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Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 37 records · Page 2Linked to original sources

Attenuated hepatosplanchnic uptake of lactate during intense exercise in humans.

We evaluated whether the increase in blood lactate with intense exercise is influenced by a low hepatosplanchnic blood flow as assessed by indocyanine green dye elimination and blood sampling from an artery and the hepatic vein in eight men. The hepatosplanchnic blood flow decreased from a resting value of 1.6 +/- 0.1 to 0.7 +/- 0.1 (SE) l/min during exercise. Yet the hepatosplanchnic O2 uptake increased from 67 +/- 3 to 93 +/- 13 ml/min, and the output of glucose increased from 1.1 +/- 0.1 to 2.1 +/- 0.3 mmol/min (P < 0.05). Even at the lowest hepatosplanchnic venous hemoglobin O2 saturation during exercise of 6%, the average concentration of glucose in arterial blood was maintained close to the resting level (5.2 +/- 0.2 vs. 5.5 +/- 0.2 mmol/l), whereas the difference between arterial and hepatic venous blood glucose increased to a maximum of 22 mmol/l. In arterial blood, the concentration of lactate increased from 1.1 +/- 0.2 to 6.0 +/- 1.0 mmol/l, and the hepatosplanchnic uptake of lactate was elevated from 0.4 +/- 0.06 to 1.0 +/- 0.05 mmol/min during exercise (P < 0.05). However, when the hepatosplanchnic venous hemoglobin O2 saturation became low, the arterial and hepatosplanchnic venous blood lactate difference approached zero. Even with a marked reduction in its blood flow, exercise did not challenge the ability of the liver to maintain blood glucose homeostasis. However, it appeared that the contribution of the Cori cycle decreased, and the accumulation of lactate in blood became influenced by the reduced hepatosplanchnic blood flow.

Adult↗

Circulating immunoreactive proANP1-30 and proANP31-67 responses to acute exercise.

The circulating immunoreactive atrial natriuretic peptide (C-terminal; alpha-ANP) increases during exercise to become suppressed in the first hours of the recovery. The response of the N-terminal ANP fragments to acute exercise is not known while proANP (31-67) appears to be elevated with chronic exercise. We evaluated the plasma concentrations of the N-terminal ANP fragments (1-30) and (31-67) in oarsmen (n=10) before and after two acute exercise bouts separated by 5 h. As control, measurements were made on a day with no exercise (n=12). At rest, the concentrations of proANP(1-30) and proANP(31-67) were 344+/-42 and 810+/-172 pmol x l(-1), respectively. Half an hour after the first exercise bout, proANP(1-30) was elevated (to 404+/-48 pmol x l(-1); P<0.05) and decreased below the pre-exercise level (to 316+/-41 pmol x l(-1); P<0.05) 4 h into the recovery period. Also, 30 min after the second exercise session, the concentration of proANP(1-30) was elevated to 408+/-45 pmol x l(-1) (P<0.05) and the pre-exercise level was re-established on the following morning. Thus, proANP(1-30), rather than proANP(31-67), responded to acute exercise. These results suggest that atrial distension and, therefore, the central blood volume changes markedly in athletes during a day with repeated exercise bouts.

Adult↗

Effects of partial neuromuscular blockade on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of central command to the resetting of the carotid baroreflex during static and dynamic exercise in humans. 2. Thirteen subjects performed 3.5 min of static one-legged exercise (20 % maximal voluntary contraction) and 7 min dynamic cycling (20 % maximal oxygen uptake) under two conditions: control (no intervention) and with partial neuromuscular blockade (to increase central command influence) using Norcuron (curare). Carotid baroreflex function was determined at rest and during steady-state exercise using a rapid neck pressure/neck suction technique. Whole-body Norcuron was repeatedly administered to effectively reduce hand-grip strength by approximately 50 % of control. 3. Partial neuromuscular blockade increased heart rate, mean arterial pressure, perceived exertion, lactate concentration and plasma noradrenaline concentration during both static and dynamic exercise when compared to control (P < 0.05). No effect was seen at rest. Carotid baroreflex resetting was augmented from control static and dynamic exercise by partial neuromuscular blockade without alterations in gain (P < 0.05). In addition, the operating point of the reflex was relocated away from the centring point (i.e. closer to threshold) during exercise by partial neuromuscular blockade (P < 0.05). 4. These findings suggest that central command actively resets the carotid baroreflex during dynamic and static exercise.

