O2 Uptake in hyperthyroidism during constant work rate and incremental exercise

To investigate the effect of hyperthyroidism on the pattern and time course of O2 uptake (VO2) following the transition from rest to exercise, six patients and six healthy subjects performed cycle exercise at an average work rate (WR) of 18 and 20 W respectively. Cardiorespiratory variables were measured breath-by-breath. The patients also performed a progressively increasing WR test (1-min increments) to the limit of tolerance. Two patients repeated the studies when euthyroid. Resting and exercise steady-state (SS) VO2 (ml.kg-1.min-1) were higher in the patients than control (5.8, SD 0.9 vs 4.0, SD 0.3 and 12.1, SD 1.5 vs 10.2, SD 1.0 respectively). The increase in VO2 during the first 20 s exercise (phase I) was lower in the patients (mean 89 ml.min-1, SD 30) compared to the control (265 ml.min-1, SD 90), while the difference in half time of the subsequent (phase II) increase to the SS VO2 (patient 26 s, SD 8; controls 17 s, SD 8) were not significant (P = 0.06). The O2 cost per WR increment (delta VO2/delta WR) in ml.min-1.w-1, measured during the incremental period (mean 10.9; range 8.3-12.2), was always within two standard deviations of the normal value (10.3, SD 1). In the two patients who repeated the tests, both the increment of VO2 from rest to SS during constant WR exercise and the delta VO2/delta WRs during the progressive exercise were higher in the hyperthyroid state than during the euthyroid state.(ABSTRACT TRUNCATED AT 250 WORDS)     

Habituation of the metabolic and ventilatory responses to cold-water immersion in humans

An experiment was undertaken to answer long-standing questions concerning the nature of metabolic habituation in repeatedly cooled humans. It was hypothesised that repeated skin and deep-body cooling would produce such a habituation that would be specific to the magnitude of the cooling experienced, and that skin cooling alone would dampen the cold-shock but not the metabolic response to cold-water immersion. Twenty-one male participants were divided into three groups, each of which completed two experimental immersions in 12 °C water, lasting until either rectal temperature fell to 35 °C or 90 min had elapsed. Between these two immersions, the control group avoided cold exposures, whilst two experimental groups completed five additional immersions (12 °C). One experimental group repeatedly immersed for 45 min in average, resulting in deep-body (1.18 °C) and skin temperature reductions. The immersions in the second experimental group were designed to result only in skin temperature reductions, and lasted only 5 min. Only the deep-body cooling group displayed a significantly blunted metabolic response during the second experimental immersion until rectal temperature decreased by 1.18 °C, but no habituation was observed when they were cooled further. The skin cooling group showed a significant habituation in the ventilatory response during the initial 5 min of the second experimental immersion, but no alteration in the metabolic response. It is concluded that repeated falls of skin and deep-body temperature can habituate the metabolic response, which shows tissue temperature specificity. However, skin temperature cooling only will lower the cold-shock response, but appears not to elicit an alteration in the metabolic response.     

Decline in peripheral chemoreceptor excitatory stimulation during acute hypoxia in the lamb

Chemoreceptor function was studied in eight 2- to 3-day-old unanesthetized lambs to sequentially assess hypoxic chemoreflex strength during an 18-min exposure to hypoxia [inspired O2 fraction (FIO2) = 0.08]. The immediate ventilatory (VE) drop in response to five breaths of pure O2 was measured at 3, 7, and 15 min during hypoxia. Each lamb was studied again at 10-11 days of age. At 2-3 days of age VE increased, with the onset of hypoxia, from 658 +/- 133 (SD) ml.min-1 X kg-1 to a peak of 1,124 +/- 177 ml.min-1 X kg-1. A dampening of the VE response then occurred, with a mean decline in VE of 319 ml.min-1 X kg-1 over the 18-min hypoxia period. Each pure O2 test (Dejours test) resulted in an abrupt fall in VE (delta VEDejours). This VE drop was 937 +/- 163, 868 +/- 244, and 707 +/- 120 ml.min-1 X kg-1 at 3, 7, and 15 min of hypoxia, respectively. Comparing the three O2 tests, delta VEDejours was significantly decreased by 15 min, indicating a loss of about one-fourth of the O2 chemoreflex drive during hypoxia. Testing at 10-11 days of age revealed a smaller VE decline during hypoxia. O2 tests at the beginning and end of the hypoxic period were not significantly different, indicating a smaller loss of hypoxic chemoreflex drive in the more mature animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynamics of hepatic lactate and glucose balances during prolonged exercise and recovery in the dog

