Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 19 recordsLinked to original sources

PubMed1992

[Anesthesiologic aspects of multiorgan donation].

As of July 1990 brain death was legally recognized in Denmark thereby rendering transplantation of heart, liver and lung possible. Brain death donors are usually treated in neurosurgical or anaesthetic intensive care units. The staff of these units influence the number of donors and also the quality of organs donated. Physiological factors pertinent to brain death donors and pre- and peroperative donor therapy in relation to multiorgan procurement are discussed from the viewpoint of the anaesthetist. Symptomatic therapy aimed at optimizing and maintaining organ function is employed; thus continuing intensive care. Sympathetic and somatic reflex responses to surgical stimulation are to be anticipated, often necessitating analgesics to blunt haemodynamic responses and neuromuscular blocking agents to inhibit movements and/or rigidity.

Anesthetics↗

PubMed1992

Recovery of pulmonary diffusing capacity after maximal exercise.

Pulmonary diffusing capacity (DICO), together with spirometric variables, arterial oxygen tension (paO2) and cardiac output were determined before and at intervals after maximal arm cranking, treadmill running and ergometer rowing. Independent of the type of exercise, D1CO increased immediately post-exercise from a median 13.6 (range 7.3-16.3) to 15.1 (9.3-19.6) mmol min-1 kPa-1 (P < 0.01). However, it decreased to 11.6 (6.9-15.5) mmol min-1 kPa-1 (P < 0.01) after 24 h with cardiac output and paO2 at resting values, and D1CO normalized after 20 h. Thoracic electrical impedance at 2.5 and 100 kHz increased slightly post-exercise, indicating a decrease in thoracic fluid balance, and there were no echocardiographic signs of left ventricular failure at the time of the decrease in D1CO. Also, active muscle (limb) circumference and volume, and an increase in haematocrit from 43.8 (38.0-47.0) to 47.1 (42.7-49.8) (P < 0.01), had normalized at the time of the decrease in D1CO. Vital capacity, forced vital capacity, forced expiratory volume in 1 s, peak and peak mid-expiratory flows did not change. However, total lung capacity increased from 6.8 (5.0-7.6) to 7.0 (5.1-7.8) litres (P < 0.05) immediately after exercise and remained elevated at 6.9 (5.1-8.7) litres (P < 0.05) when a decrease in D1CO was noted. The results demonstrate that independent of the type of maximal exercise, an approximate 15% reduction in D1CO takes place 2-3 h post-exercise, which normalizes during the following day of recovery.

Adult↗

PubMed1992

Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia.

Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3-L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8-T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats.min-1 while thoracic impedance increased from 25.5 to 26.5 ohm. End-systolic diameter (ESD) and end-diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats.min-1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head-down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol.l-1, vasopressin from 3 and 2 to 152 and 46 pmol.l-1, and aldosterone from 282 and 229 to 383 and 485 pmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Bradycardia during reversible hypovolaemic shock: associated neural reflex mechanisms and clinical implications.

1. Heart rate response to reversible central hypovolaemia can be divided into three stages. In the first stage (corresponding to a reduction of the blood volume by approximately 15%) a modest increase in heart rate (< 100 beats/min) and total peripheral resistance compensate for the blood loss, and a near normal arterial blood pressure prevails (preshock). During the second stage, a reduction of the central blood volume by approximately 30% results in a decrease in heart rate, total peripheral resistance and blood pressure due to activation of unmyelinated vagal afferents (C-fibres) from the left ventricle. In the third stage, blood pressure falls further as haemorrhage continues and tachycardia (> 120 beats/min) is manifest. This stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals. 2. Recognition of the vasodepressor-cardioinhibitory reaction to a reduced circulating blood volume is important and suggests the need for immediate treatment with volume expansion in critically ill patients.

Autonomic Nervous System↗

PubMed1992

Plasma endothelin-1 during central hypovolaemia in man.

