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Biomedical subjects

Niels H Secher

Publications and source records attributed to Niels H Secher.

At least 55 records · Page 3Linked to original sources
PubMed2004

Brain and central haemodynamics and oxygenation during maximal exercise in humans.

During maximal exercise in humans, fatigue is preceded by reductions in systemic and skeletal muscle blood flow, O(2) delivery and uptake. Here, we examined whether the uptake of O(2) and substrates by the human brain is compromised and whether the fall in stroke volume of the heart underlying the decline in systemic O(2) delivery is related to declining venous return. We measured brain and central haemodynamics and oxygenation in healthy males (n= 13 in 2 studies) performing intense cycling exercise (360 +/- 10 W; mean +/-s.e.m.) to exhaustion starting with either high (H) or normal (control, C) body temperature. Time to exhaustion was shorter in H than in C (5.8 +/- 0.2 versus 7.5 +/- 0.4 min, P < 0.05), despite heart rate reaching similar maximal values. During the first 90 s of both trials, frontal cortex tissue oxygenation and the arterial-internal jugular venous differences (a-v diff) for O(2) and glucose did not change, whereas middle cerebral artery mean flow velocity (MCA V(mean)) and cardiac output increased by approximately 22 and approximately 115%, respectively. Thereafter, brain extraction of O(2), glucose and lactate increased by approximately 45, approximately 55 and approximately 95%, respectively, while frontal cortex tissue oxygenation, MCA V(mean) and cardiac output declined approximately 40, approximately 15 and approximately 10%, respectively. At exhaustion in both trials, systemic VO(2) declined in parallel with a similar fall in stroke volume and central venous pressure; yet the brain uptake of O(2), glucose and lactate increased. In conclusion, the reduction in stroke volume, which underlies the fall in systemic O(2) delivery and uptake before exhaustion, is partly related to reductions in venous return to the heart. Furthermore, fatigue during maximal exercise, with or without heat stress, in healthy humans is associated with an enhanced rather than impaired brain uptake of O(2) and substrates.

Adenosine Triphosphate↗
PubMed2004

The CSF and arterial to internal jugular venous hormonal differences during exercise in humans.

Strenuous exercise increases the cerebral uptake of carbohydrate out of proportion to that of oxygen, but it is unknown whether such enhanced carbohydrate uptake is influenced by the marked endocrine response to exercise. During exhaustive exercise this study evaluated the a-v differences across the brain (a-v diff) of hormones that could influence its carbohydrate uptake (n= 9). In addition, neuroendocrine activity and a potential uptake of hormones via the cerebrospinal fluid (CSF) were assessed by lumbar puncture postexercise and at rest (n= 6). Exercise increased the arterial concentration of noradrenaline and adrenaline, but there was no cerebral uptake. However, following exercise CSF noradrenaline was 1.4 (0.73-5.5) nmol l(-1), and higher than at rest, 0.3 (0.19-1.84) nmol l(-1) (P < 0.05), whereas adrenaline could not be detected. Exercise increased both the arterial concentration of NH(4)(+) and its a-v diff, which increased from 1 (-12 to 5) to 17 (5-41) micromol l(-1) (P < 0.05), while the CSF NH(4)(+) was reduced to 7 (0-10) versus 11 (7-16) micromol l(-1) (P < 0.05). There was no release from, or accumulation in the brain of interleukin (IL)-6, tumour necrosis factor (TNF-alpha), heatshock protein (HSP72), insulin, or insulin-like growth factor (IGF)-I. The findings indicate that for maximal exercise, the concentration of noradrenaline is increased within the brain, whereas blood borne hormones and cytokines are seemingly unimportant. The results support the notion that the exercise-induced changes in brain metabolism are controlled by factors intrinsic to the brain.

Adult↗
PubMed2004

Carotid baroreflex function ceases during vasovagal syncope.

Despite the arterial baroreflex control of heart rate and blood pressure, vasovagal syncope is a common cause of loss of consciousness in people exposed to stimuli that reduce the central blood volume, such as head-up tilt. Carotid baroreflex function was evaluated using a rapid pulse train of neck pressure and neck suction in three conscious volunteers who developed a vasovagal episode during head-up tilt. The maximal gain of the carotid-heart rate and carotid-blood pressure baroreflex function curves were identified as measures of carotid baroreceptor responsiveness. When presyncopal symptoms developed, one further baroreflex assessment was obtained before the subjects were returned to the supine position. The bradycardia and hypotension exhibited during pre-syncope and syncope reflected a leftward and downward relocation of both the cardiac and vasomotor stimulus response curves. In addition, during the vasovagal syncope, baroreflex control was suppressed as blood pressure remained low during neck pressure stimuli. In conclusion, arterial baroreflex function ceases during vasovagal syncope.

