B RIEFLY Ne OTED Electrolytes and Their Relationship to Normal and Abnormal Muscle Function Janet A. Yu-Yahiro Electrolytes are essential to normal skele- tal muscle contraction and are thought to play a role in muscle fatigue. Excess accumulation of ammonia and hydrogen fons after strenuous bouts of physical activity are thought to slow muscle con- tractions and decrease muscle tension development. Certain disease states cause abnormal levels of such elec- trolytes as calcium, magnesium, potassi- um, or sodium. Excessively high or low levels of these ions in the serum are associated with symptoms such as mus- ole weakness or cramping. Nurses should know the effects of abnormal electrolyte levels on muscle function in the assess- ment and treatment of their patients. Janet A. Yu-Yahiro, PHD, i « Research Associate inthe Deparment of Orthopaedics at The Union Memorial Hospital, and Adjunct Assistant Professor inthe Department of Epidemiology and Preventive Medicine st the University of Maryland School of Medicine in Baltimore, Maryland Overview of skeletal muscles Each skeletal muscle is divided into bundles of muscle fibers. In ‘um, each bundle contains between 12 and 150 muscle fibers. A fiber constitutes one muscle cell, and a large fiber is about the thickness of a fine buman baie (On the cellular, or microscopic level, each muscle fiber contains slender, longitudinal structures called myofibrils. Two of these, actin ‘and myosin, play a key ole in the mechanism of muscle contraction. Each muscle fiber bas its own neural innervation. Excitation ‘occurs when a stimulus of sufficient stength is transmitted across the ‘myoneural junction (ihe meeting point of the nerve fiber and muscle fiber membrane), and an electrical current called an action potential is ‘generated. The action potential is spread along the muscle membrane, the sarcolemma, and (othe interior of the muscle fiber via the trans” verse tubules, This causes activation, the elease ofa high concentra ‘ion of calcium ions from an interior structure called the sarcoplasmic reticulum (Devries, 1966). ‘When a muscle isin a resting state the interaction between actin and myosin filaments is inhibited, The release of calcium ions by the action potential activates the attractive forces between actin and ‘myosin, and muscle contraction begins. Energy forthe contraction t0 continue is provided by the breaking down of high-energy adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and adenosine _monophosphate (AMP) (Guyton, 1981), Role of electrolytes in normal muscle fatigue Researchers suggest a positive correlation between altered levels of certain electrolytes and the development of muscle fatigue, No one is certain about the exact mechanisms by which skeletal muscles ‘become fatigued, but the most widely accepted concepts are the accu- ‘mulation and the exhaustion hypotheses (Bere & Levy, 1994; ‘Mainwood & Renaud, 1985; Simonson, 1971). The accumulation ORTHOPAEDIC NURSING — SaptomberOctobea 1994—Vol.13INo.5An understanding of a patient's electrolyte status and how it will affect muscle function is important in planning inhospital care and pre- dicting functional status after dis- charge. hypothesis states that impaired force ‘generation results from the accumula lion of excess metabolites. The exhaus- tion hypothesis proposes that fatigue is ‘due to exhaustion of energy supplies in the working muscle, ‘The specific roles of selected elec trolytes in normal muscle activity and their potential roes in the development ‘of muscle fatigue are discussed below. Ammonia ‘The most important means. by which ATP is formed to provide the ‘energy for muscular contraction is by the chemical breakdown of glicose stores by the processes of glycolysis, the citric acid eyele, and oxidative phosphorylation. Excess accumulation of hydrogen and ammonia ions disrupt these chemical processes and impair ATP production. ‘Ammonia ions are a metabolic product of working muscles. and. are released in largest quantities after activity of intense effort (Mutch & Banister, 1983). This occurs when the rate of hydrolysis of ATP exceeds the rate of rephosphorylation, resulting in the deamination of AMP to ammonia and inosine monophosphate (IMP) in an inreversible reaction (Tullson & ‘Terjung, 1991). These ammonia ions ierfere with enzymatic action in both elycolysis and the citric acid cycle and thereby deplete glucose stores. The ammonia ion concentration is propor tional to the amount of exercise done (MacLaren, Gibson, Parry-Billings, et al, 1989.) The ions are thought to bath decrease muscle tension development and prolong the length of the action potential (Washio & Inouye, 1978). In Severe states, certain abnormalities of motor dysfunction, such as convul sions, may also originate from excess ammonia levels (Mutch & Banister, 1983), Hydrogen ions Activities that require large bursts of energy for short durations, such as jumping or sprinting result in the pro- duction of lactic acid and the accumu: Tation of hydrogen ions (MacLaren, Gibson, Panry-Bilings, et al, 1989). Studies have shown that muscle pH drops from about 7.0 at rest to about 65 after maximal exercise (Herman- sen, 1979), Excess hydrogen ion inhibits phosphofructokinase activity, which is the key rate-determining enzyme in glycolysis Danforth, 1965). The reduction inthe amount of force gener ated by muscle is linearly related to the concentration of hydrogen ion (Don- aldson, Hermansen, & Bolles, 1978), ORTHOPAEDIC NURSING SeptemberiOctber 1994—Vol IN. 5 Electrolyte effects on muscles Calcium Under normal circumstances, serum calcium levels are carefully ‘maintained within a narrow range by hormonal regulation and ate not sus ‘ceptible to fluctuations due to overex- cetion. Abnormalities in serum calcium levels are most commonly found in critically ill patients as a symptom sec- ondary to 2 primary disease: hypocal- ‘cemia as a symptom of hypoparathy- roidism, vitamin D deficiency, or acute pancreatitis; or hypercalcemia as a symptom of primary. hypoparathy- roidism or malignancy. Hypocalcemia causes neuromuscular symptoms such as muscle cramps and tetany, and hypercalcemia is associated with the development of muscle weakness (Papadakis, 1993), ‘Impaired calcium release from the sarcoplasmic reticulum during a mus- cle contraction causes a decline in the development of force and an early onset of fatigue (McKenna, 1992). It has been suggested that this calcium impairment is related to decreased activity of the enzyme, calcium ATPase, Magnesium “Hypomagnesemia is found in 20 0 60 percent of critically ill patiens (Papadakis, 1993). This condition is frequently caused by infusion of large volumes of intravenous fluids, diuret- Jes, or certain medications. Among the common symptoms of hypomagne- semia are muscle cramps and weak ness. Excess magnesium can also be associated with musele weakness. This condition i almost always the result of renal insufficiency. When kidney func tion is poor, magnesium excretion declines because of a decrease in the glomerular filtration rate (Lemann, 1990) Potassium Hypokalemia is most commonly caused by inadequate dietary intake of potassium or through excess renal or gastrointestinal loses of potassium, as With diarhea or chronic use of diuret- ies (Andreoli, Carpenter, Plum, et a, 1990), Muscle weakness, fatigue, and ‘muscle cramps are common com- plaints with moderate hypokalemia, land potassium ion accumulation during intensive muscle activity contributesfatigue (Kossler, Caffier, & Lange, 1990), Primary aldosteronism is caused by a tumor of the zona glomerulosa of ‘one ofthe adrenal glands and results in excess aldosterone secretion. This in tum causes a severe decrease in extra cellular potassium and impairment of neeve conduction, which can resut in ‘musele paralysis (Guyton, 1981) Sodium Osmolality in the serum is main- tained at a. vrwally constant level under normal conditions due to the free passage of water between the intracel- Tular and extracellular uid compart- ments ‘When sodium salts are lost from the body and not replaced, extracellular fluid volume decreases. Loss of salt ‘ecurs in conditions such as exercise in extremely bot environments, or with diarthea'or vomiting. Atempts 10 replace the losses by drinking water alone cause a dilution of the body fla- ids anda reduction oftheir osmolality Dilution of serum sodium levels causes muscle or heat cramps (Brobeck, 1980 Implications for practice ‘An understanding of a patient's electrolyte status and how it will affect, ‘muscle function is important in plan- ning inospital care and predicting functional status after discharge. When evaluating a patient's general com- plaints of muscle weakness or pain, Knowledge of how specific disease processes affect serum electrolytes may provide clues as to the causes of these symptoms. References Andreoli, TE. Carpenter, CC, Plum, Ft 1. (1990). Cet essential of medicine (Gaal ed.) Philadelpis: Stands Berne, RM, & Levy, MIN. (Ed). (1993). ‘Physiology Ged). St Louis: Mosby ‘Year Book Brobeck, LR. (Bd), (1980). Best and Taylor's physiological basis of med lead practice (I0eh ed). Balimore: Wiliams & Wilkins Danforth, W. (1968). Activation ofthe gly colytic pathway in muscle. In B. Chance & -R. Estabrook (Eds), Control of energy metabolism. New ‘York: Academic Pres. Devtes, HA. (Bi). (1966). Physiology of ‘exercise (2nd ed). Dubuque, TA: Wn CBrowa, 40 Donaldson, $, Hermansen, Ly, & Boles, L (1978). 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The effect of calcium and magnesium on the spontaneous release of wansmiter at insect motor nerve terminals. Toural of Experimental Biolog. 75, 101-112. Awards Deadlines NAON Research Grants February 1, 1995 NAON Orthopaedic Industry Scholarships Fobruary 1, 1995 NAON/Howmedica Annual Congress Grants February 1, 1995 (Outstanding Orthopaedic Nurse Award February 1, 1995 Corporate Endowed Scholarships [National Associaton of| Orthopaedic Nurses February 20, 1995 ‘Outstanding Chapter Award 2 weeks before Congress a) ORTHOPAEDIC NURSING — SoplemberOctober 1994—Vo. 1380.5