Psychophysiological benefits of exercise in the treatment of fibromyalgia and myofascial pain disorder.
SUMMARY: JHP is a 36-year-old married woman, a recreational therapist and lifelong regular aerobic exerciser (running, tennis, swimming, weight training) with a history of fibromyalgia symptoms dating from eight years ago, apparently triggered by a minor injury: While rollerblading she hit a parked car and "sprained my right knee." There followed a series of visits to doctors in different specialties, varied vague diagnoses and conservative treatments that failed to stem symptoms--migrating to the neck, to the other knee and to both upper extremities--all with an accompanying and deepening mood depression.
Undiagnosed, unable to run, she became depressed and anergic. A rheumatologist finally made the diagnosis of fibromyalgia, at the same time strongly recommending that her depression was the first thing to treat. A psychiatrist prescribed Prozac. Over a six-month span, there was a gradual elevation of mood. She was able to swim more, could participate in weight training and could play some tennis. Electing to discontinue Prozac there was some return of depression but all the while she was increasing the level of exercise and within a few months did maintain the mood stabilization the Prozac had earlier brought about.
Aerobic weight training, in contrast to anaerobic weight lifting, was helpful. Personality self-description: "I am kind of compulsive so I think that I do too much and sometimes it would do the opposite." She further described herself as "a perfectionist in certain ways," and "obsessive/compulsive with exercise, an hour or two was not enough. I would exercise like a fanatic ..."
Specific traits illustrated by this patient are found in the population of those diagnosed with myofascial pain and fibromyalgia, contributing here to an overall understanding of the psychophysiologic benefits of exercise vis-a-vis myofascial pain and fibromyalgia. Among those issues is pain.
Among the things that worked for pain was any low impact exercise, e.g., swimming and lifting lighter weights. In the latter instance some modicum of strength, and, more importantly, a sense of mastery and control, evolved. Before her illness the patient could over-exert with impunity; now she had to be careful, had to emphasize the aerobic rather than the anaerobic: "I could not have gotten better without the exercise, I know that. Because of my personality, too. Sometimes I would be feeling worse and I would exercise, then feel better. It was a combination of things."
Studies support this combination of aerobic exercise and the teaching of coping skills. Accordingly, therapeutic programs in patients with myofascial pain and fibromyalgia have focused on teaching coping skills and physical exercise (6, 18, 3). Review articles document benefits in each group with the greater rewards found in patients participating in combined programs (6).
Focusing on coping skills and exercise in therapeutic programs has a psychophysiologic rationale considering the general observation of personality type, a personality configuration that may be determined, in part, by some of the theoretical underlying etiologic pathophysiology. Part of this underlying etiology is thought to involve an overactive sympathetic nervous system (3, 10, 32). The patient may then adapt to the pulling and tugging of autonomic impulses, adapt to those diffuse restive and driven feelings by organizing and sublimating these pressures into traits of compulsivity and perfectionism. The potential clinical manifestations of this over-activity might be a vague restlessness, tension or exaggerated drive, all of which the person seeks to organize and modulate, even sublimate, by compulsive personality traits. This is consistent with the composite picture offered by Grzesiak. In citing authoritative sources, among the character traits he describes are the hard working, conscientious, compulsive, responsible and self-motivated trends in chronic pain sufferers (16).
Furthermore, this over-reactivity may be mimicked by the over-response to the trauma of joint injury. For example, in our patient whose illness was apparently triggered by a rollerblade injury to one knee, her immune system then responded with a mistaken generalized and exaggerated attack on its own tissue. There is a body of literature, summarized in literature reviews (33), trying to find a link between trauma and the eruption of fibromyalgia.
The cycle of pain that led to inactivity from which flowed anergy and mood depression is a paradigm that has to be understood to give treatment regimens a sound therapeutic rationale. We still don't know whether depression is a cause or effect in fibromyalgia and myofascial pain syndromes (16).
