Plasma catecholamine concentrations of newborn piglets in thermoneutral and cold environments

Plasma epinephrine and norepinephrine concentrations were measured in seventeen unanaesthetized 3 to 4 days-old piglets while in a thermoneutral environment (31.3 degrees C) and 30, 45 and 60 min after induction of environmental cold stress (19.9-23.1 degrees C). Plasma epinephrine and norepinephrine concentrations in a warm environment were 142 +/- 26 pg/ml, and 456 +/- 44 pg/ml respectively. Environmental cold stress evoked significant increases in norepinephrine values after 30 (624 +/- 58 pg/ml), 45 (626 +/- 60 pg/ml) and 60 (626 +/- 54 pg/ml) min of cold stress. Plasma epinephrine concentrations did not significantly change during environmental cold stress. Post-hoc stratification of piglets into normothermic (deep rectal temperature 38.6 degrees C-38.8 degrees C, n = 9) and hypothermic (deep rectal temperature 37.1 degrees C-37.7 degrees C, n = 7) subgroups revealed significant increases in plasma norepinephrine concentrations only in the hypothermic subgroup. We conclude that plasma norepinephrine, but not epinephrine, is increased in newborn piglets during environmental cold stress and that the changes in norepinephrine concentrations are related to body core hypothermia. We speculate that hypothermia-mediated reductions in peripheral norepinephrine breakdown and re-uptake contribute to the rise in circulating levels.     

Influence of polycythemia on blood volume and thermoregulation during exercise-heat stress

We studied the effects of autologous erythrocyte infusion on blood volume and thermoregulation during exercise in the heat. By use of a double-blind design, nine unacclimated male subjects were infused with either 600 ml of a NaCl-glucose-phosphate solution containing a approximately 50% hematocrit (n = 6, reinfusion) or 600 ml of this solution only (n = 3, saline). A heat stress test (HST) was attempted approximately 2-wk pre- and 48-h postinfusion during the late spring months. After 30 min of rest in a 20 degrees C antechamber, the HST consisted of a 120-min exposure (2 repeats of 15 min rest and 45 min treadmill walking) in a hot (35 degrees C, 45% rh) environment while euhydrated. Erythrocyte volume (RCV, 51Cr) and plasma volume (PV, 125I) were measured 24 h before each HST, and maximal O2 uptake (VO2max) was measured 24 h after each HST. Generally, no significant effects were found for the saline group. For the reinfusion group, RCV (11%, P less than 0.01) and VO2max (11%, P less than 0.05) increased after infusion, and the following observations were made: 1) the increased RCV was associated with a reduction in PV to maintain the same blood volume as during the preinfusion measurements; 2) polycythemia reduced total circulating protein but did not alter F-cell ratio, plasma osmolality, plasma protein content, or plasma lactate at rest or during exercise-heat stress; 3) polycythemia did not change the volume of fluid entering the intravascular space from rest to exercise-heat stress; and 4) polycythemia tended to reduce the rate of heat storage during exercise-heat stress.     

Plasma volume, osmolarity, total protein and electrolytes during treadmill running and cycle ergometer exercise

While haemoconcentration due to loss of plasma volume is well established during cycling, the existence of similar changes during running remains contentious. This study compared the changes in plasma volume and associated blood indices during 60 min of running and cycling at the same relative intensity (approximately 65% VO2max), with all changes referenced to blood indices obtained after 30 min seated at rest on a cycle ergometer. Plasma osmolarity increased similarly with both forms of exercise but was less than predicted for water loss alone, such that there was a net loss of sodium during exercise and of potassium postexercise, with essentially no loss of protein. Plasma volume decreased similarly (approximately 6.5%) in both exercise trials, but while that with cycling was initiated by exercise itself and was essentially maximal within 5 min, the reduction in plasma volume in the running trial was induced by adopting the upright posture and was complete before exercise began. These data would indicate that different mechanisms are responsible for the changes in plasma volume induced by running and cycling, while the similarity of change would suggest that there is a lower limit to any reduction in plasma volume, regardless of mechanism. Furthermore, the observation that the changes in plasma volume were complete before or early in exercise, would imply that oral water ingestion during prolonged exercise, which is essential for thermoregulation, may be more concerned with homeostasis of extravascular water rather than plasma volume.     

