Tissue-Specific Exercises for the Upper Extremity



Tissue-Specific Exercises for the Upper Extremity


Lori Falkel



Tissue-specific exercise progressions can be thought of as the science of prescribing an accurate dosage of exercise. Tissue-specific exercise allows us to use our knowledge of exercise physiology to address the specific pathologic tissue conditions. When physicians prescribe medicine, they do not arbitrarily select a medication from the pharmacy and administer it. They prescribe medicine based on the pathologic condition.


With proper knowledge, exercise is the therapist’s area of expertise. For optimal outcomes, exercise dosage must not be assigned arbitrarily; it should be dosed accurately according to the physiology of the tissue(s) involved. When designing an exercise program effectively to promote the recovery of the target tissue, the therapist needs to consider multiple variables. Some of these variables are the appropriate resistance; the repetitions and sets that will promote the desired response; the speed, frequency, breaks, and duration of exercise; the appropriate positioning of the limb and/or client; and the precise range of motion. Proper exercise equipment, to provide support, can be critical for restoration of physiologic motion. The types of muscle work (for example, concentric, eccentric, and isometric) are also important considerations.


The Ola Grimsby Institute developed Scientific Therapeutic Exercise Progressions (STEP), which is a concept of dosing exercises according to the specific pathologic condition and tissue tolerance of each client. STEP is based on principles of medical exercise therapy. It was developed in Norway and has been practiced throughout Europe for many years with excellent results. STEP addresses musculoskeletal dysfunctions with respect to their histologic, biomechanical, and neurophysiologic significance.



Joint Dysfunction


Joint dysfunction occurs because of a compromise in connective tissue integrity. This may result from capsular, ligamentous, or cartilaginous causes. In cartilage, symptoms of joint dysfunction present as an inability to withstand compressive forces. If the joint dysfunction is capsular, joint swelling will be present. A ligamentous injury has point tenderness. The end result is altered mobility. Joint dysfunction can be labeled as a hypomobility, a hypermobility, or an instability. A joint is considered to be hypomobile when movement takes place about a physiologic axis but is less than normal. A hypermobile joint has greater than normal motion around a physiologic axis. Joint instability is motion around a nonphysiologic axis.1 All synovial joints can be categorized by a joint mobility grading system1 (Table 4-1).




Musculoskeletal Dysfunctions


The two main causes of musculoskeletal dysfunctions are acute trauma and cumulative trauma. Acute trauma is associated with an excessive contraction (muscle strain) or an externally applied force. Chronic overload, or cumulative trauma, is associated with prolonged static work, stress, and often reduced aerobic activity.




Comorbidities Associated with Increased Prevalence of Musculoskeletal Dysfunction


The vast majority of clients who present for treatment in a hand clinic do not have only a hand injury. The therapist must be aware of the client’s comorbidities and provide comprehensive treatment that addresses the client as a whole, rather than just an extremity. Some of the more common diseases that are associated with lowered tolerance of the musculoskeletal system are diabetes, hypothyroidism/hyperthyroidism, gastric ulcer, chronic/recurrent infections, colitis, and cardiovascular and respiratory diseases.


Diabetes causes the production and use of insulin in the body to be impaired. This results in an abundance of sugar in the bloodstream. With diabetes, the pancreas secretes little or no insulin (type I diabetes) or the body becomes resistant to the action of insulin (type II diabetes). If the disease is not treated, the level of sugar in the bloodstream builds up and leads to diabetic complications.


The thyroid gland affects all aspects of metabolism. The thyroid releases hormones that regulate heart rate, the strength of bones, how quickly calories are burned, and sensitivity to heat/cold. If the thyroid gland is underactive or overactive (hypothyroidism/hyperthyroidism), medical treatment is necessary to avoid complications.2


A gastric ulcer is an open sore that develops in the lining of the stomach. The ulcer may result from diet, stress, medication, or bacterial infection.


