Understanding Recovery: A Wound Healing Model

Understanding Recovery: A Wound Healing Model
By Dr. David H. Staplin
When subjected to high-intensity anaerobic exercise-induced trauma, skeletal muscle sustains damage at the cellular level. The literature suggests that this damage elicits an inflammatory response, and recovery time course which are related to the degree of trauma. Understanding the process of skeletal muscle recovery and repair may be enhanced utilizing models derived from the study of the acute inflammatory response and would healing. These models outline numerous sequential steps thought to be necessary for resolution of exercise-induced trauma.

Keywords: delayed on-set muscle soreness, inflammation, adaptation, skeletal muscle, eccentric force.

To understand and study the process of exercise-induced recovery and repair, it is useful to develop a model. Modeling the biochemical reactions to stress, and the observed effects such as soreness, allow for a better understanding of the events and time course necessary for muscle recovery. Such a model comes from the study of the wound healing process, particularly the inflammatory response (7, 9). Whenever muscle cells are subjected to high-intensity anaerobic training stress, damage occurs at the cellular level (1-4, 7-9). The degree of damage depends upon the degree of intensity - the higher the intensity, the greater the damage (2, 4, 5, 7, 9, 10). It is the process of healing this damage which then allows the muscle cell to adapt by becoming larger and stronger (2, 9).

Recovery from training stress requires a number of steps; each of which must proceed to completion uninterrupted for complete recovery and adaptive response (7, 9). While the exact mechanisms are unclear at the present time, and subject to further research and clarification, it is thought that acute inflammation is the initial response to muscle cell damage (7, 9, 10). This is especially the case where high intensity eccentric work is performed. Delayed-onset muscle soreness is thought to be one of the effects of this acute inflammatory response as well (1-8, 10). This sequence of events is thought to occur in the following manner and time:

1.Connective and/or contractile tissue (muscle tissue) damage occurs during intense muscular work, particularly eccentric action (1-10).
2.Within the first 24 hours, levels of neutrophils increase and migrate to the site of injury or exercise trauma (1, 6, 9).
3.At the same time, lysosomal enzymes are released which begin to digest and break down damaged tissue (3, 6, 8, 9, 10).
4.Macrophages aid lysosomes, and synthesize a variety of chemicals in response to inflammation, beginning to accumulate around 24 hours, and continuing to do so for up to several days. One of the chemicals these cells secrete, PGE2, is believed to make moves more sensitive to pain, and may help explain soreness sensations starting 24 hours or so after exercise - lasting for as long as 7 or more days (1-7, 9, 10).
5.This inflammatory response causes further damage to the affected area, and may continue for several days beyond imposition of the initial training stress damage (1, 6, 7, 9).
6.Once these initial inflammatory responses (steps 1-5) are completed, then signs of the beginnings of tissue regeneration (rebuilding of the muscle) can be observed (4, 7, 9).

It is thought that the severity of response, and so the time necessary to complete it, vary directly with the degree of trauma or the intensity of the work the muscle has been subjected to (2, 4, 5, 10). Numerous studies have examined this response process, especially with eccentric work (1-10). The time course for completion of the above 6 steps ranges from 5 days to over 6 weeks (1-10).

While not applied extensively in previous investigations, researchers are now beginning to link cellular trauma and adaptive response to exercise-induced trauma, with data derived from investigations of inflammation, delayed-onset muscle soreness and wound healing (1, 5, 7, 9). Models of the acute inflammatory response and wound healing may provide insights into the sequence and time course of events taking place in skeletal muscle cells during the recovery from high-intensity, anaerobic exercise-induced stress (7, 9). Use of such models show the time course of recovery and adaptation of skeletal muscle to be much longer than has been previously thought (1-10). This perspective provides new insights useful for the structuring of training protocols, in particular those protocols having a large eccentric component (2, 4, 5, 7, 9, 10).

With an understanding of the model described above, it is possible to more precisely match a particular workout with the appropriate recovery period. Central to this process is an understanding of the fundamental principle of INTENSITY of EFFORT.

Intensity of effort can be graphed on a line with sleep at one end, representing virtually zero muscular effort, and negative only (eccentric) reps with extremely heavy weight at the other end, representing the extreme in muscular effort. All points between these extremes represent intermediate degrees of effort which vary with their relationship to the 2 extremes. As intensity increases:
1.The time the body is able to withstand the effort DECREASES.
2.The amount of STRESS the body is subjected to INCREASES.
3.As the stress increases the disruption to FUNCTION (damage) INCREASES.
4.As the damage increases the RECOVERY and ADAPTATION time increases.

This is, in essence, what Arthur Jones has been saying for years.

