Dietary intake and biochemical, hematologic, and immune status of vegans compared with nonvegetarians.

Dietary and nutritional status of individuals habitually consuming a vegan diet was evaluated by biochemical, hematologic, and immunologic measures in comparison with a nonvegetarian group. On the basis of 4-d dietary records, the intake of female and male vegans tended to be lower in fat, saturated fat, monounsaturated fat, and cholesterol and higher in dietary fiber than that of vegetarians. With computed food and supplement intakes, vegan diets provided significantly higher amounts of ascorbate, folate, magnesium, copper, and manganese in both female and male participants. The body mass index (BMI; in kg/m(2)) of the vegans was significantly lower than that of the nonvegetarians and 9 of the 25 vegans had a BMI <19. Serum ferritin concentrations were significantly lower in vegan men but iron and zinc status did not differ between the sexes. Mean serum vitamin B-12 and methylmalonic acid concentrations did not differ; however, 10 of the 25 vegans showed a vitamin B-12 deficit manifested by macrocytosis, circulating vitamin B-12 concentrations <150 pmol/L, or serum methylmalonic acid >376 nmol/L. Vegans had significantly lower leukocyte, lymphocyte, and platelet counts and lower concentrations of complement factor 3 and blood urea nitrogen but higher serum albumin concentrations. Vegans did not differ from nonvegetarians in functional immunocompetence assessed as mitogen stimulation or natural killer cell cytotoxic activity.

Elevated plasma glucagon in amyotrophic lateral sclerosis.

This study shown an abnormality in glucagon levels that may explain the glucose intolerance, abnormal insulin reactions, and abnormal plasma amino acid levels seen in amyotrophic lateral sclerosis (ALS). We randomly administered two test meals, differing only in protein source (soy versus casein) at least 1 week apart and measured fasting and postprandial bloods for glucagon, insulin, and glucose levels in 11 ALS patients. With the soy test meal, glucagon levels were elevated in all ALS patients compared with controls: at fasting (237 +/- 111 versus 108 +/- 46 pg/ml, p less than 0.01) and 1/2 hour (389 +/- 94 versus 133 +/- 68 pg/ml, p less than 0.001), and 2 hours postprandial (379 +/- 75 versus 108 +/- 53 pg/ml, p less than 0.001). Glucagon levels after the casein test meal were also significantly elevated. Insulin was elevated by both test meals. Casein produced significant glucose intolerance.

Testing a mechanism of control in human cholesterol metabolism: relation of arginine and glycine to insulin and glucagon.

Eight men were given 2 casein meals, one with and one without a supplement of arginine and glycine, to measure the effect on plasma amino acids, insulin and glucagon. Supplementation resulted in increased levels of plasma glucagon, glycine and arginine, a tendency to decreased insulin and significantly lower insulin/glucagon ratio, tryptophan and tyrosine. The data suggest that insulin and glucagon, which control cholesterol metabolism, respond to dietary and postprandial plasma amino acid levels of arginine and glycine.

Chronic low-sodium diet in rats: responses to severe heat exposure.

To determine the effects of sodium (Na+) deficiency on the responses to severe heat stress (35.5 degrees C), immature (mean wt 150.4 g) male rats (n = 21) were fed a low-Na+ diet for 71 days. Rates of weight gain and food consumption were significantly (P less than 0.001) reduced in the low-Na+ group, whereas water consumption was unaffected. Prior to heat exposure circulating Na+ levels were unaffected by dietary Na+ restriction, but both circulating potassium (K+) and hematocrit levels were significantly (P less than 0.001) increased. After 24-h exposure to severe heat stress, circulating Na+ levels did manifest a significant (P less than 0.001) decrement in the low-Na+ group. K+ levels increased significantly (P less than 0.01) in the control group after 6 h of heat exposure but remained depressed in comparison with the low-Na+ group after 48 and 72 h. Although plasma renin activity (PRA) was not increased by chronic consumption of the low-Na+ diet or by severe heat exposure in the control group, severe heat stress in the low-Na+ group did elicit significant (P less than 0.005) increments in PRA after 24 h of exposure. Alternatively, plasma aldosterone levels were significantly (P less than 0.001) elevated by both the low-Na+ diet and heat stress. We concluded from these studies that chronic consumption of the low-Na+ diet had severe effects on hematologic, endocrinological, and thermoregulatory variables as well as thermal sensitivity to prolonged and sedentary exposure to severe heat stress.