Infections can occur when the immune system is suppressed or comes in contact with an organism to which it does not have resistance. Bones and joints become susceptible to chronic infections that originate elsewhere in the body and are passed to them via the bloodstream.3


Colitis is a painful and debilitating chronic inflammation of the digestive tract.4 Symptoms include bloating, cramping, abdominal pain, and loss of appetite. Cardiovascular and respiratory disease includes any of a multitude of problems involving the heart, lungs, and blood vessels. Some of these disease processes are preventable and are acquired over a lifetime; others are congenital. Cardiovascular disease is more prevalent than all of the previously mentioned diseases combined.5,6



Exercise Considerations


Always use caution and discretion when prescribing the intensity of exercise. A thorough evaluation provides the necessary information regarding cardiovascular compromise or risk factors, pulmonary disease, diabetes mellitus, hypertension, obesity, peripheral vascular disease, arthritis, and renal disease.5


Precaution. An exercise program may not be recommended for uncontrolled diabetes. A rigorous strengthening or aerobic exercise program, in this case, may cause a hyperglycemic effect because cellular absorption of glucose is restricted. Insulin-dependent diabetic clients may need to decrease insulin or increase carbohydrate intake when exercising. They should monitor their glucose more frequently when starting an exercise program. For this client population, the exercise should be dosed at a lower level of intensity and duration initially and should progress at a much slower rate.2



Osteoporosis


An estimated 30 million Americans have osteoporosis. This disease is responsible for 1.5 million individuals sustaining bone fractures per year (200,000 wrist fractures, 300,000 hip fractures, and 300,000 non-wrist extremity fractures). Osteoporosis costs more than $18 billion per year in health care expenses and lost productivity. Bone mass attains a peak in males and females at approximately 30 to 35 years of age, with total bone mass beginning to decline 5 to 10 years later. Boxes 4-1 and 4-2 list traits and age-related changes associated with osteoporosis.7,8




Males are less affected by osteoporosis than females. Males usually ingest more calcium and have higher levels of calcitonin. They also produce testosterone into the seventh and eighth decades of life as opposed to the decline in hormone production that females experience with menopause in the fourth or fifth decade. The increased calcium and hormone levels reduce the loss of bone mass, which in turn reduces the potential for development of osteoporosis.


Several factors can affect bone resorption levels. A lack of weight bearing and of activity in antigravity muscles changes the resorption rate, as does excessive thyroid and parathyroid hormones. Corticosteroids also have an impact.


Determinants of bone mass and loss are genetic, mechanical, or hormonal. Genetics can cause large-boned individuals to gain a relative immunity to osteoporotic fractures. The mechanics of bone density can aid in the prevention of fractures, but they also can be a possible cause. Increasing loading yields lead to increased bone mass, and decreased loading yields lead to decreased bone mass.



Exercise for Prevention/Treatment of Osteoporosis


Exercise can help prevent or slow down bone loss, improve posture, and increase overall fitness. For clients who are at risk of osteoporosis, a bone density test before beginning an exercise program is recommended. Box 4-3 lists factors to consider when selecting an exercise.7



Although walking is the best of all of the options listed in Box 4-3, those clients who are unable to tolerate walking because of comorbidities or advanced osteoporosis have other options. These options provide benefit by generating muscle tension, which provides needed stress to bone. To prevent injury to those with advanced osteoporosis, clients absolutely should avoid the exercises listed in Box 4-4.





Histology of Collagen, Bone, and Cartilage


Collagen


Collagen is the fundamental component of the connective tissues of the body, including fascia, fibrous cartilage, tendons, ligaments, bones, joint capsules, blood vessels, adipose tissue, and dermis. Collagen is the most abundant protein in the human body. It accounts for approximately 30% of all protein. Before 1970, researchers believed that all collagen was identical. Now, nineteen types of collagen are known that are differentiated by their protein composition. Type I and type II together compose approximately 90% of human connective tissue. Type III collagen is produced first, in the initial reparative phase, before type I collagen. Type III collagen also is found in arteries, the liver, and the spleen.8


Type I collagen constitutes about 90% of total body collagen. Type I collagen is found in bone, tendon, fascia, fibrous cartilage, derma, and sclera. This collagen is synthesized by fibroblasts, osteoblasts, and chondroblasts. Its primary function is to resist tension.


