Light-dark differences in the effects of ambient temperature on gaseous metabolism in newborn rats.

Body temperature (T(b)) of rat pups (7-9 days old) raised under a 12:12-h light-dark (L-D) regimen (L: 0700-1900, D: 1900-0700) was consistently higher in D than in L by approximately 1.1 degrees C. We tested the hypothesis that the L-D differences in T(b) were accompanied by differences in the set point of thermoregulation. Measurements were performed on rat pups at 7-9 days after birth. O(2) consumption (VO(2)) and CO(2) production (VCO(2)) were measured with an open-flow method during air breathing, as ambient temperature (T(a)) was decreased from 40 to 15 degrees C at the constant rate of 0.5 degrees C/min. At T(a) >/=33 degrees C, VO(2) was not significantly different between L and D, whereas VCO(2) was higher in L, suggesting a greater ventilation. Over the 33 to 15 degrees C range the VO(2) values in D exceeded those in L by approximately 30%. Specifically, the difference was contributed by differences in thermogenesis at T(a) = 30 to 20 degrees C. As T(a) was decreased, the critical temperature at which VO(2) began to rise was lower in L. We conclude that the higher T(b) of rat pups in D is accompanied by a higher set point for thermoregulation and a greater thermogenesis. These results are consistent with the idea that, in newborns, endogenous changes in the set point of thermoregulation contribute to the circadian oscillations of T(b).     

Effects of exercise and time elapsed after exercise on VO2, VCO2 and R responses to norepinephrine in rats

The effects of norepinephrine (NE) injection (300 microgram . kg-1 of body weight) on oxygen consumption (VO2), carbon dioxide production (VCO2) and respiratory exchange ratio (R) were investigated in female rats after 1 h of running on a treadmill (21.5 m . min-1) at 10% inclination. Six groups of animals were injected respectively at various times after the exercise (1, 3, 6, 9, 21, and 47 h), and were compared to six non-exercised groups injected at corresponding times. VO2 and VCO2 were monitored continuously during the 20 min preceding injection and for the 60 min following it. The increases in VO2 and VCO2, and the decrease in R were of similar magnitude in both exercised and non-exercised rats (about 30% and 20% for VO2 and VCO2, respectively, and -12% for R). Peak VO2 and R values attained after NE injection varied however with time of injection, specially in exercised animals 1 and 9 h after the run. Exercise significantly delayed time of response to NE for VO2 and VCO2 particularly 1 and 9 h after the running bout. It is concluded that time of day, exercise, and time elapsed after exercise are important factors to consider when studying metabolic responses to catecholamines. Furthermore, it is suggested that such experimental controls might be meaningful in human studies as well.     

Response of respiratory exchange ratio (R) to sinusoidal work load in humans

An examination was made of the response of respiratory exchange ratio (R), carbon dioxide output (VCO2) and oxygen uptake (VO2) to sinusoidal work load with periods (T) of 1-16 min in six healthy men to determine whether R response is sinusoidal. The influence of the ratio of the amplitude of VCO2 to that of VO2 and the phase lag between them on R response was also studied by computer simulation. The results and conclusions obtained are as follows: 1) With decrease in the period, the amplitudes of VO2 and VCO2 dropped exponentially, becoming least at T of 1 min (T = 1 min). In contrast, the amplitude of R was largest at T = 4 min and subsequently decreased progressively. 2) The peak amplitude of R at T = 4 min can be explained by the larger phase lag and relatively low of amplitude of VCO2 to VO2. 3) The smallest amplitude of R at T = 1 min was due not to the ratio of amplitude or phase lag, but to remarkably smaller amplitudes of VO2 and VCO2. 4) The phase lag of VO2 to sinusoidal work load was smaller than that of VCO2. Phase lag of R was considerably larger than that of VO2 or VCO2. 5) The response curve of VO2 and VCO2 is a sinusoidal curve with the same period as exercise. However, the response of R is not a real sinusoidal but a deformed biphasic curve with a high crest and low trough. The deformity is determined by the phase lag between VO2 and VCO2 response and also the ratio of amplitude of VCO2 to that of VO2.     

Cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in obese Zucker rats

The primary purpose of the study was to test the hypothesis that reduced leptin signaling is necessary to elicit the cardiovascular and metabolic responses to fasting. Lean (Fa/?; normal leptin receptor; n = 7) and obese (fa/fa; mutated leptin receptor; n = 8) Zucker rats were instrumented with telemetry transmitters and housed in metabolic chambers at 23 degrees C (12:12-h light-dark cycle) for continuous (24 h) measurement of metabolic and cardiovascular variables. Before fasting, mean arterial pressure (MAP) was higher (MAP: obese = 103 +/- 3; lean = 94 +/- 1 mmHg), whereas oxygen consumption (VO(2): obese = 16.5 +/- 0.3; lean = 18.6 +/- 0.2 ml. min(-1). kg(-0.75)) was lower in obese Zucker rats compared with their lean controls. Two days of fasting had no effect on MAP in either lean or obese Zucker rats, whereas VO(2) (obese = -3.1 +/- 0.3; lean = -2.9 +/- 0.1 ml. min(-1). kg(-0.75)) and heart rate (HR: obese = -56 +/- 4; lean = -42 +/- 4 beats/min) were decreased markedly in both groups. Fasting increased HR variability both in lean (+1.8 +/- 0.4 ms) and obese (+2.6 +/- 0.3 ms) Zucker rats. After a 6-day period of ad libitum refeeding, when all parameters had returned to near baseline levels, the cardiovascular and metabolic responses to 2 days of thermoneutrality (ambient temperature 29 degrees C) were determined. Thermoneutrality reduced VO(2) (obese = -2.4 +/- 0.2; lean = -3.3 +/- 0.2 ml. min(-1). kg(-0.75)), HR (obese = -46 +/- 5; lean = -55 +/- 4 beats/min), and MAP (obese = -13 +/- 6; lean = -10 +/- 1 mmHg) similarly in lean and obese Zucker rats. The results indicate that the cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in Zucker rats and suggest that intact leptin signaling may not be requisite for the metabolic and cardiovascular responses to reduced energy intake.     

Effects of human pregnancy and aerobic conditioning on alveolar gas exchange during exercise

This study examined the effects of aerobic conditioning during the second and third trimesters of human pregnancy on ventilatory responses to graded cycling. Previously sedentary pregnant women were assigned randomly to an exercise group (n = 14) or a nonexercising control group (n = 14). Data were collected at 15-17 weeks, 25-27 weeks and 34-36 weeks of pregnancy. Testing involved 20 W.min-1 increases in work rate to a heart rate of 170 beats.min-1 and (or) volitional fatigue. Breath-by-breath ventilatory and alveolar gas exchange measurements were compared at rest, a standard submaximal .VO2 and peak exercise. Within both groups, resting .V(E), .V(A), and V(T)/T(I) increased significantly with advancing gestation. Peak work rate, O2 pulse (.VO2/HR), .V(E), .V(A) respiratory rate, V(T)/T(I), .VO2, .VCO2, and the ventilatory threshold (T(vent)) were increased after physical conditioning. Chronic maternal exercise has no significant effect on pregnancy-induced changes in ventilation and (or) alveolar gas exchange at rest or during standard submaximal exercise. Training-induced increases in T(vent) and peak oxygen pulse support the efficacy of prenatal fitness programs to improve maternal work capacity.     

Diurnal variations in ventilatory and cardiorespiratory responses to submaximal treadmill exercise in females

