The etiology of a common exertional muscle cramp during the heat of
summer is not agreed upon by research because of a multiple of biochemical
aberrations that may result in neurophysiological failure. Substrates may be
depleted during extreme hyperthermal conditions imposed by prolonged energy
metabolism, which are said to affect the biochemistry of several other cellular
reactions resulting in spasms, cramps, and muscle seizure. The electrical
activity of the muscle motor neuron is subject to influence from sensory input,
spinal reflexes, inhibitory interneurons, and neural synaptic CNS input.
(Bentley 1996) Control of muscle length, posture and tone by neural receptors
(Golgi tendon organ proprioceptors) may be
"disturbed" during intense exercise, fatigue and heat, resulting in
heightened motor neuron activity producing the "rigor complex" known
as a muscle cramp. The immediate treatment for reducing a cramp is to lengthen
muscle spindles (stretch), and apply afferent pressure to the heart of the
muscle. Researchers from the literature insist that many variables affecting a
host of other variables may be isolated, but the single cause of muscle cramps
is inconclusive to date. The depletion of muscle ATP, tissue stores of
electrolytes in solution, and micronutrient energy enzymes are three such
variables which must be replenished during intense or prolonged exercise in the
heat if muscle cramps are to be avoided.
A "Rigor Complex" or muscle cramp may result when Adenosine Triphosphate (ATP) is not available within a muscle cell. ATP is the energy source produced by muscle mitochondrial cells during muscle shortening or contraction. Specific ATP binding sites (on myosin protein heads within muscle filaments) store ATP from Adenosine Diphosphate (ADP) and Phosphate (Pi), as the result of ATP breakdown after energy expenditure. Inside muscle filaments the ATP-bearing myosin head attaches itself to an actin protein head. When the myosin head binds to the actin the result is a shortening of the muscle to full state contraction, known as a "Rigor Complex". Biochemical reactions initiate a responsive release of the myosin head from its attraction to the actin head, relaxing the contractile state, restoring homeostatic balance and resupplying spent ATP from ADP and Pi byproducts of energy metabolism. Calcium bound to Troponin-C must be removed so that Tropmyosin can again move into a blocking position between the actin and myosin heads. Speculation exists that two primary causes for exertional cramps are (1) the lack of fresh reformed ATP, (2) the release of Calcium from Troponin-C for migration to sarcoplasmic retiniculum is biochemically incomplete or interrupted.
The primary fuel source for ATP synthesis is carbohydrates (muscle glycogen or blood glucose) while secondary sources are provided by fatty acids, when carbohydrate stores deplete to low levels. Very minute amounts are also cannibalized from lean muscle mass, (especially branched chain amino acids, BCAA's). The rate of ATP synthesis from carbohydrates is 1.0 mol/minute, but it is only 0.5 mol/minute from fatty acids. (Zambraski 1976) Muscle glycogen and blood glucose stores yield double the replenishing rate for ATP energy substrate metabolism. During anaerobic energy metabolism or any conditions which may raise internal temperatures, carbohydrate synthesis rates for ATP may raise to as high as 2.4 mol/minute! Researchers have found that the efficient use of fatty acid stores during recyclic transition to ATP for energy metabolism is enhanced by repeated cyclic aerobic stress. (Hermansen 1967) Application of endurance training will increase both the efficiency of fatty acid metabolism and the stores of muscle glycogen, reducing the predisposed ATP-depletion which in turn may impose a series of unwanted muscle cramps.
Chaudry (1982) stated that exogenous ATP crosses cellular membranes when depletion occurs within myosin units. ATP or ATP substrates may access human physiology orally, sublingually, or intravenously. Carbohydrates, oral ATP, or oral-sublingual ATP may be consumed for enhancing endurance performance, and preventing muscle exertion or heat stress cramps.
