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UNDERSTANDING RECOVERY: A WOUND HEALING MODEL
by Dave Staplin
To understand and study the process of muscle 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 reponse (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 makes the muscle cell 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 such as Negative Training, Hyper Training or when accentuating the Lowering of the weight during standard repetitions. 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 occurs in the following manner and time:
Connective and/or contractile tissue (muscle cell) damage occurs during intense muscular contraction, particularly eccentric action (1-10).
Within the first 24 hours, levels of neutrophils (white blood cells which respond to injury) increase and migrate to the site of injury or exercise trauma (1,6,9).
At the same time, lysosomal enzymes which digest and break down damaged tissue are released and this breakdown activity commences (3,6,8,9,10).
Macrophages (cells which aid lysosomes and synthesize a variety of chemicals in response to inflammation) begin to accumulate around 24 hours and continue to do so for up to several days. One of the chemicals these cells secrete, PGE2, is believed to make nerves , more sensitive to pain and may help explain soreness sensations starting 24 hours or so after exercise, and lasting for as long as 7 or more days (1-7,9,10).
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).
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).
The muscle cell must first rebuild to normal levels of structure and function and then, only then, and only IF allowed FURTHER TIME, will it supercompensate and build up to levels GREATER than before. The next question is: How long does this ENTIRE process take?
It must be remembered that the severity of response and so the time necessary to complete it vary according to the degree of trauma or in this case, 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 contractions (1-10). The time course for completion of the above 6 steps ranges from 5 days to over 6 weeks (1-10)! This has profound implications regarding FREQUENCY of training! The more intense your training, the longer you must allow for recovery. If you add 50% to the weight you normally use for high intensity repetitions and then proceed to perform NEGATIVE repetitions, you have just dramatically increased the stress and therefore the TIME necessary for the muscle to recover. One concrete training example may help further clarify these ideas.
From mid-July to mid-October 1997, my training partner and I increased our Squat and Deadlift poundages 49% and 70%, respectively. We used standard repetition protocol--2 seconds concentric (raising) and 4 second eccentric (lowering). We terminated sets when no more full-range, unassisted reps were possible. In other words, we performed no Forced Reps, Negatives or any other technique which would have increased the intensity of the sets. Further, we had been performing only 2 sets per workout every 7 days on Mike's Consolidation Routine.
By early November, we had experienced 2 consecutive workouts with no further progress in any of our sets. We then took 23 days off. We returned to the gym and we were now able to add 10% to the Squat poundages for the same number of reps as our previous squat workout AND we had not performed squats for 30 days!
At first, this may seem beyond belief--an absolute impossibility! Not, however, if you understand recovery from the standpoint of the inflammatory response and recovery model outlined in steps 1-6 above. It is important to never forget that high intensity anaerobic weight training stress is a study properly subsumed under the heading of MEDICAL SCIENCE. As such, medical science can teach us much, but as pioneers in the field of high intensity, anaerobic exercise, so too can we teach medical science much!
1) Clarkson, PM, Nosaka, K. Muscle function after exercise-induced muscle damage and rapid adaptation. Medicine and Science in Sports and Exercise. Vol.24, No.5, 512-20, 1992
2) Clarkson, PM, Tremblay, I. Exercise-induced muscle damage, repair and adaptation in humans. Journal of Applied Physiology. Vol.65, No.1, 1-6, 1988
3) Friden, J.,et al Myofibrillar damage following intense eccentric exercise in man. International Journal of Sports Medicine. Vol.24, No.3, 170-176,1983
4) Golden, CL, Dudley, GA., Strength after bouts of eccentric or concentric actions. Medicine and Science in Sports and Exercise. Vol.24, No.8, 926-33, 1992
5) Howell, JN, Chleboun,G., Muscle stiffness, strength loss, swelling and soreness following exercise-induced injury to humans. Journal of Physiology 464, 183-96, 1993
6) Jones, DA, Newham, JM., et al, Experimental human muscle damage: morphological changes in relation to other indices of damage. Journal of Physiology 375, 435-48, 1986
7) Mishra, DK, Friden, J., et al Anti-inflammatory medication after muscle injury. Journal of Bone and Joint Surgery, Vol. 77-A, No.10, 1510-19, 1995 8) Newman, DJ, Jones, DA., Repeated high-force eccentric exercise: effects on muscle pain and damage. Journal of Applied Physiology Vol.4, No.63, 1381-86, 1987
9) Smith, LL. Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Medicine and Science in Sports and Exercise Vol. 23, No.5, 542-51, 1991
10) Tiidus, PM, Ianuzzo, DC., Effects of intensity and duration of muscular exercise on delayed soreness and serum enzyme activities. Medicine and Science in Sports and Exercise Vol. 15, No.6, 461-5, 1983
by Dave Staplin
To understand and study the process of muscle 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 reponse (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 makes the muscle cell 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 such as Negative Training, Hyper Training or when accentuating the Lowering of the weight during standard repetitions. 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 occurs in the following manner and time:
Connective and/or contractile tissue (muscle cell) damage occurs during intense muscular contraction, particularly eccentric action (1-10).
