American College of Sports Medicine position stand. Exercise and fluid replacement.

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.

An inquiry into the role of cardiac filling pressure in acclimatization to heat.

During the first exposure of exercising subjects to hot environments (30-50 degrees C), cardiac output, heart rate, and body temperature increase over that seen in cool environments, while stroke volume decreases. If daily heat exposures occur, during the second heat exposure, heart rates and rectal temperatures are decreased from day 1 while cardiac output is maintained. This decrease in physiological strain occurs with little or no increase in evaporative heat loss. The alleviating agent appears to be an expansion of plasma volume. Several brief studies have indicated decreases in cardiac filling pressure during exercise in heat, and though inferential, it appears that the progressive increase in plasma volume during the first five to six days of heat exposure assists in maintaining cardiac filling pressure. Later, with increased evaporative heat loss due to increased sweat secretion, the mechanism of supplying increased volume to maintain cardiac filling is changed; fluid is transferred from extravascular to intravascular compartment, thus protecting venous return and cardiac filling pressure. These statements are based on limited data, and there is need of experiments designed to confirm or deny certain conclusions as to the role of cardiac filling pressure in acclimatization to heat.

The effects of body position and exercise on plasma volume dynamics.

We examined the plasma volume changes associated with a protocol of either exercise or controlled rest under identical positional and ambient conditions. Nine healthy adult males rode (E) and on another occasion sat quietly (C) on a cycle ergometer for 30 min. Ten minutes of cycle exercise immediately followed the resting C protocol. Ambient temperature was 30 degrees C (rh = 35%) and exercise load was equal to 50% of peak VO2. Venous blood samples were obtained with subjects both in the supine and seated positions prior to all experiments. Additional blood was drawn during minutes 1, 5, 10, and 30 in both experimental conditions. A final sample was taken during C after the 10 min exercise. Moving from the supine to a seated position resulted in an average loss of 162 ml of plasma across all experiments. During the E condition a further reduction in plasma volume (76 ml) occurred by one minute of exercise. Plasma volume stabilized by 5 min of exercise under the E protocol. During the C condition, subsequent fluid loss (98 ml) was not apparent until 10 min after the first seated sample and totalled 176 ml at the end of 30 min of rest. Ten minutes of cycling at the end of the C experiment resulted in a further plasma volume reduction of 137 ml. Plasma protein and albumin contents decreased by 5 min of exercise in E and by 30 min of rest in C. [Na+] and [Cl-] did not change in either condition but a rapid increase in [K+] during exercise indicated an addition of potassium to the vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exercise detraining and deacclimation to the heat on plasma volume dynamics.

The effects of the discontinuation (DET) of an endurance training/heat acclimation (T/A) program on vascular volumes were studied in 16 adult males. Resting and exercise blood volume dynamics were examined prior to and during an exercise task performed after completion of T/A (CT1) and again at the end of DET (CT2). T/A consisted of cycling at 60% of peak VO2 for 90 min per day, 6 days per week, for 4 weeks. Ambient temperature was 20 degrees C for the first 3 weeks and 40 degrees C for the last week (rh = 30-35%). Subjects were randomly assigned to one of the following DET conditions: 1) cycling one day per week at 40 degrees C, 2) cycling one day per week at 20 degrees C, 3) resting one day per week at 40 degrees C, 4) control. The exercise tasks consisted of 60 min of continuous cycle ergometer exercise at 50% of peak VO2 (Ta = 30 degrees C, rh = 35%). Although significant differences were found between CT1 and CT2, there were no interactions between the various DET conditions. Resting red cell volume decreased 98 ml and plasma volume decreased 248 ml following DET. A reduction in plasma protein content accounted for 97% of the decrease in plasma volume. Hemoconcentration occurred during exercise in both CT1 and CT2, while there were slight increases in plasma [Na+] and [Cl-] and a rapid rise in [K+]. It appears that a single exercise and/or heat exposure per week was not different from complete cessation of endurance exercise in the heat with regard to maintenance of the various vascular volumes.

Plasma volume and protein content in progressive exercise: influence of cyclooxygenase inhibitors.