Adult↗
PubMed2004

Cerebral perturbations provoked by prolonged exercise.

This review addresses cerebral metabolic and neurohumoral alterations during prolonged exercise in humans with special focus on associations with fatigue. Global energy turnover in the brain is unaltered by the transition from rest to moderately intense exercise, apparently because exercise-induced activation of some brain regions including cortical motor areas is compensated for by reduced activity in other regions of the brain. However, strenuous exercise is associated with cerebral metabolic and neurohumoral alterations that may relate to central fatigue. Fatigue should be acknowledged as a complex phenomenon influenced by both peripheral and central factors. However, failure to drive the motorneurons adequately as a consequence of neurophysiological alterations seems to play a dominant role under some circumstances. During exercise with hyperthermia excessive accumulation of heat in the brain due to impeded heat removal by the cerebral circulation may elevate the brain temperature to >40 degrees C and impair the ability to sustain maximal motor activation. Also, when prolonged exercise results in hypoglycaemia, perceived exertion increases at the same time as the cerebral glucose uptake becomes low, and centrally mediated fatigue appears to arise as the cerebral energy turnover becomes restricted by the availability of substrates for the brain. Changes in serotonergic activity, inhibitory feed-back from the exercising muscles, elevated ammonia levels, and alterations in regional dopaminergic activity may also contribute to the impaired voluntary activation of the motorneurons after prolonged and strenuous exercise. Furthermore, central fatigue may involve depletion of cerebral glycogen stores, as signified by the observation that following exhaustive exercise the cerebral glucose uptake increases out of proportion to that of oxygen. In summary, prolonged exercise may induce homeostatic disturbances within the central nervous system (CNS) that subsequently attenuates motor activation. Therefore, strenuous exercise is a challenge not only to the cardiorespiratory and locomotive systems but also to the brain.

Animals↗
PubMed2004

Reconstruction of brachial pressure from finger arterial pressure during orthostasis.

INTRODUCTION: In patients with recurrent syncope, monitoring of intra-arterial pressure during orthostatic stress testing is recommended because of the potentially sudden and rapid development of hypotension. Replacing brachial arterial pressure (BAP) by the non-invasively obtained finger arterial pressure (FinAP) has advantages because catheterization in itself may provoke a syncope. OBJECTIVE: To investigate whether reconstruction of the brachial pressure curve (ReBAP) from FinAP can account for systolic and diastolic offset in the recorded pressure on the transition from a supine to an upright position and during maintained postural stress. METHODS: In nine healthy young subjects BAP and FinAP were recorded in the supine position, during 8 min of standing and during 20 min of 70degrees passive head-up tilt (HUT70) whereafter three of the subjects fainted within 20 min of HUT. The FinAP signal was modeled off-line into a reconstructed brachial pressure curve. RESULTS: For FinAP but not for ReBAP, systolic (P < 0.05) and diastolic (P < 0.001) bias increased in the transition from the supine to the HUT position. Bias for the systolic pressure in the supine position and after 7.5 and 20 min of HUT were 2, 7 and 11 mmHg for FinAP but only 0, -2 and 1 mmHg for ReBAP (P < 0.05 for HUT). For the diastolic pressure these values were -2, 5 and 8 mmHg for FinAP and 4, 5 and 6 for ReBAP (P < 0.01 for supine). CONCLUSIONS: Brachial pressure reconstruction from the finger arterial pressure waveform accounts for the bias from the supine to the upright position, eliminates the bias for the systolic but not for diastolic finger pressure and reduces the trend in diastolic bias with increased tilt duration.

Adult↗
PubMed2004

Glucose ingestion attenuates the exercise-induced increase in circulating heat shock protein 72 and heat shock protein 60 in humans.