Diurnal variations in ventilatory and cardiorespiratory responses to submaximal treadmill exercise were analysed in 11 eumenorrhoeic women and in 10 women using monophasic oral contraceptives. Subjects performed submaximal treadmill exercise at three intensities averaging 7, 8, and 9 km x h(-1), each for 4 min at 0800, 1300 and 1700 hours, assigned randomly on 3 separate days. Rectal temperature was measured before (T(rec(b))) and after (T(rec(a))) exercise. Cardiac frequency (f(c)), ventilation (V(E)), oxygen uptake (VO(2)), carbon dioxide output (VCO(2)), and respiratory exchange ratio (R) were assessed in the last minute of each stage of the exercise. Both T(rec(b)) and T(rec(a)) increased from 0800 to 1700 hours (P < 0.001). For a given submaximal work rate, VO(2) and VCO(2) were higher in the afternoon compared to the morning. Similarly, R was increased at 1700 hours compared to 0800 hours during the recovery period following exercise (P < 0.05). However, V(E) did not vary significantly during the day at any of the running intensities. No significant interactions (group x time of day) were observed in any of the studied parameters. In contrast to ventilation, the VO(2) and VCO(2) of the females during submaximal exercise were both affected by the time of day, without any differences between eumenorrhoeic women and users of oral contraceptives.     

The effect of leptin on adrenal glands in rats with streptozotocin-induced diabetes: an experimental study

OBJECTIVE: To determine the cross-section area of adrenal medulla and the percentage of Ki-67 (a proliferation marker) of the adrenal gland in diabetic rats after leptin injection. STUDY DESIGN: Twenty-nine male Wistar rats were randomly divided into 3 groups: control (C) group (n = 9), diabetes mellitus (DM) group (n = 10) and leptin-injected diabetes mellitus (DM+L) group (n = 10). Experimental DM was induced by a single intraperitoneal dose of streptozotocin (40 mg/kg). After this, leptin (100 microg/kg) was injected subcutaneously for a period of 2 weeks in the diabetic group. RESULTS: An atrophy of adrenal medulla in the DM group was observed, and this atrophy returned to normal morphology after injection of leptin. In addition, an increase in the Ki-67 percentage was demonstrated in the zona reticularis layers in the DM+L group. CONCLUSION: Our study indicated that leptin stimulates the sympathoadrenal system and the androgen producing adrenal cortex in DM rats.     

Central stimulatory effect of leptin on T3 production is mediated by brown adipose tissue type II deiodinase

To assess whether intracerebroventricular leptin administration affects monodeiodinase type II (D2) activity in the tissues where it is expressed [cerebral cortex, hypothalamus, pituitary, and brown adipose tissue (BAT)], hepatic monodeiodinase type I (D1) activity was inhibited with propylthiouracil (PTU), and small doses of thyroxine (T4; 0.6 nmol. 100 g body wt(-1). day(-1)) were supplemented to compensate for the PTU-induced hypothyroidism. Two groups of rats were infused with leptin for 6 days, one of them being additionally treated with reverse triiodothyronine (rT3), an inhibitor of D2. Control rats were infused with vehicle and pair-fed the amount of food consumed by leptin-infused animals. Central leptin administration produced marked increases in D2 mRNA expression and activity in BAT, changes that were likely responsible for increased plasma T3 and decreased plasma T4 levels. Indeed, plasma T3 and T4 concentrations were unaltered by central leptin administration in the presence of rT3. The additional observation of a leptin-induced increased mRNA expression of BAT uncoupling protein-1 suggested that the effect on BAT D2 may be mediated by the sympathetic nervous system.     

Decreased food intake rather than zinc deficiency is associated with changes in plasma leptin, metabolic rate, and activity levels in zinc deficient rats( small star, filled)

This study investigated the hypothesis that the reduced food intake and poor weight gain in zinc deficient rats is due to: increased plasma leptin concentration, increased physical activity and/or increased metabolic rate. Weanling rats were assigned to three groups: controls fed ad libitum (C), zinc deficient (ZD), and pair-fed controls (PF), and tested in a metabolic chamber and activity monitor at baseline and weekly for four weeks. At the end of the study, all groups were compared for differences in plasma leptin concentrations. ZD and PF animals had markedly reduced food intake and weight gain. ZD had reduced stereotypic and locomotor activity compared to PF animals and both groups demonstrated an abolished peri-nocturnal activity spike and were much less active than controls. This was associated with a reduced total metabolic rate by day 30: ZD (0.73 +/- 0.07 kcal/hr, p = 0.0001) and PF (0.83 +/- 0.06 kcal/hr, p = 0.0001) groups vs. controls (1.82 +/- 0.09 kcal/hr). Plasma leptin concentrations in ZD (1.55 +/- 0.06 &mgr;g/L) were lower than controls (2.01 +/- 0.18 &mgr;g/L, p < 0.03), but neither ZD nor controls were statistically different from PF (1.68 +/- 0.05 &mgr;g/L). Both low leptin concentrations and low metabolic rates in the ZD and PF rats were associated with decreased food intake rather than zinc deficiency. The reduced food intake and poor weight gain observed in zinc deficient rats could not be explained by elevated leptin concentrations, hypermetabolism, or increased activity. Low serum leptin concentrations, hypometabolism, and decreased activity are more likely the result of the anorexia of zinc deficiency.     