Adult↗

Effects of exercise pressor reflex activation on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of the exercise pressor reflex to the resetting of the carotid baroreflex during exercise. 2. Ten subjects performed 3.5 min of static one-legged exercise (20 % maximal voluntary contraction) and 7 min dynamic cycling (20 % maximal oxygen uptake) under two conditions: control (no intervention) and with the application of medical anti-shock (MAS) trousers inflated to 100 mmHg (to activate the exercise pressor reflex). Carotid baroreflex function was determined at rest and during exercise using a rapid neck pressure/neck suction technique. 3. During exercise, the application of MAS trousers (MAS condition) increased mean arterial pressure (MAP), plasma noradrenaline concentration (dynamic exercise only) and perceived exertion (dynamic exercise only) when compared to control (P < 0.05). No effect of the MAS condition was evident at rest. The MAS condition had no effect on heart rate (HR), plasma lactate and adrenaline concentrations or oxygen uptake at rest and during exercise. The carotid baroreflex stimulus-response curve was reset upward on the response arm and rightward to a higher operating pressure by control exercise without alterations in gain. Activation of the exercise pressor reflex by MAS trousers further reset carotid baroreflex control of MAP, as indicated by the upward and rightward relocation of the curve. However, carotid baroreflex control of HR was only shifted rightward to higher operating pressures by MAS trousers. The sensitivity of the carotid baroreflex was unaltered by exercise pressor reflex activation. 4. These findings suggest that during dynamic and static exercise the exercise pressor reflex is capable of actively resetting carotid baroreflex control of mean arterial pressure; however, it would appear only to modulate carotid baroreflex control of heart rate.

Adult↗

Influence of body mass on maximal oxygen uptake: effect of sample size.

Basal metabolic rate is scaled to body mass to the power of 0.73, and we evaluated whether a similar scaling applies when the O2 transport capacity of the body is challenged during maximal exercise (i.e. at maximal O2 uptake, VO2max). The allometric relationship between VO2max and body mass (y = a.xb, where y is VO2max and x is body mass) was developed for 967 athletes representing 25 different sports, with up to 157 participants in each sport. With an increasing number of observations, the exponent approached 0.73, while for ventilation the exponent was only 0.55. By using the 0.73 exponent for VO2max, the highest value [mean (SD)] for the males was obtained for the runners and cyclists [234 (16) ml.kg-0.73.min-1], and for the females the highest value was found for the runners [189 (14) ml.kg-0.73.min-1]. For the females, aerobic power was about 80% of the value achieved by the males. Scaling may help both in understanding variation in aerobic power and in defining the physiological limitations of work capacity.

Adolescent↗

Near-infrared spectroscopy determined brain and muscle oxygenation during exercise with normal and resistive breathing.

To elevate effects of carbon dioxide (CO2) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy- (DeltaHbO2) and deoxy-haemoglobin (DeltaHb) of active muscles and the brain were determined by near-infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28-40) L min-1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end-tidal CO2 pressure (PETCO2) increased from 45 (42-48) to 48 (46-58) mmHg with a reduction of only 1% in the arterial haemoglobin O2 saturation (SaO2). During control exercise (normal breathing resistance), muscle and brain DeltaHbO2 were not different from the resting levels, and only the leg muscle DeltaHb increased (4 (-2-10) microM, P < 0.05). Moderate resistive breathing increased DeltaHbO2 of the intercostal and vastus lateralis muscles to 6 +/- (-5-14) and 1 (-7-9) microM(P < 0.05), respectively, while muscle DeltaHb was not affected. Cerebral DeltaHbO2 and DeltaHb became elevated to 6 (1-15) and 1 (-1-6) microM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO2 influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.

Adult↗

N-acetylcysteine attenuates oxidative burst by neutrophils in response to ergometer rowing with no effect on pulmonary gas exchange.