To ameliorate any pain/inactivity/depression vicious cycle, exercise treatment programs, as found in this partial sampling of original and review articles, have yielded significantly positive benefits in exercise for patients with depressive syndromes (2, 4, 5, 7, 14, 15, 21, 23, 24, 26). Benefits accrue too in population studies of exercise for prevention of depressive disorders (8, 22, 28, 29), and in studies with exercise in treating fibromyalgia patients (6, 18, 25).
Antidepressant medication has also become a staple of treatment for pain syndromes. The apparent target of both exercise and antidepressant pharmacotherapy treatment modalities is neurohormone activity, mainly that of central nervous system serotonin. Serotonin may very well be implicated in pain transmission. Serotonin activity is influenced by aerobic exercise, as seen in laboratory studies where brain tissue of the exercising animals was found to have higher levels of serotonin metabolites (9). It is also influenced by antidepressant drugs, particularly the newer generation of SSRIs.
One of the earliest antidepressants, amitriptyline, has its principal effect on serotonin. Furthermore, its side effect of drowsiness makes it an ideal drug for the sleep disturbance common to pain syndromes. And we cannot forget the universal observation that pain is perceived more intensely when a person is depressed, setting up a vicious cycle with pain and depression potentiating each other.
Accordingly, one elegant study cited improvement in the pain of fibromyalgia both with patients taking amitriptyline alone, with patients only exercising, and with patients receiving a combination of amitriptyline and aerobic exercise. Only in the exercise/amitriptyline combination group, however, was significant improvement maintained beyond three months (18).
Another example of organic illness and depression illustrates and epitomizes the therapeutic potential of vigorous exercise vis-a-vis psychophysiologic well-being. Here the example tells of exercise programs with patients suffering from traumatic brain injury (TBI) (13).
This example will hopefully be particularly illustrative because not only does sustained aerobic exercise, as seen in long-term fitness programs, have a salutary effect on mood, but it has also been shown to improve cognitive functioning (12). In this particular study (13), a combined benefit to both mood and cognitive functioning was shown in patients with TBI, in contrast to non-exercising patients with TBI (13). Especially significant is the further finding that the TBI patients who exercised were the very patients with the more severe brain injuries. They showed after their exercise regimen fewer cognitive symptoms than their non-exercising TBI counterparts. Degree of physical impediment had little relationship to a patient's ability to both participate and benefit from an exercise program (13).
Improvement in cognitive functioning has been postulated to be the effect of exercise on production of brain neurotrophic factor (27), and to the obvious increase in blood flow to the brain. Gordon (13) cites the literature demonstrating mood improvement with exercising patients with multiple sclerosis and spinal cord injuries. In those instances the improvement has been ascribed to elevated levels of beta-endorphins.
So now beta-endorphin joins the cohort of neuro-messengers such as the earlier discussed serotonin, both theorized to be involved in mood regulation and in pain transmission. Neurohormones are the grease and oil of neuron transmission, slowing or facilitating messages throughout the central nervous system. Of the endorphins, beta-endorphin is the most studied. So it is worth understanding what the endorphins are and what their role becomes, both in exercise and in psychophysiologic functioning.
Scientists had long sensed that dwelling within brain cells were natural receptor sites for opiates such as morphine. Their discovery and isolation became a journey of serendipity.
Researchers, using a new technique to cut up animal pituitary glands in order to extract ACTH, found new types of proteins other than, yet similar in configuration to, ACTH. They found too that these new proteins had strong opiate activity. Depending on their peptide structure they were classified into groups, one of them the beta-endorphins, the most widely- and easily-studied of the group.
Among the requirements to consider any of these compounds as an opiate is the nullification of endorphin pain relief by the opioid antagonist, Naloxone. Studies done to document this property serve also to illuminate the role of endorphins in the psychophysiologic benefits of exercise.
For example, in a double-blind crossover study of 12 recreational male runners, mood changes were tested before, during and after exercise. Naloxone was administered intravenously before, during and after exercise bouts to some, whereas others were given placebo injections. With the latter, significant tendencies to calmness on the Profile of Mood States and Visual Analogue Scale were recorded following prescribed exercise (usually running 45 minutes). Fatigue was specifically and positively affected in the placebo group. In those receiving Naloxone, the tendency to calmness and fatigue relief was blocked (1).