Muscle cramps are sudden electrically active contractions elicited by motor neuron hyperexcitement, or the inability of the myosin head to release from its attraction to the actin head protein. Some have assumed that exertional cramping may be the result of fluid electrolyte improprieties. Modern research science is divided on the importance of sweat losses of sodium, chloride, potassium, and magnesium and regards them as trivial, therefore not evidential as a primary cause of the "Rigor Complex". (Maughn 1986, Miles & Clarkson 1994) Chaudry (1982), however, added an interesting footnote from his unpublished observations," There is some preliminary evidence which indicates that ATP translocation is associated with sodium, potassium, -ATP-ase." Balance of fluid ratio and electrolyte intracellular to extracellular levels in the presence of Adenosine Triphosphate and its Adenosine Triphosphatase enzyme would appear mandatory for optimum muscle function. Bergeron (1996) reports of a nationally ranked tennis player who experienced unexplainably from muscle heat cramps during play. Medical examinations and history were unremarkable, and were confirmed by in-patient blood serum profiles. On court evaluation of sweat loss composition and a 3-day dietary analysis revealed that sodium loss during play far exceeded dietary intake. Increase of daily dietary sodium chloride eliminated heat cramps reoccurrence. Among the elderly, frequent cramping caused by compromised circulation may provide a model for the extreme, but similar physiological environment experience by an athlete during heat stress. Idiopathic cramping among older people was found to be directly related to electrolyte deficiencies, heat stress, metabolic myopathies, thyroid disease, dystonias, reaction to medications, and hemodialysis. (Riley & Antony 1995) These researchers have suggested treatment consisting of stretching, oral Vitamin E, and/or Quinine Sulfate supplements. They further concluded that no single treatment resulted in one effective remedy.
Dr. T.D. Noakes (1991) summarizes exertional cramps as follows: (1) Exhaustion related to glycogen depletion for fresh ATP replenishment, (2) Excessive fluid volume to electrolyte profile. He suggests intake of 16 ounces fluid using 60-120 grams carbohydrates prior to and during each hour of prolonged endurance training.
During extraordinary muscle energy metabolism, mineral flux may deplete or vary normal electrolyte homeostatic ratios. Calcium is the most abundant mineral and the 5th most abundant element found in the human body. It is therefore vital to muscle contraction, nerve transmission, blood clotting, and a multiple of metabolic functions. Bones act as a calcium reservoir, providing it when blood serum values decline below 10 mg/100ml, regulated by parathyroid hormonal controls. Over half of the serum calcium is ionized, while the remainder is protein-bound or associated with organic and inorganic acids. Protein-bound calcium acts as a weak electrolyte, while metabolically active ionized calcium is used by the blood and serum for muscle contraction.
During exercise blood calcium falls, arousing the parathyroid gland to stimulate vitamin D activation of ionized calcium release from bone stores. As calcium levels are reinstated, parathyroid stimulation halts, and calcitonin from the thyroid is released, thereby halting bone resorption/release. (Garrison & Somer 1995) Calcium depletion sensitizes neural muscle tetany. Calcium is vital to synaptic release of neurotransmitter substances which enable nerves to excite and relax during muscle contractions. The volume of neurotransmitter release is proportionate to ionized calcium concentration in the terminal membrane, and inversely proportionate to magnesium concentration. Serotonin, Acetylcholine, and Norepinephrine transmitter levels are affected by the enzymatic influences of both calcium and magnesium upon striated and smooth muscle contraction. Without substantial amounts of calcium, the glycogen enzyme, phosphorylase kinase is not able to breakdown glycogen to glucose-6-P for energy metabolism. Calcium also activates the adenosine triphosphatase enzyme for the hydrolysis of ATP. Dr. Balch (1990) stated that muscle cramps are "Commonly caused by a calcium-magnesium imbalance and/or vitamin E deficiency." He recommends a daily dietary or supplemental intake of 2:1 Calcium (1500 mg.) to Magnesium (750 mg.) and 400-1000 IU of vitamin E for prevention of muscle cramps. Substantial research noted leg cramps during pregnancy were caused by alterations of calcium metabolism.(Pitikin 1983) Studies by Hammar(1987), Knowles(1981), Odendahl(1974), and Page(1953) further suggest that supplementation of calcium or reduction of phosphorus may prevent and relieve such cramping in the legs. Possibly related to calcium balance, reduced serum magnesium has been associated with tetany and muscle cramping. (Russell 1985) Similar findings have confirmed evidence when supplemental ingestion of calcium and magnesium relieved tetanical symptoms. (Classen & Helbig 1984)
The Cations and Anions of fluid electrolyte composition are never static, but are proportionately balanced within the compensatory rates of metabolic activity both intracellularly and extracellularly. Pivotal losses of calcium and magnesium from muscle exhaustion, fluid dehydration from sweat loss, depletion of extracellular cation stores of sodium or intracellular cation stores of potassium are significant factors staged for muscle failure, I.E., a cramp event. While the previously mentioned case study of a nationally-ranked tennis player whose severe exertional muscle cramps were solved by dietary sodium supplementation, modern science considers one solution insignificant in terms of scientific methodology for settling on conclusive evidence. Muscle cramps have been associated with a hypokalemic tissue environment, and were readily relieved by potassium supplements. (Portier 1973) Glatzel (1980) was successful treating nocturnal cramps with dietary sodium chloride. Strong evidence exists for the role of electrolyte depletion associated with muscle spasms, cramps, and seizures, but inconclusive from present research literature. In fact, depletion of muscle glycogen, fluid overhydration, and the lack of vitamin substrates with enzymatic influence on fuel selection are also presently considered suspects.