Muscle oxygenation trends after tapering in trained cyclists

BACKGROUND: This study examined muscle deoxygenation trends before and after a 7-day taper using non-invasive near infrared spectroscopy (NIRS). METHODS: Eleven cyclists performed an incremental cycle ergometer test to determine maximal oxygen consumption (VO2max = 4.68 +/- 0.57 L.min-1) prior to the study, and then completed two or three high intensity (85-90% VO2max) taper protocols after being randomly assigned to a taper group: T30 (n = 5), T50 (n = 5), or T80 (n = 5) [30%, 50%, 80% reduction in training volume, respectively]. Physiological measurements were recorded during a simulated 20 km time trials (20TT) performed on a set of wind-loaded rollers. RESULTS AND DISCUSSION: The results showed that the physiological variables of oxygen consumption (VO2), carbon dioxide (VCO2) and heart rate (HR) were not significantly different after tapering, except for a decreased ventilatory equivalent for oxygen (VE/VO2) in T50 (p 相似文献   

No effect of menstrual cycle phase and oral contraceptive use on endurance performance in rowers

The aim of this study was to examine whether variables commonly used in aerobic exercise testing are influenced by menstrual cycle phases and use of oral contraceptive (OC) in female rowers. Twenty-four eumenorrheic female rowers distinguished on the basis of both menstrual status and athleticism participated in this study and were divided into competitive cyclic athletes (n = 8), recreationally trained cyclic athletes (n = 7), and recreationally trained athletes taking OC pills (ROC; n = 9). Rowers performed 2 incremental tests to voluntary exhaustion on a rowing ergometer during 2 different phases of the menstrual cycle: the follicular phase (FP) and the luteal phase (LP). The study variables were power output (Pa), heart rate (HR), oxygen consumption (VO2), carbon dioxide production (VCO2), minute ventilation (VE), the mean respiratory exchange ratio, and ventilatory equivalents of O2 (VE/VO2)) and CO2 (VE/VCO2), which were measured at maximal and at the aerobic-anaerobic transition intensities. In addition, maximal blood lactate (La) values after the test were obtained. When comparing Pa, &OV0312;o2, HR, and La values, no significant differences (p > 0.05) between FP and LP at maximal load and at threshold intensity were found in all 3 groups of the rowers studied. However, we observed higher values (p < 0.05) for VE/VCO2 at both intensities in LP compared with FP in the ROC group. In conclusion, sport-specific endurance performance was not influenced by the phase of the normal menstrual cycle and the synthetic menstrual cycle of the OC users in the rowers studied. Therefore, normally menstruating female rowers and female rowers taking OC pills should not be concerned about the timing of their menstrual cycle with regard to optimized sport-specific endurance performance.     

Cost of flight in the zebra finch ( Taenopygia guttata): a novel approach based on elimination of (13)C labelled bicarbonate