Plasma prolactin responses to acute changes in central blood volume in man

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of passive hyperthermia versus exercise-induced hyperthermia on immune responses: hormonal implications

Different stress hormones are released during prolonged exercise and passive hyperthermia. We hypothesized that these different hormonal responses could contribute to the different changes in the immune response during these two challenges. Methods: Eight subjects completed three trials in a randomized order. In the control trial (C), the subjects remained in a sitting posture for three hours in thermoneutral conditions. In the exercise hyperthermia trial (E), they exercised for two hours on a treadmill at 65% max in thermoneutral conditions, followed by 1-h recovery in thermoneutral conditions; in the passive hyperthermia trial (PH), the subjects remained in a semi-recumbent position in a climatic chamber for two hours in hot conditions, followed by 1-h recovery in thermoneutral conditions. During the E and PH trials, wind speed and thermal conditions were modulated to reach a rectal temperature (Tre) of 38.5 degrees C at 60 min and 39 degrees C at 120 min. The subjects did not drink during the experiments. Blood samples (10 mL) were taken at 0, 60, 120 and 180 min of each trial. The total white cell count and its subsets were measured; plasma catecholamines, cortisol and prolactin were assayed. In a whole blood assay, blood leukocytes were stimulated by lipopolysaccharide (LPS) or phytohemagglutinin (PHA) for 24 and 48 hours, respectively. Cytokines, such as TNF-alpha, IL-10 and INF-gamma were measured in the culture supernatant. RESULTS: The plasma levels of catecholamines were increased only during E, prolactin was increased only during PH, and cortisol was increased in both E and PH. Only the exercise caused a mobilization of blood leukocytes and leukocyte subsets. The INF-gamma and TNF-alpha production by PHA- and LPS-stimulated blood, respectively, were inhibited in a substantial way in both E and PH compared to control when Tre reached 39 degrees C. Only LPS-induced IL-10 production was enhanced during the exercise. The effects of the challenges were increased with 39 degrees C compared to 38.5 degrees C. CONCLUSIONS: Catecholamines play a major role in the mobilization of immunocompetent cells and the production of IL-10 during exercise. Prolactin and catecholamines have adverse role on the immune response, whereas cortisol exerts similar effects during both trials. The consequence could be a protection against inflammatory overshooting.     

PHYSIOLOGICAL AND LEUKOCYTE SUBSET RESPONSES TO EXERCISE AND COLD EXPOSURE IN COLD-ACCLIMATIZED SKATERS

We investigated physiological responses and changes in circulating immune cells following exercise in cold and thermoneutral conditions. Participants were short track skaters (n=9) who were acclimatized to cold conditions, and inline skaters (n=10) who were not acclimatized. All skaters were young, and skating at a recreational level three days per week for at least one year. Using a cross-over design, study variables were measured during 60 min of submaximal cycling (65% V.O₂max) in cold (ambient temperature: 5±1°C, relative humidity: 41±9%) and thermoneutral conditions (ambient temperature: 21±1°C, relative humidity: 35±5%). Heart rate, blood lactate and tympanic temperature were measured at rest, during exercise and recovery. Plasma cortisol, calprotectin and circulating blood cell numbers were measured before and after 60 min of cold or thermoneutral conditions, and during recovery from exercise. Heart rate was lower in both groups during exercise in cold versus thermoneutral conditions (P<0.05). The increase in total leukocytes during recovery was primarily due to an increase in neutrophils in both groups. The cold-acclimatized group activated neutrophils after exercise in cold exposure, whereas the non-acclimatized group activated lymphocyte and cortisol after exercise in cold exposure. Lymphocyte subsets significantly changed in both groups over time during recovery as compared to rest. Immediately after exercise in both groups, CD16+ and CD69+ cells were elevated compared to rest or before exercise in both conditions. Acclimatization to exercise in the cold does not appear to influence exercise-induced immune changes in cold conditions, with the possible exception of neutrophils, lymphocytes and cortisol concentration.     