Plasma volume expansion in rats: effects on thermoregulation and exercise.

Administration of polyethylene glycol (PEG, intraperitoneal, 3 ml, 30% solution) to adult male rats (300 g) resulted in an approximately 20% increment in plasma volume (PV) 24 h after PEG injection. When these animals were exercised (9.14 m/min, level treadmill) in a warm (30 degrees C, 30-40% relative humidity) environment, their mean endurance was increased from 67.9 (saline-treated controls, CONT) to 93.6 min (P less than 0.01). Total water loss was increased from 12.2 (CONT) to 17.2 g (PEG, P less than 0.01). Atropine administration (ATR, 200 micrograms/kg, tail vein) significantly (P less than 0.05) reduced both the endurance and the salivary water loss of CONT and PEG-treated rats, whereas it increased the heating rate (P less than 0.01) of both groups. PEG treatment reduced (P less than 0.01) the hematocrit and circulating protein levels both before and subsequent to exercise in the warm environment. Clinical chemical indexes of heat/exercise injury were generally unaffected by pharmacological intervention, whereas clinical chemical responses to exercise were related to the endurance time of each group. We concluded that expansion of PV by PEG provided significant beneficial effects on performance and thermoregulation during exercise in a warm environment.

Urinary and hematologic indexes of hypohydration.

As part of a large-scale field feeding system test we were able to collect and study hundreds of aliquots of overnight urine samples obtained immediately prior to a fasting blood sample on days 1, 20, and 44 of the field test. The large number of experimental samples (greater than 650) and concomitant collection of blood and urine aliquots along with data on body weights gave us the opportunity to assess and quantitate the sensitivity of commonly used criteria of hypohydration. Urine aliquots for all test days were initially categorized by specific gravity (SG) greater than or equal to 1.03 (n = 124) or less than 1.03 (n = 540). Creatinine levels were elevated (P less than 0.001) in the concentrated urine samples, but a decreased trend in sodium-to-potassium ratios in these samples failed to achieve statistical significance (P greater than 0.05). However, when individuals with high SG urine were subclassified by a criterion of weight loss greater than 3% from original body weight, then creatinine concentrations were elevated (P = 0.05), whereas sodium-to-potassium ratios were decreased (P = 0.05) when subjects also with high SG but weight loss less than 3% were compared. Because of the moderate altitude (2,000 m) of the field site and the time of sojourn (44 days), there occurred a slight, but significant (P less than 0.001), erythropoietic response. Hematocrit and serum osmolality were not significantly different when examined by the criteria of high or low SG urine and weight loss greater than or less than 3% original body weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma hormonal responses at graded hypohydration levels during exercise-heat stress.

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma opioid peptide responses during heat acclimation in humans.

Plasma beta-endorphin, Met-enkephalin and Peptide F immunoreactivity (ir) were measured at rest and following exercise on three days (days 1, 4, 8) of an eight day heat acclimation regime. Fourteen male subjects demonstrated physiological heat acclimation adaptations. Our data demonstrated a differential response of peripheral plasma levels of endogenous opioid peptides (EOP) to exercise in the heat. In addition, EOP did not follow the same time-course of other physiological adaptations as no differences (day 1 vs. 4 vs. 8) in resting or exercise levels were observed over the eight day heat acclimation regime. Significant increases in beta-endorphin ir (pre- to post-exercise) appear to reflect concomitant exercise-heat related changes. The increased peripheral levels of beta-endorphin were correlated to plasma levels of cortisol. Heat and exercise stress may result in a reduction of Met-enkephalin ir observed in peripheral plasma and might be due to degradation or a decrease in processing from the larger precursors. The differential responses of EOP suggest the possibility of separate physiological roles for these peptides during exercise in the heat but peripheral plasma levels of EOP do not appear to reflect acute heat acclimation changes.