Endothelin-1 (ET-1) is a potent vasoconstricting peptide with effect on resistance as well as capacitance vessels. We followed ET-1 in arterial plasma together with heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and thoracic electrical impedance (TI) in seven men during central hypovolaemia induced by 50 degrees head-up tilt. During tilting plasma ET-1 increased from 1.1 +/- 0.2 to 1.4 +/- 0.3 pmol l-1 (mean +/- SE) concomitant with an increase in total peripheral resistance (TPR) (from 15 +/- 2 to 25 +/- 3 mmHg min l-1) (P < 0.01), and HR (from 67 +/- 2 to 94 +/- 5 beats min-1) (P < 0.01) while MAP remained unchanged. CVP decreased (from 1.8 +/- 0.9 to -1.6 +/- 1.0 mmHg) (P < 0.01) during tilting and remained unchanged during sustained tilt despite further reduction of central blood volume as recorded by TI. Presyncopal symptoms occurred after 28 +/- 6 min associated with decreases in HR (to 70 +/- 6 beats min-1), MAP (from 90 +/- 3 to 52 +/- 4 mmHg) and TPR (to 11 +/- 2 mmHg min l-1) (P < 0.01). At this time plasma ET-1 reached its highest level of 1.6 +/- 0.3 pmol l-1 (P < 0.01). Data show that head-up tilt is associated with increased plasma concentrations of ET-1 which may play a role in maintaining vascular tone in situations with a reduced central blood volume.

Adult↗

PubMed1992

Heart rate during haemorrhagic shock.

In a prospective study, heart rate and mean arterial pressure were related to estimated blood loss in 34 consecutive patients aged 23-92 years during resuscitation from haemorrhagic shock. Eighteen patients with a blood loss of less than 31 (1.9 [0.9-3.0] l) (median and range), corresponding to 34 (16-46) % of estimated blood volume, had a heart rate of 83 (60-160) beats min-1 and a mean arterial pressure of 62 (35-73) mmHg. In 16 patients with a blood loss of more than 3 l (4.0 [3.3-5.0] l) corresponding to 89 (35-100) % of the estimated blood volume, heart rate was 120 (110-160) beats min-1 (P < 0.05) and mean arterial pressure 52 (0-70) mmHg (P < 0.05). Six patients died due to severe bleeding (3.1 [2.5-5.0] l) with a heart rate of 129 (110-160) beats min-1 and a mean arterial pressure of 40 (0-70) mmHg. It is concluded that reversible hypovolaemic shock is associated with a relatively low heart rate (approximately 80 beats min-1) and that tachycardia (approximately 120 beats min-1) is associated with profound bleeding. Hypovolaemic shock with tachycardia may represent a transition to an irreversible stage.

Adult↗

PubMed1992

Effect of training on insulin-mediated glucose uptake in human muscle.

During insulin stimulation whole body glucose uptake is increased in trained compared with untrained humans. However, it is not known which tissue is responsible. Seven young male subjects bicycle trained one leg for 10 wk at 70% of maximal O2 consumption (VO2max). Sixteen hours after last exercise bout, a three-step euglycemic hyperinsulinemic clamp (clamp 1) was performed (insulin levels, means +/- SE: 9 +/- 1, 53 +/- 3, 174 +/- 5, and 2,323 +/- 80 was microU/ml), with measurement of arteriovenous differences and blood flow in both legs. After 6 days of detraining subjects were restudied, having exercised the untrained leg 16 h before. VO2max for trained (T) and untrained (UT) legs was 52 +/- 2 vs. 44 +/- 2 ml.min-1.kg-1 (P < 0.05). In clamp 1 glucose uptake in T and UT legs was 1.0 +/- 0.2 vs. 0.5 +/- 0.1 mg.min-1.kg-1 (basal), 9.7 +/- 2.3 vs. 6.7 +/- 1.7 (P < 0.05) (step I), 19.2 +/- 2.8 vs. 14.3 +/- 2.0 (P < 0.05) (step II), and 22.8 +/- 2.3 vs. 18.6 +/- 2.2 (P < 0.05) (step III). During insulin infusion lactate release (P < 0.05) [8.9 +/- 1.8 vs. 2.9 +/- 0.9 mumol.min-1.kg-1 (step I), 24.6 +/- 3.1 vs. 12.5 +/- 2.6 (step III)] and glycogen storage (P < 0.1) calculated by indirect calorimetry [6.7 +/- 2.3 vs. 5.0 +/- 1.7 mg.min-1.kg-1 (step I), 16.8 +/- 2.1 vs. 14.1 +/- 1.8 (step III)] were always higher in T than in UT legs. Release of glycerol, free fatty acids, and tyrosine and clearance of insulin were not influenced by training. Insulin-mediated glucose uptake was not increased after detraining or a single bout of exercise. In conclusion, training increases sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle by local mechanisms. Glycolysis and glycogen storage are equally enhanced. The training effect represents a genuine adaptation to repeated exercise but is short lived. Insulin clearance in muscle is not influenced by training.