This study evaluated whether the reduction of the neutrophil oxidative burst by N-acetylcysteine improves pulmonary gas exchange during a six minute maximal ergometer row. Healthy trained oarsmen were double-blinded randomized to either N-acetylcysteine (6 g daily for three days) or placebo groups. As determined by the relative changes of the zymosan-stimulated luminol-enhanced chemiluminescence response, N-acetylcysteine suppressed the exercise-induced enhanced neutrophil oxidative burst response to rowing (-7 +/- 6% vs. 17 +/- 8%; P < 0.05). This was the case although the concentration of neutrophils remained similarly elevated above the pre-exercise level in both trials (to 5.4+/-0.5 vs. 5.9+/-0.6 x 10(9) cells x l(-1), respectively, P>0.05). In the placebo and N-acetylcysteine groups, pulmonary ventilation increased and the arterial CO2 partial pressure decreased to the same extent during exercise. Also, at the end of exercise the arterial O2 partial pressure (77 1 vs. 78+/-1 mmHg), haemoglobin O2 saturation (92 +/- 1% vs. 93 +/- 1%) and O2 uptake (5.0 +/- 0.2 vs. 4.9 +/- 0.21 x min(-1)) were not significantly affected by N-acetylcysteine. Equally, two hours after exercise, the pulmonary diffusion capacity was reduced by 7 +/- 2% below the pre-exercise with no significant influence of N-acetylcysteine. We conclude that the neutrophil oxidative burst to exercise does not influence pulmonary gas exchange during and after maximal rowing.

Acetylcysteine↗

Neural blockade during exercise augments central command's contribution to carotid baroreflex resetting.

This investigation was designed to determine central command's role on carotid baroreflex (CBR) resetting during exercise. Nine volunteer subjects performed static and rhythmic handgrip exercise at 30 and 40% maximal voluntary contraction (MVC), respectively, before and after partial axillary neural blockade. Stimulus-response curves were developed using the neck pressure-neck suction technique and a rapid pulse train protocol (+40 to -80 Torr). Regional anesthesia resulted in a significant reduction in MVC. Heart rate (HR) and ratings of perceived exertion (RPE) were used as indexes of central command and were elevated during exercise at control force intensity after induced muscle weakness. The CBR function curves were reset vertically with a minimal lateral shift during control exercise and exhibited a further parallel resetting during exercise with neural blockade. The operating point was progressively reset to coincide with the centering point of the CBR curve. These data suggest that central command was a primary mechanism in the resetting of the CBR during exercise. However, it appeared that central command modulated the carotid-cardiac reflex proportionately more than the carotid-vasomotor reflex.

Adult↗

Anatomical and functional characteristics of carotid sinus stimulation in humans.

Transmission characteristics of pneumatic pressure to the carotid sinus were evaluated in 19 subjects at rest and during exercise. Either a percutaneous fluid-filled (n = 12) or balloon-tipped catheter (n = 7) was placed at the carotid bifurcation to record internal transmission of external neck pressure/neck suction (NP/NS). Sustained, 5-s pulses, and rapid ramping pulse protocols (+40 to -80 Torr) were recorded. Transmission of pressure stimuli was less with the fluid-filled catheter compared with that of the balloon-tipped catheter (65% vs. 82% negative pressure, 83% vs. 89% positive pressure; P < 0.05). Anatomical location of the carotid sinus averaged 3.2 cm (left) and 3.6 cm (right) from the gonion of the mandible with a range of 0-7.5 cm. Transmission was not altered by exercise or Valsalva maneuver, but did vary depending on the position of the carotid sinus locus beneath the sealed chamber. These data indicate that transmission of external NP/NS was higher than previously recorded in humans, and anatomical variation of carotid sinus location and equipment design can affect transmission results.

Adult↗

Arterial baroreflex control of sympathetic nerve activity during acute hypotension: effect of fitness.