Plasma volume expansion in humans after a single intense exercise protocol.

We used intense intermittent exercise to produce a 10% expansion of plasma volume (PV) within 24 h and tested the hypothesis that PV expansion is associated with an increase in plasma albumin content. The protocol consisted of eight 4-min bouts of exercise at 85% maximal O2 uptake with 5-min recovery periods between bouts. PV, plasma concentrations of albumin and total protein (TP), and plasma osmolality were measured before and during exercise and at 1, 2, and 24 h of recovery from exercise. During exercise, PV decreased by 15%, while plasma TP and albumin content remained at control levels. At 1 h of recovery, plasma albumin content was elevated by 0.17 +/- 0.04 g/kg body wt, accounting for the entire increase in plasma TP content. PV returned to control level at 1 h of recovery without fluid intake by the subjects, despite a 820 +/- 120-g reduction in body weight. At 2 h of recovery, plasma TP content remained significantly elevated, and plasma TP and albumin concentration were significantly elevated. At 24 h of recovery, PV was expanded by 4.5 +/- 0.7 ml/kg body wt (10 +/- 1%), estimated from hematocrit and hemoglobin changes, and by 3.8 +/- 1.3 ml/kg body wt (8 +/- 3%), measured by Evans blue dye dilution. Plasma albumin content was increased by 0.19 +/- 0.05 g/kg body wt at 24 h of recovery. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body wt expansion of the PV. No significant changes in plasma osmolality occurred during recovery, but total plasma osmotic content increased in proportion to PV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circulating leptin response to feeding and exogenous infusion of insulin in sheep exposed to thermoneutral and cold environments

Leptin has been shown to regulate feed intake and energy expenditure. Insulin stimulates leptin secretion in rodents, but its action on leptin secretion is still obscure in ruminants. If insulin stimulates leptin secretion in ruminants, circulating leptin concentrations may change during exposure to cold, because of fluctuating insulin secretion and action in the cold environment. The present experiment was designed to determine whether feeding or exogenous administration of insulin affects circulating leptin levels in sheep exposed to thermoneutral and cold environments. Suffolk rams that were shorn and fed a diet once daily were subjected to a thermoneutral (20 degrees C) or cold (0 degrees C) environment for at least 1 week. Overall mean concentrations of plasma leptin in the feeding experiment were lower (P<0.05) in the cold environment than in the thermoneutral environment. Plasma leptin levels remained relatively unchanged after feeding in both environments, though plasma insulin response to feeding in both environments increased (P<0.01). The euglycemic clamps (insulin infusion rate: 4 mUkgBW(-1)min(-1) for 2 h) increased (P<0.01) circulating leptin concentrations in the thermoneutral, but not in the cold environment. These results suggest that lower circulating leptin levels in ruminants exposed to the cold environment could be partly due to the depressed insulin action on leptin secretion.     

The effect of repeated acute mental stress on habituation and recovery responses in hemoconcentration and blood cells in healthy men

Acute mental stress elicits hemoconcentration and polycytosis. We investigated whether haematological response to repeated acute mental stress would habituate and be sustained 45 min and 105 min after stress. Twenty-four men underwent a 13-min stressor three times, one week apart; hematological variables were measured at week one and three. Hematocrit, hemoglobin, leukocytes, lymphocytes, erythrocytes, and thrombocytes all increased from rest to immediately post-stress (p's<.001). After 105 min of recovery, leukocytes and platelets both were higher, and hematocrit, hemoglobin, lymphocytes, and erythrocytes were all lower than at rest (p's<.001 to <.05). At all time points, hematocrit (p=.005) and erythrocytes (p=.006) were lower at week three than at week one. In contrast to an attenuation in systolic blood pressure increase from rest to immediately post-stress (p<.001), and in cortisol recovery from immediately post-stress to 45 min post-stress (p<.001), the magnitude of change in hemoconcentration and cell counts in stress and recovery experienced no habituation. Adjustment for stress-induced plasma volume shift altered findings: Elevated leukocytes post-stress persisted at 105 min (p<.001); any changes in lymphocytes became insignificant; erythrocytes decreased from rest to post-stress (p<.001) to increase again during recovery (p's<.05); platelets increased linearly between rest and 105 min of recovery (p=.005). We conclude that the magnitude of changes in hemoconcentration and blood cells during acute mental stress and recovery failed to habituate to stress repeats and, in part, sustained up to 105 min. Plasma volume shift accompanying stress affects the time course of stress polycytosis.     