Adult↗

PubMed1992

Pituitary-adrenal responses to head-up tilt in humans: effect of H1- and H2-receptor blockade.

Effects of the histamine H1- or H2-receptor antagonists mepyramine (Mep) and cimetidine (Cim) on neuroendocrine and cardiovascular responses to 50 degrees head-up tilt were evaluated in seven human males. Central hypovolemia was characterized by two phases. The first is a normotensive phase with increases in heart rate (HR), total peripheral resistance (TPR), and decrease in cardiac output. Plasma adrenocorticotropic hormone, beta-endorphin, cortisol, catecholamines, and renin activity increased moderately. Normotension lasted 39 +/- 7 min during infusion of saline but was reduced by Mep [18 +/- 3 min, F(2,12) = 9.60, P less than 0.01] and was unaffected by Cim (44 +/- 4 min). The second is a hypotensive phase associated with presyncopal symptoms (hypovolemic shock) and decreases in HR and TPR and a further increase in pituitary-adrenal and sympathoadrenal activity. Decreases in mean arterial pressure and TPR were augmented by Mep, which inhibited release of norepinephrine. Cim inhibited epinephrine release without affecting the development of hypovolemic shock. It is concluded that histaminergic mechanisms are involved in activation of the sympathoadrenal system but not in the pituitary-adrenal axis during central hypovolemia in humans.

Adult↗

PubMed1992

Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans.

Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.

Adult↗

PubMed1992

Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans.

Transcranial Doppler ultrasound-determined middle (MCA) and anterior (ACA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes (PI) were measured during "no-load" [21, 60, and 102 revolutions/min (rpm)] and loaded cycling (30, 60, and 149 W) at approximately 60 rpm. At rest Vmean MCA was 51 (36-55) cm/s (median and range; n = 10) and Vmean ACA was 41 (36-49) cm/s (n = 7; P < 0.05). With no load on the cycle Vmean MCA increased 4 (2-36), 10 (0-47), and 27% (4-58) (P < 0.05) at the three pedaling frequencies, respectively; arterial PCO2 (PaCO2) remained constant. During loaded cycling the increases were 19 (6-42), 25 (2-45), and 32% (12-67) (P < 0.01), respectively, with only a minimal change in PaCO2. No significant changes were observed in Vmean ACA. Changes in Vmean MCA were similar to those recorded by the initial slope index (ISI) of the 133Xe clearance method (n = 11), which in turn were smaller than increases recorded by the fast-compartment flow. PI ACA followed PI MCA during no-load as well as loaded exercise and increased with work rate, perhaps reflecting an increase in pulse pressure from 56 (48-63) mmHg at rest to 109 (88-123) mmHg at 149 W (P < 0.01). Data demonstrate a graded increase in regional cerebral perfusion during dynamic exercise corresponding to the MCA territory.

Adult↗

PubMed1992

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Effects of axillary blockade on regional cerebral blood flow during dynamic hand contractions.

Regional cerebral blood flow (rCBF) was measured at orbitomeatal (OM) plane +5.0 and +9.0 cm in 10 subjects at rest and during dynamic hand contractions before and after axillary blockade. Handgrip strength was significantly reduced, and rating of perceived exertion increased after blockade. During hand contractions before blockade, contralateral hemispheric cerebral blood flow (CBF) at OM +9.0 increased from a resting value of 58 (49-75) to 63 (52-82) ml.100 g-1.min-1; contralateral motor sensory rCBF at OM +9 from 58 (50-77) to 71 (64-84); motor sensory rCBF at OM +5 from 67 (54-76) to 77 (64-87) and 70 (62-84) contralaterally and ipsilaterally, respectively; and supplementary motor area (SM) rCBF from 64 (53-69) to 75 (67-88) ml.100 g-1.min-1. During dynamic hand contractions after axillary blockade, CBF did not increase at OM +5 or in the SM. Furthermore, contralateral motor sensory rCBF at OM +9 increased much less. Axillary blockade had no effect on resting CBF, rCBF, or increases in the two during hand contractions of the opposite hand. Thus neural feedback from the contracting muscle is necessary for the increases in SM bilateral OM +5 motor sensory rCBF and the maximal increase in contralateral OM +9 motor sensory rCBF during dynamic hand contractions.

