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The aetiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood. This review focuses on the physiological basis for skeletal muscle relaxation, a historical perspective and analysis of the commonly postulated causes of EAMC, and known facts about EAMC from recent clinical studies. Historically, the causes of EAMC have been proposed as (1) inherited abnormalities of substrate metabolism ('metabolic theory') (2) abnormalities of fluid balance ('dehydration theory'), (3) abnormalities of serum electrolyte concentrations ('electrolyte theory') and (4) extreme environmental conditions of heat or cold ('environmental theory'). Detailed analyses of the available scientific literature including data from recent studies do not support these hypothesis for the causes of EAMC. In a recent study, electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex. In two animal studies, abnormal reflex activity of the muscle spindle (increased activity) and the Golgi tendon organ (decreased activity) has been observed in fatigued muscle. We hypothesize that EAMC is caused by sustained abnormal spinal reflex activity which appears to be secondary to muscle fatigue. Local muscle fatigue is therefore responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity. Muscles which cross two joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping. Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.
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PMID:Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis. 923 53

It is the position of the American College of Sports Medicine that adequate fluid replacement helps maintain hydration and, therefore, promotes the health, safety, and optimal physical performance of individuals participating in regular physical activity. This position statement is based on a comprehensive review and interpretation of scientific literature concerning the influence of fluid replacement on exercise performance and the risk of thermal injury associated with dehydration and hyperthermia. Based on available evidence, the American College of Sports Medicine makes the following general recommendations on the amount and composition of fluid that should be ingested in preparation for, during, and after exercise or athletic competition: 1) It is recommended that individuals consume a nutritionally balanced diet and drink adequate fluids during the 24-hr period before an event, especially during the period that includes the meal prior to exercise, to promote proper hydration before exercise or competition. 2) It is recommended that individuals drink about 500 ml (about 17 ounces) of fluid about 2 h before exercise to promote adequate hydration and allow time for excretion of excess ingested water. 3) During exercise, athletes should start drinking early and at regular intervals in an attempt to consume fluids at a rate sufficient to replace all the water lost through sweating (i.e., body weight loss), or consume the maximal amount that can be tolerated. 4) It is recommended that ingested fluids be cooler than ambient temperature [between 15 degrees and 22 degrees C (59 degrees and 72 degrees F])] and flavored to enhance palatability and promote fluid replacement. Fluids should be readily available and served in containers that allow adequate volumes to be ingested with ease and with minimal interruption of exercise. 5) Addition of proper amounts of carbohydrates and/or electrolytes to a fluid replacement solution is recommended for exercise events of duration greater than 1 h since it does not significantly impair water delivery to the body and may enhance performance. During exercise lasting less than 1 h, there is little evidence of physiological or physical performance differences between consuming a carbohydrate-electrolyte drink and plain water. 6) During intense exercise lasting longer than 1 h, it is recommended that carbohydrates be ingested at a rate of 30-60 g.h(-1) to maintain oxidation of carbohydrates and delay fatigue. This rate of carbohydrate intake can be achieved without compromising fluid delivery by drinking 600-1200 ml.h(-1) of solutions containing 4%-8% carbohydrates (g.100 ml(-1)). The carbohydrates can be sugars (glucose or sucrose) or starch (e.g., maltodextrin). 7) Inclusion of sodium (0.5-0.7 g.1(-1) of water) in the rehydration solution ingested during exercise lasting longer than 1 h is recommended since it may be advantageous in enhancing palatability, promoting fluid retention, and possibly preventing hyponatremia in certain individuals who drink excessive quantities of fluid. There is little physiological basis for the presence of sodium in n oral rehydration solution for enhancing intestinal water absorption as long as sodium is sufficiently available from the previous meal.
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PMID:American College of Sports Medicine position stand. Exercise and fluid replacement. 930 99