Within the first 24 hours, levels of neutrophils (white blood cells which respond to injury) increase and migrate to the site of injury or exercise trauma (1,6,9).
At the same time, lysosomal enzymes which digest and break down damaged tissue are released and this breakdown activity commences (3,6,8,9,10).
Macrophages (cells which aid lysosomes and synthesize a variety of chemicals in response to inflammation) begin to accumulate around 24 hours and continue to do so for up to several days. One of the chemicals these cells secrete, PGE2, is believed to make nerves , more sensitive to pain and may help explain soreness sensations starting 24 hours or so after exercise, and lasting for as long as 7 or more days (1-7,9,10).
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).
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).
The muscle cell must first rebuild to normal levels of structure and function and then, only then, and only IF allowed FURTHER TIME, will it supercompensate and build up to levels GREATER than before. The next question is: How long does this ENTIRE process take?
It must be remembered that the severity of response and so the time necessary to complete it vary according to the degree of trauma or in this case, 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 contractions (1-10). The time course for completion of the above 6 steps ranges from 5 days to over 6 weeks (1-10)! This has profound implications regarding FREQUENCY of training! The more intense your training, the longer you must allow for recovery. If you add 50% to the weight you normally use for high intensity repetitions and then proceed to perform NEGATIVE repetitions, you have just dramatically increased the stress and therefore the TIME necessary for the muscle to recover. One concrete training example may help further clarify these ideas.
From mid-July to mid-October 1997, my training partner and I increased our Squat and Deadlift poundages 49% and 70%, respectively. We used standard repetition protocol--2 seconds concentric (raising) and 4 second eccentric (lowering). We terminated sets when no more full-range, unassisted reps were possible. In other words, we performed no Forced Reps, Negatives or any other technique which would have increased the intensity of the sets. Further, we had been performing only 2 sets per workout every 7 days on Mike's Consolidation Routine.
By early November, we had experienced 2 consecutive workouts with no further progress in any of our sets. We then took 23 days off. We returned to the gym and we were now able to add 10% to the Squat poundages for the same number of reps as our previous squat workout AND we had not performed squats for 30 days!
At first, this may seem beyond belief--an absolute impossibility! Not, however, if you understand recovery from the standpoint of the inflammatory response and recovery model outlined in steps 1-6 above. It is important to never forget that high intensity anaerobic weight training stress is a study properly subsumed under the heading of MEDICAL SCIENCE. As such, medical science can teach us much, but as pioneers in the field of high intensity, anaerobic exercise, so too can we teach medical science much!
1) Clarkson, PM, Nosaka, K. Muscle function after exercise-induced muscle damage and rapid adaptation. Medicine and Science in Sports and Exercise. Vol.24, No.5, 512-20, 1992
2) Clarkson, PM, Tremblay, I. Exercise-induced muscle damage, repair and adaptation in humans. Journal of Applied Physiology. Vol.65, No.1, 1-6, 1988
3) Friden, J.,et al Myofibrillar damage following intense eccentric exercise in man. International Journal of Sports Medicine. Vol.24, No.3, 170-176,1983
4) Golden, CL, Dudley, GA., Strength after bouts of eccentric or concentric actions. Medicine and Science in Sports and Exercise. Vol.24, No.8, 926-33, 1992
5) Howell, JN, Chleboun,G., Muscle stiffness, strength loss, swelling and soreness following exercise-induced injury to humans. Journal of Physiology 464, 183-96, 1993
6) Jones, DA, Newham, JM., et al, Experimental human muscle damage: morphological changes in relation to other indices of damage. Journal of Physiology 375, 435-48, 1986
7) Mishra, DK, Friden, J., et al Anti-inflammatory medication after muscle injury. Journal of Bone and Joint Surgery, Vol. 77-A, No.10, 1510-19, 1995 8) Newman, DJ, Jones, DA., Repeated high-force eccentric exercise: effects on muscle pain and damage. Journal of Applied Physiology Vol.4, No.63, 1381-86, 1987
9) Smith, LL. Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Medicine and Science in Sports and Exercise Vol. 23, No.5, 542-51, 1991
10) Tiidus, PM, Ianuzzo, DC., Effects of intensity and duration of muscular exercise on delayed soreness and serum enzyme activities. Medicine and Science in Sports and Exercise Vol. 15, No.6, 461-5, 1983