The present experiments were undertaken to assess dynamics of hepatic lactate and glucose balance in the over-night-fasted dog during 150 min of moderate-intensity treadmill exercise and 90 min of exercise recovery. Catheters were implanted chronically in an artery and portal and hepatic veins 16 days before experimentation. 3-3H-glucose was infused to determine hepatic glucose uptake, as well as tracer-determined glucose production by isotope dilution (Ra). At rest, net hepatic lactate output was 0.33 +/- 0.15 mg.kg-1.min-1 and increased to 2.26 +/- 0.82 mg.kg-1.min-1 after 10 min of exercise, after which it fell such that the liver was a net lactate consumer by the end of exercise and through recovery. In contrast to the rapid release of lactate, net hepatic glucose output rose gradually from 2.58 +/- 0.20 mg.kg-1.min-1 at rest to 8.87 +/- 0.85 mg.kg-1.min-1 after 60 min of exercise, beyond which it did not change significantly until the cessation of exercise. Hepatic glucose uptake at rest was 1.38 +/- 0.42 mg.kg-1.min-1 and did not change appreciably during exercise or recovery. Absolute hepatic glucose output (net glucose output plus uptake) rose from 3.96 +/- 0.45 mg.kg-1.min-1 at rest to 10.20 +/- 1.09 mg.kg-1.min-1 after 60 min of exercise and was 9.65 +/- 1.15 mg.kg-1.min-1 at 150 min of exercise. Ra rose from 3.34 +/- 0.21 mg.kg-1.min-1 to 7.58 +/- 0.73 and 8.59 +/- 0.77 mg.kg-1.min-1 at 60 and 150 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rectal and rectal vs. esophageal temperatures in paraplegic men during prolonged exercise

This study investigated the rectal (Tre), esophageal (Tes), and skin (Tsk) temperature changes in a group of trained traumatic paraplegic men pushing their own wheelchairs on a motor-driven treadmill for a prolonged period in a neutral environment. There were two experiments. The first experiment (Tre and Tsk) involved a homogeneous group (T10-T12/L3) of highly trained paraplegic men [maximum O2 uptake (VO2max) 47.5 +/- 1.8 ml.kg-1.min-1] exercising for 80 min at 60-65% VO2max.Tre and Tsk (head, arm, thigh, and calf) and heart rate (HR) were recorded throughout. O2 uptake (VO2), minute ventilation (VE), CO2 production (VCO2), and heart rate (HR) were recorded at four intervals. During experiment 1 significant changes in HR and insignificant changes in VCO2, VE, and VO2 occurred throughout prolonged exercise. Tre increased significantly from 37.1 +/- 0.1 degrees C (rest) to 37.8 +/- 0.1 degrees C after 80 min of exercise. There were only significant changes in arm Tsk. Experiment 2 involved a nonhomogeneous group (T5-T10/T11) of active paraplegics (VO2max 39.9 +/- 4.3 ml.kg-1.min-1) exercising at 60-65% VO2max for up to 45 min on the treadmill while Tre and Tes were simultaneously recorded. Tes rose significantly faster than Tre during exercise (dT/dt 20 min: Tes 0.050 +/- 0.003 degrees C/min and Tre 0.019 +/- 0.005 degrees C/min), and Tes declined significantly faster than Tre at the end of exercise. Tes was significantly higher than Tre at the end of exercise. Our results suggest that during wheelchair propulsion by paraplegics, Tes may be a better estimate of core temperature than Tre.     