Hypohydration impairs endurance exercise performance in temperate but not cold air.

This study compared the effects of hypohydration (HYP) on endurance exercise performance in temperate and cold air environments. On four occasions, six men and two women (age = 24 +/- 6 yr, height = 170 +/- 6 cm, weight = 72.9 +/- 11.1 kg, peak O2 consumption = 48 +/- 9 ml.kg(-1).min(-1)) were exposed to 3 h of passive heat stress (45 degrees C) in the early morning with [euhydration (EUH)] or without (HYP; 3% body mass) fluid replacement. Later in the day, subjects sat in a cold (2 degrees C) or temperate (20 degrees C) environment with minimal clothing for 1 h before performing 30 min of cycle ergometry at 50% peak O2 consumption followed immediately by a 30-min performance time trial. Rectal and mean skin temperatures, heart rate, and ratings of perceived exertion measurements were made at regular intervals. Performance was assessed by the total amount of work (kJ) completed in the 30-min time trial. Skin temperature was significantly lower in the cold compared with the temperate trial, but there was no independent effect of hydration. Rectal temperature in both HYP trials was higher than EUH after 60 min of exercise, but the difference was only significant within the temperate trials (P < 0.05). Heart rate was significantly higher at 30 min within the temperate trial (HYP > EUH) and at 60 min within the cold trial (HYP > EUH) (P < 0.05). Ratings of perceived exertion increased over time with no differences among trials. Total work performed during the 30-min time trial was not influenced by environment but was less (P < 0.05) for HYP than EUH in the temperate trials. The corresponding change in performance (EUH-HYP) was greater for temperate (-8%) than for cold (-3%) (P < 0.05). These data demonstrate that 1) HYP impairs endurance exercise performance in temperate but not cold air but 2) cold stress per se does not.     

Hyperhydration with glycerol solutions

Glycerol was tested as an agent to promote hyperhydration of male and female subjects. Series I experiments involved ingesting 0.5, 1.0, or 1.5 g glycerol/kg body wt and within 40 min drinking 0.1% NaCl, 21.4 ml/kg. In series II, 1.0 g glycerol/kg body wt was ingested at time 0, and 25.7 ml/kg of 0.1% NaCl was ingested over a 3.5-h period. Experiments were of 4-h duration and included controls without glycerol as each subject served as his/her control. Blood samples were taken at 40- or 60-min intervals for hemoglobin (Hb), hematocrit (Hct), plasma osmolality, glycerol, and multiple blood chemistry analyses. Urine was collected at 60-min intervals. Glycerol ingestion increased plasma osmolality for 2 h and reduced the total 4-h urine volume. There were no significant changes in Hb or Hct as a result of the glycerol or excess fluid intake. This study demonstrates that glycerol plus excess fluid intake can produce hyperhydration for at least 4 h.     