Physostigmine: dose-response effects on endurance and thermoregulation during exercise.

We previously reported that the administration of 200 micrograms/kg of physostigmine (PH) to rats exercising on a treadmill resulted in decrements in both endurance (decreased running time to exhaustion) and thermoregulation. However, it was necessary to determine the dose-response effects of PH administration before PH-treated exercising rats could be used as a model with which to examine the relative anticholinergic potency of drugs. In the present work saline, 50, 100, or 200 micrograms/kg of physostigmine salicylate (0%, 40%, 50%, and 60% whole blood cholinesterase inhibition) was administered to rats (N = 12/group) prior to treadmill exercise (26 degrees C, 50% rh, 11 m/min, 6 degrees incline). The saline control group ran for 67 +/- 6 min (mean +/- SE) with a rate of rise of core temperature of 0.051 +/- 0.007 degrees C/min. The run times declined (80%, 64% and 48% of control) as rate of rise of core temperature increased (116%, 180%, and 214% of control) in a dose-dependent manner (50, 100, 200 micrograms/kg PH). Cholinergic symptoms such as salivation, tremors, and defecation were also affected in a dose-dependent manner by PH administration. Since cholinergic symptoms, thermoregulatory effects, and endurance decrements all vary in a dose-dependent manner with physostigmine administration, the exercising rat represents a useful model for examining the relative potency of cholinergic therapies.

Atropine, diazepam, and physostigmine: thermoregulatory effects in the heat-stressed rat.

We have previously reported that administration of atropine (A) to unrestrained, sedentary, heat-stressed rats resulted in a dose-dependent increase in heating rate (rate of rise of core temperature, degree C/min). Additionally, we have demonstrated that the decrements in treadmill endurance and increments in heating rate of physostigmine (PH)-treated running rats can both be restored to control levels by pretreating the animals with A and diazepam (D). Our objective in the present work was to determine if the administration of D + PH to A-treated unrestrained, sedentary, heat-stressed rats (N = 16/group, 510-530 g) could improve their thermal tolerance. The following drugs were administered singly (at 10 min intervals) via lateral tail vein: vehicle-control (C), A (200 micrograms/kg), D (500 micrograms/kg), and PH (200 micrograms/kg). After drug administration, the rats were heat-stressed (Tamb = 41.5 degrees C) until a core temperature of 42.6 degrees C was attained when they were removed to a 26 degrees C chamber. The heating rates (degrees C/min) and tolerance times (min) of the respective groups were: C- 0.02, 235; A- 0.08, 58; A D- 0.06, 94; and A + D + PH- 0.04, 143. Administration of D with A significantly decreased heating rate, and D + PH more than doubled the thermal tolerance of A-treated rats. Thus, the combination of A + D + PH not only restores PH-induced performance and thermoregulatory decrements of rats exercised in a moderate environment, but also reduces A-induced heat intolerance.

Carbamates, atropine, and diazepam: effects on performance in the running rat.

We have reported that when rats (500 g, male) are exercised to exhaustion on a treadmill, pretreatment with the centrally acting carbamate physostigmine reduced endurance (run time, RT) and increased the rate of rise of core temperature (Tc+). Both RT and Tc+ were restored to control levels by pretreatment with either or a combination of atropine (A), and diazepam (D). Our objective in the present work was to determine whether A+D could also restore the performance and thermoregulatory decrements induced by the peripherally acting carbamate pyridostigmine (PY). After drug administration, rats were run (11 m/min, 6 degrees elevation, Ta = 26 degrees C) to exhaustion. PY treatment resulted in a reduced RT and an increased heat gain that neither A nor D alone (A+PY and D+PY) could restore to control levels. On the other hand, a combination of both A and D restored these variables to control levels. In conclusion, A+D can restore the performance and thermoregulatory decrements resulting from the administration of either a centrally or a peripherally acting carbamate.

