Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 163 records · Page 9Linked to original sources

PubMed1993

Effect of diazepam on endocrine and cardiovascular responses to head-up tilt in humans.

Effects of the GABAergic drug diazepam (0.15 mg kg-1, i.v.) on cardiovascular and endocrine responses to 50 degrees head-up tilt were evaluated in seven men. During the initial phase of tilt (normotensive phase), increases in heart rate (HR) and total peripheral resistance (TPR) and decreases in cardiac output were unaffected by diazepam. Also the associated increase in plasma noradrenaline did not change, while response in plasma ACTH was diminished and in plasma cortisol abolished by diazepam (F(1,10) = 6.45; P < 0.03). After 42 +/- 4 min of sustained tilt with saline (control) and 47 +/- 6 min (n.s.) after diazepam, presyncopal symptoms appeared (hypotensive phase) associated with decreases in HR, MAP, and TPR (P < 0.01). This episode induced a 2-3-fold increase in plasma ACTH, beta-endorphin, prolactin, cortisol (< 0.01), and a moderate increase in plasma adrenaline (P < 0.05). Diazepam did not significantly change cardiovascular and endocrine responses to the hypotensive phase of tilt. Results indicate that diazepam attenuates the cortisol part of pituitary-adrenal responses to moderate, but not to severe, central hypovolaemia in humans with no effect on cardiovascular tolerance.

Adult↗

PubMed1993

Effect of serotonin receptor blockade on endocrine and cardiovascular responses to head-up tilt in humans.

Effects of blockade of serotonin (5-HT) receptors on the integrated cardiovascular and endocrine adaptations during head-up tilt were investigated in normal men. In control experiments 50 degrees head-up tilt increased heart rate (HR), total peripheral resistance (TPR), plasma renin activity (PRA) and sympathetic activity (plasma noradrenaline; NA). A moderate increase in pituitary-adrenal hormones (plasma ACTH, beta-END and cortisol) was observed. After a mean tilt time of 30 +/- 5 min (n = 20) presyncopal symptoms associated with decreases in HR, TPR and arterial pressure occurred. At this time pituitary hormones, cortisol, adrenomedullary (plasma adrenaline; A) as well as vagal activity (plasma pancreatic polypeptide) were markedly increased, whereas sympathetic activity (plasma NA) decreased. The 5-HT1+2 receptor antagonist methysergide did not significantly interfere with cardiovascular variables but attenuated the response of NA, prolactin (PRL), beta-endorphin (beta-END) and PRA (P < 0.02). The 5-HT2-receptor antagonist ketanserin reduced the tolerated tilt time (10 +/- 4 vs. 32 +/- 2 min; P < 0.0003, n = 7) but had no significant effects on hormonal variables. The 5-HT3-receptor antagonist ondansetron abolished the adrenomedullary response to hypotension without affecting cardiovascular tolerance or the activity of the pituitary-adrenal axis. The results suggest that serotonergic mechanisms may be involved in the integrated cardiovascular and endocrine responses to central blood volume depletion in humans.

Adrenocorticotropic Hormone↗

PubMed1993

Enhanced heart rate response to haemorrhage by ileus in the pig.

Effects of ileus on cardiovascular and hormonal responses to haemorrhage were evaluated in 10 anaesthetized pigs. Ileus was induced and the bleeding sequence repeated on the following day. Before ileus, a resting heart rate (HR) of 105 (range 83-140) beats min-1 remained unchanged until haemorrhage amounted to 15% of the blood volume. With a blood loss of 28% HR increased to a maximum of 162 (126-245) beats min-1. In contrast, ileus increased HR upon initiation of haemorrhage from a similar resting value to a maximum of 200 (152-250) beats min-1 (P < 0.0005). There were neither statistical differences in mean arterial pressure, cardiac output, central venous pressure, thoracic electrical impedance, pulmonary arterial mean pressure, pulmonary wedge pressure, pulmonary and systemic vascular resistances, nor in plasma concentrations of dopamine, adrenaline, vasopressin and aldosterone during haemorrhage before and after ileus. Plasma noradrenaline increased more with haemorrhage after than before ileus: from 2.8 (1.2-5.0) to 13 (2.3-59.0) vs. 3.0 (1.5-4.2) to 3.6 (2.7-17.5) nmol l-1 (P < 0.005). Also, the pancreatic polypeptide response to haemorrhage was enlarged with ileus (29 (0-60) to 90 (45-145) vs. 23 (0-64) to 57 (27-106) pmol l-1 (P < 0.005)). No significant differences could be detected in cardiovascular and hormonal responses to haemorrhage before and after a sham-operation in three pigs. Results demonstrate an immediate and enhanced HR response to haemorrhage in the pig with ileus, reflected in sympathetic activation as indicated by plasma noradrenaline.