Non-steroidal anti-inflammatory compounds such as ibuprofen and naproxen reduce volume loss in sheep following injection of endotoxin. We investigated whether these drugs would change the course of plasma volume reduction during progressive exercise on a cycle ergometer. Subjects [15 males; age (mean +/- SD), 26.3 +/- 8.3 yr; height, 180.3 +/- 4.5 cm; weight, 76.8 +/- 8.0 kg; peak VO2, 3.8 +/- 0.6 l.min-1] exercised for 5 min at 20, 30, 40, 50, 60, and 70% of peak VO2 with and without a 24-h pre-treatment with either ibuprofen or naproxen. The two tests for each subject were done a week apart. Blood samples were drawn before and after each exercise level. Based on blood analysis, cyclooxygenase inhibitors significantly altered the retention of protein within the vascular volume during exercise. That is, the degree of concentration of protein per unit of plasma volume loss during exercise was less with drug treatment. In spite of this, ibuprofen and naproxen did not influence fluid shifts during exercise. Use of cyclooxygenase inhibitors probably increased the permeability of vascular endothelium to large molecules, which was only evident when hydrostatic and osmotic events in muscle capillaries caused an increase in bulk flow across the capillary walls.

Changes in blood pressure, heart rate and blood constituents during heat exposure in men with elevated blood pressure.

Although the vascular volume response of hypertensive men during exercise has been rather well characterized, the effect of resting heat exposure in this patient population has not been examined. This was done in the present report in seven men with high blood pressure (BP) (i.e., diastolic pressure greater than 12 kPa (90 mmHg) upon initial interview) and 5 normotensive control subjects. 50 min after each subject had consumed an amount of water equal to 1% of his body weight, he reclined on a cot. 10 min later the subject was carried into an environmental chamber equilibrated at Tdb = 45 degrees C, Twb = 28 degrees C. Free-flowing venous blood samples were obtained from a cubital vein, and BP and heart rate were measured, before the heat exposure and at 15 min intervals during the experiment. Within 30 min systolic, diastolic and mean BP of the high BP subjects had decreased to normal levels; no BP changes were detected in normotensive subjects. Accompanying this depressor response was an exaggerated elevation in plasma glucose concentration. No alterations were found with haematocrit, plasma osmolality or electrolytes, or total protein and albumin. The data suggest that heat exposure may have been more stressful for the subjects with high BP than for their controls. This finding implies that phasic depressor responses may be as important as phasic pressor episodes in the aetiology of established essential hypertension.

Effect of arginine vasopressin, acetazolamide, and angiotensin II on CSF pressure at simulated altitude.

To test the hypothesis that arginine vasopressin (AVP) in the cerebral spinal fluid (CSF) influences CSF dynamics at simulated altitudes, cannulae were bilaterally implanted into the lateral ventricles of rabbits and rats. Recordings of CSF pressures at ambient and at various reduced barometric pressures identified an increase in CSF pressure in animals at simulated altitudes. Samples of CSF collected before and immediately after altitude exposures and assayed for AVP did not show a significant change in AVP concentration. Brain water content did not change after 6-8 h of reduced barometric pressure. Intraarterial injections of acetazolamide reduced CSF pressures, whereas intraventricular injection had no effect. Intraventricular angiotensin II (AII) elevated CSF pressures both at ambient (744-755 mm Hg) and reduced barometric pressures. When AII was preceded by saralasin, an AII blocker, the rise in CSF pressure with AII injection was prevented. Indeed, saralasin given alone, reduced or prevented the rise in CSF pressure seen at simulated altitudes. Intraventricular AVP did not influence CSF pressures nor did prostaglandins E2 and F1 alpha and norepinephrine. In AVP-deficient (Brattleboro) rats, response to intraventricular AVP depended on barometric pressure; i.e. CSF pressure rose when the rat was exposed to reduced barometric pressures and fell when the rat was exposed to ambient pressure. We suggest that hypobaric stress could cause an increase in AII content of the central nervous system which, in turn, would lead to an increase in CSF pressure. The exact mechanism of CSF pressure increase after AII increase remains to be investigated.

Vascular volume changes during cycling and stepping in women at two hydration levels.

Five female Caucasians were studied in a hot, wet environment (32.2 degrees C dry bulb, 30 degrees C wet bulb) during both cycle ergometer exercise and block stepping at exercise intensities (30-40% of the subjects's VO2 max) which produced similar heart rates. During each type of exercise, the women were studied once following 24 h water deprivation and once 60 min after ingestion of an amount of water equal to 1% of their body weight. Venous blood samples were obtained before, and at 10 min intervals during each of the four 60-min exercise session. Hemoconcentration and osmoconcentration were observed during both types of exercise, with more rapid increases in these variables occurring during ergometer exercise compared to block stepping. While the fluid status manipulation was effective in altering the pre-exercise osmolalities by an average of 9 mosmol . kg-1, it had little effect on vascular volume dynamics during either type of exercise. Similarly, increases in heart rate and body temperature during exercise were not altered by the water balance of the subject. The pattern of vascular volume changes during exercise in women, therefore, seems more sensitive to exercise mode than to pre-exercise water balance.

A subcutaneous capsule for long-term studies.