Adult↗

PubMed1992

Neural influence on cardiovascular and endocrine responses to static exercise in humans.

At the onset of exercise, signals from the central nervous system result in immediate vagal withdrawal and resulting increases in heart rate and arterial blood pressure. From the second heart beat peripheral nerve (reflex) influence from exercising muscle can be detected. With continued exertion, especially with large muscle groups, this influence becomes increasingly important. Sympathetic nerve signals to resting muscle can be influenced by the central nervous system, but are dominated by influence from 'metaboreceptors' in exercising muscle, while sympathetic nerve signals to skin are more influenced by the central nervous system. Cardiovascular responses to static contractions increase with the percentage of maximum contraction intensity as well as with the muscle mass involved. Plasma catecholamines rise in proportion to increases in cardiovascular variables and are influenced by a central nervous mechanism early in the contraction. Furthermore, during static contractions the increase in plasma adrenaline (epinephrine) is larger relative to that of noradrenaline than during dynamic exercise. Both catecholamine responses and the responses of pituitary hormones depend on the active muscle mass, but are small compared to those established during dynamic exercise. Experiments designed to enhance central command, resulting in increased cardiovascular and endocrine responses compared to control experiments and experiments in which an attenuation of peripheral nerve influence resulted in reduced changes in these variables during exercise, contrast with the notion that the 2 neural control mechanisms are redundant. Rather, the 2 neural influences on the autonomic nervous system work in concert in eliciting the responses manifest during static exercise.

Cardiovascular Physiological Phenomena↗

PubMed1992

The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.

Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Maximal oxygen uptake and work capacity after inspiratory muscle training: a controlled study.

The effect of inspiratory muscle training for 10 min twice a day for 27.5 days was evaluated in 20 human subjects, of whom 10 formed a training group and 10 a sham training group. The maximal oxygen uptake (VO2 max), maximal ventilation, breathing frequency during maximal exercise and the distance run in 12 min on a track were determined in addition to resting peak expiratory flow, forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1), with alveolar oxygen tension (pAO2) during maximal exercise being calculated. Inspiratory muscle training increased maximal inspiratory pressure from 93 (range 38-118) to 110 (65-165) mmHg in the training group (P less than 0.0005), but did not affect VO2 max, ventilation during maximal exercise, peak expiratory flow, FEV1 or FVC. However, breathing frequency during maximal exercise decreased slightly from 56 (44-87) to 53 (38-84) breaths min-1 (P less than 0.05) in the training group only; but the calculated pAO2 did not increase from the pre-training value of 126 (116-132) mmHg. The maximal distance run during 12 min increased similarly in the training and sham training groups by 8% (3-12%) and 6% (2-12%), respectively (P less than 0.01). The results of this study show that inspiratory muscle training resulting in a 32% (0-85%) increase in maximal inspiratory pressure does not change FEV1, FVC, peak expiratory flow, VO2 max or work capacity.

Adult↗

PubMed1991

Thoracic impedance as an index of body fluid balance during cardiac surgery.