On three separate occasions, five zebra finches ( Taenopygia guttata) were injected intraperitoneally with 0.2 ml 0.29 M NaH(13)CO(3)solution and placed immediately into respirometry chambers to explore the link between (13)C elimination and both O(2) consumption (VO(2)) and CO(2) production (VCO(2)). Isotope elimination was best modelled by a mono-exponential decay. The elimination rate (k(c)) of the (13)C isotope in breath was compared to VO(2) (ml O(2)/min) and VCO(2) (ml CO(2)/min) over sequential 5-min time intervals following administration of the isotope. Elimination rates measured 15-20 min after injection gave the closest relationships to VO(2) ( r(2) =0.82) and VCO(2) ( r(2)=0.63). Adding the bicarbonate pool size (N(c)) into the prediction did not improve the fit. A second group of birds ( n=11) were flown for 2 min (three times in ten birds and twice in one) between 15 min and 20 min following an injection of 0.2 ml of the same NaH(13)CO(3) solution. Breath samples, collected before and after flight, were used to calculate k(c) over the flight period, which was converted to VO(2) and VCO(2) using the equation generated in the validation experiment for the corresponding time period. The energy expenditure (watts) during flight was calculated from these values using the average RQ measured during flight of 0.79. The average flight cost measured using the bicarbonate technique was 2.24+/-0.11 W (mean+/-SE). This average flight cost did not differ significantly from predictions generated by an allometric equation formulated by Masman and Klaassen (1987 Auk 104:603-616). It was however substantially higher than the predictions based on the aerodynamic model of Pennycuick (1989 Oxford University Press), which assumes an efficiency of 0.23 for flight. The flight efficiency in these birds was 0.11 using this model. Flight cost was not related to within-individual variation [general linear model (GLM) F(1,31)=1.16, P=0.29] or across-individual variations in body mass (GLM F(1,31)=0.26, P=0.61), wingspan (regression F(1,10)=0.01, P=0.94) or wing loading (regression F(1, 31)=0.001, P=0.99) in this sample of birds.     

Leptin and prolactin, but not corticosterone, modulate body weight and thyroid function in protein-malnourished lactating rats.

To understand the role of hormonal changes in the lower food ingestion and body weight in protein-restricted lactating rats as well as the higher serum T (3), higher deiodination, iodide and T (3) milk transfer, we measured maternal serum prolactin, leptin, TSH and corticosterone, which are hormones that could influence those parameters. After birth, dams were separated into: control-fed with a 23 % protein diet (n = 12) and PR (protein-restricted)-fed with an 8 % protein diet (n = 12). At the 4 (th) and 21 (st) day of lactation, half of the animals in each group were sacrificed. PR dams presented hyperleptinemia (day 4: + 20 %; day 21: + 19 %; p < 0.05) and hypoprolactinemia (day 4: - 85 %; day 21: - 92 %; p < 0.05), which could help explain the lower food consumption and body weight in lactating PR rats since leptin is anorexigenic and prolactin is orexigenic. Also, this hyperleptinemia could contribute for the increase in serum T (3) of PR dams, since leptin stimulates T (3) production, especially acting on deiodinases. Serum corticosterone was not different between PR and C groups, and TSH was lower only at the end of lactation. Thus, we suggest that both leptin and prolactin could play an important role in the body weight and thyroid hormone changes observed in protein-malnourished lactating rats.     

The relationship between the ventilation and lactate thresholds following normal, low and high carbohydrate diets

Five men performed an incremental exercise test following a normal, low and high carbohydrate dietary regimen over a 7-day period, to examine the influence of an altered carbohydrate energy intake on the relationship between the ventilation (VET) and lactate (LaT) thresholds. VET and LaT were determined from the ventilatory equivalents for O2 (VE.VO2(-1) and CO2 (VE.VCO2(-1) and the log-log transformation of the lactate (La) to power output relationship, respectively. The total duration of the incremental exercise test, carbon dioxide output (VCO2), respiratory exchange ratio, blood La values and arterialized venous partial pressure of CO2 (PCO2) were reduced, and VE.VCO2(-1), the slope of the VE-VCO2 relationship, blood beta-hydroxybutyrate and pH were increased during the low carbohydrate trial compared with the other conditions. Total plasma protein and Na+, K+, and Cl- were similar across conditions. LaT and VET were unaffected by the altered proportions of carbohydrate in the diets and occurred at a similar oxygen consumption (mean VO2 across trials was 1.98 L.min-1 for VET and 2.01 L.min-1 for LaT). A significant relationship (r = 0.86) was observed for the VO2 that represented individual VET and LaT values. The increased VE.VCO2(-1) and slope of the VE-VCO2 relationship could be accounted for by the lower PCO2. It is concluded that alterations in carbohydrate energy intake do not produce an uncoupling of VET and LaT as has been reported previously.     