Effect of short-term energy intake level and exercise on oxygen consumption in men

The influence of short-term energy intake and cycle exercise on oxygen consumption in response to a 1.5 MJ test meal was investigated in ten young, adult men. On the morning after a previous day's "low-energy" intake (LE regimen) of 4.5 MJ, the mean resting oxygen consumption increased by 0.7 ml X kg-1 X min-1 after the test meal (P less than 0.025). After a "high-energy" intake (HE regimen) of 18.1 MJ, the resting measurement was unchanged (+0.4 ml X kg-1 X min-1) after the meal (n.s.). These trends are the reverse of what would be expected if oxygen consumption in response to feeding is a factor in the acute control of body weight. The mean fasting oxygen consumption during cycle exercise at 56% of VO2max (constant work) for both LE and HE prior intakes was not different at 31.1 ml X kg-1 X min-1. Oxygen consumption during exercise increased after feeding by 0.5 ml X kg-1 X min-1 on the LE regimen (n.s.) and decreased by 1.2 ml X kg-1 X min-1 on the HE regimen (n.s.). These results are also the reverse of what would be expected if oxygen consumption in response to exercise is related to short-term energy intake.     

Effects of body mass and morphology on thermal responses in water

Ten male volunteers were divided into two groups based on body morphology and mass. The large-body mass (LM) group (n = 5) was 16.3 kg heavier and 0.22 cm2 X kg-1 X 10(-2) smaller in surface area-to-mass ratio (AD X wt-1) (P less than 0.05) than the small-body mass (SM) group (n = 5). Both groups were similar in total body fat and skinfold thicknesses (P greater than 0.05). All individuals were immersed for 1 h in stirred water at 26 degrees C during both rest and one intensity of exercise (metabolic rate approximately 550 W). During resting exposures metabolic rate (M) and rectal temperature (Tre) were not different (P greater than 0.05) between the LM and SM groups at min 60. Esophageal temperature (Tes) was higher (P less than 0.05) for the SM group at min 60, although the change in Tes during the 60 min between groups was similar (LM, -0.4 degrees C; SM, -0.2 degrees C). Tissue insulation (I) was lower (P less than 0.05) for SM (0.061 degrees C X m-2 X W-1) compared with the LM group (0.098 degrees C X m-2 X W-1). During exercise M, Tre, Tes, and I were not different (P greater than 0.05) between groups at min 60. These data illustrate that a greater body mass between individuals increases the overall tissue insulation during rest, most likely as a result of a greater volume of muscle tissue to provide insulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Core temperature "null zone".

An experimental protocol was designed to investigate whether human core temperature is regulated at a "set point" or whether there is a neutral zone between the core thresholds for shivering thermogenesis and sweating. Nine male subjects exercised on an underwater cycle ergometer at a work rate equivalent to 50% of their maximum work rate. Throughout an initial 2-min rest period, the 20-min exercise protocol, and the 100-min recovery period, subjects remained immersed to the chin in water maintained at 28 degrees C. On completion of the exercise, the rate of forehead sweating (Esw) decayed from a mean peak value of 7.7 +/- 4.2 (SD) to 0.6 +/- 0.3 g.m-2.min-1, which corresponds to the rate of passive transpiration, at core temperatures of 37.42 +/- 0.29 and 37.39 +/- 0.48 degrees C, as measured in the esophagus (Tes) and rectum (Tre), respectively. Oxygen uptake (VO2) decreased rapidly from an exercising level of 2.11 +/- 0.25 to 0.46 +/- 0.09 l/min within 4 min of the recovery period. Thereafter, VO2 remained stable for approximately 20 min, eventually increased with progressive cooling of the core region, and was elevated above the median resting values determined between 15 and 20 min at Tes = 36.84 +/- 0.38 degrees C and Tre = 36.80 +/- 0.39 degrees C. These results indicate that the core temperatures at which sweating ceases and shivering commences are significantly different (P less than 0.001) regardless of whether core temperature is measured within the esophagus or rectum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Work capacity during 30 days of bed rest with isotonic and isokinetic exercise training

