Health Matters

Pains, Strains, and Automobiles: Muscle Injury and Recovery Whether from exercise, repetitive use, physical trauma, or an odd sleeping position, muscle soreness is something most of us will have experienced. The questions naturally arise: What happens to cause that pain? How does the body respond if there is an injury? What can the reader do to address both the discomfort and the usually accompanying tightness as well as when? And, finally, what preventative steps can be taken to avoid future pain? As facilitators of movement, muscles play a pivotal part in our day-to-day lives. Ideally, they should be kept in a state of dynamic flexibility, meaning basically that they should be strong yet supple. Unfortunately, the ideal is frequently not the norm. Rather, certain overused muscles become shortened while others become lax from being underused or to accommodate tightening elsewhere. The ensuing repositioning of joints generates biomechanical distortions, all of which may predispose either set of muscles to injury under certain conditions. One such category of activity is a particular way one uses one’s muscles to do something. Using the example of the elbow flexors while taking groceries to the car, there may be three types of contractions involved: to raise the bags off the floor, they are shortened as they are contracted — concentric contraction; to lower the bags to the ground smoothly, they are kept taut while they are lengthened — eccentric contraction; and to push the bags to the back of the trunk, they may tighten without a change in length — isometric contraction. Whereas discomfort can arise from each, injury usually occurs with the eccentric type. That is especially true for muscles which span two joints and tend to have a higher proportion of fast-twitch fibres. (see the article, “Tension Headaches” in this issue for details about pain associated with concentric contractions) Muscle Injury and Repair Several interrelated factors will determine the specific pattern of signs and symptoms of as well as the body’s response to an injury: how tight the muscle was prior to the incident; what was the nature of the force involved — i.e., the specifics of a motor vehicle accident vs. the duration, type and intensity of a certain exercise; the state of other related tissues to a joint (ligaments, tendons, other associated muscles...); and the orientation of the joint, determining the position of the muscle sustaining the injury. Nevertheless, general characteristics have been found in terms of both structural change and recovery processes as well as the associated symptomology. Conceptually, one can liken muscle remodeling to adding an extension onto one’s home while renovating the adjacent, deteriorating room. In that analogy, the deteriorating room is muscle cell — the sarcomere — which has been damaged while the extension is new cells. The removal of debris or necrotic tissue is part of the inflammatory process by which specialised cells like macrophages consume the unwanted tissue. During the process, fibrous scar tissue is put in place thereby allowing new muscle tissue to be formed properly by anchoring the tears. Further support may be lent by an increase in resting or passive tension within the muscle as a whole; however, the presence of localised taut bands within which the damage may have occurred may impede healing. As satellite cells migrate and differentiate into new muscle cells, the need for the scar tissue is reduced and the ‘scaffolding comes down.’ Lastly, localised nerve damage may necessitate some ‘rewiring.’ Signs and Symptoms of the Recovery Process Perhaps the most obvious symptom of muscle injury is soreness — clinically named, “delayed-onset muscle soreness” (DOMS). Beginning between 6 and 8 hours after the incident and peaking within 48 hours, DOMS seems secondary to the inflammatory process resulting from damage to the portions of the muscle cell. One possible initiator is the rupture of the reservoirs of calcium (Ca2+), an ion essential in the process of muscle contraction. Under specific conditions it has been implicated in the activation of certain enzymes, notably calpain, which breaks down the protein desmin used in the structure (the Z disk) which binds muscles cells to each other in series. Another indication of damage is the elevation of levels of fibronectin which points to lesions in the muscle’s membrane. While the associated inflammatory process is too detailed to discuss here, the outcome is believed to include sensitising pain receptors (nociceptors) and recruiting certain receptors in the muscle which respond to pressure (mechanoreceptors) and spindles to signal pain. After an initial decrease in resting tension, a subsequent increase within 24 hours in the muscle is yet another sign of injury. Basically, that has been linked to a rise in calcium levels throughout the muscle as a whole including in undamaged cells. Finally, there is an associated fatigue and weakness. Rather than due to an ‘energy crisis’ in the muscle (i.e., with decreased stores/production of CP and ATP) or a reduction in calcium release, with injury this sign is related to mechanical damage to the structure of the functional part of the muscle cell as well as that aforementioned structure which binds them in series (the Z disk). It appears that in some cells the stretch causes one half to become lengthened while the the other is shortened as is that next muscle cell in the series. Under normal circumstances, the muscle cell would ‘recoil’ or interdigitate and allow normal functioning during the next contraction; however, in response to too much force, the arrangement of these proteins is irreversibly compromised, leading to new and more cells being laid down to replace them. Within this context, one preventative measure the reader can take is making sure that one’s muscles are not taut under day-to-day conditions, especially if eccentric exercises are part of one’s weekly routine. Appropriate stretching is a must because the resting tension which builds under concentric contractions (shortening of muscles) has been found to lower the number of muscle cells in a given muscle as a whole. If, from the outset of activity a muscle is already shortened, then it is de facto relatively predisposed to injury. Decreasing resting tension after injury has occurred is also of benefit for the very same reason. In some cases, though, either certain muscles are too tight or their attachments make them difficult to stretch, even though they are an essential part of daily life. In that case shiatsu, acupuncture or registered massage therapy are all recognised forms of manual therapy which can bring a person to a state where needed stretches can take over in a relatively short period of time by lengthening the muscles for the person.