Heat shock protein (Hsp) 72 is a cytosolic stress protein that is highly inducible by several factors including exercise. Hsp60 is primarily mitochondrial in cellular location, plays a key role in the intracellular protein translocation and cytoprotection, is increased in skeletal muscle by exercise, and is found in the peripheral circulation of healthy humans. Glucose deprivation increases Hsp72 in cultured cells, whereas reduced glycogen availability elevates Hsp72 in contracting human skeletal muscle. To determine whether maintained blood glucose during exercise attenuates the exercise-induced increase in intramuscular and circulating Hsp72 and Hsp60, 6 males performed 120 minutes of semirecumbent cycling at approximately 65% maximal oxygen uptake on 2 occasions while ingesting either a 6.4% glucose (GLU) or sweet placebo (CON) beverage throughout exercise. Muscle biopsies, obtained before and immediately after exercise, were analyzed for Hsp72 and Hsp60 protein expression. Blood samples were simultaneously obtained from a brachial artery, a femoral vein, and the hepatic vein before and during exercise for the analysis of serum Hsp72 and Hsp60. Leg and hepatosplanchnic blood flow were measured to determine Hsp72-Hsp60 flux across these tissue beds. Neither exercise nor glucose ingestion affected the Hsp72 or Hsp60 protein expression in, or their release from, contracting skeletal muscle. Arterial serum Hsp72 increased (P < 0.05) throughout exercise in both trials but was attenuated (P < 0.05) in GLU. This may have been in part because of the increased (P < 0.05) hepatosplanchnic Hsp72 release in CON, being totally abolished (P < 0.05) in GLU. Serum Hsp60 increased (P < 0.05) after 60 minutes of exercise in CON before returning to resting levels at 120 minutes. In contrast, no exercise-induced increase in serum Hsp60 was observed in GLU. We detected neither hepatosplanchnic nor contracting limb Hsp60 release in either trial. In conclusion, maintaining glucose availability during exercise attenuates the circulating Hsp response in healthy humans.

Adult↗
PubMed2003

A reduced cerebral metabolic ratio in exercise reflects metabolism and not accumulation of lactate within the human brain.

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 approximately 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.

Adult↗
PubMed2003

Central command is capable of modulating sweating from non-glabrous human skin.

Isometric handgrip exercise (IHG) increases sweating rate without changing core or skin temperatures. The contribution of central command resulting in increases in sweating rate during IHG is unknown. To investigate this question, seven subjects performed IHG (35 % maximum voluntary contraction (MVC) for 2 min) followed by 2-min of post-exercise ischaemia (PEI), with and without partial neuromuscular blockade (PNB). PNB was performed to augment central command during the IHG bout. These trials were conducted while the subject was normothermic, mildly heated, and moderately heated. On the non-exercising arm, forearm sweating rate was monitored over a microdialysis membrane perfused with neostigmine (acetylcholinesterase inhibitor), and at an adjacent untreated site. In normothermia with PNB, despite reduced force production during IHG (17 +/- 9 versus 157 +/- 13 N; P < 0.001), the elevation in sweating rate at the neostigmine-treated site was greater relative to the control IHG bout (P < 0.05). During subsequent PEI, for the PNB trial mean arterial blood pressure (MAP) and sweating rate returned towards pre-IHG levels, while during the control trial these variables remained elevated. During IHG while mildly heated, the elevation in sweating rate was greater during the PNB trial relative to the control trial. In contrast, during moderate heating sweating increased during IHG for both trials, however the elevation in sweating rate during the PNB trial was not greater than during the control trial. These results suggest that central command is capable of modulating sweating rate in all thermal conditions, however its effect is reduced when body temperatures and/or sweating rate are substantially elevated.

Adult↗
PubMed2003

Glucose ingestion blunts hormone-sensitive lipase activity in contracting human skeletal muscle.

To examine the effect of attenuated epinephrine and elevated insulin on intramuscular hormone sensitivity lipase activity (HSLa) during exercise, seven men performed 120 min of semirecumbent cycling (60% peak pulmonary oxygen uptake) on two occasions while ingesting either 250 ml of a 6.4% carbohydrate (GLU) or sweet placebo (CON) beverage at the onset of, and at 15 min intervals throughout, exercise. Muscle biopsies obtained before and immediately after exercise were analyzed for HSLa. Blood samples were simultaneously obtained from a brachial artery and a femoral vein before and during exercise, and leg blood flow was measured by thermodilution in the femoral vein. Net leg glycerol and lactate release and net leg glucose and free fatty acid (FFA) uptake were calculated from these measures. Insulin and epinephrine were also measured in arterial blood before and throughout exercise. During GLU, insulin was elevated (120 min: CON, 11.4 +/- 2.4, GLU, 35.3 +/- 6.9 pM, P < 0.05) and epinephrine suppressed (120 min: CON, 6.1 +/- 2.5, GLU, 2.1 +/- 0.9 nM; P < 0.05) compared with CON. Carbohydrate feeding also resulted in suppressed (P < 0.05) HSLa relative to CON (120 min: CON, 1.71 +/- 0.18, GLU, 1.27 +/- 0.16 mmol.min-1.kg dry mass-1). There were no differences in leg lactate or glycerol release when trials were compared, but leg FFA uptake was lower (120 min: CON, 0.29 +/- 0.06, GLU, 0.82 +/- 0.09 mmol/min) and leg glucose uptake higher (120 min: CON, 3.16 +/- 0.59, GLU, 1.37 +/- 0.37 mmol/min) in GLU compared with CON. These results demonstrate that circulating insulin and epinephrine play a role in HSLa in contracting skeletal muscle.

