Running Injuries: how to approach recovery training

Running places specific demands on the body, which lead to structural and functional adaptations

At a glance

In this article Matt Lancaster considers the management of the (often difficult) transition from injury to full training.

Like any sport, running places specific demands on the body, which lead to structural and functional adaptations. A key difference between running and many other sports is the magnitude of recycled elastic energy and the demand for eccentric muscle work.

In sprinting, the magnitude of this eccentric muscle demand is high. Maximum hamstring muscle force coincides with eccentric activity, and occurs as the swinging leg approaches its greatest extension, which is also the phase of running where sprinters are most likely to injure their hamstrings(1,2).

Eccentric muscle activity is associated with post-exercise muscle soreness. A study of endurance athletes found that muscle soreness after running reached similar levels to an experimental group performing specific fatiguing exercises(3). Post-exercise muscle damage can affect the way we move, including the way we run(4).

Activities such as cycling and swimming do not place the same high eccentric demand on key lower-limb running muscles. A Dutch group investigating the relatively low energy cost of increasing power output during running found the prevalence of low energy cost eccentric muscle activity helped explain this efficiency(5). Conversely, the poorer efficiency observed in cycling was attributed to the prevalence of higher metabolic cost concentric muscle actions.

Eccentric muscle action and energy absorption within our tendons help to dampen ground reaction forces. However, adaptation to impact is still clearly noticeable in other tissues. In a study of bone density in recreational athletes, the total body bone density was significantly greater in runners than cyclists (6). Likewise, recreational swimmers and climbers have a low total body bone density, though the relative density of their arms is high compared to their spine or legs, due to the effect of muscle action on bones (7). Unsurprisingly, not only do endurance runners have higher total bone densities than swimmers, the relative density is even more pronounced in their legs (7).

However, considering all runners as a single group is perhaps insufficient to accurately describe these specific adaptations. A Greek research team, investigating bone density among national and international standard runners and swimmers found that the intensity, as well as type, of activity was important (8) (see table 1). This specificity is also seen in the inherent stiffness of the Achilles tendon, which is greater in sprinters than non-athletes (9). The same adaptation is not seen in endurance runners.

Table 1

It’s in the genes…

Our body adapts to traumatic events, such as running, by focusing tension, compression and sheer forces on specific molecules, which convert mechanical stresses into biological events (10). This process is called mechanotransduction, and results in adaptive changes to the structure of the extracellular matrix (ECM)(11,12). While the exact mechanisms of mechanotransduction are still emerging, fibroblasts can increase the genetic expression and manufacturing of ECM building blocks in response to mechanical loading(12).

Mechanotransduction occurs in a dose dependant manner(12). The type, magnitude, duration and frequency of loading determine the change in tissue structure. Significantly, if we do not maintain a minimal threshold of loading, our ECM structure is down-regulated and our tissues decondition (11).

Bone mass can reduce by 50%, or more, in 12 weeks without weight bearing activity, while other soft tissues show signs of degradation much earlier(11). In a study on rats, muscle function returned more quickly than bone density following a period of inactivity, but clearly reduced loading or immobilisation during times of injury has consequences for healthy, as well as injured, tissue(13).

Injury

In simple terms, disease, and by extension, injury, reflect the consequence of defects in our genetic machinery to accommodate environmental stresses and demands (14). An increased injury risk may reflect inadequate adaptation of our tissues to the repetitive mechanical loading imposed by running (see figure 1). Failure of tissues to adapt may also involve general health, nutrition and medical issues.

Figure 1

It is probably not surprising that evidence is emerging that some individuals have an increased genetic risk of soft tissue injury, and that the genes involved are associated with the chemicals and mechanisms we see in mechanotransduction (15). But, although injuries remain complex and multifactorial, there is certainly no suggestion that people with certain genes will develop a particular musculoskeletal injury.

Connective tissue injury triggers a cascade of events that promote tissue repair (16). Acute inflammation sensitises pain receptors, encouraging us to protect the injured site and avoid further damage. A proliferation of new cells and building materials form a scar at the site of injury, which initially is weaker than the original tissue (11,16). Under the correct conditions, the scar enters a remodelling phase to maximise its structure and function, which may continue for a year or more(11).