Improvement of alveolar-capillary membrane diffusing capacity with exercise training in chronic heart failure.

Chronic heart failure (CHF) may impair lung gas diffusion, an effect that contributes to exercise limitation. We investigated whether diffusion improvement is a mechanism whereby physical training increases aerobic efficiency in CHF. Patients with CHF (n = 16) were trained (40 min of stationary cycling, 4 times/wk) for 8 wk; similar sedentary patients (n = 15) were used as controls. Training increased lung diffusion (DlCO, +25%), alveolar-capillary conductance (DM, +15%), pulmonary capillary blood volume (VC, +10%), peak exercise O2 uptake (peak VO2, +13%), and VO2 at anaerobic threshold (AT, +20%) and decreased the slope of exercise ventilation to CO2 output (VE/VCO2, -14%). It also improved the flow-mediated brachial artery dilation (BAD, from 4.8 +/- 0.4 to 8.2 +/- 0.4%). These changes were significant compared with baseline and controls. Hemodynamics were obtained in the last 10 patients in each group. Training did not affect hemodynamics at rest and enhanced the increase of cardiac output (+226 vs. +187%) and stroke volume (+59 vs. +49%) and the decrease of pulmonary arteriolar resistance (-28 vs. -13%) at peak exercise. Hemodynamics were unchanged in controls after 8 wk. Increases in DlCO and DM correlated with increases in peak VO2 (r = 0.58, P = 0.019 and r = 0.51, P = 0.04, respectively) and in BAD (r = 0.57, P < 0.021 and r = 0.50, P = 0.04, respectively). After detraining (8 wk), DlCO, DM, VC, peak VO2, VO2 at AT, VE/VCO2 slope, cardiac output, stroke volume, pulmonary arteriolar resistance at peak exercise, and BAD reverted to levels similar to baseline and to levels similar to controls. Results document, for the first time, that training improves DlCO in CHF, and this effect may contribute to enhancement of exercise performance.     

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.     

Effects of prolonged exercise in highly trained traumatic paraplegic men

This study investigated the cardiovascular and metabolic responses to prolonged wheelchair exercise in a group of highly trained, traumatic paraplegic men. Six endurance-trained subjects with spinal cord lesions from T10 to T12/L3 underwent a maximal incremental exercise test in which they propelled their own track wheelchairs on a motor-driven treadmill to exhaustion to determine maximal O2 uptake (VO2max) and related variables. One week later each subject exercised in the same wheelchair on a motorized treadmill at 60-65% of VO2max for 80 min in a thermoneutral environment (dry bulb 22 degrees C, wet bulb 17 degrees C). Approximately 10 ml of venous blood were withdrawn both 20 min and immediately before exercise (0 min), after 40 and 80 min of exercise, and 20 min postexercise. Venous blood was analyzed for hematocrit (Hct), hemoglobin (Hb), and lactate, and the separated plasma was analyzed for glucose, K+, Na+, Cl-, free fatty acid (FFA), and osmolality. VO2, CO2 production (VCO2), minute ventilation (VE), respiratory exchange ratio (R), net efficiency, and wheelchair strike rate were determined at four intervals throughout the exercise period. Data were analyzed with an analysis of variance repeated-measures design and a Scheffé post hoc test. VO2max was 47.5 +/- 1.8 (SE) ml.min-1.kg-1 with maximal VE BTPS and maximal heart rate (HR) being 100.1 +/- 3.8 l/min and 190 +/- 1 beats/min, respectively. During prolonged exercise there were no significant changes in VO2, VCO2, VE, R, net efficiency, wheelchair strike rate, and lactate, glucose, and Na+ concentrations. Significant increases occurred in HR, FFA, K+, Cl-, osmolality, Hb, and Hct throughout exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Leptin,NPY, Melatonin and Zinc Levels in Experimental Hypothyroidism and Hyperthyroidism: The Relation to Zinc

