Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 19 recordsLinked to original sources

PubMed2006

Brain-derived neurotrophic factor (BDNF) and type 2 diabetes.

AIMS/HYPOTHESIS: Decreased levels of brain-derived neurotrophic factor (BDNF) have been implicated in the pathogenesis of Alzheimer's disease and depression. These disorders are associated with type 2 diabetes, and animal models suggest that BDNF plays a role in insulin resistance. We therefore explored whether BDNF plays a role in human glucose metabolism. SUBJECTS AND METHODS: We included (Study 1) 233 humans divided into four groups depending on presence or absence of type 2 diabetes and presence or absence of obesity; and (Study 2) seven healthy volunteers who underwent both a hyperglycaemic and a hyperinsulinaemic-euglycaemic clamp. RESULTS: Plasma levels of BDNF in Study 1 were decreased in humans with type 2 diabetes independently of obesity. Plasma BDNF was inversely associated with fasting plasma glucose, but not with insulin. No association was found between the BDNF G196A (Val66Met) polymorphism and diabetes or obesity. In Study 2 an output of BDNF from the human brain was detected at basal conditions. This output was inhibited when blood glucose levels were elevated. In contrast, when plasma insulin was increased while maintaining normal blood glucose, the cerebral output of BDNF was not inhibited, indicating that high levels of glucose, but not insulin, inhibit the output of BDNF from the human brain. CONCLUSIONS/INTERPRETATION: Low levels of BDNF accompany impaired glucose metabolism. Decreased BDNF may be a pathogenetic factor involved not only in dementia and depression, but also in type 2 diabetes, potentially explaining the clustering of these conditions in epidemiological studies.

Adult↗

PubMed2006

Preload maintenance and the left ventricular response to prolonged exercise in men.

This study examined whether left ventricular function was reduced during 3 h of semi-recumbent ergometer cycling at 70% of maximal oxygen uptake while preload to the heart was maintained via saline infusion. Indices of left ventricular systolic function (end-systolic blood pressure-volume relationship, SBP/ESV) and diastolic filling (ratio of early to late peak filling velocities into the left ventricle, E:A) were calculated during recovery and compared with baseline resting data. During exercise in seven healthy, trained male subjects, an arterial catheter allowed continuous assessment of arterial pressure, stroke volume (SV), cardiac output ( ) and an index of contractility (dP/dt(max)). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 +/- 5 to 185 +/- 19 mmHg and from 66 +/- 9 to 135 +/- 23 beats min(-1); increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise ( approximately 150 mmHg), while heart rate only increased by 8 +/- 9 beats min(-1) (means +/- s.d.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP ( approximately 5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, and dP/dt(max) were all increased with the onset of exercise (from 85 +/- 8 to 120 +/- 18 ml, from 5.4 +/- 1.3 to 16.5 +/- 3.3 l min(-1) and from 14.4 +/- 4 to 28 +/- 8 mmHg s(-1); values from rest to the end of the first 5 min of exercise for SV, and dP/dt(max), respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 +/- 0.4 to 1.6 +/- 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r(2) = 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.

Adaptation, Physiological↗

PubMed2006

Flow-related techniques for preoperative goal-directed fluid optimization.

BACKGROUND: Improved postoperative outcome has been demonstrated by perioperative maximization of cardiac stroke volume (SV) with fluid challenges, so-called goal-directed therapy. Oesophageal Doppler (OD) has been the most common technique for goal-directed therapy, but other flow-related techniques and parameters are available and they are potentially easier to apply in clinical practice. The objective of this investigation was therefore to use OD for preoperative SV maximization and compare the findings with a Modelflow determined SV, with an OD estimated corrected flow time (FTc), with central venous oxygenation ( Svo2 ) and with muscle and brain oxygenation assessed with near infrared spectroscopy (NIRS). METHODS: Twelve patients scheduled for radical prostatectomy were anaesthetized before optimization of SV estimated by OD. A fluid challenge of 200 ml colloid was provided and repeated if at least a 10% increment in OD SV was obtained. Values were compared with simultaneously measured values of Modelflow SV, FTc, Svo2 and muscle and cerebral oxygenation estimated by NIRS. RESULTS: Based upon OD assessment, optimization of SV was achieved after the administration of 400-800 ml (mean 483 ml) of colloid. The hypothetical volumes administered for optimization based upon Modelflow and Svo2 differed from OD in 10 and 11 patients, respectively. Changes in FTc and NIRS were inconsistent with OD guided optimization. CONCLUSION: Preoperative SV optimization guided by OD for goal-directed therapy is preferable compared with Modelflow SV, FTc, NIRS and Svo2 until outcome studies for the latter are available.

