by Ryan A. Hall, originally presented at the 2003 SuperSlow Medical Resource Symposium
Scientifically, stress is defined as the nonspecific responses of an organism to any demand made upon it (Selye, 1974). Viewed in this light, exercise is nothing more than a physical stressor imposed upon the body to produce an adaptive response. The extent of the adaptation is dependent upon balancing the severity of the stressor (intensity, frequency, and duration) with an adequate recovery interval. Exercise does not produce the adaptation directly. Rather, it serves as a stimulus for the body to produce the adaptive response.
McGuff (1997) has outlined this process in the following schematic:
Stimulus > Organism > X-days > Response
In this model, the stimulus (exercise) is imposed upon the organism (human body), followed by a recovery period (x-days) in order to produce a response (increase in muscular strength and hypertrophy). Moreover, further questions arise from this model. What are the mechanisms of the stimulus? What effect does the stimulus have on the organism? What occurs during the recovery period (x-days)? How much recovery time is required? What happens if the recovery interval is interrupted? Does the recovery interval change with alterations in the stimulus or organism? What is the desired response?
Most of these questions can be answered by looking at existing physiology and medical research literature. A multitude of data is available concerning exercise stress and recovery. This presentation will review research on many aspects of the stimulus and recovery process of skeletal muscle in order to develop a biochemical adaptation model. When viewed together, this data supports the attached biochemical model (Fig 1) of the stimulus and growth process of skeletal muscle.
Following the model, it can be seen that the initial stimulus is a mechanical stressor to the muscle tissue caused by high-tension, low-velocity contractions, occurring during the eccentric (negative or lowering) phase of an exercise (Armstrong RB, Warren GL, Warren JA, 1991). The high-tension eccentric contractions cause disruption or micro-trauma of the myofilaments (contractile proteins), and cytoskeleton of the muscle fibers, usually in the largest fast glycolytic fibers (Friden J, Sjostrom M, Ekblom B, 1983). This initial mechanical damage is followed by an inflammatory response resulting in further protein turnover. Serum levels of creatine kinase are used as a measure of protein damage / turnover. Depending upon the severity of myofiber disruption, serum creatine kinase can increase to very high levels over the next five days, and not return to baseline for 10 or more days (Pedersen BK, Ostrowski K, Rohde T, Bruunsgaard H, 1998). This process must be left uninterrupted or protein synthesis and regeneration of the damaged fibers will not be complete. If an adequate recovery interval is allowed, the body will enter an anabolic state and the disrupted fibers will enhance their composition of contractile protein by increasing the number of myofibrils within the muscle fibers. The previously disrupted fibers will hypertrophy, increasing the resistance to further damage at similar intensities (Armstrong et al., 1991).
However, if another stimulus (workout) is introduced before recovery is complete, a cascade of negative biochemical reactions occurs in the body. Protein turnover will be incomplete, thus causing further disruption to previously damaged tissue. This imbalance between stimulus and recovery leads to an overstressed condition and an increase in the production of cortisol, a major catabolic hormone. An overabundance of cortisol upsets the balance between catabolism (breakdown of tissue) and anabolism (build-up of tissue), favoring the catabolic process (Urhausen A, Gabriel H, Kindermann W, 1995). If this occurs, the organism is now in a chronic state of degeneration called overtraining. Overtrained individuals experience a wide range of conditions, including: muscle soreness / stiffness, tendonitis, suppressed immune system, increased frequency of upper respiratory tract infections, depression, lethargy, weakness, reductions in testosterone, greatly reduced sperm count in men, depressed muscle glycogen reserves, insomnia, decreased exercise performance, and symptoms of Cushing’s disease (Budgett R, 1990; Fry RW, Morton AR, Keast D, 1991). Research indicates that chronically overtrained individuals may require up to three to six months to fully recover after cessation of training (Kuipers H, Keizer HA, 1988). At this point, further results from exercise are not possible.
Results from exercise are dependent upon the proper manipulation of stimulus and recovery. Research indicates that high intensity exercise may require an extended recovery interval. Further evidence shows that as the intensity of exercise increases, greater micro-trauma accumulates, requiring a greater recovery interval (Ploutz-Snyder LL, Tesch PA, Dudley GA, 1998). Details of the biochemical model and application to exercise prescription will be covered in the presentation and in report format at a later date.
Copyright 2003, Ryan A. Hall.
Armstrong RB, Warren GL, Warren JA. Mechanisms of exercise-induced muscle fibre injury. Sports Med 1991 Sep;12(3):184-207.
Budgett R. Overtraining syndrome. Br J Sports Med 1990 Dec;24(4):231-236.
Friden J, Sjostrom M, Ekblom B. Myofibrillar damage following intense eccentric exercise in man. Int J Sports Med 1983 Aug;4(3):170-6.
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McGuff, D. The dose-response relationship of exercise. Ultimate Exercise: Bulletin Number 1, 1998.
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Ploutz-Snyder LL, Tesch PA, Dudley GA. Increased vulnerability to eccentric exercise-induced dysfunction and muscle injury after concentric training. Arch Phys Med Rehabil 1998 Jan;79(1):58-61.
Selye, Hans. Stress Without Distress. Signet, New York, 1974.