In assessing interstitial fluid dynamics, perforated capsules have a limited existence because of the ingrowth of connective tissue. A permanently patent capsule (1 yr) can be obtained by implanting 1.9-cm lengths of Tygon tubing (OD 7.9 mm, ID 4.8 mm). After implant, the capsule is invested in connective tissue, and a thin strand of connective tissue invades both ends of the capsule. In 2-3 wk, the connective tissue joins in the capsule and there is no further ingrowth of connective tissue. This tissue bridge through the center of the capsule is richly vascularized, eventually containing small central arteries and veins. Protein content of capsule fluid was 50-60% of plasma, with albumin proportionately higher in the capsule. Intracapsule pressures averaged -2.08 mmHg. Communication between capsule contents and vascular volume appeared to be size-dependent in that the [35S]sulfate and [3H]inulin count could be measured in tail blood 5 min after intracapsule injection and it increased over 30 min. This did not occur with [14C]dextran (mol wt 70,000) and [14C]globulins (mol wt 150,000). This capsule appears to lend itself to long-term studies related to interstitial fluid dynamics and/or capillary exchange.

Lipofibromatous hamartoma of median nerve and ulnar nerve: surgical treatment.

Seven cases of lipofibromatous hamartomas of the median and ulnar nerve wee seen. Three were treated conservatively, and four had radical surgical excision. The three conservatively treated patients, seen over 20 years ago, were lost to follow-up. Four hand centers stated that these masses do not regress on conservative treatment. Follow-up evaluation of 1, 4, 9, and 20 years of the patients treated by radical surgery indicated that all patients had a useful, functional hand. All had complete range of motion in flexion and extension. Moving two-point discrimination was normal in two and abnormal in the older patient and in the patient whose tumor was resected at the wrist. If surgical treatment is decided upon for the large tumor masses, it is recommended that it be done early, distal to the wrist, and at age 2. Electromyographic studies do not demonstrate sensory nerve regeneration. Compensatory sensibility results obtained must be due to the reeducational capability in children. Radical surgical excision without nerve grafting is not recommended in adults because the potential for reeducation is limited. Some surgeons recommend and do nerve grafting following resection of the tumor when there are no remaining identifiable nerve fibers.

Influence of exercise type, hydration, and heat on plasma volume shifts in men.

Four male Caucasians were studied during cycle ergometer exercise and stair stepping in a hot wet environment (32 degrees C db, 30 degrees C wb) after exertion was equated by matching heart rates during training. With each exercise, one session was conducted after 24 h of water deprivation, the other 50 min after ingestion of an amount of water equal to 1% body weight. Venous blood samples were obtained 24 h before each exercise and before and at 10-min intervals during each exercise. No changes in osmolality were found during stair stepping. A progressive osmoconcentration, however, occurred during cycling after dehydration and an initial osmoconcentration with little subsequent change accompanied ergometer exercise after hydration. This latter effect was due to a consistent osmodilution in all subjects, but occurring at different times during the session in each. All attained an osmolality of 290 mosmol/kg before dilution. Because this value is above the threshold of arginine vasopressin release, this hormone may have been responsible for the osmodilution. Therefore, the preexercise osmolality and the rate at which the threshold for vasopressin release is attained may determine whether osmodilution, osmoconcentration, or both occur during exercise.

Effect of training and heat acclimation on exercise responses of sedentary females.

In an attempt to explain why females experience greater strain than males during exercise in the heat, we studied the responses of nine females to moderate exercise (40% VO2 max) on a cycle ergometer in a cool (16--20 degrees C, 30% rh) and a hot (45 degrees C, 30% rh) environment. Venous blood was sampled during rest, at the 40th min of exercise, and 25 min after exercise. Test runs were then performed during a 4-wk training program (phase 2) and during heat acclimation (phase 3). Except for K+, changes in plasma constituents during exercise were not altered by training or acclimation. A greater mean decrease in plasma volume occurred during exercise in a hot (11.9%) than in a cool (3.9%) environment. Plasma osmolality and protein concentration increased due to the loss of plasma water. The most striking response to training was a significant expansion of resting plasma volume (9.7%) and total protein content (11.6%). During acclimation, sweat rates increased and mean skin temperatures significantly decreased. Hemodilution reported in heat-acclimated men was not seen. The factor primarily responsible for improved cardiovascular fitness in these women during acclimation may have been the maintenance of a larger central blood volume.

Temperature regulation and hypohydration: a singular view.

