Mixed findings regarding the effects of whole-body heat stress on central blood volume have been reported. This study evaluated the hypothesis that heat stress reduces central blood volume and alters blood volume distribution. Ten healthy experimental and seven healthy time control (i.e. non-heat stressed) subjects participated in this protocol. Changes in regional blood volume during heat stress and time control were estimated using technetium-99m labelled autologous red blood cells and gamma camera imaging. Whole-body heating increased internal temperature (> 1.0• C), cutaneous vascular conductance (approximately fivefold), and heart rate (52 ± 2 to 93 ± 4 beats min −1 ), while reducing central venous pressure (5.5 ± 07 to 0.2 ± 0.6 mmHg) accompanied by minor decreases in mean arterial pressure (all P < 0.05). The heat stress reduced the blood volume of the heart (18 ± 2%), heart plus central vasculature (17 ± 2%), thorax (14 ± 2%), inferior vena cava (23 ± 2%) and liver (23 ± 2%) (all P ≤ 0.005 relative to time control subjects). Radionuclide multiple-gated acquisition assessment revealed that heat stress did not significantly change left ventricular end-diastolic volume, while ventricular end-systolic volume was reduced by 24 ± 6% of pre-heat stress levels (P < 0.001 relative to time control subjects). Thus, heat stress increased left ventricular ejection fraction from 60 ± 1% to 68 ± 2% (P = 0.02). We conclude that heat stress shifts blood volume from thoracic and splanchnic regions presumably to aid in heat dissipation, while simultaneously increasing heart rate and ejection fraction.

During maximal exercise lactate taken up by the human brain contributes to reduce the cerebral metabolic ratio, O 2 /(glucose + 1/2 lactate), but it is not known whether the lactate is metabolized or if it accumulates in a distribution volume. In one experiment the cerebral arterio-venous differences (AV) for O 2 , glucose (glc) and lactate (lac) were evaluated in nine healthy subjects at rest and during and after exercise to exhaustion. The cerebrospinal fluid (CSF) was drained through a lumbar puncture immediately after exercise, while control values were obtained from six other healthy young subjects. In a second experiment magnetic resonance spectroscopy ( 1 H-MRS) was performed after exhaustive exercise to assess lactate levels in the brain (n = 5). Exercise increased the AV O2 from 3.2 ± 0.1 at rest to 3.5 ± 0.2 mM (mean ± S.E.M.; P < 0.05) and the AV glc from 0.6 ± 0.0 to 0.9 ± 0.1 mM (P < 0.01). Notably, the AV lac increased from 0.0 ± 0.0 to 1.3 ± 0.2 mM at the point of exhaustion (P < 0.01). Thus, maximal exercise reduced the cerebral metabolic ratio from 6.0 ± 0.3 to 2.8 ± 0.2 (P < 0.05) and it remained low during the early recovery. Despite this, the CSF concentration of lactate postexercise (1.2 ± 0.1 mM; n = 7) was not different from baseline (1.4 ± 0.1 mM; n = 6). Also, the 1 H-MRS signal from lactate obtained after exercise was smaller than the estimated detection limit of ∼1.5 mM. The finding that an increase in lactate could not be detected in the CSF or within the brain rules out accumulation in a distribution volume and indicates that the lactate taken up by the brain is metabolized.

These findings demonstrate that during combined arm and leg and exercise in the upright position the CBR resets to a lower blood pressure than during arm cranking likely because the central blood volume is enhanced by the muscle pump of the legs.

During arm exercise (A), mean arterial pressure (MAP) is higher than during leg exercise (L).We evaluated the effect of central blood volume on the MAP response to exercise by determining plasma atrial natriuretic peptide (ANP) during moderate upright and supine A, L and combined arm and leg exercise (A + L) in 11 male subjects. In the upright position, MAP was higher during A than at rest (102 ± 6 versus 89 ± 6 mmHg; mean ± S.D.) and during L (95 ± 7 mmHg; P < 0.05), but similar to that during A + L (100 ± 6 mmHg). There was no significant change in plasma ANP during A, while plasma ANP was higher during L and A + L (42.7 ± 12.2 and 43.3 ± 17.1 pg ml −1 , respectively) than at rest (34.6 ± 14.3 pg ml −1 , P < 0.001). In the supine position, MAP was also higher during A than at rest (100 ± 7 versus 86 ± 5 mmHg) and during L (92 ± 5 mmHg; P < 0.01) but similar to that during A + L (102 ± 6 mmHg). During supine A, plasma ANP was higher than at rest and during L but lower than during A + L (73.1 ± 22.5 versus 47.2 ± 15.9, 67.4 ± 18.3 and 78.1 ± 25.0 pg ml −1 , respectively; P < 0.05). Thus, upright A was the exercise mode that did not enhance plasma ANP, suggesting that central blood volume did not increase. The results suggest that the similar blood pressure response to A and to A + L may relate to the enhanced central blood volume following the addition of leg to arm exercise.