Vitamin E supplementation was shown to relieve muscle cramping in several clinical observations by Lotzof (1977) and Cathcart (1972). Two separate experimental studies by Ayres (1969 & 1974) confirmed the findings of Cathcart and Lotzof. Dr. Balch's research of the literature (1990) recently was added to the aforementioned scholarship. Nocturnal muscle spasms and distal/peripheral small muscle cramps were relieved by oral ingestion of vitamin B-6(Pyrodoxine) in the studies performed by Ellis and Presley (1973).
Depletion of the immediate and most easily converted fuels for ATP conversion (Carbohydrate stores: muscle glycogen & blood glucose) may prompt a temporary deficiency which results in muscle failure or "Rigor Complex". Similar deficiencies in calcium spent during extreme exercise may further trigger imbalances in its ideal ratio of 2:1 to magnesium associated with muscle spasms and cramping. Too much or too little tissue fluid volume affect the working ratios of intracellular potassium to extracellular sodium, which also affects substrate anion stores in both. For example, exertional dehydration and electrolyte sweat loss per hour are as follows: (Electrolyte per volume of fluid) Sodium=2grams/liter, Chloride=1gram/liter, Potassium=0.2gram/liter, Magnesium=0.1gram/liter. While these electrolyte losses are trivial, depletion levels after 3 hours are significant, resulting in inefficient muscle contraction, spasms, or cramps in athletes who have not conditioned themselves to endure such deficiencies.
Fluid replacement and fuel replacement are primary for prolonging endurance and preventing muscle failure. Few athletes realize that metabolism of muscle glycogen releases as much as 2 liters fluid during prolonged endurance activity. Back-of-the-pack ultrarunners, who linger, drinking while at aid stations, predispose themselves to dilutional hyponatremia from too much water intake, while those at the front-of-the-pack tend to dehydrate (Noakes 1990). Runners who severely suffer from dilutional hyponatremia may be dangerously exposed to total muscle failure, and death. During excessive rates of exertional metabolism, depletion of fuel sources, fluid loss or fluid intake, mineral imbalances, electrolyte ratio flux, and enzymatic vitamin expenditure must be replenished in order to prevent a muscle from seizing.
A. Subject physiology to specific training and preparatory conditioning.
B. Replenish carbohydrate losses before, during, and after training. The body can metabolize ingestion of 60-120 grams per hour for storage of fuel source.
C. Fluid intake of 16 ounces per hour, or 4 ounces fluid every 15 minutes will prevent dehydration and hyponatremia, which may result when too much fluid is consumed.
D. After 3 hours exercise, precise, balanced electrolyte replacement is required and necessary in order to prevent muscle cramping.
E. Intake of Amino Acids (especially branched-chain Amino Acids, BCAA's) before, during and after exercise may contribute to reduced muscle failure or spasms.
F. A balanced exact ratio of chelated vitamins is necessary for antioxidant and enzymatic activity during high rates of energy demands contributes to efficient muscle function and endurance during heat stress conditions.
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Everyone has felt the sharp pain of a muscle that contracts suddenly and refuses to relax. Usually muscle cramps last only a few minutes. Sometimes they occur at night. You might have called it a "Charley horse."
These cramps or spasms are caused by one or
more of the following:
· working a muscle too hard,
· staying in the same position too long,
· not drinking enough water while exercising or working,
· doing a new activity that your muscles are not used to,
· poor nutrition, and
· not stretching before and after a physical activity.
Regular exercise and drinking water will prevent most of this type of cramping.
Sometimes muscle
cramps or spasms mean you have a more serious medical problem. You may need
immediate medical attention. See a health care professional if you have any of
the following:
· frequent muscle cramps or spasms,
· cramps in the abdominal area,
· muscle cramps after overheating, or
· cramps or spasm that do not relax.
Some treatments for muscle spasm and cramps include:
· Gentle massage to the cramped muscle.
· Stretch the muscle out of the spasm slowly.
· Alternate heat and cold on the muscle for 1 to 2 minutes for a total of 15 minutes. Then massage and stretch again.