I have been experimenting with various combinations of intensity and recovery with 4 experienced trainees, ranging in age from 26 to 42. All of these individuals have trained seriously for over 8 years (the 42 yr. old for over 20 years), and have tried virtually every training program ever used. Through a slow, evolutionary process taking place throughout the past 9 months or so, this group is now alternating between the following 2 protocols:
Protocol 1 - Negative only reps with weights of 150% of 6 rep max., 10 seconds negative rep speed: including 1) negative squats on Smith machine, negative underhand chins, and 2) negative Hammer Strength deadlifts, negative Hammer Strength chest press or negative dips.

Protocol 2 - Standard repetitions, 2 seconds raising, and 4 seconds lowering (2 second pause with all single joint exercises) to a point where the weight ceases motion, including: 1) barbell squat, flat bench press, Hammer Strength pullover super-setted with underhand chins, and 2) Hammer Strength or barbell deadlift with a shrug at the top of the movement, pec deck super-setted with Hammer Strength incline press, dumbbell biceps curl.

(Note: TOTAL time for a super set equals time for a regular set. For example, if chins are carried out for 60 seconds of time under load prior to momentary muscular failure, the pullovers super-setted with chins are allotted only the same 60 seconds. Otherwise, we are extending the EFFORT, not increasing the intensity.) Weights are selected such that the time under load is approximately 60 seconds by the time momentary muscular failure is reached. None of these trainees use steroids, creatine, 'Testosterone boosting supplements,' or caloric intakes greater than 10% above calculated maintenance levels.

Protocol 1 is followed by Protocol 2 in an alternating fashion. Each workout of each protocol is followed by a minimum of 21 days complete rest - no aerobics, no 'active recovery' (a contradiction in terms); nothing but daily living activities. I am beginning to think that 4 or more weeks would be better after the negative protocol. Certainly this would be necessary as strength increases.

I have taken these trainees through 1 cycle each of these protocols. They have been able to increase weights by ~10% relative to the last time these same exercises were performed. Whether, and for how long, this rate of increase is able to be sustained remains to be seen; but these results are not surprising when the recovery model discussed above is considered.

If this sounds fantastic, or impossible, remember the reaction Arthur Jones has 'enjoyed' for his concepts, and the reaction most high-intensity trainees must tolerate from the 'flat-worlders' around them. Should you decide to experiment with the above protocols, keep precise records, and contact me with your experiences and observations. I can be reached by calling (612) 377-1769, or e-mailing me at [email protected]. Finally, I would like to thank Dr. Lucille L. Smith at Appalachian State University for her comments and insights.

In Part I of this series on understanding recovery, a wound healing model was presented. This model outlines several factors important for understanding cellular recovery. First, when muscle cells are subjected to high intensity training stress, cellular damage occurs, with the degree dependent upon the degree of intensity. Second, an inflammatory response occurring as a result of trauma causes further damage to muscle cells for as much as several days after the imposition of the initial training stress. Third, full cellular recovery requires each of several additional steps to be completed sequentially, and without interruption. This, however, is not the full story regarding overall recovery.

It must be remembered that the wound healing model is limited to a discussion of events taking place at the cellular level only. High intensity training stresses not just the skeletal muscle cells, but numerous other body structures and systems as well. Connective tissue, bones, ligaments, and tendons are subject to mechanically induced stress as a result of the load imposed, while the endocrine system produces various hormonal responses affecting numerous glands and organs in an attempt to return the body to a state of homeostasis. The nervous system must recover from exercise induced fatigue, while immediate, short, and long-term energy stores must be replenished. The processes taking place to insure this multi-level recovery takes time, and a coordinated effort of virtually all systems of the body. The rate and efficiency with which this recovery takes place in any given individual is dependent upon a number of factors which, within limits, will vary from person to person. These factors, and their influence, represent something of an unknown at this point.

Several lines of inquiry, with as yet unanswered questions pertaining to high intensity, anaerobic training stress present themselves as possibilities for future research:

1) What is the impact of various muscle fiber types, and their distribution regarding recovery time?
2) What do fiber types tell us about the correct application of training stress as it relates to time under load? (Arthur Jones' Inroad Testing Procedure is an approach to answering this question.)
3) What is the relationship between the damage caused by overtraining and free radical type cellular damage?
4) Is there a relationship between the damage caused by overtraining and free radical type cellular damage?

These questions, and numerous others, are those science hopes to answer in the future. While it is not necessary to be able to answer all of these questions to develop and apply an effective approach to training, these answers should allow for even greater precision in any individual application of training principles.

At this time, no precise equation or formula is available to help design training programs for each and every individual as it is in many other sciences. For example, when building a traffic bridge, estimates of the load per unit time the bridge will carry, distance to be spanned, materials available, funds, life span of the bridge, weight of the bridge itself, and many other variables can be measured precisely, and used in final equations to design the bridge. Because of the many unknowns mentioned above, each trainee must take the fundamental principles of training briefly, training infrequently, and training intensely, and define, on an individual basis, what these terms mean. As this series continues, we will be discussing our experiences, and those of trainees with which we consult, in an effort to provide more precise answers to designing training programs and enhancing recovery.