The aim of this study was to examine whether ingesting water alone, or dextrose (7.5 g x 100 ml(-1)) with electrolytes, or fructose/corn solids (7.5 g x 100 ml(-1)) (400 ml every 20 min) would reduce the perceived exertion associated with 16 km (3 h) walking/running in the heat compared with that perceived during exercise with no fluid intake. Perceived exertion was assessed at 1-h intervals during exercise. Blood samples, required for analysis of blood glucose, plasma sodium, plasma osmolality and plasma volume, were obtained prior to exercise and at 1-h intervals during the exercise; further samples were obtained 1-h intervals for 3 h following the exercise. Drinking fluids at regular intervals reduced the level of perceived exertion. In the test during which no fluid was ingested, body mass decreased by 4.9 (0.4) kg [mean (SEM)], but decreased less with ingestion of either the dextrose/electrolytes or fructose/corn solids solutions, or water alone [1.3 (0.2) kg, 1.6 (0.3) kg and 2.0 (0.1) kg, respectively]. Plasma volume fell by 17% when taking no fluid, but fell less when ingesting fluids. Blood glucose fell significantly (P < 0.01) when taking no fluid and rose to 8.4 (1.3) mmol x l(-1) (P < 0.001) and 6.8 (1.1) mmol x l(-1) (P < 0.01) with ingestion of the dextrose/electrolytes or fructose/corn solids solutions, respectively. Urine output was greater with ingestion of water than with any of the other drinks. Six subjects experienced fatigue during exercise with no fluid and failed to complete the exercise. These results suggest that fatigue was caused by several interacting factors: a fall in blood glucose and plasma volume, dehydration, and neuroglycopenia. Taking fluids during exercise reduced the strain and the rating of perceived exertion; this was better achieved by ingesting a dextrose/electrolytes solution.
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PMID:Dehydration in soldiers during walking/running exercise in the heat and the effects of fluid ingestion during and after exercise. 940 63

Many types of drugs are used by athletes to improve performance. This paper reviews the literature on 3 categories of drugs: those that enhance performance as stimulants (amphetamines, ephedrine, and cocaine), those that are used to reduce tremor and heart rate (beta-blockers) and those involved in bodyweight gain or loss (anabolic-androgenic steroids, growth hormone, beta 2-agonists, and diuretics). Limitations of research on these drugs as they relate to performance enhancement are also discussed. The numerous studies that have assessed the effects of amphetamines on performance report equivocal results. This may be due to the large interindividual variability in the response to the drug and the small sample sizes used. Most studies, however, show that some individuals do improve exercise performance when taking amphetamines, which may be attributed to their role in masking fatigue. As a stimulant, ephedrine has not been found to improve performance in the few studies available. More recently, ephedrine has been purported to be effective as a fat burner and used by athletes to maintain or improve muscle mass. Although research on individuals with obesity supports the use of ephedrine for fat loss, no studies have been done on athletes. The few studies of cocaine and exercise suggest that little to no performance gains are incurred from cocaine use. Moreover, the sense of euphoria may provide the illusion of better performance when, in actuality, performance was not improved or was impaired. beta-Blockers have been found to reduce heart rate and tremor and to improve performance in sports that are not physiologically challenging but require accuracy (e.g. pistol shooting). However, there is evidence that some individuals may be high responders to beta-blockers to the extent that their heart rate response is so blunted as to impair performance. Although equivocal, several studies have reported that anabolic-androgenic steroids increase muscle size and strength. However, most studies are not well controlled and use insufficient drug doses. One recent well controlled study did find an increase in muscle mass and strength with supraphysiological doses, and the improvements were greater in participants who were also resistance training. There is little information available on the effects of growth hormone on muscle mass or performance in athletes, although data suggest that growth hormone administration does not increase muscle protein synthesis. beta 2-Agonists, such as clenbuterol and salbutamol, when administered orally appear to improve muscular strength due to their potential role in increasing muscle mass. However, studies have not been done using athletes. Diuretics results in a loss of body water and hence bodyweight that can be advantageous for sports with strict bodyweight classifications. There is insufficient evidence on possible performance decrements in the field that could result from dehydration induced by the diuretics. Overall, the most significant concern in studies of drug use is the large inter-individual variability in responses to a drug. Further studies are needed to understand why some individuals are more responsive than others and to assess whether the responses are consistent for a given individual. Most studies of drug effectiveness have not used athletes. The effectiveness of many drugs may be reduced in highly trained athletes because there is a lower margin for improvement.
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PMID:Drugs and sport. Research findings and limitations. 942 62