Sympathetic neural responses to increased osmolality in humans

The purpose of this study was to examine the relationship between osmolality and efferent sympathetic outflow in humans. We hypothesized that increased plasma osmolality would be associated with increases in directly measured sympathetic outflow. Muscle sympathetic outflow was successfully recorded in eight healthy subjects during a 60-min intravenous hypertonic saline infusion (HSI; 3% NaCl) on one day and during a 60-min intravenous isotonic saline (ISO) infusion (0.9% NaCl) on a different day. The HSI provides an osmotic and volume stimulus, whereas the ISO infusion provides a volume-only stimulus. Muscle sympathetic nerve activity was quantified using the technique of peroneal microneurography. Plasma osmolality increased during the HSI but not during the ISO infusion (ANOVA, P < 0.05). Sympathetic outflow differed between the trials (ANOVA, P < 0.05); during the HSI burst, frequency initially increased from 14.6 +/- 2.5 to 18.1 +/- 1.9 bursts/min; during the ISO infusion, burst frequency initially declined from 14.7 +/- 2.5 to 12.0 +/- 2.1 bursts/min. Plasma norepinephrine concentration was greater at the end of the HSI compared with the end of the ISO infusion (HSI: 297 +/- 64 vs. ISO: 202 +/- 49 pg/ml; ANOVA, P < 0.05). We conclude that HSI-induced increases in plasma osmolality are associated with increases in sympathetic activity in humans.     

Age and hypohydration independently influence the peripheral vascular response to heat stress

Seven young (Y, 22-28 yr) and seven middle-aged (MA, 49-60 yr) normotensive men of similar body size, fatness, and maximal oxygen uptake (VO2max) were exposed to a heat challenge in an environmental chamber (48 degrees C, 15% relative humidity). Tests were performed in two hydration states: hydrated (H, 25 ml water/kg body wt 1 h before the test, 2.5 h before exercise) and hypohydrated (Hypo, after 18-20 h of water deprivation). Each test began with a 90-min rest period during which the transiently increased plasma volume and decreased osmolality after drinking in the H condition returned to base line. This period was followed by 30 min of cycle exercise at a mean intensity of 43% VO2max and a 60-min resting recovery period with water ad libitum. Although prior drinking caused no sustained changes in plasma osmolality, Hypo increased plasma osmolality by 7-10 mosmol/kg in both groups. There were no significant age differences in water intake, urine output or osmolality, overall change in body weight, or sweating rate. In the H state, the percent change in plasma volume was less (P less than 0.01) during exercise for the Y group (-5.9 +/- 0.7%) than for the MA group (-9.4 +/- 0.6%). Esophageal temperature (Tes) was higher in the Hypo condition for both groups with no age-related differences. Throughout the 3-h period, mean skin temperature was higher in the Y group and significantly so (P less than 0.05) in the Hypo condition.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sensitive assay for midazolam and its metabolite 1′-hydroxymidazolam in human plasma by capillary high-performance liquid chromatography

A sensitive high-performance liquid chromatographic method is described for the quantification of midazolam and 1′-hydroxymidazolam in human plasma. Sample (1 ml plasma) preparation involved a simple solvent extraction step with a recovery of approximately 90% for both compounds. An aliquot of the dissolved residue was injected onto a 3 μm capillary C₁₈ column (150 mm×0.8 mm I.D.). A gradient elution was used. The initial mobile phase composition (phosphate buffer–acetonitrile, 65:35) was maintained during 16 min and was then changed linearly during a 1-min period to phosphate buffer–acetonitrile, 40:60. The flow-rate of the mobile phase was 16 μl/min and the eluate was monitored by UV detection. The limits of quantification for midazolam and 1′-hydroxymidazolam were 1 ng/ml and 0.5 ng/ml, respectively. The applicability of the method was demonstrated by studying the pharmacokinetics of midazolam, and its major metabolite 1′-hydroxymidazolam, in human volunteers following i.v. bolus administration of a subtherapeutic midazolam dose (40 μg/kg).     

Effect of acute hyperglycemia on basal, secretin and secretin + cholecystokinin stimulated exocrine pancreatic secretion in humans