Chronic vs acute carbamate administration in exercising rats.

Physostigmine (PH), alone, and pyridostigmine (PY), in combination with atropine and 2-PAM, have been shown to protect animals against organophosphate poisoning. While acute administration of either of these carbamates increased heating rates and decreased endurance of exercising rats, chronically administered PY did not induce these decrements, and we hypothesized that chronic administration of PH could also result in similar attenuation of these effects. Thus, PH was administered acutely (iv) or chronically (osmotic mini-pump) in the following 4 groups (510-530g, male, N = 10/group): C (control, saline iv), AC-200 (acute, 200 ug/kg, 58% whole blood cholinesterase (ChE) inhibition), CH-7 (chronic, 125 ug/hr, 7 days, 60% inhib.), and CH-14 (chronic, 125 ug/hr, 14 days, 56% inhib.). Rats were run (11 m/min, 26 degrees C) to exhaustion. The run times and heating rates (% of control) were: AC-200 - 47, 213%; CH-7 - 60, 157%; CH-14 - 92, 109%. Additionally, ultrastructural changes noted in diaphragms of acutely treated animals were less evident in chronically treated animals. Thus, the decremental effects of acute PH administration on endurance, thermoregulation, and ultrastructure were attenuated with chronic administration at similar levels of ChE inhibition.

Effects of water temperature and flavoring on voluntary dehydration in men.

Effects of water temperature and flavoring on fluid consumption and body weight losses were studied in fourteen unacclimatized men (21-33 years) during 6 hr of treadmill exercise (4.8 km.hr-1, 5% grade for 30 min.hr-1) in a hot environment. Subjects consumed each of four beverages (15 degrees C water, 40 degrees C water, 15 degrees C flavored water, and 40 degrees C flavored water) on four nonconsecutive days. We identified two groups of individuals by body weight (BW) loss during the cool water trial: drinkers (D) who lost less than 2% initial BW (0.80 +/- 0.15%) and reluctant drinkers (RD) who lost more than 2% (2.53 +/- 0.12%). Although sweat losses were not different between the two groups, D consumed 31% more cool water than RD and experienced 68% less BW loss. Compared to the warm water trial, 6 hr consumption of cool water was significantly increased in both D (59%) and RD (141%) and BW loss was dramatically reduced in both groups. Flavoring significantly enhanced warm water consumption and reduced BW loss in RD only. Reduced consumption of warm water increased rectal temperature, heart rate and plasma osmolality in both groups. The results of this study indicate that either flavoring or cooling warm water will enhance fluid intake and reduce body weight deficits in men reluctant to drink.

Heatstroke pathophysiology: the energy depletion model.

This symposium focuses on exertional heatstroke, with emphasis on predisposing factors, clinical observations, diagnosis, treatment and recovery. The serious challenge to cardiovascular stability presented by exercise hyperthermia and some aspects of regulatory failure was reviewed in the introduction. The intent of this review, to understand how heat stress is translated into heat strain at the cellular level, is not to downplay the seriousness of the systemic condition. If we are successful, this may stimulate further interest on the impact of heat on the cell as a model for other factors which alter membrane integrity and permeability, lead to new experimental paradigms, and improve the diagnosis and treatment of other disorders such as toxic, hypovolemic, or ischemic shock. This review may also stimulate interesting research regarding more subtle threats to homeostasis such as chronic exercise, hypohydration and thirst, ion imbalance, and sleep deprivation. Since the original article on heat stroke pathophysiology was published (39), we have discussed the relationship of this concept to carbohydrate metabolism (40), thirst (41), and the cellular aspects of heat illness treatment (99). This article will attempt to integrate and extend some of those ideas.