Cold weather injury (CWI) reports covering 272 U.S. Army soldiers from September 1990 to May 1995 were reviewed. First- and second-degree frostbite accounted for 99.3% of all injuries. Although some soldiers had extensive lost duty time from their injuries, no one suffered tissue loss during the 5-year period. Fifty-one percent of injuries occurred during field training. Thirty-six percent occurred while engaging in garrison activities, including physical training, which accounted for 15% of all CWIs. Twelve percent of all injuries occurred during off-duty time. Seventy-one percent of CWIs occurred when the wind-chill factor was at or below -20 degrees F (-29 degrees C). Male African-American soldiers appear to be significantly more susceptible to frostbite than male Caucasian soldiers, especially with regard to frostbite of the distal extremities (relative risk = 3.94; 95% confidence interval = 2.77-5.59). Other identified risk factors include inadequate clothing, wet clothing, dehydration, inactivity, fatigue, and previous CWIs.
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PMID:Cold weather injuries among U.S. soldiers in Alaska: a five-year review. 943 82

To examine the effects of rapid dehydration on isometric muscular strength and endurance, seven men were tested at baseline (control) and after a dehydration (dHST) and a euhydration (eHST) heat stress trial. The dHST consisted of intermittent sauna exposure until 4% of body mass was lost, whereas the eHST consisted of intermittent sauna exposure (same duration as dHST) with water replacement. Peak torque was determined for the knee extensors and elbow flexors during three isometric maximal voluntary contractions. Time to fatigue was determined by holding a maximal voluntary contraction until torque dropped below 50% peak torque for 5 s. Strength and endurance were assessed 3.5 h after the HSTs (no food or water intake). Body mass was decreased 3.8+/-0.4% post dHST and 0.4+/-0.3% post eHST. Plasma volume was decreased 7.5+/-4.6% and 5.7+/-4.4%, 60 and 120 min post dHST, respectively. A small (1.6 mEq x L[-1]) but significant increase was found for serum Na+ concentration 60 min post dHST but had returned to predehydration level 120 min post dHST. Serum K+ and myoglobin concentrations were not affected by HSTs. Peak torque was not different (P > 0.05) among control, dHST, and eHST for the knee extensors (Mean (Nm)+/-SD, 285+/-79, 311+/-113, and 297+/-79) and elbow flexors (79+/-12, 83+/-15, and 80+/-12). Time to fatigue was not different (P > 0.05) among control, dHST and eHST for the knee extensors (Mean (s)+/-SD. 42.4+/-11.5, 45.3+/-7.6, and 41.8+/-6.0) and elbow flexors (48.2+/-8.9, 44.0+/-9.4, and 46.0+/-6.4). These results provide evidence that isometric strength and endurance are unaffected 3.5 h after dehydration of approximately 4% body mass.
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PMID:Effects of dehydration on isometric muscular strength and endurance. 950 58