A similar study and similar result was obtained in a study using another opioid antagonist, Naltrexone (11). Here, in the placebo group, mood states became calmer, more relaxed and pleasant, tending away from depression, anger and confusion. Positive mood changes were not detected in those preloaded with Naltrexone (11).
These studies hint that activity generated mood changes are mediated, at least in part, through endorphinergic mechanisms. Note, however, what is not claimed, and that is the production of an "endorphin high." The exerciser becomes more relaxed, calmer, but not "high."
Not high but challenged, if not stressed. The knowledge of how much exercise it takes to stimulate the production of endorphins, their chemical structure and the location of their secretory centers will provide a teleologic clue as to why increased endorphin output (along with monoamines, e.g., serotonin, norepinephrine) contributes to psychophysiologic benefits for the exerciser.
To further understand the role of the endorphin messenger neurohormone in relation to exercise, look at quality and quantity of exercise, particularly as found in animal studies. For example, stimulation of rats' sciatic nerves for 30-minute intervals caused an increased pain threshold persisting long after the 30 minutes. That increase could be blocked by Naloxone (31). Furthermore, review articles tell of rats trained to run spontaneously that showed an increase both in beta-endorphin and in monoamine concentration in their cerebrospinal fluid (1, 9). (Intense bouts of resistance training can also elicit an enhanced endorphin response (19).)
It is the stressful intensity of the exercise bouts that stimulates an endorphin response, a response that modulates not only pain but also the excesses of the overall stress response itself. Consider again the chemical composition of beta-endorphin, i.e., similar to ACTH, produced in the pituitary gland in concert with the endorphins, and secreted into the bloodstream in equimolar amounts in response to challenges of stress adaptation (17, 20).
Consider too the role of ACTH (by way of adrenocortical stimulation) in conserving, e.g., sodium retention to prevent any loss of fluids in the stress response. The sites of production of endorphins also give a further clue to their role. Their main sites are the pituitary secreting into the periphery and the hypothalamic secretion that in turn hooks up with projections to forebrain and hind-brain receptors (modulation of pain and a modifying influence, particularly upon nerve fiber connections within the autonomic nervous system).
This neurohormone messenger endorphin influence is more of a balancing act. Their role is not unlike that of ACTH stimulation serving to calm the stress response. Clinical examples of this balancing role of the endorphins, in concert with ACTH with which it shares that similar molecular configuration, were discussed above in the studies with Naloxone and Naltrexone where the subjective response was more one of calm and relaxation rather than a "high" (1, 11).
EXAMPLE: 1984 Women's Olympic Marathon: Joan Benoit, comfortably in first place, nears the L.A. Coliseum with less than a half-mile to go. "... the goal is in sight, the pain is secondary," remarks commentator Marty Liquori. "Those knees are like glass, she's picking them up and putting them down, but it hurts a lot less when you're winning the gold medal," adds Kathy Switzer. Benoit finishes, then continues to run a victory lap. Liquori characterizes the changed running style: "Once crossing the finish line she broke into a different stride ... a more natural stride for a person that is running because of the joy and the happiness ..."
To say Joan Benoit was excited would be to understate the myriad ecstatic emotions surging through this first-time marathon winner. Those feelings, I contend, or any over-reaction that has to be balanced, trigger the increased production of endorphins. The endorphins released serve to calm the reaction so that it does not lead to total depletion: not only excitement but any intense feeling--happy or unhappy--that unchecked could result in exhaustion and total depletion of reserves. In fact, that increased production of neurohormones like serotonin and norepinephrine, leading to feelings of elation and excitement, may be the signal for the balancing function of the endorphins.
In capsule form, too, we see the journey of patients with myofascial pain, injured, debilitated, the darkness of their despair partially lifted by the sight of the end of the painful journey, here translated to the clarification of the diagnosis. So many things in life are that way, even the stock market that is elevated by the pronounced declaration of bad news. Then with mastery in full view, excitement and jubilation become tempered by the outpouring of calming and pain-numbing endorphin flow.