The role of exercise in the etiology of exertional heatstroke.

Exertional heatstroke usually occurs among healthy, fit individuals who are motivated to perform strenuous exercise because of peer pressure, discipline, or athletic competition. In fact, exertional heatstroke deaths among high school athletes in the United States (ranked third only to head and neck injuries and heart failures), and the reluctance of race directors to cancel or postpone mass participation road races during periods of severe heat and humidity, emphasize a continuing need for widespread dissemination of information. The purposes of this symposium are 1) to convey essential information to the members of ACSM who are involved in exercise prescription, patient care, or athletic training; and 2) to disseminate recent scientific theories and research concerning exertional heatstroke.

Time course of recovery and heat acclimation ability of prior exertional heatstroke patients.

Our understanding of the time course of recovery from exertional heatstroke (EH) and the heat acclimation ability of prior EH patients is limited. This manuscript reviews previous findings regarding recovery from EH and presents original research involving the heat acclimation ability of 10 prior EH patients (PH) and 5 control subjects. Heat acclimation, by definition, distinguishes heat-intolerant from heat-tolerant prior heatstroke patients. Nine PH exhibited normal heat acclimation adaptations (40.1 degrees C, 7 d, 90 min.d-1), thermoregulation, sweat gland function, whole-body sodium and potassium balance, and blood values at 61 +/- 7 d after EH. One PH (subject A) did not adapt to exercise in the heat, was defined heat intolerant, but subsequently was declared heat tolerant (11.5 months post-EH). Three PH exhibited large, unexpected increases in serum CPK levels, which resolved upon subsequent testing, and were probably related to their detrained state and the exercise which they performed. It was concluded that: 1) sleep loss and generalized fatigue were the most common predisposing factors for PH; 2) recovery from EH was idiosyncratic and may require up to 1 year in severe cases; 3) PH were not hereditarily heat intolerant, prior to EH; 4) no measured variable predicted recovery from EH, or heat acclimation responses; 5) heat intolerance occurs in a small percentage of prior heatstroke patients, and may be transient or persistent.

Heat acclimatization during summer running in the northeastern United States.

Five highly trained distance runners (DR) were observed during controlled 90-min thermoregulation trials in spring (T1) and late summer (T2) to document the nature of heat acclimatization in the northeastern United States. These trials simulated environmental (30.3 +/- 0.1 degrees C dry bulb, 34.9 +/- 0.5% relative humidity, 4.47 m X s-1 wind speed) and exercise (treadmill running at 80, 120, 160, and 200 m X min-1) stresses encountered by DR during summer training in the northeastern United States. Between T1 and T2, DR trained outdoors for 14.5 +/- 0.4 wk, but consequently exhibited few physiological adaptations classically associated with heat acclimatization. Statistical comparison of T1 and T2 indicated no significant differences in mean heart rate, rectal temperature, sweat Na+ and K+, plasma Na+ and K+, or change in plasma volume during exercise. Mean weighted skin temperature was unchanged except at 50 min of exercise, and sweat rate was also unchanged except during the initial 30 min segment: 73 +/- 6 vs 93 +/- 8 ml X m-2 X h-1. Significant decreases (P less than 0.05) in submaximal VO2 were observed: T1 vs T2 values were 13.97 +/- 0.27 vs 10.19 +/- 1.19, 31.38 +/- 1.15 vs 27.91 +/- 1.45, and 44.97 +/- 0.85 vs 41.24 +/- 0.97 ml X kg-1 X min-1, at treadmill speeds of 80, 120, and 200 m X min-1, respectively. We conclude that DR did not require 14.5 wk of summer training to maintain safe rectal temperatures (less than or equal to 38.4 degrees C) during T1, which simulated the hottest days of summer in the northeastern United States.