1. Magnocellular neurosecretory cells (MNCs) in the rat hypothalamus adopt a phasic pattern of spike discharge under conditions demanding enhanced vasopressin release, such as during dehydration or hemorrhage. The emergence of phasic firing minimizes the occurrence of secretory fatigue from the axon terminals of MNCs, thereby maximizing vasopressin release from the neurohypophysis. 2. Intracellular and whole-cell recordings from hypothalamic slices or explants in vitro have shown that phasic firing is supported by the presence of a plateau potential which arises from the summation of spike depolarizing afterpotentials (DAPs). Modulatory actions of neurotransmitters on the amplitude of the DAP, therefore, represent possible mechanisms by which the expression of phasic firing may be regulated in vivo. 3. Here we review the basis for phasic firing in MNCs of the rat supraoptic nucleus and present recent findings concerning the direct and indirect mechanisms through which selected neurotransmitters have been found to regulate the amplitude of DAPs.
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PMID:Extrinsic modulation of spike afterpotentials in rat hypothalamoneurohypophysial neurons. 952 26

During endurance exercise in the heat athletes lose 1-21/h of fluid due to thermoregulatory sweating. The ensuing dehydration is accompanied by higher and faster increases in core temperature, which per se can cause fatigue. The main cardiovascular consequences of combined dehydration and hyperthermia [1 degree C higher core temperature and 3-4 kg (4%) body weight loss] are the significant reductions in cardiac output (3 l/min), muscle blood flow, skin blood flow and blood pressure. Separately, however, hyperthermia (i.e., 39.3 C) and dehydration do not significantly reduce cardiac output or blood pressure. In conclusion, the superimposition of dehydration on hyperthermia during exercise in the heat causes greater alterations in cardiovascular function that make the dehydrated athlete much less able to cope with hyperthermia.
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PMID:Separate and combined influences of dehydration and hyperthermia on cardiovascular responses to exercise. 969 13

Many approaches have been undertaken to understand Alzheimer's disease (AD) but the heterogeneity of the etiologic factors makes it difficult to define the clinically most important factor determining the onset and progression of the disease. However, there is increasing evidence that the previously so-called "secondary factors" such as a disturbed glucose metabolism, oxidative stress and formation of "advanced glycation endproducts" (AGEs) and their interaction in a vicious cycle are also important for the onset and progression of AD. AGEs are protein modifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia. Oxidative modifications are formed by a complex cascade of dehydration, oxidation and cyclisation reactions, subsequent to a non-enzymatic reaction of sugars with amino groups of proteins. Accumulation of AGE-crosslinked proteins throughout life is a general phenomenon of ageing. However, AGEs are more than just markers of ageing since they can also exert adverse biologic effects on tissues and cells, including the activation of intracellular signal transduction pathways, leading to the upregulation of cytokine and free radical production (oxidative stress). Oxidative stress is involved in various divergent events leading to cell damage, including an increase in membrane rigidity, DNA strand breaks and an impairment in glucose uptake. In addition, other age-related metabolic changes such as depletion of antioxidants or decreased energy production by a disturbed glucose metabolism diminish the ability of the cell to cope with the effects of radical-induced membrane, protein and DNA damage. With our improving understanding of the molecular basis for the clinical symptoms of dementia, it is hoped that the elucidation of the etiologic causes, particularly the positive feedback loops involving radical damage and a reduced glucose metabolism, will help to develop novel "neuroprotective" treatment strategies able to interrupt this vicious cycle of oxidative stress and energy shortage in AD.
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PMID:Alzheimer's disease--synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. 972 Sep 73

Two patients, men aged 47 and 64 years, were found in a comatose condition in their homes, after a period of fatigue, polyuria and polydipsia. They had not been known to suffer from diabetes mellitus, but now displayed a hyperglycaemic hyperosmolar non-ketoacidotic disorder as the first manifestation of diabetes mellitus type 2. In that condition, just sufficient insulin is present to counteract ketone production, but not enough to prevent hyperglycaemia. Neurological and thromboembolic manifestations, possibly fatal, may result from severe dehydration brought about by a vicious circle in which osmotic diuresis reduces the effective circulating volume, causing renal function to decrease and hyperglycaemia to increase even more. Both patients recovered fully after adequate treatment with solutions of NaCl and glucose.
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PMID:[The hyperglycemic dehydration syndrome]. 986 7


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