Injured muscle tissue undergoes this same connective tissue scar formation, in addition to regeneration of muscle fibres and nerves (16). The process in tendons is somewhat different and will be considered in a later article. Time scales for healing are determined by the specific tissue injured and the degree of damage (see box 1).

Loading healing tissues

The balance between rest and activity is often the most crucial decision in managing the successful return from injury to training, and largely depends on the tissue damaged and severity of injury. A study of rats with experimental calf-muscle injuries found that a group which remained active regained full muscle bulk in 21 days, while a sedentary group still had reduced muscle mass 42 days after the injury (17).

A similar investigation of the effect of rest and activity on tissue healing in rats found that, while prolonged immobilisation and rest limited the size of the scar, the new tissue did not mature properly, and there was a failure to regain full tissue strength(16). However, commencing activity immediately following injury led to denser scars, which also prohibited muscle fibre regeneration.

The best results were obtained with a short period of immobilisation (in this case 3-5 days) followed by early active mobility(16). This protocol led to optimal orientation of new fibres and better penetration of muscle fibres into the scar.

For a range of connective tissue injuries, including ligament, muscle and bone, a brief period of immobilisation (probably corresponding to the inflammatory and early repair phases of healing) followed by early active loading has been shown to produce the best overall healing results(11,16).

Premature or excessive loading may exceed the loading capacity of fragile new tissue, and delay, or even cause failure of, the healing process (11,18). But rest alone is not an effective way to manage the transition from injury back to training. Controlled exercise and appropriately timed loading, depending on the severity of the injury, provides us with a powerful mechanism to enhance healing at a cellular level.

What loading dose is best for injured tissues?

An investigation into chronic Achilles tendon problems in soccer players found that net collagen synthesis increased in the injured tendon tissues in response to a specific loading programme (19). Significantly, there was no increase in the rate of collagen production in a group with healthy tendons that performed the same exercise programme. In general, loading of injured tissue at thresholds below those required to produce adaptation in healthy tissues is sufficient to promote healing.

This represents a sophisticated system of self-regulation within our tissues. Optimising healing of injured tissues in response to stresses that are not sufficient to cause further damage is advantageous. However, there is no obvious benefit to increasing collagen production in healthy tissues in response to such stresses.

Consideration should be given to the total loading volume (magnitude, repetition and intensity) and not merely the number of repetitions(20). The initial loading progression may be quite slow and frustrating for many runners. However, as tissue health improves, the rate of progression can usually increase, coinciding with tissue remodelling (see figure 2).

Figure 2

Different mechanical stimuli alter the specific gene expression in recovering tissue and the type of loading is also important (21). Loading should reflect the tensile or compressive stresses the injured tissue is subjected to in its usual function. Dense fibrous tissues, such as ligaments, respond to tension(11). Muscle tension can be applied through gentle contraction, initially with the muscle in a relatively protected range to protect the immature scar (18).

Progressing to full training

Progression to full training requires a broad approach to rehabilitation, best illustrated by considering the same four training categories advocated for developing running robustness.

Strength training – As tissues become healthier and stronger, loading exercises should become increasingly running-specific and reflect a training, rather than tissue healing, stimulus (see figure 2). Failure to regain full strength and tissue function may pose a significant risk of reinjury (18). For instance, the incidence of hamstring injury is less in athletes who undergo high load eccentric hamstring training, reflecting the function of the muscle group during running (22,23).

Consideration should also be given to maintaining strength in uninjured body segments, which will otherwise decondition with rest. At the very least, rehabilitation should aim to return you to the level of strength training you were able to perform prior to injury, if not beyond. However, the reality is that, even with a successful recovery from injury, regaining full strength may take a considerable period of time and it is not uncommon for a subtle strength deficit to remain.

Finally, it is worth remembering that the tissue remodelling process may extend for a year or more, even if your recovery seems complete well before then. Maintaining some form of repetitive loading of injured tissues outside a normal strength training programme may encourage optimal long-term healing of the tissue.