Such is not to trivialize this whole equation to mere biochemical terms. Rather, it is the neuro-messengers that become conduits of the human spirit. It is determination and attitude that call forth the biochemical responses. Perhaps the strivings and (theorized) unbalanced autonomic drive that typify many patients with this illness become powerful assets in overcoming pain, debility and despair--assets in crossing the finish line of recovery.
Within the wisdom of teleologic adaptation and survival lies a key to understanding the functions of pain relief and mood depression. Much can be illuminated by returning to the original case study, a case study that, in turn, illustrates an essential link to the total understanding of the role of exercise as part of the psychophysiologic benefit for the pain of fibromyalgia and myofascial pain syndromes. That last link has to do with the universal human need for mastery and self-esteem. That last link is the psyche part of psychophysiologic.
Now to put all of the pieces together and to propose a unifying thesis to the overall fibromyalgia picture.
Dr. John Greist and colleagues at the University of Wisconsin were among the first to prescribe exercise for "mild" to "moderate" depressions (14, 15). He cautioned that goals should be at first modest so that patients can make incremental gains over time and feel a sense of accomplishment, of mastery, and above all of self-esteem (14, 15). That was demonstrated in JHP, who learned to eschew heavy weights in favor of lighter weights. In so doing she earned the beginnings of a sense of strength, mastery and control.
Such is a human need but particularly so in this high-energy productive woman whose personality traits mirror others similarly affected for whom vigorous exercise translates into a way of life. This attitude and approach to living may, I postulate, be partially grounded constitutionally in an overactive sympathetic nervous system around which compulsive personality traits evolve in order to organize and sublimate what otherwise would be restive feelings.
But then the patient is suddenly attacked by a mysterious illness. One of the characteristics of this illness is a diffuse generalized response in the joints and tissues, an over-response too that may be constitutionally determined. Once in the throes of what is first a mystery, an illness that ironically impairs this person's particular avenue of expression, she feels a loss of independence, mastery and control. Gone with it are any sense of security and self-esteem. An all-encompassing depression sets in.
The human mind poorly tolerates a puzzle. We all need some sense of certainty. Therefore no headway can be made in treatment until a diagnosis, even just a label, is determined.
Managing pain, once the diagnosis was made and once a ray of light could shine through the darkness of uncertainty and melancholy, the first step was to treat the depression. The rheumatologist's words were insightful and incisive: "... if you don't work on her depression, nothing will help."
Here the antidepressant drugs make serotonin more available. Serotonin, in turn, is in some undetermined way involved in modulating pain transmission. Its availability may lessen the pain of depression. Certainly pain is more troublesome when the mood is low.
Here too the antidepressant jump-started a neurohormone response that enabled this patient to resume further activity. A return to more vigorous activity augmented the neurohormone response and added one more neuromessenger group to the arsenal of adaptation, namely the endorphins.
Endorphins (i.e., endogenous morphine), through their connection to the hind-brain, are strong inhibitors of pain. Through their connection to the hypothalamus they may also have a calming effect on the underlying overactive sympathetic nervous system. Vigorous exercise stimulates endorphin production within the central nervous system and in the periphery. The result is pain relief and a feeling of calm and relaxation.
The reduction of symptoms, probably the initial benefit accrued from just making the diagnosis and then the antidepressive medication (allowing serotonin and other neurohormones to flow again) eased her return to exercise. Exercise intense in quality and in time allowed then the benefits of the endorphin response. The endorphin response was the glue that materially neutralized pain and created a feeling of calm and relaxation. And relaxation or tension relief in muscles allowed for a better blood supply to the tissues involved.
Breaking down psychophysiologic into its component parts, exercise benefits the psychic as the patient perseveres and gains a sense of mastery, a sense of control, a sense of orientation and of self-esteem. It is similar to the runner reaching near the destination, knowing the goal is in sight. It is the horse sensing the stable and feeling a surge of strength. It is the patient's beginning awareness of what lies ahead and what must be done to reach the ultimate goal.