Animals↗

PubMed1993

The effect of epidural anaesthesia with 1% lidocaine on the pressor response to dynamic exercise in man.

1. In order to examine the sensitivity to local anaesthetics of afferent neural feedback from working muscle during dynamic exercise, sixteen subjects cycled for 12 min before and after epidural anaesthesia using 1% lidocaine. The presence of afferent neural blockade was verified by elimination of the blood pressure response to a cold pressor test, laser-induced evoked potentials and increases in pain detection and tolerance thresholds of the foot. Conversely, epidural anaesthesia had no effect on these variables in the unblocked skin areas or on electrically evoked potentials in blocked or unblocked skin. 2. During dynamic exercise, heart rate increased as did mean arterial pressure and cardiac output. Mean arterial pressure remained at the exercise level during post-exercise ischaemia, but heart rate and cardiac output decreased while total peripheral resistance increased. Epidural anaesthesia did not significantly affect these variables during rest, dynamic exercise, post-exercise ischaemia or recovery. 3. The results of this study show that, in order to affect blood pressure during dynamic exercise, epidural anaesthesia must block the pressor response to post-exercise ischaemia. The implication of these data is that complete or almost complete block of group III and/or group IV muscle afferents is necessary to inhibit the pressor response to dynamic exercise in man.

Adult↗

PubMed1993

Neural control of cardiovascular responses and of ventilation during dynamic exercise in man.

1. Nine subjects performed dynamic knee extension by voluntary muscle contractions and by evoked contractions with and without epidural anaesthesia. Four exercise bouts of 10 min each were performed: three of one-legged knee extension (10, 20 and 30 W) and one of two-legged knee extension at 2 x 20 W. Epidural anaesthesia was induced with 0.5% bupivacaine or 2% lidocaine. Presence of neural blockade was verified by cutaneous sensory anaesthesia below T8-T10 and complete paralysis of both legs. 2. Compared to voluntary exercise, control electrically induced exercise resulted in normal or enhanced cardiovascular, metabolic and ventilatory responses. However, during epidural anaesthesia the increase in blood pressure with exercise was abolished. Furthermore, the increases in heart rate, cardiac output and leg blood flow were reduced. In contrast, plasma catecholamines, leg glucose uptake and leg lactate release, arterial carbon dioxide tension and pulmonary ventilation were not affected. Arterial and venous plasma potassium concentrations became elevated but leg potassium release was not increased. 3. The results conform to the idea that a reflex originating in contracting muscle is essential for the normal blood pressure response to dynamic exercise, and that other neural, humoral and haemodynamic mechanisms cannot govern this response. However, control mechanisms other than central command and the exercise pressor reflex can influence heart rate, cardiac output, muscle blood flow and ventilation during dynamic exercise in man.

Adult↗

PubMed1993

Regulation of hepatic glucose production during exercise in humans: role of sympathoadrenergic activity.

