Rehabilitation by Mark Rippetoe
BY MARK RIPPETOE | JULY 05, 2017
Shoulder rehab after rotator cuff repair.
All athletes who 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 involves pushing past previous barriers to new levels of performance. To the extent 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. Also, accidents happen, both related and unrelated to training.
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. The dead tissue 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, provided that you fail to die.
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 for weeks and months until the force of contraction is counterbalanced by the tensile strength of the collagen scar, completing the remodeling process. The end result is the recovery of the heart’s ability to generate contractile force even having lost some of its original muscle irrecoverably. The change in contractile geometry of the ventricle will not actually allow the return to 100% of normal function. 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. And in fact, the resumption of normal activities is what drives the ability to resume normal activities.
Severe muscle damage in other parts of the body constitutes a similar but less dire situation. 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, but the surrounding muscles that normally aid the damaged muscle in its biomechanical role will assume 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 (usually in frogs, not people) and the underlying soleus and plantaris muscles rapidly adapt and assume the load once carried by the gastrocnemius. It is well documented that these newly stressed muscles change dramatically, both chemically and structurally, after ablation in order to return the whole 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.
In both 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 an increasing 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 under a higher relative load. The adaptation that facilitates the return to normal function is a response to the stress to the system produced by the injured area’s decrease in function. 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, just as no adaptation ever occurs in the absence of stress.
While caution is necessary 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. Again, we have evolved over time to be able to remodel damaged tissue while it is being utilized – heart, liver, kidney, bone, and muscle are necessary for sustained existence, and had we not been able to heal it without bed rest, hospitals, and doctors, we would have been eaten by the hyenas a long time ago.
Most injuries experienced in the weight room, on the field, and in daily life do not rise to the severity of necrosis. 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 injured tissue from healing fully. This is accomplished by the enforcement of very strict technique during exercise of the injured area. It hurts more 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 this load will not be stressful enough systemically to maintain advanced fitness levels. When the athlete is released to unrestricted activity, enough detraining has occurred that a change in programming will be required. Six to eight weeks in rehabilitation can result in the loss of enough overall performance to warrant return to a program of simple progression, even for an advanced athlete. Once pre-injury or pre-disease performance levels have been regained, a return to normal training at that level can follow. As discussed earlier, strength is a resilient quality, and strength lost through detraining can be recovered much more rapidly than it was initially gained.
Remember our definition of the stress/recovery/adaptation process: Stress is an event that produces a significant change in the environment of an organism, sufficient to disrupt the physiological state that exists within an organism in equilibrium with its current environmental conditions. Adaptation to the stress event is the organism’s modification of its physiology to compensate for the new environmental conditions as it recovers from the stress.
This definition provides an insight into effective rehab: it must be sufficiently stressful to cause an adaptation if it is to yield a return to a state that is better than before, the process of which facilitates a return to the previously high level of performance. The state of the injured athlete is lower than before he was injured, so the current/injured level of performance must be challenged if improvement upon it is to occur. This is the same training process that yielded the heightened performance before the injury, and it must be undertaken again, as unpleasant a prospect as that may be for the injured athlete.
The biggest mistake made by therapists is the incorrect application of this concept. Many of them seem to regard the injury itself as the stressor, and fail to realize that 1) the stress of injury has already been adapted to, that 2) the subsequent lack of training (detraining) stimulus is a stress that has likewise been adapted to, and 3) that the rehab they provide must be sufficiently intense to produce the stress/recovery/adaptation response that took the athlete to his previous level of performance.
“Rehab” – in the sense an athlete uses the term – cannot do its job unless it provides sufficient stress to cause the adaptation to that stress, just like it did the first time, and mistaking the stress of the injury that occurred days, weeks, or months in the past for something that must be allowed to rest more or heal a little bit longer is a failure to understand the fundamental processes that govern performance.
Excerpted from Practical Programming for Strength Training, 3rd ed.