Aged↗

PubMed2006

The plasma atrial natriuretic peptide response to arm and leg exercise in humans: effect of posture.

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.

Adaptation, Physiological↗

PubMed2006

The postural reduction in middle cerebral artery blood velocity is not explained by PaCO2.

In the normocapnic range, middle cerebral artery mean velocity (MCA Vmean) changes approximately 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO2) and a decrease in PaCO2 will reduce the cerebral blood flow by vasoconstriction (the CO2 reactivity of the brain). When standing up MCA Vmean and the end-tidal carbon-dioxide tension (PETCO2) decrease, suggesting that PaCO2 contributes to the reduction in MCA Vmean. In a fixed body position, PETCO2 tracks changes in the PaCO2 but when assuming the upright position, cardiac output (Q) decreases and its distribution over the lung changes, while ventilation (VE) increases suggesting that PETCO2 decreases more than PaCO2. This study evaluated whether the postural reduction in PaCO2 accounts for the postural decline in MCA Vmean). From the supine to the upright position, VE, Q, PETCO2, PaCO2, MCA Vmean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO2Hb) were followed in seven subjects. When standing up, MCA Vmean (from 65.3+/-3.8 to 54.6+/-3.3 cm s(-1) ; mean +/- SEM; P<0.05) and cO2Hb (-7.2+/-2.2 micromol l(-1) ; P<0.05) decreased. At the same time, the VE/Q ratio increased 49+/-14% (P<0.05) with the postural reduction in PETCO2 overestimating the decline in PaCO2 (-4.8+/-0.9 mmHg vs. -3.0+/-1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA Vmean seems to be explained by the reduction in PETCO2 but the small decrease in PaCO2 makes it unlikely that the postural decrease in MCA Vmean can be accounted for by the cerebral CO2 reactivity alone.

Adult↗

PubMed2005

Effect of carbohydrate ingestion on brain exchange of amino acids during sustained exercise in human subjects.

AIM: This study investigated the effect of prolonged exercise with and without carbohydrate intake on the brain exchange of amino acids, especially focussing on tryptophan and branched-chain amino acids (BCAA). METHODS: Five male subjects exercised for 3 h on a cycle ergometer at 200 +/- 7 W on two occasions; either supplemented with a 6% carbohydrate solution or with flavoured water (placebo). Catheters were inserted into the right internal jugular vein and the radial artery of the non-dominant arm. The brain exchange of amino acids during exercise was calculated from the arterial-jugular venous concentration difference multiplied by plasma flow. RESULTS: About 106 micromol (22 mg) of tryptophan was taken up by the brain during exercise in the placebo trial, whereas no significant uptake was observed in the carbohydrate trial. In accordance, the arterial concentration of free tryptophan increased from 12 +/- 1 to 20 +/- 2 micromol L(-1) during the placebo trial and was significantly higher compared with the glucose trial (14 +/- 1 micromol L(-1) at the end of exercise). Also, the arterial concentration of total tryptophan (free and albumin-bound) increased during the first 30 min of exercise in both trials, but returned to the basal level at 180 min of exercise. In both trials, BCAA were taken up by the brain while glutamine was released. CONCLUSION: The present data show that both tryptophan and BCAA are taken up by the brain during prolonged exercise, and we suggest that the cerebral uptake of tryptophan may relate to increased synthesis of serotonin (5-HT) in the brain.

Adult↗

PubMed2005

Venous oxygen saturation during normovolaemic haemodilution in the pig.