The purpose was to test the hypothesis that twice daily, short-term, variable intensity isotonic and intermittent high-intensity isokinetic leg exercise would maintain peak O2 uptake (VO2) and muscular strength and endurance, respectively, at or near ambulatory control levels during 30 days of -6 degrees head-down bed rest (BR) deconditioning. Nineteen men (aged 32-42 yr) were divided into no exercise control (peak VO2 once/wk, n = 5), isokinetic (Lido ergometer, n = 7), and isotonic (Quinton ergometer, n = 7) groups. Exercise training was conducted in the supine position for two 30-min periods/day for 5 days/wk. Isotonic training was at 60-90% of peak VO2, and isokinetic training (knee flexion-extension) was at 100 degrees/s. Mean (+/- SE) changes (P less than 0.05) in peak VO2 (ml.m-1.kg-1) from ambulatory control to BR day 28 were 44 +/- 4 to 36 +/- 3, -18.2% (3.27-2.60 l/m) for no exercise, 39 +/- 4 to 40 +/- 3, +2.6% (3.13-3.14 l/min) for isotonic, and 44 +/- 3 to 40 +/- 2, -9.1% (3.24-2.90 l/min) for isokinetic. There were no significant changes in any groups in leg peak torque (right knee flexion or extension), leg mean total work, arm total peak torque, or arm mean total work. Mean energy costs for the isotonic and isokinetic exercise training were 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1) and 214 kcal/h (8.9 +/- 0.5 ml.m-1.kg-1), respectively. Thus near-peak, variable intensity, isotonic leg exercise maintains peak VO2 during 30 days of BR, while this peak, intermittent, isokinetic leg exercise protocol does not.     

Carnitine metabolism during exercise in patients with peripheral vascular disease

The distribution between carnitine and the acyl derivatives of carnitine reflects changes in the metabolic state of a variety of tissues. Patients with peripheral vascular disease (PVD) develop skeletal muscle ischemia with exertion. This impairment in oxidative metabolism during exercise may result in the generation of acylcarnitines. To test this hypothesis, 11 patients with PVD and 7 age-matched control subjects were evaluated with graded treadmill exercise. Subjects with PVD walked to maximal claudication pain at a peak O2 consumption (VO2) of 19.9 +/- 1.3 ml X kg-1 X min-1 (mean +/- SE). Control subjects were taken to a near-maximal work load at a VO2 of 31.3 +/- 1.0 ml X kg-1 X min-1. In patients with PVD, the plasma concentration of total acid-soluble, long-chain acylcarnitine and total carnitine was increased at peak exercise compared with resting values. Four minutes postexercise, the plasma short-chain acylcarnitine concentration was also increased. In control subjects taken to the higher work load, only the long-chain acylcarnitine concentration was increased at peak exercise. In patients with PVD, plasma short-chain acylcarnitine concentration at rest was negatively correlated with subsequent maximal walking time (r = -0.51, P less than 0.05). In conclusion, acylcarnitines increased in patients with PVD who walked to maximal claudication pain, whereas control subjects did not show equivalent changes even when taken to a higher work load. The relationship between short-chain acylcarnitine concentration at rest and subsequent exercise performance suggests that repeated episodes of ischemia may cause chronic accumulation of short-chain acylcarnitine in plasma in proportion to the severity of disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Decreased reliance on lactate during exercise after acclimatization to 4,300 m