We examined arterial baroreflex control of muscle sympathetic nerve activity (MSNA) during abrupt decreases in mean arterial pressure (MAP) and evaluated whether endurance training alters baroreflex function. Acute hypotension was induced nonpharmacologically in 14 healthy subjects, of which 7 were of high fitness (HF) and 7 were of average fitness (AF), by releasing a unilateral arterial thigh cuff after 9 min of resting ischemia under two conditions: control, which used aortic and carotid baroreflex (ABR and CBR, respectively) deactivation; and suction, which used ABR deactivation alone. The application of neck suction to counteract changes in carotid sinus transmural pressure during cuff release significantly attenuated the MSNA response (which increased 134 +/- 32 U/14 s) compared with control (which increased 195 +/- 43 U/14 s) and caused a greater decrease in MAP (19 +/- 2 vs. 15 +/- 2 mmHg; P < 0.05). Furthermore, during both trials, the HF subjects exhibited a greater decrease in MAP compared with AF subjects despite an augmented baroreflex control of MSNA. These data indicate that the CBR contributes importantly to the MSNA response during acute systemic hypotension. Additionally, we suggest that an impaired control of vascular reactivity hinders blood pressure regulation in HF subjects.

Adult↗

Fatty acid kinetics and carbohydrate metabolism during electrical exercise in spinal cord-injured humans.

Motor center activity and reflexes from contracting muscle have been shown to be important for mobilization of free fatty acids (FFA) during exercise. We studied FFA metabolism in the absence of these mechanisms: during involuntary, electrically induced leg cycling in individuals with complete spinal cord injury (SCI). Healthy subjects performing voluntary cycling served as controls (C). Ten SCI (level of injury: C5-T7) and six C exercised for 30 min at comparable oxygen uptake rates (approximately 1 l/min), and [1-14C]palmitate was infused continuously to estimate FFA turnover. From femoral arteriovenous differences, blood flow, muscle biopsies, and indirect calorimetry, leg substrate balances as well as concentrations of intramuscular substrates were determined. Leg oxygen uptake was similar in the two groups during exercise. In SCI, but not in C, plasma FFA and FFA appearance rate fell during exercise, and plasma glycerol increased less than in C (P < 0.05). Fractional uptake of FFA across the working legs decreased from rest to exercise in all individuals (P < 0.05) but was always lower in SCI than in C (P < 0.05). From rest to exercise, leg FFA uptake increased less in SCI than in C subjects (14 +/- 3 to 57 +/- 20 vs. 41 +/- 13 to 170 +/- 57 micromol x min(-1) x leg(-1); P < 0.05). Muscle glycogen breakdown, leg glucose uptake, carbohydrate oxidation, and lactate release were higher (P < 0.05) in SCI than in C during exercise. Counterregulatory hormonal changes were more pronounced in SCI vs. C, whereas insulin decreased only in C. In conclusion, FFA mobilization, delivery, and fractional uptake are lower and muscle glycogen breakdown and glucose uptake are higher in SCI patients during electrically induced leg exercise compared with healthy subjects performing voluntary exercise. Apparently, blood-borne mechanisms are not sufficient to elicit a normal increase in fatty acid mobilization during exercise. Furthermore, in exercising muscle, FFA delivery enhances FFA uptake and inhibits carbohydrate metabolism, while carbohydrate metabolism inhibits FFA uptake.

Adult↗

Muscle tensing during standing: effects on cerebral tissue oxygenation and cerebral artery blood velocity.

BACKGROUND AND PURPOSE: When standing up causes dizziness, tensing of the leg muscles may alleviate the symptoms. We tested the hypothesis that leg tensing improves orthostatic tolerance via enhanced cerebral perfusion and oxygenation. METHODS: In 10 healthy young adults, the effects of leg tensing on transcranial Doppler-determined middle cerebral artery (MCA) mean blood velocity (V(mean)) and the near-infrared spectroscopy-determined frontal oxygenation (O(2)Hb) were assessed together with central circulatory variables and an arterial pressure low-frequency (LF) (0.07 to 0.15 Hz) domain evaluation of sympathetic activity. RESULTS: Standing up reduced central venous pressure by (mean+/-SEM) 4.3+/-2.6 mm Hg, stroke volume by 49+/-7 mL, cardiac output by 1.9+/-0.4 L/min, and mean arterial pressure at MCA level by 9+/-4 mm Hg, whereas it increased heart rate by 30+/-4 beats per minute (P<0.05). MCA V(mean) declined from 67+/-4 to 56+/-3 cm/s, O(2)Hb decreased by 7+/-2.8%, and LF spectral power increased (P<0.05). Leg tensing increased central venous pressure by 1.4+/-2.7 mm Hg and cardiac output by 1.8+/-0.4 L/min with no significant effect on blood pressure, whereas heart rate decreased by 11+/-3 beats per minute (P<0.05). MCA V(mean) increased to 63+/-3 cm/s and O(2)Hb increased by 2.1+/-2.6%, whereas LF power declined (P<0.05). Within 2 minutes after leg tensing, these effects had disappeared. CONCLUSIONS: During standing, tensing of the leg muscles attenuates a reduction in cerebral perfusion and oxygenation as it stabilizes central circulatory variables and reduces sympathetic activity.