Thoracic impedance at 2.5 (TI2.5) and 100 kHz (TI100), central venous pressure (CVP), and body fluid balance were recorded together with rectal temperature and arterial haematocrit in 15 consecutive patients subjected to coronary artery bypass grafting. I.v. fluid and blood were administered in an excess of 3.18 (1.38-9.35) 1 during the operation. TI2.5 decreased from 51.7 (39.2-66.4) to 34.9 (21.1-45.7) ohm (P = 0.001), while TI100 decreased from 41.9 (31.4-55.0) to 30.3 (18.3-40.8) ohm (P = 0.002). CVP, 6 (3-11) mmHg [0.8 (0.4-1.5) kPa], was the same before and after surgery. Temperature decreased during cardiopulmonary bypass from 35.4 (34.1-36.6) to 26.7 (22.9-31.0) degrees C and haematocrit from 39 (34-46)% to a lowest value of 27 (23-32)% (P = 0.0001). A close linear correlation between TI and body fluid balance was observed (TI2.5: r = -0.96, TI100: r = -0.95, P = 0.0001). Corrections of TI for temperature and/or haematocrit improved the correlation between TI and fluid balance to 0.99 (TI2.5) and 0.98 (TI100). The data indicate that changes in thoracic impedance can be used to monitor body fluid balance during cardiac surgery.

Aged↗

PubMed1991

Blood volume distribution during head-up tilt induced central hypovolaemia in man.

We evaluated regional electrical impedance (Z degree) at 2.5 and 100 kHz to separate intra- and extracellular fluid changes and correlated Z degree over the thorax (TI) to relative changes in the central blood volume (CBV) induced by head-up tilt. In nine experiments head-up tilt resulted in normotensive central hypovolaemia associated with a 3.7 +/- 0.4 Ohm (mean +/- SE) increase in TI100 kHz after 60 min. In 24 experiments pre-syncopal symptoms were induced after 43 +/- 2 min, when TI100 kHz had increased 4.2 +/- 0.2 Ohm. Head-up tilt instantly decreased the activity of technetium labelled erythrocytes (99Tcm) over the thorax by 24 +/- 2%, and increased 99Tcm over the thigh by 68 +/- 10% (P less than 0.01, n = 8) with no further changes during the sustained tilt. Haematocrite increased during head-up tilt from 43.1 +/- 0.3 to 47.9 +/- 0.6% (P less than 0.01, n = 8). Accordingly, the increase in TI (6.3 +/- 0.6 vs. 4.5 +/- 0.4 Ohm, n = 6) and the decrease in Z degree through one leg (7.2 +/- 1.2 vs. 2.8 +/- 0.5 Ohm, n = 6) at 2.5 kHz was more pronounced than at 100 kHz. Also the changes in TI were correlated to CBV as calculated from 99Tcm and haematocrite (r = 0.90, P less than 0.01). The results suggest that: (1) Hypovolaemic shock is associated with a faster increase of TI than normotensive head-up tilt. (2) Head-up tilt is characterized by an initial decrease in CBV followed by a further decrease in plasma volume, which eventually leads to hypovolaemic shock. (3) Blood volume changes during head-up tilt are reflected in regional Z degree.

Adult↗

PubMed1991

Effect of training on central factors in fatigue following two- and one-leg static exercise in man.

Leg strength and fatigue developed during 150 repeated two- and one-leg isometric maximal voluntary contractions were determined before and after a 5-week one- (n = 6) or two- (n = 7) leg training programme including a control group of five subjects. Two- and one-leg training increased two- and one-leg strength by 59 (range 8-107) and 36% (-1-69) respectively (P less than 0.01) with no significant difference between the two groups. Two-leg training decreased (P less than 0.05) fatigue only during two-leg maximal voluntary contractions (from 20 [11-26] to 13% [6-27]); and one-leg training fatigue only during one-leg maximal voluntary contractions (from 20 [15-23] to 11% [9-24]) despite the fact that both legs were trained. Surface electromyographic activity decreased during both repeated two- and one-leg maximal voluntary contractions (P less than 0.01) but a reduction in electromyographic decay was seen (P less than 0.05) during two-leg maximal voluntary contractions after two-leg training. Training increased fast-twitch b fibre size (P less than 0.01), and glycogen depletion was seen in fast-twitch (a and b) fibres, but the relative fast-twitch b area did not increase significantly. No training effects were seen in the control group. The results show that an approximately 47% increase in muscle strength may take place without a significant change in the relative percentage of muscle fibre types or in the average muscle fibre size. Furthermore, the specificity of the training response to fatigue developed during repeated two- and one-leg maximal voluntary contractions suggests a change in the nervous influence on the motor units.

Adult↗