Type II collagen is found in hyaline and elastic cartilage and intervertebral disks. Type II collagen is synthesized by chondroblasts. Its primary function is to resist intermittent pressure.


Fibroblasts produce type I collagen fibers that are found in tendons, ligaments, and joint capsules. Procollagen, the precursor of collagen, is produced in the endoplasmic reticulum and is made up of polypeptide chains of lysine, glycine, and proline. Tropocollagen is the basic molecular unit of collagen fibrils and is found in the interstitial spaces; this collagen is the building block of collagen. The bonds of procollagen and tropocollagen are weak and easily deformed or ruptured. One must understand that collagen bonds are remodeled from mobilization or exercise.


Fibroblasts also produce glycosaminoglycans. These are proteoglycans, the fundamental components of connective tissue, which make up the extracellular matrix of tendons, ligaments, and articular cartilage. Imbibition is the primary nutritional source for avascular tissues, such as tendons, ligaments, cartilage, and vertebral disks. When tension/pressure increase, fluid is forced out of tissue and the volume of the tissue decreases. This causes an increase in the concentration of proteoglycan substances and an increase in osmotic pressure, which in turn produces imbibition. Glycosaminoglycans provide the fibers with nutrition via imbibition and lubrication. They allow space for elastic deformity of the tissue.8 The half-life of glycosaminoglycans is 1.7 to 7 days. Immobilization for more than 1.7 to 7 days causes a 50% decrease in glycosaminoglycans. Therefore lubrication is decreased and the elastic range of collagen is decreased. A decrease in glycosaminoglycans causes a decrease in nutrition, which damages the tissue.



Bone


Bone is the protective and supportive framework that has rigid and static, elastic and dynamic properties. The properties and geometry of bone can be altered in response to internal and external stress and also in response to mineral demands. Bone has plastic qualities; it absorbs and stores compressional forces and transmits tensile forces. Bone also has elastic qualities. Long bone can deform up to 5%. The ability of bone to deform decreases with age.


Bone is composed of approximately 5% water and approximately 70% minerals (calcium hydroxyapatite, phosphate, magnesium, sodium, potassium, and fluoride carbonate); approximately 20% organic compounds, mostly type I collagen; and approximately 5% noncollagenous proteins. Osteoblasts are the functional building blocks of the osteoid matrix; they are located only at the surface of bone tissue. Osteocytes are mature osteoblasts. Osteoclasts are responsible for bone dissolution and absorption. Bone homeostasis balances synthesis, dissolution, and absorption with the forces that are applied on the skeleton.9



Cartilage


Cartilage is a semirigid connective tissue that is less dense and more elastic than bone. The functional unit of cartilage is the chondrocyte. Chondroblasts are immature chondrocytes, and they produce the ground substance or extracellular matrix of cartilage. This extracellular matrix consists of glycosaminoglycans and type II collagen. Water composes 65% to 80% of articular cartilage. Like fibroblasts, chondroblasts synthesize collagen and glycosaminoglycans when stimulated by mechanical tension. Mature cartilage is avascular and lacks nerve supply. Cartilage gets nutrition through imbibition. The mechanical forces of motion stimulate imbibition and removal of waste products.


The three types of cartilage are the following:



The two primary functions of articular cartilage are to promote motion between two opposing bones with minimal friction and wear and to distribute the load applied to the joint surfaces over as great an area as possible.10



Optimal Stimulus for Regeneration of Collagen, Bone, and Cartilage


Collagen


The optimal stimulus for fibroblastic function in the regeneration of collagen is modified tension along the line of stress. This modified tension is not to exceed the level of tension that the newly formed polar bonds of tropocollagen can withstand. The tropocollagen is an immature precursor to the stronger, more resilient collagen. Once a certain level of tension is exceeded, tissue breakdown will occur instead of proliferation.