Adult↗

Lactate, glucose and O2 uptake in human brain during recovery from maximal exercise.

The metabolic activity of the brain has not been evaluated during physical exercise. In six volunteers substrate uptake by the brain was determined during graded exercise and recovery from maximal exercise by measuring the arterial-internal jugular venous concentration differences(a-v differences). The a-v difference for lactate increased from 0.02 +/- 0.08 mmol l-1 at rest to 0.39 +/- 0. 13 mmol l-1 during exercise and remained positive during 30 min of recovery (P < 0.05). The a-v difference for glucose (0.55 +/- 0.06 mmol l-1 at rest) did not change significantly during exercise, but during the initial 5 min of recovery it increased to 0.83 +/- 0.10 mmol l-1 (P < 0.05). The O2 a-v difference at rest of 3.11 +/- 0.30 mmol l-1 remained stable during exercise, then increased during the initial 5 min of recovery (3.77 +/- 0.52 mmol l-1) and remained high during the subsequent 30 min recovery period (3.62 +/- 0.64 mmol l-1; P < 0.05). Thus the O2/glucose uptake ratio did not change during exercise (pre-exercise 5.95 +/- 0.68; post-exercise 6.02 +/- 1.39) but decreased to 4.93 +/- 0.99 during the initial 5 min of recovery (P < 0.05). When lactate uptake was included, the resting O2/carbohydrate uptake ratio of 5.84 +/- 0.73 was reduced to 4.42 +/- 0.25 during exercise and decreased further during the recovery phase (to 3.79 +/- 0.30; P < 0.05). In contrast, in the resting and immobilised rat, lactate infusion to a level similar to that obtained during maximal exercise in humans did not affect the a-v difference for lactate. The large carbohydrate uptake by the brain during recovery from maximal exercise suggests that brain glycogen metabolism is important in the transition from rest to exercise, since this would explain the significant post-exercise decrease in the O2/carbohydrate uptake ratio.

Adult↗

An electrical admittance based index of thoracic intracellular water during head-up tilt in humans.

During 50 degrees head-up tilt (HUT), the number of erythrocytes within the thorax has been shown to be reduced by approximately 25% and this level is retained during a maintained tilt, whilst that in the thigh increases by approximately 70%. To evaluate whether the electrical admittance of intracellular water (ICW) may be used to monitor this redistribution of red cells in humans, we determined the regional difference in the reciprocal value of the impedance at 1.5 and 100 kHz for the thorax (thoraxICW) and for the leg (legICW). In ten subjects all variables remained unchanged during head-down tilt but during HUT, presyncopal symptoms were induced in eight subjects after a mean of 27 (SEM 7) min as mean heart rate dropped from 85 (SEM 4) to 66 (SEM 3) beats x min(-1), mean arterial blood pressure from 80 (SEM 3) to 60 (SEM 5) mmHg, and mean oxygen saturation of venous blood from 76 (SEM 2)% to 73 (SEM 3)% (P < 0.05). The mean haematocrit increased from 50 (SEM 5)% to 52.5 (SEM 3.5)% (P < 0.01) and mean central venous pressure decreased during tilting (from a mean of 1 (SEM 1) to a mean of -1 (SEM 1) mmHg; P < 0.05) and returned to value at rest during the maintained tilt. Mean thoracic impedances increased by 7.0 (SEM 1.0) ohms (1.5 kHz) and 5.4 (SEM 1.2) ohms (100 kHz), and mean leg impedances decreased by 9.3 (SEM 1.2) ohms (1.5 kHz) and 3.1 (SEM 1.0) ohms (100 kHz) (P < 0.01). Mean thoraxICW decreased at 40 degrees HUT and remained reduced by 11 (SEM 2) S x 10(-4) (P < 0.05) until the presyncopal symptoms developed, at which time it was lower by 16 (SEM 2) S x 10(-4) (P < 0.01). Mean legICW increased from 97 (SEM 15) to 99 (SEM 15) S x 10(-4) (P = 0.08) during HUT but decreased during maintained tilt (to 94 (SEM 15) S x 10(-4); P < 0.05). The results suggested that during HUT, the difference in electrical admittance at a high and a low frequency current reflects the reduced number of red cells within the thorax.