The physiologic is an adaptive outpouring of serotonin and related monamine neuro-messengers, earned through sustained aerobic effort. The main aerobic effort for this patient was swimming. Swimming and water exercises are probably the best sports for any patient similarly afflicted. They are low impact and work the entire musculature. A feeling of elation breaks through. The very feeling that comes about through the prolonged aerobic work (whose physiologic concomitant is the outpouring of neurohormones) is then joined by the modulating and balancing function of the flowing endorphins. They bring with them a sense of calm and well-being, and--most importantly for the myofascial pain--actual, if not natural, analgesia.
1. Allen M.E., Coen D. Naloxone Blocking of Running-Induced Mood Changes. Annals of Sports Medicine 1987; 3:190-195.
2. Anthony J. Psychologic Aspects of Exercise. Clin Sports Med 1991; 10:171-180.
3. Bennet R.M. Beyond Fibromyalgia: Ideas on Etiology and Treatment. J Rhematol 1989; 16 Suppl. 19:185-91.
4. Berger B.G., Owen D.R. Mood Alteration with Swimming--Swimmers Really Do "Feel Better." Psychosomatic Medicine 1983; 45:425-432.
5. Brown R.S., Ramirez D.E., Taub J.M. The Prescription of Exercise for Depression. Physician and Sports Medicine 1978; 6:34-45.
6. Burckhardt C.S., Mannerkorpi K., Hedenberg L., Bjelle A. A Randomized, Controlled Clinical Trial of Education and Physical Training for Women with Fibromyalgia. Rheumatol 1994; 714-20.
7. Byrne A., Byrne D.G. The Effect of Exercise on Depression, Anxiety and Other Mood States. A Review Journal of Psychosomatic Research 1993; 37:565-574.
8. Camacho T.C., Roberts R.E., Lazarus N.B., Kaplan G.A., Cohen R.D. Physical Activity and Depression: Evidence from the Alameda County Study. Am J Epidemiol 1991; 134:220-231.
9. Chaouloff F. Physical Exercise and Brain Monoamines: A Review. Acta Physiol Scand 1989; 137:1-13.
10. Cohen H., Neumann L., Shore M., Amir M., Cassuto Y., Buskila D. Autonomic Dysfunction in Patients with Fibromyalgia: Application of Power Analysis of Heart Rate Variables. Semin Arthritis Rheum 2000; 29(4):217-27.
11. Daniel, M., Martin A.D., Carter J. Opiate Receptor Blockade by Naltrexone and Mood State after Acute Physical Activity. Br J Sports Med (England) 1992; 26:111-115.
12. Dustman R.E., Ruhling R.O., Russell E.M., Shearer D.E., Bonekat H.W., Shigeoka J.W., Wood J.S., Bradford D.C. Aerobic Exercise Training and Improved Neuropsychological Functions in Older Individuals. Neurobiology of Aging 1984; 5:35-42.
13. Gordon W.A., Sliwinski M., Echo J., McLoughlin M., Sheerer, M., Meili T.E. The Benefits of Exercise in Individuals with Traumatic Brain Injury: A Retrospective Study. J Head Trauma Rehabil 1998; 13(4):58-67.
14. Greist J.H., Eischens R.R., Klein M.H., Eischens R.R., Faris J., Gurman A.S., Morgan W.P. Running Through Your Mind. J Psychosom Res 1978; 22(4):259-94.
15. Greist J.H., Klein M.H., Eischens R.R., Faris J., Gurman A.S., Morgan W.P. Running as Treatment for Depression. Comprehensive Psychiatry 1979; 20:41-53.
16. Grzesiak R.C. Psychological Considerations in Myofascial Pain. In Rachlin, E, editor: Myofascial Pain and Fibromyalgia: Trigger Point Management St. Louis, 1994; Mosby 61-90.
17. Heitkamp H., Schmid K., Scheib K.B. Endorphin and Adrenocorticotropic Hormone Production During Marathon and Incremental Exercise. European Journal of Applied Physiology 1993; 66:269-274.