Precaution. If tension exceeds this critical level, the signs and symptoms will be pain, inflammatory reaction, muscle guarding, decreased range of motion or loss of flexibility, and secondary scarring.8




Cartilage


The optimal stimulus in the regeneration of cartilage is intermittent compression/decompression with glide. Joint movement (shear) is necessary to distribute synovial fluid over the cartilaginous surface and provide oxygen and other necessary nutrients. Intermittent compression forces the extracellular fluid within the joint to be compressed into the cartilage matrix. With joint immobilization, an alteration in joint mechanics and a decrease in the normal contact areas of cartilage occur. This eventually leads to joint dysfunction, hypomobility or hypermobility, and muscle guarding.


Precaution. The body responds to the stresses placed upon it. With abnormal stresses, there will be dysfunctional remodeling. This manifests as joint degeneration, osteophytes, bone spurs, or pseudarthrosis.9



Effects of Immobilization versus Early Mobilization




After 9 weeks of immobilization, there is 14% loss of total collagen, and by 12 weeks there is a 28% loss. The half-life of glycosaminoglycans is 1.7 to 7 days. The half-life of collagen is 300 to 500 days. For this reason, under normal physiologic conditions, it takes between 1 to 2 years for full healing to occur. Immobilization of cartilage causes a decrease in thickness and number of collagen bundles, a decrease in proteoglycan content, an increase in water content, a decrease in load-bearing capacity, softening of the articular surface, decrease in tensile strength of cartilage, and a decrease in oxygen content. To decrease these adverse effects of immobilization, one should institute an exercise model of high repetitions with low to no resistance. This model increases the oxygen content within the tissues by improving blood flow and imbibition. For maximal benefit, mobilization exercises should be performed several times a day.8 A home exercise program helps accomplish these goals. Box 4-5 lists the qualities of a good home exercise program.




Neurophysiology


Muscle Spindles


Muscle spindles are proprioceptors that consist of intrafusal muscle fibers enclosed in a sheath (spindle). They run parallel to the extrafusal muscle fibers and act as receptors that provide information on muscle length and the rate of change in muscle length. The spindles are stretched when the muscle lengthens. This stretch causes the sensory neuron in the spindle to transmit an impulse to the spinal cord, where it synapses with alpha motor neurons. This causes activation of motor neurons that innervate the muscle. The muscle spindles determine the amount of contraction necessary to overcome a given resistance. When the resistance increases, the muscle is stretched further, and this causes spindle fibers to activate a greater muscle contraction.11




Joint Mechanoreceptors


Four types of mechanoreceptors are found in the synovial joint capsules. Mechanoreceptors have a significant effect on muscle tone and pain sensation locally and distally along segmental innervations. The number of mechanoreceptors decreases with age. By age 70 the total number of receptors has decreased by about 50%, depending on factors such as genetics and activity level.12


Type I mechanoreceptors are found in the superficial layers of the joint capsule between the collagen fibers. A large percentage of the type I mechanoreceptors is found in the joints of the neck, hip, and shoulder. They have a great effect on the coordination of the tonic muscle fibers. They are slow-adapting and inhibit pain. They fire during movement and for about 1 minute after movement stops. They provide postural and kinesthetic awareness (awareness of the position of the body or body part in space). They are active in the beginning and end-range of collagen tension.


Type II mechanoreceptors are found in deep layers of joint capsules. A high concentration of the type II mechanoreceptors is found in the joints of the lumbar spine, hand, foot, and temporomandibular joint. They are fast adapting and pain inhibiting. They fire during movement and continue to fire until about ½ second after movement stops. They do not respond to stretch but are activated in beginning and midrange of collagen tension. They have more effect on the phasic muscle fibers and kinesthesia.