Carbohydrate Metabolism↗
PubMed2003

Partial blockade of skeletal muscle somatosensory afferents attenuates baroreflex resetting during exercise in humans.

During exercise, the carotid baroreflex is reset to operate around the higher arterial pressures evoked by physical exertion. The purpose of this investigation was to evaluate the contribution of somatosensory input from the exercise pressor reflex to this resetting during exercise. Nine subjects performed seven minutes of dynamic cycling at 30% of maximal work load and three minutes of static one-legged contraction at 25% maximal voluntary contraction before (control) and after partial blockade of skeletal muscle afferents with epidural anaesthesia. Carotid baroreflex function was assessed by applying rapid pulses of hyper- and hypotensive stimuli to the neck via a customised collar. Using a logistic model, heart rate (HR) and mean arterial pressure (MAP) responses to carotid sinus stimulation were used to develop reflex function stimulus-response curves. Compared with rest, control dynamic and static exercise reset carotid baroreflex-HR and carotid baroreflex-MAP curves vertically upward on the response arm and laterally rightward to higher operating pressures. Inhibition of exercise pressor reflex input by epidural anaesthesia attenuated the bi-directional resetting of the carotid baroreflex-MAP curve during both exercise protocols. In contrast, the effect of epidural anaesthesia on the resetting of the carotid baroreflex-HR curve was negligible during dynamic cycling whereas it relocated the curve in a laterally leftward direction during static contraction. The data suggest that afferent input from skeletal muscle is requisite for the complete resetting of the carotid baroreflex during exercise. However, this neural input appears to modify baroreflex control of blood pressure to a greater extent than heart rate.

Adult↗
PubMed2003

Carotid baroreflex responsiveness to head-up tilt-induced central hypovolaemia: effect of aerobic fitness.

This investigation examined the interaction between carotid baroreflex (CBR) responsiveness during head-up tilt (HUT)-induced central hypovolaemia and aerobic fitness. Seven average fit (AF) individuals, with a mean maximal oxygen uptake (VO2max) of 49 +/- 1 (ml O2) kg-1 min-1, and seven high fit (HF) individuals, with a VO2max of 61 +/- 1 (ml O2) kg-1 min-1, voluntarily participated in the investigation. After 10-15 min supine, each subject was exposed to nine levels of progressively increasing HUT by 10 deg increments from -20 deg to +60 deg. During the final 3 min of each stage of HUT, the CBR responsiveness was measured using a rapid pulse (500 ms) train of neck pressure (NP) and neck suction (NS) ranging from +40 to -80 Torr. The maximal gain of the carotid-HR (Gmax-HR) and carotid-MAP (Gmax-MAP) baroreflex function curves was identified as measures of CBR responsiveness. During HUT-induced decreases in thoracic admittance, an index of central blood volume (CBV), the Gmax-HR and Gmax-MAP of the AF subjects increased more than the Gmax-HR and Gmax-MAP of the HF subjects (P < 0.05). The data demonstrate that the increase in the CBR responsiveness during a tilt-induced progressive unloading of the cardiopulmonary baroreceptors was attenuated in endurance-trained subjects. These findings provide an explanation for the predisposition to orthostatic hypotension and intolerance in well-trained athletes.

Adult↗
PubMed2003

Baroreflex-mediated changes in cardiac output and vascular conductance in response to alterations in carotid sinus pressure during exercise in humans.

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex (CBR)-mediated changes in mean arterial pressure (MAP) during mild to heavy exercise. CBR function was determined in eight subjects (25 +/- 1 years) at rest and during three cycle exercise trials at heart rates (HRs) of 90, 120 and 150 beats min-1 performed in random order. Acute changes in carotid sinus transmural pressure were evoked using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to -80 Torr (+5.33 to -10.67 kPa). Beat-to-beat changes in HR and MAP were recorded throughout. In addition, stroke volume (SV) was estimated using the Modelflow method, which incorporates a non-linear, three-element model of the aortic input impedance to compute an aortic flow waveform from the arterial pressure wave. The application of NP and NS did not cause any significant changes in SV either at rest or during exercise. Thus, CBR-mediated alterations in Q were solely due to reflex changes in HR. In fact, a decrease in the carotid-HR response range from 26 +/- 7 beats min-1 at rest to 7 +/- 1 beats min-1 during heavy exercise (P = 0.001) reduced the contribution of Q to the CBR-mediated change in MAP. More importantly, at the time of the peak MAP response, the contribution of TVC to the CBR-mediated change in MAP was increased from 74 +/- 14 % at rest to 118 +/- 6 % (P = 0.017) during heavy exercise. Collectively, these findings indicate that alterations in vasomotion are the primary means by which the CBR regulates blood pressure during mild to heavy exercise.