To investigate the role of sympathoadrenergic activity on glucose production (Ra) during exercise, eight healthy males bicycled 20 min at 41 +/- 2 and 74 +/- 4% maximal O2 uptake (VO2max; mean +/- SE) either without (control; Co) or with blockade of sympathetic nerve activity to liver and adrenal medulla by local anesthesia of the celiac ganglion (Bl). Epinephrine (Epi) was in some experiments infused during blockade to match (normal Epi) or exceed (high Epi) Epi levels during Co. A constant infusion of somatostatin and glucagon was given before and during exercise. At rest, insulin was infused at a rate maintaining euglycemia. During intense exercise, insulin infusion was halved to mimic physiological conditions. During exercise, Ra increased in Co from 14.4 +/- 1.0 to 27.8 +/- 3.0 mumol.min-1.kg-1 (41% VO2max) and to 42.3 +/- 5.2 (74% VO2max; P < 0.05). At 41% VO2max, plasma glucose decreased, whereas it increased during 74% VO2max. Ra was not influenced by Bl. In high Epi, Ra rose more markedly compared with control (P < 0.05), and plasma glucose did not fall during mild exercise and increased more during intense exercise (P < 0.05). Free fatty acid and glycerol concentrations were always lower during exercise with than without celiac blockade. We conclude that high physiological concentrations of Epi can enhance Ra in exercising humans, but normally Epi is not a major stimulus. The study suggests that neither sympathetic liver nerve activity is a major stimulus for Ra during exercise. The Ra response is enhanced by a decrease in insulin and probably by unknown stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Effect of limb anesthesia on middle cerebral response to handgrip.

Transcranial Doppler ultrasound was used to measure middle cerebral arterial mean flow velocity (Vmean) on both sides of the brain in 12 subjects during hand contractions before and during regional anesthesia of the left arm. At rest Vmean was 49 (36-104) cm/s (median and range) and was unaffected by regional anesthesia. During right-hand contractions Vmean remained unchanged on the right side of the brain, whereas it increased 20 (4-37)% (P < 0.01) on the left side of the brain. Similarly, during left-hand contractions Vmean increased 24 (2-42)% (P < 0.01) on the right side of the brain, while it remained unchanged on the left side of the brain. Regional anesthesia did not quantitatively affect Vmean during right-hand contractions. In contrast, during left-hand contractions, both right and left Vmean tended to decrease. Increases in Vmean appeared despite a decrease in arterial carbon dioxide tension (P < 0.01). Heart rate and blood pressure responses to hand contractions were enhanced during regional anesthesia (P < 0.01), but left-hand contractions resulted in a less pronounced increase in blood pressure (P < 0.01). These data demonstrate a contralateral increase in cerebral perfusion during hand contractions that is dependent on intact afferent input from the working limb.

Adult↗

PubMed1993

Middle cerebral artery blood velocity and cerebral blood flow and O2 uptake during dynamic exercise.

Results obtained by the 133Xe clearance method with external detectors and by transcranial Doppler sonography (TCD) suggest that dynamic exercise causes an increase of global average cerebral blood flow (CBF). These data are contradicted by earlier data obtained during less-well-defined conditions. To investigate this controversy, we applied the Kety-Schmidt technique to measure the global average levels of CBF and cerebral metabolic rate of oxygen (CMRO2) during rest and dynamic exercise. Simultaneously with the determination of CBF and CMRO2, we used TCD to determine mean maximal flow velocity in the middle cerebral artery (MCA Vmean). For values of CBF and MCA Vmean a correction for an observed small drop in arterial PCO2 was carried out. Baseline values for global CBF and CMRO2 were 50.7 and 3.63 ml.100 g-1.min-1, respectively. The same values were found during dynamic exercise, whereas a 22% (P < 0.0001) increase in MCA Vmean was observed. Hence, the exercise-induced increase in MCA Vmean is not a reflection of a proportional increase in CBF.

Adult↗

PubMed1993

Physiological and biomechanical aspects of rowing. Implications for training.

