes suggestive of osteoarthritis (Spector et al. 1996). But athletes did not
report pain any more frequently than did non-athletes, who generally had fewer
radiological signs of osteoarthritis. Interestingly, it appears that women are
more likely than men to develop osteoarthritis when exposed to high levels of
habitual physical loading of their joints (Imeokparia et al. 1994).
In summary, people who participate in regular, vigorous, competitive
athletics for most of their lives are at increased risk of developing
osteoarthritis. The risk is increased if they also develop a joint injury during
their sporting careers or if they also load their joints during their work.
Sports that involve both impact and torsional loading, such as soccer, racket
sports, and track and field, are associated with greater risk than long-distance
running. Competitive long-distance running at an elite level appears to increase
the risk only of hip osteoarthritis. But for those more sedentary patients who
develop osteoarthritis, a supervised walking program reduces symptoms and
improves functional capacity (Kovar et al. 1992; Ettinger et al. 1997).
FROM: LORE OF RUNNING by Tim Noakes, MD--CHAPTER 14: Staying Injury Free