We hypothesized that the increased exercise arterial lactate concentration on arrival at high altitude and the subsequent decrease with acclimatization were caused by changes in blood lactate flux. Seven healthy men [age 23 +/- 2 (SE) yr, wt 72.2 +/- 1.6 kg] on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-2D]glucose (Brooks et al. J. Appl. Physiol. 70:919-927, 1991) and [3-13C]lactate and rested for a minimum of 90 min followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 consumption (VO2peak; 65 +/- 2% of both acute altitude and acclimatization). During rest at sea level, lactate appearance rate (Ra) was 0.52 +/- 0.03 mg.kg-1.min-1; this increased sixfold during exercise to 3.24 +/- 0.19 mg.kg-1.min-1. On acute exposure, resting lactate Ra rose from sea level values to 2.2 +/- 0.2 mg.kg-1.min-1. During exercise on acute exposure, lactate Ra rose to 18.6 +/- 2.9 mg.kg-1.min-1. Resting lactate Ra after acclimatization (1.77 +/- 0.25 mg.kg-1.min-1) was intermediate between sea level and acute exposure values. During exercise after acclimatization, lactate Ra (9.2 +/- 0.7 mg.kg-1.min-1) rose from resting values but was intermediate between sea level and acute exposure values. The increased exercise arterial lactate concentration response on arrival at high altitude and subsequent decrease with acclimatization are due to changes in blood lactate appearance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of hematocrit reduction on hormonal and metabolic responses to exercise

We wished to determine the effect of a 25% hematocrit reduction on glucoregulatory hormone release and glucose fluxes during exercise. In five anemic dogs, plasma glucose fell by 21 mg/dl and in five controls by 7 mg/dl by the end of the 90-min exercise period. After 50 min of exercise, hepatic glucose production (Ra) and glucose metabolic clearance rate (MCR) began to rise disproportionately in anemics compared with controls. By the end of exercise, the increase in Ra was almost threefold higher (delta 15.1 +/- 3.4 vs. delta 5.2 +/- 1.3 mg X kg-1 X min-1) and MCR nearly fourfold (delta 24.6 +/- 8.8 vs. delta 6.5 +/- 1.3 ml X kg-1 X min-1). Exercise with anemia, in relation to controls resulted in elevated levels of glucagon [immunoreactive glucagon (IRG) delta 1,283 +/- 507 vs delta 514 +/- 99 pg/ml], norepinephrine (delta 1,592 +/- 280 vs. delta 590 +/- 155 pg/ml), epinephrine (delta 2,293 +/- 994 vs. delta 385 +/- 186 pg/ml), cortisol (delta 6.7 +/- 2.2 vs. delta 2.1 +/- 1.0 micrograms/dl) and lactate (delta 12.1 +/- 2.2 vs. delta 4.2 +/- 1.8 mg/dl) after 90 min. Immunoreactive insulin and free fatty acids were similar in both groups. In conclusion, exercise with a 25% hematocrit reduction results in 1) elevated lactate, norepinephrine, epinephrine, cortisol, and IRG levels, 2) an increased Ra which is likely related to the increased counterregulatory response, and 3) we speculate that a near fourfold increase in MCR is related to metabolic changes due to hypoxia in working muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma volume during heat stress and exercise in women

Five women were studied during exercise and passive heating to determine whether PV dynamics were affected by the menstrual cycle. The exercise bout (80% VO2 peak) on a modified cycle ergometer and the passive heat stress were done in a hot environment (Ta = 50 degrees C, Pw = 1.61 kPa) during the follicular and luteal phase. Esophageal temperature (Tes) was measured continuously. Blood samples were drawn after each 0.2 degree C increase in Tes and VO2 was measured at that time. Initial PV was estimated at rest during the follicular phase. PV changes from rest were calculated at each Tes from Hb and Hct. During passive heating, PV decreased by a mean volume of 156 (+/- 80) ml to 2.83 (+/- 0.09) l in the follicular phase. During the luteal phase, there was a larger volume reduction (300 +/- 100 ml) during passive heating, and the final PV was lower than in the follicular phase and averaged 2.47 +/- 0.18 l. During exercise, PV decreased 463 (+/- 90) ml to 2.50 (+/- 0.11) l in the follicular and 381 (+/- 70) ml to 2.50 (+/- 0.23) l in the luteal phase. These data indicate that there is a menstrual cycle effect on PV dynamics during passive heating such that more fluid is shifted out of the vasculature during the luteal phase. During severe exercise there is a greater fluid loss during the follicular phase, yet the final PV is not different between phases.     

