All athletes that train hard enough to compete will get injured. This is the sorry truth of the matter, and anyone dissuaded from competition by this fact would not have made a good competitor anyway. Progress involves hard training, and hard training eventually involves pushing past previous barriers to new levels of performance. In the sense that this can cause injury, successful competitive athletics is dangerous. It is a danger that can and must be managed, but it is important to recognize the fact that athletes get hurt. If they want to continue to be athletes afterwards, it is equally important to understand how to manage and rehabilitate injuries successfully so that they don’t end a career.
Severely damaged tissue cannot be repaired through rehabilitation. Rather, the surrounding healthy tissue is strengthened in order to take over the load once carried by the now non-functional tissue. If someone has a survivable heart attack, such as a myocardial infarction, part of the heart muscle dies (figure 9-4). The dead muscle no longer contributes to the contraction of the heart, but the heart continues to beat and deliver blood. Immediately after the infarction, the efficiency with which the heart delivers blood is low but, without missing a beat, the remaining healthy, functional heart muscle begins to adapt because it continues to be loaded. In order to adapt to the missing force generation capacity of the damaged tissue, the remaining muscle contracts more forcefully and rapidly increases in mass. The end result is the recovery of the entire heart's ability to generate contractile force even having lost some of its original muscle through irrecoverable damage. The change in contractile geometry of the ventricle will not actually allow the return to 100% of normal function; instead of the geometry of a normal heart, the post-infarcted heart is shaped like a Chinese tea-cup on its side, with the necrotic tissue forming a lid. This altered geometry, even with thicker walls after hypertrophy, is inherently less efficient than the original ventricle, but it functions well enough that normal activities can eventually be resumed.
With severe muscle damage in other parts of the body a similar but less dire situation exists. If a muscle is severely damaged to the point of necrosis, not only will the remaining tissue adapt to the loss of function of the damaged tissue by increasing its functional capacity, the surrounding muscles that normally aid the damaged muscle in its biomechanical role will contribute to the recovery of function by assuming part of the workload. This is classically illustrated in the scientific and medical literature in 'ablation' experiments where the gastrocnemius muscle (major calf muscle) is removed and the underlying soleus and plantaris muscles rapidly adapt and assume the load once carried by the gastrocnemius (figure 9-5).
It is well documented that these newly-stressed muscles change dramatically, both chemically and structurally, after ablation in order to return the mechanical system to 'normal' function. The recovered structures are not as good as the original equipment, but they function at a high percentage of the original capacity.
Figure 9-4. If a coronary artery is blocked through atherosclerosis or, as in the case above, experimentally blocked by tying off the left main coronary artery in the rat (A), the muscle tissue that loses its circulatory supply (B1) will be irreversibly damaged. The tissue immediately surrounding the injured tissue (B2) and any other undamaged tissue will immediately become overloaded and assume the pressure generation load once uniformly distributed over the entire ventricular mass (Selye’s Stage 1). Although the heart’s function is reduced and an enforced period of recovery is needed, the surviving healthy tissues continue to carry an overload during convalescence resulting in an increase in strength and mass of the surviving muscle (Selye’s Stage 2).
Figure 9-5. In ablation experiments, a muscle is surgically removed (A, B, and C). In most hypertrophy experiments, the ablated muscle of choice is the gastrocnemius (C - both heads), leaving the underlying plantaris and soleus to carry the walking load once carried by the gastrocnemius. In this case, the surgical removal of the gastrocnemius places the rat, and specifically the rat’s leg, in Selye’s Stage 1. Rats undergoing this procedure begin walking on the operated leg within 24 hours and within one to two weeks their activity level and gait are the same as un-operated rats. The overloaded soleus and plantaris have adapted (Selye’s Stage 2). It is normal to see about a 75% increase in soleus and plantaris mass with this type of overload.
In both of the previous scenarios recovery of function occurred after only a short period of reduced loading, essentially the duration of time needed for the resolution of inflammation and any other blatant pathology. A rapid return to full functional load is required to induce adaptation and recovery. Even in the infarcted heart, a return to normal load represents a functional overload of the remaining tissue – the same amount of force must initially be generated by a smaller muscle mass, so it is a higher relative load. The adaptation that facilitates the return to normal function is due to the stress to the system produced by the decrease in function of the injured area. The injury that necessitates the compensation is the source of the stress to the surrounding tissues, and they respond by adapting to the new demands placed on them. Without the injury the adaptation would not occur, and in the absence of stress no adaptation ever occurs. While caution is advised in order to avoid further injury, the belief that rehabilitation can occur in the absence of overload represents a failure to comprehend the basic tenets of the physiology and mechanics of the living human body.
Most injuries experienced in the weight room, on the field, or in life do not rise to the severity of necrosis of any tissue. They are inconvenient, painful, aggravating, and potentially expensive to deal with, but they do not alter the quality of life for a significant period of time. But the same principles apply to healing them that apply to more severe injuries, because the mechanisms that cause them to heal are the same. The concept of letting an injury heal beyond an initial few days reflects a lack of understanding of the actual processes that cause the return to function. A less severe injury that does not involve tissue necrosis nonetheless involves an overload of the immediate ability of the compromised tissue, thus stimulating the processes that cause repair. In this particular instance, care must be taken to ensure that the structure that is healing receives its normal proportion of the load, because the object is to return this particular structure to full function, not to allow the adjacent structures to assume the load and thus preventing the injury from healing fully. This is accomplished by the enforcement of very strict technique during exercise of the injured area. It hurts worse this way, but the long term return to full function depends on the correct amount of stress to the injured area.
During supervised rehabilitation, the workloads used should be light enough to allow recovery of function locally, within the injured tissue, but that this load is not stressful enough systemically to maintain advanced fitness levels. When the athlete is released to unrestricted activity, enough detraining has occurred systemically that it will require a change in programming. Six to eight weeks in rehabilitation can result in the loss of enough overall performance to warrant the use of simple progression, even for an elite athlete. Once pre-injury or pre-disease performance levels have been regained, a return normal training at that level can follow. As discussed earlier, strength is a resilient quality, and the recovery of strength lost through detraining is possible much faster than it was initially gained.
