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
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
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
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
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.
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.
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.
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).