Pancreatico-biliary secretion is reduced during acute hyperglycemia. We investigated whether alterations in pancreatico-biliary flow or volume output are responsible for the observed reduction in duodenal output of pancreatic enzymes and bilirubin during hyperglycemia. Eight healthy subjects were studied on two occasions during normoglycemia and hyperglycemia (15 mmol/l). Pancreatico-biliary output was measured by aspiration using a recovery marker under basal conditions (60 min), during secretin infusion (0.1 CU/kg.h) for 60 min and during secretin + CCK (0.5 IDU/kg.h) infusion for 60 min. Secretin was infused to stimulate pancreatico-biliary flow and volume output. Secretin significantly (P<0.005-P<0.05) increased volume and bicarbonate output and CCK significantly (P<0.01) increased the output of bilirubin, pancreatic enzymes, bicarbonate and volume, both during normoglycemia and hyperglycemia. During hyperglycemia basal, secretin stimulated and secretin + CCK stimulated total pancreatico-biliary output were significantly (P<0.005-P<0.05) reduced compared to normoglycemia. The incremental outputs, however, were not significantly different between hyper- and normoglycemia. Pancreatic volume output was significantly (P<0.05) reduced during hyperglycemia compared to normoglycemia under basal conditions (31+/-16 m/h versus 132+/-33 m/h) during secretin infusion (130+/-17 ml/h versus 200+/-34 m/h) and during secretin + CCK infusion (370+/-39 ml/h versus 573+/-82 ml/h). Plasma PP levels were significantly (P<0.05) reduced during hyperglycemia. It is concluded that 1) hyperglycemia significantly reduces basal pancreatico-biliary output 2) the incremental pancreaticobiliary output in response to secretin or secretin + CCK infusion is not significantly affected during hyperglycemia, 3) a reduction in volume output contributes to the inhibitory effect of hyperglycemia on pancreatico-biliary secretion, 4) hyperglycemia reduces PP secretion suggesting vagal-cholinergic inhibition of pancreatico-biliary secretion and volume during hyperglycemia.     

Temperature regulation during rest and exercise in the cold in premenarcheal and menarcheal girls.

Temperature regulation during exercise in the cold was examined in 13 adolescent female individuals, aged 13-18 yr. Six girls with established menstrual cycles comprised the eumenorrheic menarcheal (EM) group, and seven nonmenstruating girls comprised the premenarcheal (PM) group. During the first visit, maximal oxygen consumption (Vo(2 max)), height, weight, and percent body fat were measured. The second visit included a determination of metabolic rate in thermoneutrality (21 degrees C), consisting of a 10-min rest period and 20 min of cycling (30% of Vo(2 max)), and a cold test (5 degrees C, 40% humidity, <0.3 m/s air velocity) involving a 20-min rest period and 40 min of cycling (30% of Vo(2 max)). Subjects in the EM group were tested twice in the chamber: once during the follicular and once during the luteal phase. Heat production per kilogram in thermoneutrality and in the cold was significantly (P < 0.05) higher in the PM compared with the EM girls. However, the PM girls had a significantly (P < 0.05) lower core temperature in the cold than the EM group. PM girls also had a significantly higher body surface area-to-mass ratio compared with the EM girls. Although percent body fat between groups was not significantly different, within the PM group percent body fat explained 79% (P < 0.01) of the variance in the decrease of core temperature. There were no menstrual phase-related differences in temperature regulation in either the thermoneutral or cold environment. In conclusion, menstrual phase does not influence temperature regulation in female individuals during adolescence. EM girls had lower metabolic heat production but maintained their core temperature more effectively in the cold than did the PM girls. This thermoregulatory difference between PM and EM girls is mainly a function of geometric differences with maturation-related peripheral vasoconstrictive differences maybe limiting the effectiveness of the mechanism of increased heat storage in younger female individuals.     

Glycerol hyperhydration improves cycle time trial performance in hot humid conditions

Eight competitive cyclists [mean peak oxygen consumption, (VO2(peak)) = 65 ml x min(-1) x kg(-1)] undertook two 60-min cycle ergometer time trials at 32 degrees C and 60% relative humidity. The time trials were split into two 30-min phases: a fixed-workload phase and a variable-workload phase. Each trial was preceded by ingestion of either a glycerol solution [1 g x kg(-1) body mass (BM) in a diluted carbohydrate (CHO)-electrolyte drink] or a placebo of equal volume (the diluted CHO-electrolyte drink). The total fluid intake in each trial was 22 ml x kg(-1) BM. A repeated-measures, double blind, cross over design with respect to glycerol was employed. Glycerol ingestion expanded body water by approximately 600 ml over the placebo treatment. Glycerol treatment significantly increased performance by 5% compared with the placebo group, as assessed by total work in the variable-workload phase (P < 0.04). There were no significant differences in rectal temperature, sweat rate or cardiac frequency between trials. Data indicate that the glycerol-induced performance increase did not result from plasma volume expansion and subsequently lower core temperature or lower cardiac frequencies at a given power output as previously proposed. However, during the glycerol trial, subjects maintained a higher power output without increased perception of effort or thermal strain.     