Painful Menstruation and Acupuncture With the new year comes a new, regular feature to “Health Matters” devoted to women’s health. In the current issue a condition affecting some 50% of menstruating women will be addressed, notably painful menstruation or dysmenorrhea. “Cramping,” “tiring,” “aching,” “tender,” “miserable,” and “nagging” are all words typically used to describe dysmenorrhea. While some are clearly directly associated with the uterus — i.e., cramping —, others are not so restricted. That in part relates to the ability of the body to sensitise neurons receiving signals from other areas and/or amplify pain from these tissues. Notably, certain muscles and organs may become painful or more painful, resulting in pain states associated with the abdomen and the pelvis. As with pain in general, it has the ability to diminish (if only temporarily) a woman’s physical and emotional quality of life, revealed here by the use of the words “tiring” and “miserable,” respectively. The causes of dysmenorrhea fall within one of two general categories: Primary: not involving any pelvic abnormalities; Acquired: secondary to another condition. In both instances the underlying mechanisms sustaining the pain as well as the treatment prescribed differ yet are all complex. In the case of the primary type, the severity of cramping seems to directly relate to the levels of an inflammatory substance in the endometrium and menstrual fluid, called “prostaglandin” (PGf2a). The more that is present, the more cramps occur. Such a relationship seems true of pain too. The specifics of location, quality and intensity, however, vary over the course of the menstrual cycle and in response to different stimuli (types of pressure, heat, and so on). Overall, skin of the abdomen and limbs seems most sensitive to pain around ovulation while the tissue under the skin and muscles particularly of the left abdomen seem most sensitive around menstruation. Part of that may relate to a process readers will recall from articles in previous issues: that of central sensitisation. That process involves certain second-order neurons in the spinal cord becoming ‘jumpy’ and requiring fewer ‘messages’ from their associated tissues to signal pain to higher centres of the brain. Indeed, as with other types of referred pain, it ‘spreads’ beyond the spinal levels originally stimulated. Hormonal changes may be another factor in changes in the sensitivity of the central nervous system. In the case of acquired dysmenorrhea, other conditions may need be addressed first: gynæcological disease: endometriosis, adhesions, pelvic congestion syndrome, leiomyoma (fibroids of the uterus), and adenomyosis; gastrointestinal disease: constipation, irritable bowel syndrome, diverticulitis, diverticulosis, chronic appendicitis, and Meckel’s diverticulum; genitourinary disease: interstitial cystitis and chronic urethritis; musculoskeletal diseases: fasciitis, nerve entrapments, hernias (inguinal, femoral, umbilical, incisional), low back scoliosis, L1 to L2 disc disorders and spondylolisthesis; and psychological considerations: depression, a history of sexual abuse, psychosexual dysfunction, and somatisation. Whereas detailing the treatments for concurrent conditions is beyond the scope of this article, that which is usually used to diminish the pain is not: non-steroidal anti-inflammatory drugs (NSAIDs). In Canada, the NSAIDs most frequently used for dysmenorrhea are: Arthrotec (a combination of Diclofenac sodium and Misoprostol) Celebrex Entrophen (enteric coated aspirin) Naprosyn (Naproxen) In addition Rofecoxib (Vioxx) is also being used. Each of those drugs works by inhibiting one or two enzymes, COX-1 or COX-2, which help produce certain prostagladins and, thus, the inflammation and pain. In each case, though, there are risks of adverse side-effects, notably with the gastrointestinal tract. For more details, the reader is directed to the National Library of Medicine’s http://www.nlm.nih.gov/medlineplus/druginformation.html as well as Health Canada’s Adverse Drug Reaction Newsletter http://www.hc-sc.gc.ca/hpb-dgps/therapeut/htmleng/cadrnwsletter.html Depending upon the ætiology, acupuncture can also be an effective tool in relatively painlessly reducing painful menstruation without the adverse side-effects, however, within the context of a multidisciplinary approach including the participation of a gynæcologist. Traditional Chinese gynæcological theory dates to the Shang dynasty (1500-1000 BC), since which time it has classified 8 main patterns of dysmenorrhea based on cause and symptomology. Each class differentiates between type and onset of pain; characteristics of the menses including flow, colour, presence of clots; emotional state; and associated signs and symptoms such as headache, dizziness, distension of the breasts, feeling hot or cold and so on. Additionally, for each class there is an acupuncture protocol. Specifically, the pain patterns are: lower abdominal pain 1-2 days prior to or during the period; intense, stabbing pain before or during the period; lower abdominal pain before or after the period; central pain; pain relieved by the application of heat; sore back; (including a scanty flow and feeling cold); hypogastric pain before the period or sometimes at mid-cycle; burning sensation extending to the sacrum; abdominal pain before or during the period; (including a heavy flow and a feeling of heat); dull, hypogastric pain towards the end of or after the period; pain relieved by pressure and massage; (including being tired); dull, abdominal pain after the period; abdominal pain relieved by pressure and application of heat; and dull, hypogastric pain towards the end of or after the period; sore back; pain relieved by pressure and massage; (including being exhausted). While acupuncture is frequently used in combination with Traditional Chinese herbal therapy, it can be effective when solely used (as is practiced at the Kingsway Therapeutic Centre). Should the reader have any questions on whether acupuncture may be helpful, please call Carrie Anderson (D.Ac.) at the Centre. * * * * * * * *