The drag force on a racing shell increases with the square of velocity corresponding to a 3.2 power increase in energy expenditure. However, the metabolic cost increases with only an approximately 2.4 power function of shell velocity. During international races the metabolic cost corresponds to an oxygen uptake of 6.7 to 7.0 L/min over 6.5 min. The relative anaerobic contribution to 6.5 min of 'all-out' rowing has not been determined but is estimated to range from 21 to 30%. Because of the large muscle mass involved in rowing, blood variables reach extreme values: adrenaline 19 nmol/L; noradrenaline 74 nmol/L; pH 7.1; and bicarbonate 9.8 mmol/L. Because of the static component of the rowing stroke at the catch, blood pressure increases to near 200mm Hg, and the heart of oarsmen has adapted to this load by increasing wall thickness and internal diameters. The maximal oxygen uptake of oarsmen may reach 6.6 L/min and ventilation 243 L/min. Arterial oxygen tension decreases by 20mm Hg during 'all-out' rowing corresponding to a decrease in pulmonary diffusion capacity. A force of approximately 800 to 900N is developed on the oar. Force generation during rowing is relatively slow, 0.3 to 0.4 sec. Oarsmen are strongest in low velocity movement with 70 to 75% slow twitch fibres in skeletal muscle. Data indicate that rowing technique and training may improve explaining why results become approximately 0.7 sec faster per year.

Altitude↗

PubMed1993

Peripheral venous oxygen saturation during head-up tilt induced hypovolaemic shock in humans.

We followed central, median cubital and dorsal metacarpal venous oxygen saturations (SvO2) during 50 degrees head-up tilt (anti-Trendelenburg's position) induced central hypovolaemia in eight males. Head-up tilt resulted in slight tachycardia of 101 (60-120) beats min-1 (median with range) and a stable mean arterial pressure (MAP) of 100 (88-114) mmHg. After 13 (6-23) min presyncopal symptoms appeared, accompanied by decreases in heart rate to 75 (51-97) beats min-1 and in MAP to 59 (49-76) mmHg (p < 0.01). Cardiac output decreased 0.9 (0.3-1.6) 1 min-1 while thoracic electrical impedance increased 3.4 (-1.2-5.9) Ohm (p < 0.01). Tilt-up decreased central venous pressure, but during sustained tilt it remained unchanged. Arterial oxygen saturation did not change. Head-up tilt decreased central SvO2 by 12 (5-24)% (p < 0.01). Median cubital SvO2 decreased 8 (-5-25)% (p < 0.02) during tilting, and it remained at this level during sustained tilt. Only five of eight samples from the dorsal metacarpal vein could be obtained. In these samples SvO2 was lowered by 15 (7-26)% (p = 0.01) at the onset of presyncopal symptoms. The results indicate that loss of central blood volume is reflected in central as well as peripheral SvO2. However, for reliable monitoring of blood volume changes, central SvO2 is the most useful variable, as this SvO2 changed consistently with the central blood volume, and blood samples could be obtained readily from the central venous catheter.

Adult↗

PubMed1993

Natural killer cell activity during head-up tilt-induced central hypovolemia in humans.

Changes in immunological competent blood cells were evoked in seven humans during passive head-up tilt (50 degrees anti-Trendelenburg's position maintained until appearance of presyncopal symptoms). Blood samples were collected after 60 min of rest, when presyncopal symptoms appeared during tilt, and 105 min after tilt-down. Natural killer (NK) cell activity increased during head-up tilt due to a three to four-fold increase in CD16+ NK cells in blood. In support NK cell activity boosted with interferon-alpha and interleukin 2 (IL-2) rose in parallel with unboosted NK cell activity. This effect on NK cells disappeared during recovery but was not suppressed when compared to prevalues. Lymphocyte concentration also increased during head-up tilt. Concentrations of CD3+ and CD4+ T cells were almost stable during head-up tilt, whereas the percentage of CD3+ T cells in relation to blood mononuclear cell (BMNC) concentration decreased, due to a diminished percentage of CD4+ T cells and the marked simultaneous increase in the percentage of CD16+ NK cells. Although changes in the BMNC composition occurred, the proliferative responses of BMNC following stimulation with phytohemagglutinin, purified derivative of tuberculin, or IL-2 did not change significantly. We conclude that head-up tilt induced marked changes in subpopulations of BMNC, especially the CD16+ NK cells, as they were recruited to the blood.

Adult↗

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↗