Body temperatures of exercising humans who have been denied water are elevated when compared to hydrated controls. The simplest "explanation" for the elevated temperature is a decrease in sensitivity of the sweating mechanism. This and similar "explanations" do not direct attention to basic causes but only the result(s) of more fundamental aspects of regulatory physiology. Among the items considered in this speculative presentation are influences of changes in osmolarity, specific ions, peptide hormones, fluid shifts, and muscular contractions during exercise. A hypothesis is offered for consideration in explaining elevations of body temperature in exercise with and without water replacement. In general, the hypothesis relates changes in hypothalamic osmotic pressure and/or ionic constituents with fluid and ionic events in muscle during exercise. The fluid and ionic shifts are probably proportional to the amount of lean body mass engaged in dynamic exercise. Since blood volume has also been shown to be related to lean body mass, similar relative work loads should lead to similar changes in the osmotic and/or ionic environment of the hypothalamus, thus resulting in similar increases in body temperature during exercise. Hypohydration is superimposed on this basic response. Increases in body temperature of resting hypohydrated subjects appear to be due to increases in osmotic pressure and/or specific ion concentrations. During exercise, these changes are added to those induced by muscle contraction. The focal point of all such ionic and osmotic changes is thought to be neural processes within the hypothalamus.

Effects of exercise in the heat on body fluid distribution.

Experimental findings as to body fluid shifts during exercise appear to be greatly influenced by the mode of exercise (bicycle ergometer, treadmill, etc) and by the state of subject hydration. Endurance training has been shown to increase resting plasma (blood) volume. Also, endurance training results in modification of vascular volume dynamics during exercise, i.e. for a set task, plasma volume becomes stabilized. In the untrained individual, heat exposure exaggerates body fluid shifts during exercise. With training, stability of vascular volume is attained during heat exposure, but maximum protective responses towards exercise in heat is only gained upon heat acclimatization. Two items benefit the individual: an increase in the capacity of the sweat mechanism and an expansion of plasma volume. Benefits of training as to body fluid shifts are probably a result of metabolic changes within the active muscle mass.

Early response of plasma contents on exposure of working men to heat.

Twelve men block-stepped (35 W) 4 h/day for 12 days and were divided into two similar groups on the basis of Vo2max. All were exposed to 33.8 degrees C dry bulb, 32.7 degrees C wet bulb for 2 h (E1) while working (30% Vo2max). Venous blood was obtained at 10-min intervals during hour 1 and at 20-min intervals during hour 2. Group 1 was acclimatized to heat. Group II continued to train. The test exposure was repeated (E2). During E1 a trend toward hemodilution was evident but not significant for either group. Protein moved into the vascular volume and a decrease in plasma osmolarity was significant only after 30 min. For both groups during E2 significant hemodilution occurred during the first 10 min. Only group I remained significantly hemodiluted for 2 h. Protein movement and osmodilution again occurred in both groups. These results support earlier suggestions as to the mechanisms of hemodilution based on 1-h blood samples. Conflicting evidence as to the pressure or absence of hemodilution upon heat exposure is noted, and a hypothesis is proposed which appears to reconcile divergent results.

Acclimatization in a hot, humid environment: energy exchange, body temperature, and sweating.

Four trained young men, worked for 4 h/day at 43-50% of their maximum aerobic capacity for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Their thermal status was assessed using direct calorimetry. As a group, the men showed classical acclimization responses, but there were marked individual differences. The calorimetric analysis revealed that reductions in strain were associated with minor changes in heat balance confined to the first and last hours of exposure. Events occurring within the first 4 days appeared to have little effect on body temperatures. Significant decreases in body temperature took place only when sweat and evaporation rate increased. A 10% increase in evaporation rate was accompanied by a 30% increase in sweat rate and a 200% increase in unevaporated sweat; thus, there is a wasteful overproduction of sweat. By the 10th day skin temperature was confined to the level necessary to evaporate sufficient sweat to achieve thermal balance with a fully wet body surface. The efficiency of heat transport within the body did not change with acclimatization.

Acclimization in a hot, humid environment: cardiovascular adjustments.

Four trained young men worked for 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb, and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. This portion of the study was mainly concerned with central circulatory changes during acclimatization. The central circulatory adaptation to work in heat could be divided into four distinct phases: phase I (day 1) was characterized by a progressive fall in stroke volume (SV) during heat exposure but cardiac output (CO) was maintained above control values by high heart rates. Phase II (days 2 and 3) was marked by increases in SV ande decreases in heart rate but with little change in CO from phase I. During phase III (days 4-8 of acclimatization), CO increased due to increases in SV. Phase IV (days 6-8) was associated with decreases in rectal and skin temperature towards control levels. SV and HR both decline in this phase so that CO was not elevated greatly above control levels. The results indicated that central circulatory and temperature regulating events are not casually associated in acclimatization.