BACKGROUND: Hypovolaemia may be considered to represent a volume-restricted cardiac output (CO), but CO varies inversely with the haemoglobin concentration (Hb) and a maximal mixed venous oxygen saturation (SvO2) may be a better target for volume administration than a maximal CO. METHODS: In 10 anaesthetized pigs, volume loading with 6% hydroxyethyl starch was performed to obtain a maximal SvO2 followed by normovolaemic haemodilution with 6% hydroxyethyl starch. RESULTS: Volume loading increased SvO2 from 55.0+/-5.2% to 64.8+/-9.0% (mean+/-SD) associated with an increase in CO (2.3+/-0.4 to 3.5+/-0.9 l/min) and central venous oxygen saturation (ScvO2; 68.2+/-9.3% to 79.4+/-7.2%; P<0.05). Heart rate (HR), mean arterial (MAP), central venous (CVP), pulmonary arterial mean (PAMP), and occlusion pressures (PAOP) increased as well (P<0.05). In contrast, during progressive haemodilution, SvO2 and ScvO2 remained statistically unchanged until the haemoglobin concentration had decreased from 5.5+/-0.4 to 2.9+/-0.2 mM, while CO and HR increased at a haemoglobin value of 4.4+/-0.4 and 4.0+/-0.4 mM and CVP and PAOP decreased at a haemoglobin of 4.0+/-0.4 and 2.9+/-0.2 mM, respectively (P<0.05) leaving MAP unaffected. CONCLUSION: This study found that volume loading increased cardiac output and mixed and central venous oxygen saturations in parallel, but during normovolaemic haemodilution an increase in cardiac output left mixed and central venous oxygen saturations statistically unchanged until haemoglobin concentration was reduced by approximately 50%. Accordingly, volume therapy should be directed to maintain a high venous oxygen saturation rather than a change in cardiac output.

Animals↗

PubMed2005

Stroke volume of the heart and thoracic fluid content during head-up and head-down tilt in humans.

BACKGROUND: The stroke volume (SV) of the heart depends on the diastolic volume but, for the intact organism, central pressures are applied widely to express the filling of the heart. METHODS: This study evaluates the interdependence of SV and thoracic electrical admittance of thoracic fluid content (TA) vs. the central venous (CVP), mean pulmonary artery (MPAP) and pulmonary artery wedge (PAWP) pressures during head-up (HUT) and head-down (HDT) tilt in nine healthy humans. RESULTS: From the supine position to 20 degrees HDT, SV [112 +/- 18 ml; mean +/- standard deviation (SD)], TA (30.8 +/- 7.1 mS) and CVP (3.6 +/- 0.9 mmHg) did not change significantly, whereas MPAP (from 13.9 +/- 2.7 to 16.1 +/- 2.5 mmHg) and PAWP (from 8.8 +/- 3.4 to 11.3 +/- 2.5 mmHg; P < 0.05) increased. Conversely, during 70 degrees HUT, SV (to 65 +/- 24 ml) decreased, together with CVP (to 0.9 +/- 1.4 mmHg; P < 0.001), MPAP (to 9.3 +/- 3.8 mmHg; P < 0.01), PAWP (to 0.7 +/- 3.3 mmHg; P < 0.001) and TA (to 26.7 +/- 6.8 mS; P < 0.01). However, from 20 to 50 min of HUT, SV decreased further (to 48 +/- 21 ml; P < 0.001), whereas the central pressures did not change significantly. CONCLUSIONS: During both HUT and HDT, SV of the heart changed with the thoracic fluid content rather than with the central vascular pressures. These findings confirm that the function of the heart relates to its volume rather than to its so-called filling pressures.

Adult↗

PubMed2004

Standing up to the challenge of standing: a siphon does not support cerebral blood flow in humans.