Symptomatic hyponatremia during prolonged exercise in heat.

Although hyponatremia (HN) has been reported among endurance athletes, its etiology often remains uncertain and of great interest to clinicians and physiologists. This case report presents physiologic evidence regarding the etiology and development of HN during exercise in the heat. A 21-yr-old male volunteer (K.G.) unexpectedly experienced symptomatic HN during a research investigation that involved controlled sodium (Na+) intake (137 mEq Na+.d-1 for 7d) and exercise-heat acclimation (41 degrees C; 30 min.h-1, 8 h.d-1 for 10 d). Fluid balance, physiologic variables, and hematologic/hormone data were measured before and after the HN episode, with similar measurements recorded for nine unaffected volunteers. The results indicated: 1) HN was verified in K.G. (plasma Na+ < 130 mEq.l-1) after only 4 h of mild, intermittent exercise in heat; 2) K.G.'s heart rate, rectal temperature, blood pressure, and Na+ losses in sweat and urine were < or = control subjects at all times; 3) between hours 4-7, an inappropriately large release of vasopressin coincided with a decrease of urine volume to 0 ml.h-1. It was concluded that a large intake (10.3 l.7h-1) and retention (2.77 l.7h-1) of water and a "low normal" initial plasma Na+ (134 mEq.l-1) were primary factors in the development of HN in K.G., whereas Na+ losses in sweat and urine were normal and served only to exacerbate HN.

American College of Sports Medicine position stand. Heat and cold illnesses during distance running.

Many recreational and elite runners participate in distance races each year. When these events are conducted in hot or cold conditions, the risk of environmental illness increases. However, exertional hyperthermia, hypothermia, dehydration, and other related problems may be minimized with pre-event education and preparation. This position stand provides recommendations for the medical director and other race officials in the following areas: scheduling; organizing personnel, facilities, supplies, equipment, and communication; providing competitor education; measuring environmental stress; providing fluids; and avoiding potential legal liabilities. This document also describes the predisposing conditions, recognition, and treatment of the four most common environmental illnesses: heat exhaustion, heatstroke, hypothermia, and frostbite. The objectives of this position stand are: 1) To educate distance running event officials and participants about the most common forms of environmental illness including predisposing conditions, warning signs, susceptibility, and incidence reduction. 2) To advise race officials of their legal responsibilities and potential liability with regard to event safety and injury prevention. 3) To recommend that race officials consult local weather archives and plan events at times likely to be of low environmental stress to minimize detrimental effects on participants. 4) To encourage race officials to warn participants about environmental stress on race day and its implications for heat and cold illness. 5) To inform race officials of preventive actions that may reduce debilitation and environmental illness. 6) To describe the personnel, equipment, and supplies necessary to reduce and treat cases of collapse and environmental illness.

Thyroid stimulating hormone and prolactin responses to thyrotropin releasing hormone in nondepressed alcoholic inpatients.

Thyroid stimulating hormone (TSH) and prolactin (PRL) responses to thyrotropin releasing hormone (TRH) stimulation are sometimes blunted in alcoholic subjects; however, the mechanisms involved in these phenomena have not been established. We hypothesized that elevations in free thyroid concentrations might be related to these abnormal responses and then tested that hypothesis in a sample of nondepressed alcoholic inpatients (n = 21). Four alcoholic patients had delta max TSH responses that were < 7 mIU/l; three had PRL responses at or below 8 micrograms/l. Baseline TSH was the only significant predictor of peak TSH; however, free thyroxine (FT4) and baseline TSH both were significant predictors of peak PRL. The average baseline FT4 concentration in alcoholic patients was significantly higher than that in healthy control subjects (n = 10). Our data, thus, suggest that small elevations of FT4 play a role in the inhibition of TSH and PRL responses to TRH among nondepressed, abstinent alcoholic patients.