18. Isomeri R., Mikkkelsson M., Latikka, P. Effects of Amitriptyline and Cardiovascular Fitness Training on the Pain of Fibromyalgia Patients: Scand J Rheumatol 1992; Suppl 94:47.
19. Kraemer W.J., Dziados J.E., Marchitelli L.J., Gordon S.E., Harman E.A., Mello R., Fleck S.J., Frykman P.N., Triplett N.T. Effects of Different Heavy-Resistance Exercise Protocols on Plasma B-Endorphin Concentrations. J. App. Physiol 1993; 74:450-459.
20. Kraemer W.J., Fleck S.J., Callister R., Shealy M., Dudley G.A., Maresh, C.M., Marchitelli L., Cruthirds C., Murray T., Faikel J.E. Training Responses of Plasma Beta-Endorphin, Adrenocorticotropin, and Cortisol. Med Sci. Sports Exerc 1989; 21:146-153.
21. LaFontaine, T.P., DiLorenzo T.M., Frensch P.A., Stucky-Ropp R.C., Bargman, E.P., McDonald D.G. Aerobic Exercise and Mood: A Brief Review (1985-1990). Sports Medicine 1992; 13: 160-170.
22. Lee I-M, Hsieh C-c, Paffenbarger R.S., Jr. Exercise Intensity and Longevity in Men: The Harvard Alumni Health Study. JAMA 1995; 273:1179-1184.
23. Martinsen E.W., Medhus A., Sandvik L. Effects of Aerobic Exercise on Depression: A Controlled Study. Brit Med J 1985; 291:109.
24. Martinsen E.W. Physical Activity and Depression: Clinical Experience. Acta Psychiatr Scand 1994; Suppl 377: 23-27.
25. McCain G.A., Bell D.A., Mai F.M., Halliday P.D. A Controlled Study of the Effects of a Supervised Cardiovascular Fitness Training Program on the Manifestations of Primary Fibromyalgia. Arthritis and Rheumatism 1988; 31:9, 1135-1141.
26. McCann L., Holmes D. Influence of Aerobic Exercise on Depression. Journal of Personality and Social Psychology 1984; 46:1142-1147.
27. Neeper, E.A., Gomez-Pinilla, Choi, J., Cotman, C. Exercise and Brain Neurotrophins. Nature 1995; 373:109.
28. Nicoloff G., Schwenk, T.L. Using Exercise to Ward Off Depression. Physician and Sports Medicine 1995; 23:44-56.
29. Paffenbarger R.S., Jr., Lee I-M, Leung R. Chronic Disease in Former College Students: LIII. Physical and Personal Characteristics Associated with Depression and Suicide in American College Men 1994; In J. Lonnqvist and T. Sahi, eds., Acta Psychiatr Scand 89 (Suppl 377): 16-22.
30. Sandstrom, M.J., Keefe, F.J. Self-Management of Fibromyalgia: The Role of Formal Coping Skills Training and Physical Exercise Training Programs. Arthritis Care and Research 1998; 432-447.
31. Thoren P., Floras J.S., Hoffmann P., Seals D.R. Endorphins and Exercise: Physiological Mechanisms and Clinical Implications. Medicine in Science in Sports and Exercise 1990; 22:417-428.
32. Vaeroy H., Qiao Z-G, Morkrid L., Forre O. Altered Sympathetic Nervous System Responses in Patients with Fibromyalgia (fibositis syndrome). J Rhematol 1989; 16:1460-5.
33. White K.P., Carette S., Harth M., Tessell R.W. Trauma and Fibromyalgia: Is There an Association and What Does It Mean? Semin Arthritis Rheum 2000; 4:200-16.
by Paul J. Kiell, M.D.
|Printer friendly Cite/link Email Feedback|
|Author:||Kiell, Paul J.|
|Date:||Sep 22, 2003|
|Previous Article:||Chicago Marathon hosts inaugural meeting of American Road Race Medical Society: group working to standardize medical care at athletic events.|
|Next Article:||Back to Boston in 2004!|
|Fibromyalgia Research: Challenges and Opportunities.|
|Questions and Answers About Fibromyalgia.|