Type III mechanoreceptors are located in the deep and superficial layers of the joint capsules and ligaments. They are slow adapting and inhibit muscle tone in response to stretch at the extreme end-range of tension. They provide kinesthetic information, but their role is less understood than the type I and II mechanoreceptors.


Type IV mechanoreceptors are located in joint capsules, blood vessels, articular fat pads, anterior dura mater, ligaments of the spine, and connective tissue. They are not found in muscle. They fire when excessive levels of tension are reached in the collagen, and they warn of tissue trauma. They function as pain-provoking, nonadapting, high-threshold receptors. They fire continuously until the injurious stimulus is removed. They are provoked by excessive stretch, inflammation, high temperature (38° C to 42° C or 100.4° F to 107.6° F), or respiratory and cardiovascular distress.12


Pain has been defined by the International Association for the Study of Pain as an unpleasant emotional disorder evoked by sufficient activity in the nociceptive system and associated with real or potential tissue damage.13 The irritation causing the pain may be due to immobilization, physical trauma, infection, or emotional tension.


Precaution. Pain is a protective mechanism. Pain is not a warning that something is about to go wrong; it has already gone wrong! Pain is the way the body alerts the brain that an irritation to the tissue has occurred. For this reason, one must remember to exercise within a pain-free range of motion. In this case, feeling bad is a good thing because it is how your body communicates. Listen to the body.



Traumatology


The response of the body to trauma is predictable and consistent, regardless of the tissue involved or the mechanism of injury. Trauma sets off a highly organized response involving chemical, metabolic, permeability, and vascular changes at a cellular level in preparation for tissue repair.



Phases and Time Frames of Healing


The initial response to a traumatic event is irritation. This lasts for 5 to 6 hours. Vasomotor constriction occurs in the first few seconds. An immediate release of chemical vasodilators occurs. These dilators are also transmitters for the nociceptive (pain) system. The vasodilation increases the hydrostatic pressure because of increased capillary permeability. Clinicians rarely can influence this phase because of its immediate occurrence.


The next stage of healing is the acute stage, which lasts for 1 to 3 days depending on the vascularity of the tissue. During this time frame, a migration of the larger cell bodies through the wall of the vessel occurs. Subsequently, blood flow increases to the area, increasing hydrostatic pressure and increasing bleeding. The large proteins leak out of the capillary, causing a shift in osmotic pressure with resultant pulling of fluid out of the capillary. Venous stasis occurs distal to the traumatized area, and edema results (see Chapter 3).


The third stage of healing is the subacute stage. The subacute stage begins with the settled stage, where muscle spasming occurs over the next 3 to 5 days. Bleeding is no longer present. Oxygen and macrophages are present. Walling off of the capillary occurs, which makes waste removal difficult. This leads to secondary healing or scarring. Externally applied heat in the settled stage promotes stasis and inflammatory exudates. The preferred method of heating tissue is internally. Initiating movement with low resistance exercise produces friction and naturally generates heat. This promotes increased blood flow.


The final stage is the chronic stage. Tissue becomes strongly chemical bonded (covalent bonds) and mature at 9 to 12 months. At this stage the tissue becomes nonelastic and cannot be deformed. Mature scar tissue may cause pain. Clinically, concentrate on increasing the tolerance of the tissue to tension about the scar by use of controlled stress through properly dosed exercises.


Tissue-specific exercise in the subacute stage provides the optimal stimulus for the removal of metabolites, which are products of metabolism, from the tissue. Muscle contraction is necessary to transport metabolites from the cell and provide oxygen/nutrition to the area. Increased vascularization accomplishes this goal. This is achieved through many repetitions of properly dosed exercise with minimal resistance while avoiding excessive tissue tension. In other words, the muscle contractions with proper exercise facilitate formation of capillaries, blood flow, and removal of metabolites.

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Sep 9, 2016 | Posted by in MANUAL THERAPIST | Comments Off on Tissue-Specific Exercises for the Upper Extremity

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