Since zinc mediates the effects of many hormones or is found in the structure of numerous hormone receptors, zinc deficiency leads to various functional impairments in the hormone balance. And also thyroid hormones have important activity on metabolism and feeding. NPY and leptin are affective on food intake and regulation of appetite. The present study is conducted to determine how zinc supplementation and deficiency affect thyroid hormones (free and total T3 and T4), melatonin, leptin, and NPY levels in thyroid dysfunction in rats. The experiment groups in the study were formed as follows: Control (C); Hypothyroidism (PTU); Hypothyroidism+Zinc (PTU+Zn); Hypothyroidism+Zinc deficient; Hyperthyroidism (H); Hyperthyroidism+Zinc (H+Zn); and Hyperthyroidism+Zinc deficient. Thyroid hormone parameters (FT₃, FT₄, TT₃, and TT₄) were found to be reduced in hypothyroidism groups and elevated in the hyperthyroidism groups. Melatonin values increased in hyperthyroidism and decreased in hypothyroidism. Leptin and NPY levels both increased in hypo- and hyperthyroidism. Zinc levels, on the other hand, decreased in hypothyroidism and increased in hyperthyroidism. Zinc supplementation, particularly when thyroid function is impaired, has been demonstrated to markedly prevent these changes.     

Evaluation of a microprocessor-controlled exercise testing system

We evaluated a new exercise-testing system (Beckman Horizon MMC), incorporating a microprocessor that controls the acquisition of data, corrects for time delays, applies calibration factors, ensures quality control, and presents results in a variety of formats. Precision of measurements of ventilation (VE) and mixed expired gas concentrations was high. In steady-state exercise (n = 100) VO2 was measured with a precision (+/- SD) of 66 ml/min (4.3%), (r = 0.991); there was a small (4.62%) systematic underestimation of VCO2, but precision was comparable with VO2, with SD being 67 ml/min (4.55%) (r = 0.993). Good agreement was obtained between measurements made in progressive incremental exercise in healthy subjects with correlation coefficients of 0.997 for VE, 0.995 for VO2, and 0.994 for VCO2. Agreement in patients with cardiorespiratory disorders (n = 10) was similar, except in three patients in whom a variable pattern of breathing limited strict comparisons. Comparison with a breath-by-breath analysis system (n = 5) showed that rapid changes in VE, VCO2, and VO2 were followed accurately; the half time for a change in VO2 was not systematically different between the two systems (SD, 3.34 s, r = 0.951). The incorporation of microprocessor-controlled calibration procedures, which are simple to carry out frequently, was judged to be an important feature of this system.     

Delayed kinetics of respiratory gas exchange in the transition from prior exercise

The kinetics of oxygen uptake (VO2), carbon dioxide output (VCO2), and expired ventilation (VE) in the transition from rest or from prior exercise were studied in response to step increases in power output (PO). The data were modeled with a single-component exponential function incorporating a time delay (TD). Each subject exercised on four occasions. Test 1 was an incremental test for determination of ventilatory anaerobic threshold (AT). Step increase tests were rest to 80% of PO at AT (test 2), rest-40% AT (3a), 40-80% AT (3b), rest-40% AT (4a), and 40-120% AT (4b). Respiratory gas exchange was monitored by open-circuit techniques. The VO2 kinetics showed the time constant (tau) to be longer in the transitions from prior exercise [tests 3b and 4b were 60.6 +/- 10.8 (SD) and 79.2 +/- 17.4 s] than from rest (tests 2, 3a, and 4a were 37.8 +/- 7.2, 30.0 +/- 7.8, and 39.6 +/- 17.4 s). The mean response time (MRT = tau + TD) was also longer for these tests. Kinetic analysis for VCO2 showed a tendency for tau to be shorter for the tests from prior exercise, but neither tau nor tau + TD were significantly different between tests. In contrast to VCO2, VE kinetics showed a significantly longer tau + TD for test 3b (P less than 0.05) and test 4b (P less than 0.01). This study has shown the VO2 kinetics to be delayed when a given increment in PO occurred from prior exercise, whether the final PO was below or above the AT. Further, the dissociation of VCO2 and VE kinetics does not support a direct link between these two variables as the sole control factor in exercise hyperpnea.