Adult↗

Influence of temperature on the distribution of blood in humans as assessed by electrical impedance.

This study investigated whether ambient temperature influences the distribution of blood as indicated by electrical impedance. In ten supine humans, the room temperature was raised from 14 to 35 degrees C. Skin temperature and blood flow on the thorax increased by 3.6 (SD 0.3) degrees C and 84 (SD 40)%, respectively, and by 9.8 (SD 1) degrees C and 115 (SD 45)%, respectively, on the extremities (P < 0.05). Cardiac output remained unchanged, ear temperature and heart rate became elevated, and the oesophageal temperature and mean arterial pressure decreased (P < 0.05). At five discrete frequencies (1.5. 5, 50, 100, 200 kHz) thoracic impedance was increased by 1.2 (SD 1) to 1.5 (SD 1) omega (P < 0.05). In contrast, total body impedance was reduced by 16.4 (SD 5) omega and leg impedance was reduced by 4.0 (SD 2) omega, while an index of intracellular water within the thorax (the difference between the admittances at 100 kHz and 1.5 kHz) was decreased by 10 (SD 1) x 10(-4)S (P < 0.05). The results would suggest that total body impedance is dominated by the impedance of the extremities. The increase in thoracic impedance and a decrease in leg impedance (as in total body impedance) could be explained by a redistribution of blood from the thorax to the extremities during heating. Such a translocation of blood was confirmed by a reduced impedance based index of intracellular water within the thorax.

Adult↗

Cerebral blood flow and metabolism during exercise.

During exercise regional cerebral blood flow (rCBF), as blood velocity in major cerebral arteries and also blood flow in the internal carotid artery increase, suggesting an increase in blood flow to a large part of the brain. Such an increase in CBF is independent of the concomitant increase in blood pressure but is modified by the alteration in arterial carbon dioxide tension (PaCO(2)). Also, the increase in middle cerebral artery mean blood velocity (MCA V(mean)) reported with exercise appears to depend on the ability to increase cardiac output (CO), as demonstrated in response to beta-1 blockade and in patients with cardiac insufficiency or atrial fibrillation.Near-infrared spectroscopy (NIRS) determined cerebral oxygenation supports the alterations in MCA V(mean) during exercise. Equally, the observation that the cerebrovascular CO(2)-reactivity appears to be smaller in the standing than in the sitting and especially in the supine position could relate to the progressively smaller CO. In contrast, during exercise "global" cerebral blood flow (gCBF), as determined by the Kety-Schmidt technique is regarded as being constant. One limitation of the Kety-Schmidt method for measuring CBF is that blood flow in the two internal jugular veins depends on the origin of drainage and it has not been defined which internal jugular venous flow is evaluated. Such a consideration is equally relevant for an evaluation of cerebral metabolism during exercise. While the regional cerebral uptake of oxygen (O(2)) increases during exercise, the global value is regarded as being constant. Yet, during high intensity exercise lactate is taken up by the brain and its O(2) uptake also increases. Furthermore, in the initial minutes of recovery immediately following exercise, brain glucose and O(2) uptake are elevated and lactate uptake remains high.A maintained substrate uptake by the brain after exercise suggests a role for brain glycogen in cerebral activation, but the fate of brain substrate uptake has not yet been determined.

Blood Pressure↗