Conditioning – First, along with strength training, a targeted approach to conditioning should maintain a minimum loading level in healthy tissues to try to maintain tissues in the adapted state you have trained so hard to achieve. Where appropriate, this should include impact loading and exercises that reflect the eccentric and energy recycling demands of running.

Second, careful assessment may reveal specific areas of relative deconditioning, which may have either contributed to the initial injury, or continue to contribute to excessive stress on the injured tissue during normal movements. Targeted exercises could involve conditioning lower-leg muscles for foot or ankle injuries, or improving trunk muscle endurance in cases of low-back pain.

Coordination – Adaptation in the way we move is a primary consequence of injury and pain. Coordination and motor learning are crucial in the transition back to full training, with a clear relationship between small-scale movement patterns and larger scale running mechanics.

Experimental knee-joint swelling inhibits quadriceps muscle activity, and increases ground reaction forces for single-legged landing, while the excitability of nerves supplying ankle muscles increases following experimental swelling, possibly in an attempt to stabilise the joint (24,25).

Pain can lead to changes in the way we recruit muscles and affect our ability to learn a new motor task (26,27). Significantly, changes in muscle recruitment persist in people with chronic back pain who are pain free at the time of testing, while anticipation of pain has also been shown to alter muscle recruitment, emphasising the need to look beyond just tissue injury when planning rehabilitation (26).

Training proprioception and balance is a crucial aspect of rehabilitating many lower-limb injuries. Muscle retraining is now an accepted form of treatment for low-back pain. Even for specific muscle injuries, progressive agility and trunk stabilisation exercises have been shown to be more effective than isolated stretching and strengthening alone (28). Running drills provide a useful transition from small-scale motor recruitment exercises to the specific coordination demands of running, such as developing appropriate spring stiffness.

Running – As we have seen, running produces specific tissue adaptations, occurring at the most fundamental biological level, and these adaptations can be down-regulated with rest. Cycling and swimming are useful ways to maintain some level of overall fitness during a rehabilitation period, but they do not prepare tissues for the impact, eccentric demand or specific loading requirements of running.

Running progression should consider the intensity of running and not just time or distance. The faster we run, the greater the magnitude of muscle activity, while ground reaction forces are also greater with increased body weight and running velocity (29,30). Running on hills and different surfaces will also affect impact forces and our requirement to produce leg stiffness. These variables should all be phased in carefully, with a slow initial progression, and any symptoms monitored over a 24-hour-period after each session.

References

1. Med & Sci in Sports & Ex 2005; 37 (1): 108-113
2. Clinical Biomechanics 2005; 20: 1072-1078
3. BMC Musculoskeletal Disorders 2001; 2:5
4. Gait & Posture 2007; 25: 236-242
5. Eur J Appl Physiol 2002; 87: 556-561
6. Metabolism 2008; 57: 226-232
7. Osteoporosis Int 2001; 12: 152-157
8. Int J Sports Med 2007; 28: 773-779
9. J Biomech 2007; 40: 1946-1952
10. FASEB J 2006; 20: 811-827
11. J Am Acad Ortho Surg 1999; 7: 291-299
12. Gene 2007; 391: 1-15
13. J Musculoskeletal Neuronal Interact 2006; 6 (3): 217-225
14. Molecular Systems Biol 2007; 3 (124): 1-11
15. Br J Sports Med 2007; 41: 241-246
16. Scan J Med Sci Sports 2003; 13: 150-154
17. Am J Physiol Cell Physiol 2007; 294: 467-476
18. Clin J Sports Med 2002; 12: 3-5
19. Scand J Med Sci Sport 2007; 17: 61-66
20. Sports Med 2008; 38 (2): 139-160
21. J Ortho Research 2000; 18: 524-531
22. Scand J Med Sci Sport 2008; 18 (1): 40-48
23. Am J Sports Med 2006; 34: 1297-1306
24. Am J Sports Med 2007; 35: 1269-1276
25. Br J Sports Med 2004; 38: 26-30
26. Brain 2004; 127: 2339-2347
27. Pain 2007; 132: 169-178
28. J Ortho Sports Phys Ther 2004; 34 (3): 116-125
29. J Sports Sciences 2005; 23 (10): 1101-1109
30. Biomechanics 2005; 38: 445-452

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