Short-term training attenuates muscle TCA cycle expansion during exercise in women.

Muscle glycogenolytic flux and lactate accumulation during exercise are lower after 3-7 days of "short-term" aerobic training (STT) in men (e.g., Green HJ, Helyar R, Ball-Burnett M, Kowalchuk N, Symon S, and Farrance B. J Appl Physiol 72: 484-491, 1992). We hypothesized that 5 days of STT would attenuate pyruvate production and the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise, because of reduced flux through the reaction catalyzed by alanine aminotransferase (AAT; pyruvate + glutamate <--> 2-oxoglutarate + alanine). Eight women [22 +/- 1 yr, peak oxygen uptake (Vo2 peak) = 40.3 +/- 4.6 ml. kg-1. min-1] performed seven 45-min bouts of cycle exercise at 70% Vo2 peak over 9 days (1 bout/day; rest only on days 2 and 8). During the first and last bouts, biopsies (vastus lateralis) were obtained at rest and after 5 and 45 min of exercise. Muscle glycogen concentration was approximately 50% higher at rest after STT (493 +/- 38 vs. 330 +/- 20 mmol/kg dry wt; P 相似文献   

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

To find out whether endurance training influences the kinetics of the increases in heart rate (fc) during exercise driven by the sympathetic nervous system, the changes in the rate of fc adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%-70% of maximal oxygen uptake (VO2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuous fc recording. At the completion of the training programme, the subjects' VO2max had increased significantly (39.2 ml.min-1.kg-1, SD 4.7 vs 46 ml.min-1.kg-1, SD 5.6) and the steady-state fc at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-state fc was found at 150 W (146 beats.min-1, SD 10 vs 169 beats.min-1, SD 9) but the difference between the steady-state fc at 150 W and that at 100 W (delta fc) did not decrease significantly (26 beats.min-1, SD 7 vs 32 beats.min-1, SD 6). The time constant (tau) of the fc increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P less than 0.01) and the acceleration index (A = 0.63.delta fc.tau-1) decreased from 0.20 beats.min-1.s-1, SD 0.05 to 0.14 beats.min-1.s-1, SD 0.04 (P less than 0.02). The major part of the changes in tau and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Human thermoregulatory responses during serial cold-water immersions

This studyexamined whether serial cold-water immersions over a 10-h period wouldlead to fatigue of shivering and vasoconstriction. Eight men wereimmersed (2 h) in 20°C water three times (0700, 1100, and 1500) in1 day (Repeat). This trial was compared with single immersions(Control) conducted at the same times of day. Before Repeat exposuresat 1100 and 1500, rewarming was employed to standardize initial rectaltemperature. The following observations were made in the Repeatrelative to the Control trial: 1)rectal temperature was lower and heat debt was higher(P < 0.05) at 1100; 2) metabolic heat production waslower (P < 0.05) at 1100 and 1500;3) subjects perceived the Repeattrial as warmer at 1100. These data suggest that repeated coldexposures may impair the ability to maintain normal body temperaturebecause of a blunting of metabolic heat production, perhaps reflectinga fatigue mechanism. An alternative explanation is that shiveringhabituation develops rapidly during serially repeated cold exposures.