Passive heat exposure leads to delayed increase in plasma levels of atrial natriuretic peptide in humans.

The effects of passive heat exposure on atrial natriuretic peptide (ANP) were studied in six healthy men staying in a Finnish sauna at +92 degrees C for 20 min. Their rectal temperature increased by 0.4 degrees C, and evaporative water loss was 0.92 +/- 0.14 (SD) kg. Heart rate and systolic blood pressure increased significantly during the 20-min exposure. Serum osmolality and plasma arginine vasopressin levels increased during the exposure, then declined, and increased significantly again at 90-120 min. Plasma renin activity and aldosterone increased by two- to fourfold in 20 min. Plasma ANP levels rose from 13 +/- 7 to 39 +/- 15 ng/l at 60 min and to 41 +/- 13 ng/l at 120 min (P less than 0.01 for both). We conclude that transient increases in heart rate and systolic blood pressure or changes in blood volume as inferred from the weight loss do not contribute to the increased plasma ANP levels observed after the heat exposure. Instead, increased secretions of pressor hormones could explain the elevated plasma ANP levels observed after the thermal stress.     

Hematological variations at rest and during maximal and submaximal exercise in a cold (0°C) environment

The affect of negative thermal stress on hematological variables at rest, and during submaximal (sub ex) and maximal exercise (max ex) were observed for young males who volunteered in two experimental sessions, performed in cold (0°C) and in normal room temperature (20°C). At rest, hematological variables such as RBC and derivates Hb and Hct were significantly increased (P<0.05) during cold stress exposure, while plasma volume decreased. The findings of this study suggest that the major factor inducing hypovolemia during low thermal stress can be imputed to local plasma water-shift mechanisms and especially to a transient shift of plasma water from intrato extravascular compartments. Rest values for WBC and platelets (Pla) were also slightly increased during cold stress exposure. However this increase can partly be related to hemoconcentration but also to the cold induced hyperventilation activating the lung circulation. Maximal exhaustive exercise induced, in both experimental temperatures, significant (P<0.05) increments of RBC, Hb, Hct, and WBC while plasma volume decreased. However, Pla increase was less marked. On the other hand, cold stress raised slightly the observed variations of the different hematological variables. Submaximal exercise induced a similar, though non-significant, pattern for the different hematological variables in both experimental conditions. Observed plasma volume ( PV%) reduction appears during exercise. However cold stress induced resting plasma volume variations that are transferred at every exercise level. Neither exercise nor cold inducement significantly modified the hematological indices (MCH, MCV, MCHC). In conclusion hematological variables are affected by cold stress exposure, even when subjects perform a physical activity.     

Plasma volume change during heavy-resistance weight lifting

Blood samples were obtained from six young men before, and over a 60-min period following a bout of heavy-resistance weight lifting to determine changes in plasma volume. Weight lifting consisted of three sets of four exercises (arm curl, bench press, bent-arm row, and squat) performed using 70% of one-repetition maximum for as many repetitions as possible. Plasma volume change was determined from haematocrit and haemoglobin concentration. During weight lifting, mean oxygen uptake and heart rate were 1.96 L X min-1 and 158 bt X min-1, respectively. Plasma volume was decreased -14.3% (p less than 0.05) immediately following exercise and -7.0% (p less than 0.05) at 15 min into recovery, but had returned to the resting level within 30 min. It was concluded that heavy-resistance weight lifting elicits a significant decrease in plasma volume, which is similar in magnitude to that observed during running and cycling at 80-95% of maximal oxygen uptake.