Arthritic Pain, Part 3: Rheumatoid Arthritis Following the general introduction (part 1) and subsequent article on osteoarthritis (part 2), this issue addresses rheumatoid arthritis (RA) — a chronic, autoimmune, inflammatory disorder affecting some 300 000 Canadians and women twice as often as men. “Normally the balance between destruction and repair [of bone] is carefully regulated. However,if the instigator cannot be removed, or the inflammatory reaction persists and is not downsized appropriately, disease may be the outcome.” Weyand, C.M.; Goronzy, J.J. (1997) “The molecular basis of rheumatoid arthritis.” Journal of Molecular Medicine 75:772-785. Clinically, RA presents itself predominantly as joint swelling, pain and stiffness (usually lasting at least 1 hour in the morning), weakness, deformity, fatigue, malaise, fever, weight loss, and depression. In particular it affects the more distal joints on both sides of the body: the wrist and ankle the elbow and knee the shoulder and hip the joint one commonly considers to be the knuckle (MCP) and the adjacent joint in the finger (PIP) and those corresponding ones in the feet (MTP and PIP, respectively) Typically the process of destruction of the involved bone and cartilage predates of the onset of signs and symptoms. Indeed, by the time they are evident, the damage may be irreversible. Finally, RA may also involve different organs such as the lungs, heart, liver, vasculature and so on. While it is not possible to speak of definitive answers to the “why?” and “how?,” the current understanding reflects a better knowledge of: the way the immune system responds to external and internal prompters (antigens) generally; the ways in which this varies from person to person; the ability of people to respond differently to the same antigen; the ability of a person to respond in numerous ways to the same antigen; and the ways in which different symptomology of RA may also be reflected in different immunological responses. As variable and daunting as that may sound, some tendencies in study findings have emerged which shed light on the factors which orchestrate the destructive process. (see “Recent Findings” for details) Until recently treatment typically included the use of glucocorticoids, non-steroidal anti-inflammatories (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs, i.e., methotrexate) to control the inflammatory process and slow the process of joint degradation. In 1999 the US Food and Drug Administration approved three new DMARDs: leflunomide, etanercept (designed to neutralise TNF-a), and infliximab (an antibody against TNF-a). Additionally, it approved a new NSAID, celecoxib. Because of the anti-TNF approach to two of the drugs, there is a risk of infection (sometimes life-threatening) because of its inhibitory action on the immune system. Acupuncture, Shiatsu and Registered Massage Therapycan also have a beneficial effect but upon muscles which have become taut and further restricted range of motion of their associated joints (particularly those of the wrist, elbow, knee and ankle for RA). By gently loosening them, diminished muscular pain may too be had in addition to less compression, torsion or sheering of the weight-being joints in the leg. That has the benefit of making needed exercise more comfortable to perform. Recent Findings about RA development: Physically there is an invasion into the joint of a pannus, a tissue with numerous new blood vessels and two types of cells which contribute to the inflammation (amongst other cells). This helps bring oxygen and nutrients to foster the disease process in its early stages. While RA sufferers may have some 100 different types of T cells (involved in protecting the body against disease) active in affected joints, only a small number may be important in the disease process. There is, however, an abundance of a specific class of T cells (CD4+) which has the abilities to stimulate its own growth and to resist being broken down. The degree to which they have spread throughout the body reflects the severity of signs and symptoms. Those specific T cells produce a number of molecules which promote inflammation and degrade the joint, notably with TNF-a having a wide range of individual and combined effects. Specifically, TNF-a stimulates certain cells in the pannus to produce adhesion molecules which bind T cells with B cells, inducing the latter to produce rheumatoid factor (RF). It also stimulates production of messenger cells (cytokines) such as IL-1 and IL-6, both of which promote inflammation. It promotes the growth of a group of cells called osteoclasts which help to consume the surface layer of bone so new layers can be produced. When it works with IL-1, it induces production of compounds called metalloproteinases which are capable of breaking down almost every protein making up the joint and inhibits their inhibitors. Lastly there seems to be a genetic predisposition to developing RA. 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