Adult↗
PubMed2003

Glucose ingestion attenuates interleukin-6 release from contracting skeletal muscle in humans.

To examine whether glucose ingestion during exercise affects the release of interleukin-6 (IL-6) from the contracting limb, seven men performed 120 min of semi-recumbent cycling on two occasions while ingesting either 250 ml of a 6.4 % carbohydrate (GLU trial) or sweet placebo (CON trial) beverage at the onset of, and at 15 min intervals throughout, exercise. Muscle biopsies obtained before and immediately after exercise were analysed for glycogen and IL-6 mRNA expression. Blood samples were simultaneously obtained from a brachial artery and a femoral vein prior to and during exercise and leg blood flow was measured by thermodilution in the femoral vein. Net leg IL-6 release, and net leg glucose and free fatty acid (FFA) uptake, were calculated from these measurements. The arterial IL-6 concentration was lower (P < 0.05) after 120 min of exercise in GLU, but neither intramuscular glycogen nor IL-6 mRNA were different when comparing GLU with CON. However, net leg IL-6 release was attenuated (P < 0.05) in GLU compared with CON. This corresponded with an enhanced (P < 0.05) glucose uptake and a reduced (P < 0.05) FFA uptake in GLU. These results demonstrate that glucose ingestion during exercise attenuates leg IL-6 release but does not decrease intramuscular expression of IL-6 mRNA.

Administration, Oral↗
PubMed2003

Cardiovascular control during exercise: insights from spinal cord-injured humans.

BACKGROUND: We studied the role of the central nervous system, neural feedback from contracting skeletal muscles, and sympathetic activity to the heart in the control of heart rate and blood pressure during 2 levels of dynamic exercise. METHODS AND RESULTS: Spinal cord-injured individuals (SCI) with (paraplegia, n=4) or without (tetraplegia, n=6) sympathetic innervation to the heart performed electrically induced exercise. Responses were compared with those established by able-bodied individuals (control, n=6) performing voluntary exercise at a similar pulmonary oxygen uptake. In all subjects, cardiac output and leg blood flow increased, but in SCI they reached a maximal value. The increase in cardiac output was mainly elicited by an increase in stroke volume in individuals with tetraplegia, whereas in individuals with paraplegia it was by heart rate. The increase in SCI was slow compared with that in controls. During exercise, blood pressure was stable in controls, whereas it decreased over time in SCI and especially in individuals with tetraplegia. CONCLUSIONS: The autonomic nervous system provides for acceleration of the heart at the onset of exercise, but a slow increase in heart rate is established even without central command, neural feedback from working muscles, or autonomic influence on the heart. Yet an intact autonomic nervous system is a prerequisite for a large rise in cardiac output and in turn leg blood flow during exercise. Thus, when the sympathetic nervous system is injured at a level where it influences the heart, vasodilatation in working muscles challenges blood pressure.

Blood Pressure↗
PubMed2003

Cerebral metabolism is influenced by muscle ischaemia during exercise in humans.

Maximal exercise reduces the cerebral metabolic ratio (O2/(glucose + 1/2 lactate)) to < 4 from a resting value close to 6, and only part of this decrease is explained by the 'intent' to exercise. This study evaluated whether sensory stimulation of brain by muscle ischaemia would reduce the cerebral metabolic ratio. In 10 healthy human subjects the cerebral arterial-venous differences (a-v differences) for O2, glucose and lactate were assessed before, during and after three bouts of 10 min cycling with equal workload: (1) control exercise at light intensity, (2) exercise that elicited a high rating of perceived exertion due to a 100 mmHg thigh cuff, and (3) exercise followed by 5 min of post-exercise muscle ischaemia that increased blood pressure by approximately 20 %. Control exercise did not significantly affect the a-v differences. However, during the recovery from exercise with thigh cuffs the cerebral metabolic ratio decreased from a resting value of 5.4 +/- 0.2 to 4.0 +/- 0.4 (mean +/- S.E.M.; P < 0.05) as a discrete lactate efflux from the brain at rest shifted to a slight uptake. Also, following post-exercise muscle ischaemia, the cerebral metabolic ratio decreased to 4.5 +/- 0.3 (P < 0.05). The results support the hypothesis that during exercise, cerebral metabolism is influenced both by the mental effort to exercise and by sensory input from skeletal muscles.

Adult↗