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Background and Aim: The neurotransmitter histamine is involved in the regulation of appetite and in the development of age-related obesity in mice. Furthermore, histamine is a mediator of the anorexigenic action of leptin. The aim of the present study was to investigate a possible role of histamine in the development of high-fat diet (HFD)-induced obesity. Methods: Histamine-deficient histidine decarboxylase knock-out (HDC-KO) mice and C57BL/6J wild-type (WT) mice were given either a standard diet (STD) or HFD for 8 weeks. Body weight, 24-hour caloric intake, epididymal adipose tissue size, plasma leptin concentration and quantitative expression of leptin receptor (Ob-R) mRNA were measured. Results: Both HDC-KO and WT mice fed an HFD for 8 weeks increased their body weight significantly more than STD-fed mice. A significant difference in body weight gain between HDC-KO mice fed an HFD or an STD was seen after 2 weeks, whereas a significant difference in body weight gain was first observed after 5 weeks in WT mice. After 8 weeks 24-hour caloric intake was significantly lower in HFD- than in STD-fed WT mice. In HDC-KO mice no difference in caloric intake was observed between HFD- and STD-fed mice. After 8 weeks epididymal adipose tissue size and plasma leptin concentration had increased significantly in HFD-fed WT and HDC-KO mice compared to their STD-fed controls. Epididymal adipose tissue size was higher in HDC-KO than WT mice, both in STD- and HFD-fed mice. A significant decrease in Ob-R mRNA in HFD-fed HDC-KO mice compared to STD-fed HDC-KO mice was observed, while no such difference was observed in WT mice. Conclusion: Based on our results, we conclude that histamine plays a role in the development of HFD-induced obesity.

Background: Brain natriuretic peptide (BNP) is increased in heart failure; however, the relative contribution of the right and left ventricles is largely unknown. Aim: To investigate if right ventricular function has an independent influence on plasma BNP concentration. Methods: Right (RVEF), left ventricular ejection fraction (LVEF), and left ventricular end-diastolic volume index (LVEDVI) were determined in 105 consecutive patients by first-pass radionuclide ventriculography (FP-RNV) and multiple ECG-gated equilibrium radionuclide ventriculography (ERNV), respectively. BNP was analyzed by immunoassay. Results: Mean LVEF was 0.51 (range 0.10-0.83) with 36% having a reduced LVEF (b0.50). Mean RVEF was 0.50 (range 0.26-0.78) with 43% having a reduced RVEF (b 0.50). The mean LVEDVI was 92 ml/m 2 with 22% above the upper normal limit (117 ml/m 2 ). Mean BNP was 239 pg/ml range (0.63-2523). In univariate linear regression analysis LVEF, LVEDVI and RVEF all correlated significantly with log BNP (p b 0.0001). In a multivariate analysis only RVEF and LVEF remained significant. The parameter estimates of the final adjusted model indicated that RVEF and LVEF influence on log BNP were of the same magnitude. Conclusion: BNP, which is a strong prognostic marker in heart failure, independently depends on both left and right ventricular systolic function. This might, at least in part, explain why BNP holds stronger prognostic value than LVEF alone.

The aim of the present investigation was to examine how 8 weeks of intense endurance training influenced right and left ventricular volumes and mass in obese untrained subjects. Ten overweight subjects (19-47 years; body mass index of 34+/-5 kg/m(2)) underwent intensive endurance training (rowing) three times 30 min/week for 8 weeks at a relative intensity of 72+/-8% of their maximal heart rate response (mean+/-SD). Before and after 8 weeks of endurance training, the left and the right end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF), stroke volume (SV) and ventricular mass (VM) were measured by Magnetic resonance imaging (MRI). Submaximal heart rate decreased from 126+/-5 to 113+/-3 b.p.m. (10%; P<0.01), and from 155+/-5 to 141+/-4 b.p.m. (9%; P<0.001) at submaximal workloads of 70 and 140 W (110 W for women), respectively (mean+/-SEM). Resting ventricular parameters increased significantly: left ventricular SV, EDV and VM increased by 6%, 7% and 13%, respectively (P<0.01). The right side of the heart showed significant changes in SV, EDV and VM with increase of 4%, 4% and 12%, respectively (P<0.05). Eight weeks of endurance training significantly increased left ventricular SV and right ventricular SV, due to an increase in left ventricular EDV and right ventricular EDV. Furthermore, left VM and right VM increased. We conclude that using MRI and a longitudinal design it was possible to demonstrate similar and balanced changes in the right and left ventricle in response to training.