Model studies have been advanced to suggest both that a siphon does and does not support cerebral blood flow in an upright position. If a siphon is established with the head raised, it would mean that internal jugular pressure reflects right atrium pressure minus the hydrostatic difference from the brain. This study measured spinal fluid pressure in the upright position, the pressure and the ultrasound-determined size of the internal jugular vein in the supine and sitting positions, and the internal jugular venous pressure during seated exercise. When the head was elevated approximately 25 cm above the level of the heart, internal jugular venous pressure decreased from 9.5 (SD 2.8) to 0.2 (SD 1.0) mmHg [n = 15; values are means (SD); P < 0.01]. Similarly, central venous pressure decreased from 6.2 (SD 1.8) to 0.6 (SD 2.6) mmHg (P < 0.05). No apparent lumen was detected in any of the 31 left or right internal veins imaged at 40 degrees head-up tilt, and submaximal (n = 7) and maximal exercise (n = 4) did not significantly affect internal jugular venous pressure. While seven subjects were sitting up, spinal fluid pressure at the lumbar level was 26 (SD 4) mmHg corresponding to 0.1 (SD 4.1) mmHg at the base of the brain. These results demonstrate that both for venous outflow from the brain and for spinal fluid, the prevailing pressure approaches zero at the base of the brain when humans are upright, which negates that a siphon supports cerebral blood flow.

Adult↗

PubMed2004

Arterial blood pressure and carotid baroreflex function during arm and combined arm and leg exercise in humans.

AIM: During arm cranking (A) blood pressure is higher than during combined arm and leg exercise (A + L), while the carotid baroreflex (CBR) is suggested to reset to control a higher blood pressure in direct relation to work intensity and the engaged muscle mass. METHOD: This study evaluated the function of the CBR by using neck pressure and neck suction during upright A, L and A + L in 12 subjects and, in order to evaluate a potential influence of the central blood volume on the CBR, also during supine A in five subjects. Exercise intensities for A and L were planned to elicit a heart rate response of c. 100 and 120 beats min(-1), respectively, in the upright position and both workloads were maintained during A + L and supine A. RESULTS: The CBR operating point, corresponding to the pre-stimulus blood pressure, was 88 +/- 6 mmHg (mean +/- SE) at rest. During upright A, L and A + L and supine A it increased to 109 +/- 9, 95 +/- 7, 103 +/- 7 and 104 +/- 4 mmHg, respectively, and it was thus higher during upright A than during A + L and supine A (P < 0.05). In addition, the CBR threshold and saturation pressures, corresponding to the minimum and maximum carotid sinus pressure, respectively, were higher during upright A than during supine A, A + L, L and at rest (P < 0.05) with no significant change in the maximal reflex gain. CONCLUSION: 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.

Adult↗

PubMed2004

Exercise induces the release of heat shock protein 72 from the human brain in vivo.

The present study tested the hypothesis that in response to physical stress the human brain has the capacity to release heat shock protein 72 (Hsp72) in vivo. Therefore, 6 humans (males) cycled for 180 minutes at 60% of their maximal oxygen uptake, and the cerebral Hsp72 response was determined on the basis of the internal jugular venous to arterial difference and global cerebral blood flow. At rest, there was a net balance of Hsp72 across the brain, but after 180 minutes of exercise, we were able to detect the release of Hsp72 from the brain (335 +/- 182 ng/min). However, large individual differences were observed as 3 of the 6 subjects had a marked increase in the release of Hsp72, whereas exercise had little effect on the cerebral Hsp72 balance in the remaining 3 subjects. Given that cerebral blood flow was unchanged during exercise compared with values obtained at rest, it is unlikely that the cerebral Hsp72 release relates to necrosis of specific cells within the brain. These data demonstrate that the human brain is able to release Hsp72 in vivo in response to a physical stressor such as exercise. Further study is required to determine the biological significance of these observations.

Adult↗

PubMed2003

Effect of fitness on arm vascular and metabolic responses to upper body exercise.

We investigated arm perfusion and metabolism during upper body exercise. Eight average, fit subjects and seven rowers, mean +/- SE maximal oxygen uptake (VO2 max) 157 +/- 7 and 223 +/- 14 ml O2. kg(-0.73).min(-1), respectively, performed incremental arm cranking to exhaustion. Arm blood flow (ABF) was measured with thermodilution and arm muscle mass was estimated by dual-energy X-ray absorptiometry. During maximal arm cranking, pulmonary VO2 was approximately 45% higher in the rowers compared with the untrained subjects and peak ABF was 6.44 +/- 0.40 and 4.55 +/- 0.26 l/min, respectively (P < 0.05). The arm muscle mass for the rowers and the untrained subjects was 3.5 +/- 0.4 and 3.3 +/- 0.1 kg, i.e., arm perfusion was 1.9 +/- 0.2 and 1.4 +/- 0.1 l blood.kg(-1).min(-1), respectively (P < 0.05). The arteriovenous O2 difference was 156 +/- 7 and 120 +/- 8 ml/l, respectively, and arm VO2 was 0.98 +/- 0.08 and 0.60 +/- 0.04 l/min corresponding with 281 +/- 22 and 181 +/- 12 ml/kg, while arm O(2) diffusional conductance was 49.9 +/- 4.3 and 18.6 +/- 3.2 ml.min(-1).mmHg(-1), respectively (P < 0.05). Also, lactate release in the rowers was almost three times higher than in the untrained subjects (26.4 +/- 1.1 vs. 9.5 +/- 0.4 mmol/min, P < 0.05). The energy requirement of an approximately 50% larger arm work capacity after long-term arm endurance training is covered by an approximately 60% increase in aerobic metabolism and an almost tripling of the anaerobic capacity.

Adult↗

PubMed2003

Severe intracellular magnesium and potassium depletion in patients after treatment with cisplatin.

The purpose of this study is (1) to evaluate skeletal muscle magnesium (Mg) and potassium (K) during treatment with cisplatin; (2) to evaluate the predictive value of plasma (P)-Mg for intracellular Mg during cisplatin treatment; and (3) to evaluate whether changes in intracellular K influence skeletal muscle Na,K-ATPase. In all, 65 patients had a needle muscle biopsy obtained before and 26 patients both before and after cisplatin treatment. Biopsies were analysed for Mg, K, and Na,K-ATPase concentrations, and P-Mg and P-K determined. Treatment with a total dose of approximately 500 mg (270 mg m(-2) surface area) cisplatin over 80 days was associated with reductions in muscle [Mg] (95% CI) (8.95 (8.23-9.63) to 7.76 (7.34-8.18) mumol g(-1) wet wt. (P<0.01), and muscle [K] (90.81 (83.29-98.34) to 82.87 (78.74-87.00) mumol g(-1) wet wt. (P<0.05), as well as in P-Mg 0.82 (0.80-0.85) to 0.68 (0.64-0.73) mmol l(-1) (P<0.01 but not in P-K (4.0 (3.8-4.1) vs 3.8 (3.7-4.0) mmol l(-1)). No simple correlations were observed between P-Mg and muscle [Mg], or between P-K and muscle [K], either before (n=65) or after (n=26) treatment with cisplatin. The changes in [Mg] and [K] were not associated with changes in the muscle Na,K-ATPase concentration. Following treatment with cisplatin, an approximately 15% decline in P-Mg was accompanied by an approximately 15% loss of muscle [Mg], as well as an approximately 10% reduction of muscle [K] and fatigue and muscle weakness previously ascribed to hypomagnesaemia may therefore also be well explained by muscle K depletion observed despite normal levels of P-K. There was no correlation between P-Mg and SM-Mg or between P-K and SM-K. Thus, P-Mg and P-K are not reliable indicators for Mg and K depletion during treatment with cisplatin. However, the majority of patients will present Mg and K depletion after cisplatin therapy and of these only very few patients will present a low P-Mg or P-K. Therefore, routine supplementation should be considered in all patients receiving cisplatin.

Adenosine Triphosphatases↗

PubMed2003

Arm blood flow and oxygenation on the transition from arm to combined arm and leg exercise in humans.

The cardiovascular response to exercise with several groups of skeletal muscle implies that work with the legs may reduce arm blood flow. This study followed arm blood flow (Yarm) and oxygenation on the transition from arm cranking (A) to combined arm and leg exercise (A+L). Seven healthy male subjects performed A at approximately 80 % of maximum work rate (Wmax) and A at ~80 % Wmax combined with L at approximately 60 % Wmax. A transition trial to volitional exhaustion was performed where L was added after 2 min of A. The Yarm was determined by constant infusion thermodilution in the axillary vein and changes in biceps muscle oxygenation were measured with near-infrared spectroscopy. During A+L Yarm was lowered by 0.38 +/- 0.06 l min-1 (10.4 +/- 3.3 %, P < 0.05) from 2.96 +/- 1.54 l min-1 during A. Total (HbT) and oxygenated haemoglobin (HbO2) concentrations were also lower. During the transition from A to A+L Yarm decreased by 0.22 +/- 0.03 l min-1 (7.9 +/- 1.8 %, P < 0.05) within 9.6 +/- 0.2 s, while HbT and HbO2 decreased similarly within 30 +/- 2 s. At the same time mean arterial pressure and arm vascular conductance also decreased. The data demonstrate reduction in blood flow to active skeletal muscle during maximal whole body exercise to a degree that arm oxygen uptake and muscle tissue oxygenation are compromised.

Adult↗

PubMed2003

Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise.

AIM: This study evaluated if the fatigue and apathy arising during exercise with hypoglycaemia could relate to a lowering of the cerebral metabolic rates of glucose and oxygen. METHODS AND RESULTS: Six males completed 3 h of cycling with or without glucose supplementation in random order. Cerebral blood flow, metabolism and interleukin-6 (IL-6) release were evaluated with the Kety-Schmidt technique. Blood glucose was maintained during the glucose trial, while it decreased from 5.2 +/- 0.1 to 2.9 +/- 0.3 mmol L-1 (mean +/- SE) after 180 min of exercise in the placebo trial with a concomitant increase in perceived exertion (P < 0.05). During hypoglycaemia, the cerebral glucose uptake was reduced from 0.34 +/- 0.05 to 0.28 +/- 0.04 micromol g(-1) min(-1), while the cerebral uptake of beta-hydroxybutyrate increased to 5 +/- 1 pmol g(-1) min(-1) (P < 0.05). The reduced glucose uptake was accompanied by a lowering of the cerebral metabolic rate of oxygen from 1.84 +/- 0.19 mmol g(-1) min(-)1 during exercise with glucose supplementation to 1.60 +/- 0.16 mmol g(-1) min(-1) during hypoglycaemia (P < 0.05). In addition, the cerebral IL-6 release was reduced from 0.4 +/- 0.1 to 0.0 +/- 0.1 pg g(-1) min(-1) (P < 0.05). CONCLUSIONS: Exercise-induced hypoglycaemia limits the cerebral uptake of glucose, exacerbates exercise, reduces the cerebral metabolic rate of oxygen and attenuates the release of IL-6 from the brain.

3-Hydroxybutyric Acid↗

PubMed2002

Arm blood flow and metabolism during arm and combined arm and leg exercise in humans.

The cardiovascular response to exercise with several groups of skeletal muscle suggests that work with the arms may decrease leg blood flow. This study evaluated whether intense exercise with the legs would have a similar effect on arm blood flow (Y(arm)) and O(2) consumption (V(O(2))(,arm)). Ten healthy male subjects (age 21 +/- 1 year; mean +/- S.D.) performed arm cranking at 80 % of maximum arm work capacity (A trial) and combined arm cranking with cycling at 60 % of maximum leg work capacity (A + L trial). The combined trial was a maximum effort for 5-6 min. Y(arm) measurement by thermodilution in the axilliary vein and arterial and venous blood samples permitted calculation of V(O(2))(,arm). During the combined trial, Y(arm) was reduced by 0.58 +/- 0.25 l min(-1) (19.1 +/- 3.0 %, P < 0.05) from the value during arm cranking (3.00 +/- 0.46 l min(-1)). The arterio-venous O(2) difference increased from 122 +/- 15 ml l(-1) during the arm trial to 150 +/- 21 ml l(-1) (P < 0.05) during the combined trial. Thus, V(O(2))(,arm) (0.45 +/- 0.06 l min(-1)) was reduced by 9.6 +/- 6.3 % (P < 0.05) and arm vascular conductance from 27 +/- 4 to 23 +/- 3 ml min(-1) (mmHg)(-1) (P < 0.05) as noradrenaline spillover from the arm increased from 7.5 +/- 3.5 to 13.8 +/- 4.2 nmol min(-1) (P < 0.05). The data suggest that during maximal whole body exercise in humans, arm vasoconstriction is established to an extent that affects oxygen delivery to and utilisation by working skeletal muscles.

Adult↗

PubMed2002

New insights into differential baroreflex control of heart rate in humans.

Recent data indicate that bilateral carotid sinus denervation in patients results in a chronic impairment in the rapid reflex control of blood pressure during orthostasis. These findings are inconsistent with previous human experimental investigations indicating a minimal role for the carotid baroreceptor-cardiac reflex in blood pressure control. Therefore, we reexamined arterial baroreflex [carotid (CBR) and aortic baroreflex (ABR)] control of heart rate (HR) using newly developed methodologies. In 10 healthy men, 27 +/- 1 yr old, an abrupt decrease in mean arterial pressure (MAP) was induced nonpharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) after 9 min of resting leg ischemia under two conditions: 1) ABR and CBR deactivation (control) and 2) ABR deactivation. Under control conditions, cuff release decreased MAP by 13 +/- 1 mmHg, whereas HR increased 11 +/- 2 beats/min. During ABR deactivation, neck suction was gradually applied to maintain carotid sinus transmural pressure during the initial 20 s after cuff release (suction). This attenuated the increase in HR (6 +/- 1 beats/min) and caused a greater decrease in MAP (18 +/- 2 mmHg, P < 0.05). Furthermore, estimated cardiac baroreflex responsiveness (DeltaHR/DeltaMAP) was significantly reduced during suction compared with control conditions. These findings suggest that the carotid baroreceptors contribute more importantly to the reflex control of HR than previously reported in healthy individuals.

Adult↗

PubMed2002

Bicarbonate attenuates intracellular acidosis.

BACKGROUND: This study was prompted by concern that administration of bicarbonate for correction of lactate acidosis aggravates a low intracellular pH (pHi). In healthy subjects we evaluated skeletal muscle pHi using 31P-magnetic resonance spectroscopy during 5-minute rhythmic handgrip to provoke intracellular acidosis. METHODS: Subjects were randomized to treatment with bicarbonate or saline infused intravenously in a cross-over study design with 1 h between trials. RESULTS: In response to rhythmic handgrip, muscle venous O(2) hemoglobin saturation decreased from 51 +/- 4% to 36 +/- 2% and lactate increased from 1.0 +/- 0.1 to 4.9 +/- 0.5 mmol/l with a reduction in pH from 7.43 +/- 0.01-7.23 +/- 0.01 (P<0.05). pHi decreased from 7.06 +/- 0.02-6.36 +/- 0.08 (P<0.05). Infusion of bicarbonate increased the arterial blood concentration from 26 +/- 1 to 39 +/- 1 mmol/l (P<0.05). The arterial CO(2) partial pressure decreased from 5.6 +/- 0.2 to 5.2 +/- 0.3 kPa during rhythmic handgrip, whereas it increased to 5.9 +/- 0.2 kPa (P<0.05) during infusion of bicarbonate. Bicarbonate treatment also increased pH of arterial and venous blood (7.55 +/- 0.01 vs. 7.44 +/- 0.02 and 7.31 +/- 0.01 vs. 7.23 +/- 0.02, respectively; P<0.05). In the last min of rhythmic handgrip the decrease in pHi was attenuated by the administration of bicarbonate (6.60 +/- 0.11 vs. 6.40 +/- 0.12; P<0.05). CONCLUSION: During exercise-induced metabolic acidosis, intravenous administration of bicarbonate increased the buffering capacity of blood and attenuated the decrease in intracellular muscle pH, although there was a small increase in the arterial carbon dioxide pressure.

Acidosis↗