     

Mobilization of circulating leucocyte and lymphocyte subpopulations during and after short, anaerobic exercise

A group of 11 healthy athletes [age, 27.4 (SD 6.7) years; body mass, 75.3 (SD 9.2) kg; height, 182 (SD 8) cm; maximal oxygen uptake, 58.0 (SD 9.9) ml.kg-1.min-1] conducted maximal exercise of 60-s duration on a cycle ergometer [mean exercise intensity, 520 (SD 72) W; maximal lactate concentration, 12.26 (SD 1.35) mmol.l-1]. Adrenaline and noradrenaline, and leucocyte subpopulations were measured flow cytometrically at rest, after 5-min warming up at 50% of each individual's anaerobic threshold (followed by 5-min rest), immediately after (0 min), 15 min, 30 min, and 1, 2, 4 and 24 h after exercise. Granulocytes showed two increases, the first at 15 min and, after return to pre-exercise values, the second more than 2 h after exercise. Eosinophils also increased at 15 min but decreased below pre-exercise values 2 h after exercise. Total lymphocytes and monocytes had their maximal increases at 0 min. Out of all lymphocyte subpopulations CD3-CD16/CD56(+)- and CD8+CD45RO--cells increased most and had their maximal cell counts at 0 min. The CD3(+)-, CD4+CD45RO(+)-, CD8+CD45RO(+)-, and CD19(+)- increased at 0 min, but had their maximum at 15 min. During the hours after exercise CD3-CD16/CD56(+)-, CD3+CD16/CD56(+)-, CD8+CD45RO(+)- and CD8+CD45RO--cells were responsible for the lymphocytopenia. The CD3(+)- and CD3-CD16/CD56(+)-cells were lower 24 h after exercise than before exercise. Adrenaline and noradrenaline increased during exercise. In conclusion, short anaerobic exercise led to a sequential mobilization of leucocyte subpopulations. The rapid increase of natural killer cells and monocytes may have been due to increased blood flow and catecholamine concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute anemia increases lactate production and decreases clearance during exercise

We evaluated whether elevated blood lactate concentration during exercise in anemia is the result of elevated production or reduced clearance. Female Sprague-Dawley rats were made acutely anemic by exchange transfusion of plasma for whole blood. Hemoglobin and hematocrit were reduced 33%, to 8.6 +/- 0.4 mg/dl and 26.5 +/- 1.1%, respectively. Blood lactate kinetics were studied by primed continuous infusion of [U-14C]lactate. Blood flow distribution during rest and exercise was determined from injection of 153Gd- and 113Sn-labeled microspheres. Resting blood glucose (5.1 +/- 0.2 mM) and lactate (1.9 +/- 0.02 mM) concentrations were not different in anemic animals. However, during exercise blood glucose was lower in anemic animals (4.0 +/- 0.2 vs. 4.6 +/- 0.1 mM) and lactate was higher (6.1 +/- 0.4 vs. 2.3 +/- 0.5 mM). Blood lactate disposal rates (turnover measured with recyclable tracer, Ri) were not different at rest and averaged 136 +/- 5.8 mumol.kg-1.min-1. Ri was significantly elevated in both control (260.9 +/- 7.1 mumol.kg-1.min-1) and anemic animals (372.6 +/- 8.6) during exercise. Metabolic clearance rate (MCR = Ri/[lactate]) did not differ during rest (151 +/- 8.2 ml.kg-1.min-1); MCR was reduced more by exercise in anemic animals (64.3 +/- 3.8) than in controls (129.2 +/- 4.1). Plasma catecholamine levels were not different in resting rats, with pooled mean values of 0.45 +/- 0.1 and 0.48 +/- 0.1 ng/ml for epinephrine (E) and norepinephrine (NE), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of menstrual cycle and physical training on heat loss responses during dynamic exercise at moderate intensity in a temperate environment

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal O2 uptake of 36.7+/-1.1 vs. 49.4+/-1.7 ml.kg-1.min-1, respectively; P<0.05) performed a cycling exercise at 50% maximal O2 uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25 degrees C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature (Tes) during exercise were significantly higher during the midluteal than during the midfollicular phase (P<0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. Tes threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. Tes threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase; however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase.