"Supraspinal locomotor centers do/do not contribute significantly to the hyperpnea of dynamic exercise in humans".
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Carbon Dioxide↗
Biomedical subjects
Niels H Secher
Publications and source records attributed to Niels H Secher.
"In health and in a normoxic environment, VO2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow".
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Animals↗
Muscular performance after concentric and eccentric exercise in trained men.
PURPOSE: We studied previously resistance-trained men and compared the effects of concentric and eccentric training on performance and structural muscle parameters. METHODS: Seventeen trained individuals (age 26.9 +/- 3.4 yr) participated in 12 wk of either maximum concentric (N = 8) or eccentric (N = 9) resistance training of the elbow flexors. The functional performance was measured as the maximum concentric and eccentric strength and angular velocity at standard loads. Muscle cross-sectional area and cross-sectional area of single cells were used as measures of muscular hypertrophy. Fiber-type proportions were assessed by staining cells for myofibrillar ATPase. RESULTS: Both eccentric and concentric training increased concentric strength to a similar extent (14 vs 18%), whereas eccentric training led to greater increases in eccentric strength than concentric training did (26 vs 9%). The maximum angular velocity at all loads was enhanced equally in both training groups. The cross-sectional area of both the elbow flexors (+11%) and of the type I and type IIA fibers increased only after the eccentric training. In addition, the relative cross-sectional area occupied by the type II fibers increased from 64 to 73% after the eccentric training. There were only minor changes in the fiber-type proportions. CONCLUSION: The present data suggest that for resistance-trained men, increases in concentric strength and velocity performance after eccentric training are largely mediated by changes in fiber and muscle cross-sectional area. However, hypertrophy alone could not explain the increase in eccentric strength. Because the increases in strength and velocity performance after concentric training could not be ascribed to muscular adaptations alone, we suggest that they may be attributable to additional neural factors.
Adult↗
Are the arms and legs in competition for cardiac output?
Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.
Arm↗
The interaction of central command and the exercise pressor reflex in mediating baroreflex resetting during exercise in humans.
Central command and the exercise pressor reflex can independently reset the carotid baroreflex (CBR) during exercise. The present investigation assessed the interactive relationship between these two neural mechanisms in mediating baroreflex resetting during exercise. Six men performed static leg exercise at 20% maximal voluntary contraction under four conditions: control, no perturbation; neuromuscular blockade (NMB) induced by administration of the neuromuscular blocking agent Norcuron (central command activation); MAST, application of medical antishock trousers inflated to 100 mmHg (exercise pressor reflex activation); and Combo, NMB plus MAST (concomitant central command and exercise pressor reflex activation). With regard to CBR control of heart rate (HR), both NMB and Combo conditions resulted in a further resetting of the carotid-cardiac stimulus-response curve compared to control conditions, suggesting that CBR-HR resetting is predominately mediated by central command. In contrast, it appears that CBR control of blood pressure can be mediated by signals from either central command or the exercise pressor reflex, since both NMB and MAST conditions equally augmented the resetting of the carotid-vasomotor stimulus-response curve. With regard to the regulation of both HR and blood pressure, the extent of CBR resetting was greater during the Combo condition than during overactivation of either central command or the exercise pressor reflex alone. Therefore, we suggest that central command and the exercise pressor reflex interact such that signals from one input facilitate signals from the other, resulting in an enhanced resetting of the baroreflex during exercise.
Adult↗
Brain glucose and lactate uptake during exhaustive exercise.
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Brain↗
Kidneys extract BNP and NT-proBNP in healthy young men.
Renal metabolism of the cardiac marker NH2-terminal-pro-brain natriuretic peptide (NT-proBNP) has been suggested. Therefore, we determined the renal extraction ratios of NT-proBNP and its bioactive coproduct brain natriuretic peptide (BNP) at rest and during exercise. In addition, the cerebral ratios were evaluated. Ten young healthy men were investigated at baseline, during moderate cycle exercise (heart rate: 140, Borg scale: 14-15), and in the recovery with BNP and NT-proBNP measured from the brachial artery and the jugular and renal veins, and the renal and cerebral extraction ratios (Ext-Ren and Ext-Cer, respectively) were calculated. Cardiac output, stroke volume, heart rate, mean arterial pressures, and estimated glomerular filtration were determined. BNP and NT-proBNP were extracted by the kidneys but not by the brain. We observed no effect of exercise. The mean values (+/- SE) of Ext-Ren of NT-proBNP were similar (0.19 +/- 0.05, 0.21 +/- 0.06, and 0.12 +/- 0.03, respectively) during the three sessions (P > 0.05). Also the Ext-Ren of BNP were similar (0.18 +/- 0.07, 0.15 +/- 0.11, and 0.14 +/- 0.06, respectively; P > 0.05). There were no significant differences between Ext-Ren of BNP and NT-proBNP during the three sessions (P > 0.05). The Ext-Cer of both peptides varied insignificantly between -0.21 +/- 0.15 and 0.11 +/- 0.08. The renal extraction ratio of both BNP and NT-proBNP is approximately 0.15-0.20. There is no cerebral extraction, and short-term moderate exercise does not affect these values. Our findings suggest that the kidneys extract BNP and NT-proBNP to a similar extent in healthy young men.
Adult↗
Autonomic nervous system influence on arterial baroreflex control of heart rate during exercise in humans.
A combination of sympathoexcitation and vagal withdrawal increases heart rate (HR) during exercise, however, their specific contribution to arterial baroreflex sensitivity remains unclear. Eight subjects performed 25 min bouts of exercise at a HR of 90, 120, and 150 beats min-1, respectively, with and without metoprolol (0.16 +/- 0.01 mg kg(-1); mean +/- S.E.M.) or glycopyrrolate (12.6 +/- 1.6 microg kg-1). Carotid baroreflex (CBR) function was determined using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to -80 Torr, while transfer function gain (GTF) was calculated to assess the linear dynamic relationship between mean arterial pressure and HR. Spontaneous baroreflex sensitivity (SBR) was evaluated as the slope of sequences of three consecutive beats in which systolic blood pressure and the R-R interval of the ECG either increased or decreased, in a linear fashion. The beta-1 adrenergic blockade decreased and vagal cardiac blockade increased HR both at rest and during exercise (P < 0.05). The gain at the operating point of the modelled reflex function curve (GOP) obtained using NP and NS decreased with workload independent of beta-1 adrenergic blockade. In contrast, vagal blockade decreased GOP from -0.40 +/- 0.04 to -0.06 +/- 0.01 beats min-1 mmHg-1 at rest (P < 0.05). Furthermore, as workload increased both GOP and SBR, and GOP and GTF were correlated (P < 0.001), suggesting that the two dynamic methods applied to evaluate arterial baroreflex (ABR) function provide the same information as the modelled GOP. These findings suggest that during exercise the reduction of arterial baroreceptor reflex sensitivity at the operating point was a result of vagal withdrawal rather than an increase in sympathetic activity.
Adrenergic beta-Antagonists↗
Limitations to systemic and locomotor limb muscle oxygen delivery and uptake during maximal exercise in humans.
Reductions in systemic and locomotor limb muscle blood flow and O2 delivery limit aerobic capacity in humans. To examine whether O2 delivery limits both aerobic power and capacity, we first measured systemic haemodynamics, O2 transport and O2 uptake during incremental and constant (372 +/- 11 W; 85% of peak power; mean +/- S.E.M.) cycling exercise to exhaustion (n = 8) and then measured systemic and leg haemodynamics and during incremental cycling and knee-extensor exercise in male subjects (n = 10). During incremental cycling, cardiac output and systemic O2 delivery increased linearly to 80% of peak power (r2 = 0.998, P < 0.001) and then plateaued in parallel to a decline in stroke volume (SV) and an increase in central venous and mean arterial pressures (P < 0.05). In contrast, heart rate and increased linearly until exhaustion (r2 = 0.993; P < 0.001) accompanying a rise in systemic O2 extraction to 84 +/- 2%. In the exercising legs, blood flow and O2 delivery levelled off at 73-88% of peak power, blunting leg per unit of work despite increasing O2 extraction. When blood flow increased linearly during one-legged knee-extensor exercise, per unit of work was unaltered on fatigue. During constant cycling, , SV, systemic O2 delivery and reached maximal values within approximately 5 min, but dropped before exhaustion (P < 0.05) despite increasing or stable central venous and mean arterial pressures. In both types of maximal cycling, the impaired systemic O2 delivery was due to the decline or plateau in because arterial O2 content continued to increase. These results indicate that an inability of the circulatory system to sustain a linear increase in O2 delivery to the locomotor muscles restrains aerobic power. The similar impairment in SV and O2 delivery during incremental and constant load cycling provides evidence for a central limitation to aerobic power and capacity in humans.
Adult↗
Central command and the cutaneous vascular response to isometric exercise in heated humans.
Cutaneous vascular conductance (CVC) decreases during isometric handgrip exercise in heat stressed individuals, and we hypothesized that central command is involved in this response. Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction) followed by postexercise ischaemia in normothermia and during heat stress (increase in internal temperature approximately 1 degrees C). To augment the contribution of central command independent of force generation, on a separate day the protocol was repeated following partial neuromuscular blockade (PNB; i.v. cisatracurium). Forearm skin blood flow was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pressure. The PNB attenuated force production despite encouragement to attain the same workload. During the heat stress trials, isometric exercise decreased CVC by approximately 12% for both conditions, but did not change CVC in either of the normothermic trials. During isometric exercise in the heat, the increase in mean arterial pressure (MAP) was greater during the control trial relative to the PNB trial (31.0+/-9.8 versus 18.6+/-6.4 mmHg, P<0.01), while the elevation of heart rate tended to be lower (19.4+/-10.4 versus 27.4+/-8.1 b.p.m., P=0.15). During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB trial but remained reduced in the control trial. These findings suggest that central command, as well as muscle metabo-sensitive afferent stimulation, contributes to forearm cutaneous vascular responses in heat stressed humans.
Adult↗
"Central command" and insular activation during attempted foot lifting in paraplegic humans.
The relationship between cardiovascular regulation and brain activation was investigated during attempted foot lifting in paraplegic subjects and during rhythmic handgrip exercise at one-third of maximum voluntary contraction force. Brain areas of interest were the primary sensory-motor area and the insula, a hypothesized center for a central nervous feed-forward mechanism involved in cardiovascular control ("central command"). This mechanism is complementary to the usual known feedback pathways such as skeletal muscle afferent signals. Regional cerebral blood flow (rCBF) was measured in eight normal and three paraplegic subjects using positron emission tomography (PET) and oxygen-15-labeled water. Statistical parametric maps were calculated from the images comparing rest and handgrip. Paraplegics were also scanned during attempted foot lifting, a condition without sensory feedback. During activation tasks, heart rate and mean arterial pressure increased. PET activation responses (P < 0.05, corrected for multiple comparisons) were found in the contralateral primary sensory-motor area, the supplementary motor area, ipsilateral cerebellum, and bilaterally in the insula. A conjunction analysis showing responses common to handgrip and attempted foot lifting revealed activation in the right central insula (P < 0.05, corrected) in concordance with the concept of a central command feed-forward hypothesis.
Adult↗
Maintained cerebral and skeletal muscle oxygenation during maximal exercise in patients with liver cirrhosis.
BACKGROUND/AIMS: In cirrhotic patients, insufficient redistribution of blood from splanchnic organs to the central circulation could limit blood supply to skeletal muscles and the brain during exercise. METHODS: Eight cirrhotic patients performed incremental cycling to exhaustion (74 (49-123) W; median with range). RESULTS: Heart rate increased from 68 (62-88)beats/min at rest to 142 (116-163)beats/min, cardiac output from 5.1 (3.3-7.2) to 12.9 (8.5-15.9)l/min, and mean arterial pressure from 89 (75-104) to 115 (92-129)mmHg (P<0.05), while the indocyanine green elimination determined hepatosplanchnic blood flow declined from 0.97 (0.55-1.46) to 0.62 (0.36-1.06)l/min (P<0.05). As assessed by near-infrared spectrophotometry, cerebral oxygenation (NIRS) was 61% (48-85%) and increased to 72% (57-86%) during exercise (P<0.05). The NIRS determined oxygenation of the vastus lateralis muscle also increased: the concentrations of oxygenated haemoglobin by 5.9 (0.57-9.47)micromol/l, deoxygenated haemoglobin by 7.2 (1.8-12.0)micromol/l, and thus total haemoglobin by 12.1 (3.6-21.5)micromol/l (P<0.05). CONCLUSIONS: In patients with cirrhosis, exercise reduces hepatosplanchnic blood flow, while O(2) supply to muscle and brain appears to increase indicating that blood redistribution from splanchnic organs does not limit blood flow to working muscles and the brain.
Adult↗
Normovolaemia defined by central blood volume and venous oxygen saturation.
1. The intravenous administration of fluid and blood has to balance the danger of unexpected death in response to a reduction of central blood volume (CBV) against that of developing pulmonary and/or peripheral oedema. 2. The initial cardiovascular response to haemorrhage is similar to that developed in response to standing. In the upright position, adults are subjected to a reduction of CBV of approximately 0.5 L and can therefore tolerate a blood loss of approximately 1 L when supine. 3. However, volume administration directed by cardiovascular variables is seldom precise, even with integration of the bradycardia and hypotension developed when CBV decreases by approximately 30%. Immediate intervention is needed because such a reduction in CBV raises the lower limit of cerebral autoregulation to approximately 80 mmHg compared with the commonly considered value of approximately 60 mmHg with an associated risk of developing brain ischaemia and irreversible shock. 4. Alternatively, the volume load can be monitored both directly and accurately by means of thoracic electrical admittance. A functional definition of normovolaemia may be the filling of the heart that ensures cardiac output and oxygen delivery. From that perspective, supine humans are normovolaemic in that a maximal venous oxygen saturation (Svo2) is established. 5. Conversely, Svo2 decreases in the upright position and, with a blood loss of approximately 100 mL, Svo2 is reduced by 1%. It is suggested that, in supine humans and guided by Svo2, normovolaemia may be established to an accuracy of approximately 100 mL and that its adequacy is controlled by recording cerebral oxygenation.
Animals↗
Cerebral ammonia uptake and accumulation during prolonged exercise in humans.
We evaluated whether peripheral ammonia production during prolonged exercise enhances the uptake and subsequent accumulation of ammonia within the brain. Two studies determined the cerebral uptake of ammonia (arterial and jugular venous blood sampling combined with Kety-Schmidt-determined cerebral blood flow; n = 5) and the ammonia concentration in the cerebrospinal fluid (CSF; n = 8) at rest and immediately following prolonged exercise either with or without glucose supplementation. There was a net balance of ammonia across the brain at rest and at 30 min of exercise, whereas 3 h of exercise elicited an uptake of 3.7 +/- 1.3 micromol min(-1) (mean +/-s.e.m.) in the placebo trial and 2.5 +/- 1.0 micromol min(-1) in the glucose trial (P < 0.05 compared to rest, not different across trials). At rest, CSF ammonia was below the detection limit of 2 microm in all subjects, but it increased to 5.3 +/- 1.1 microm following exercise with glucose, and further to 16.1 +/- 3.3 microm after the placebo trial (P < 0.05). Correlations were established between both the cerebral uptake (r2 = 0.87; P < 0.05) and the CSF concentration (r2 = 0.72; P < 0.05) and the arterial ammonia level and, in addition, a weaker correlation (r2 = 0.37; P < 0.05) was established between perceived exertion and CSF ammonia at the end of exercise. The results let us suggest that during prolonged exercise the cerebral uptake and accumulation of ammonia may provoke fatigue, e.g. by affecting neurotransmitter metabolism.
Adult↗
Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans.
Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V(s)), diastolic (V(d)). and mean (V(m)) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P < 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V(m) and V(s) (P < 0.05) but tended to decrease MCA V(d) (P = 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V(m) and between SBP and MCA V(s) remained unchanged from rest to exercise, whereas that between DBP and MCA V(d) increased from rest to heavy exercise (P < 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V(m), even during high-intensity exercise.
Adult↗
Dynamic cerebral autoregulation during exhaustive exercise in humans.
We investigated whether dynamic cerebral autoregulation is affected by exhaustive exercise using transfer-function gain and phase shift between oscillations in mean arterial pressure (MAP) and middle cerebral artery (MCA) mean blood flow velocity (V(mean)). Seven subjects were instrumented with a brachial artery catheter for measurement of MAP and determination of arterial Pco(2) (Pa(CO(2))) while jugular venous oxygen saturation (Sv(O(2))) was determined to assess changes in whole brain blood flow. After a 10-min resting period, the subjects performed dynamic leg-cycle ergometry at 168 +/- 5 W (mean +/- SE) that was continued to exhaustion with a group average time of 26.8 +/- 5.8 min. Despite no significant change in MAP during exercise, MCA V(mean) decreased from 70.2 +/- 3.6 to 57.4 +/- 5.4 cm/s, Sv(O(2)) decreased from 68 +/- 1 to 58 +/- 2% at exhaustion, and both correlated to Pa(CO(2)) (5.5 +/- 0.2 to 3.9 +/- 0.2 kPa; r = 0.47; P = 0.04 and r = 0.74; P < 0.001, respectively). An effect on brain metabolism was indicated by a decrease in the cerebral metabolic ratio of O(2) to [glucose + one-half lactate] from 5.6 to 3.8 (P < 0.05). At the same time, the normalized low-frequency gain between MAP and MCA V(mean) was increased (P < 0.05), whereas the phase shift tended to decrease. These findings suggest that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in Pa(CO(2)).
Adult↗
Cerebral metabolism during upper and lower body exercise.
When continuation of exercise calls for a "will," the cerebral metabolic ratio of O2 to (glucose + lactate) decreases, with the largest reduction (30-50%) at exhaustion. Because a larger effort is required to exercise with the arms than with the legs, we tested the hypothesis that the reduction in the cerebral metabolic ratio would become more pronounced during arm cranking than during leg exercise. The cerebral arterial-venous differences for blood-gas variables, glucose, and lactate were evaluated in two groups of eight subjects during exhaustive arm cranking and leg exercise. During leg exercise, exhaustion was elicited after 25 +/- 6 (SE) min, and the cerebral metabolic ratio was reduced from 5.6 +/- 0.2 to 3.5 +/- 0.2 after 10 min and to 3.3 +/- 0.3 at exhaustion (P < 0.05). Arm cranking lasted for 35 +/- 4 min and likewise decreased the cerebral metabolic ratio after 10 min (from 6.7 +/- 0.4 to 5.0 +/- 0.3), but the nadir at exhaustion was only 4.7 +/- 0.4, i.e., higher than during leg exercise (P < 0.05). The results demonstrate that exercise decreases the cerebral metabolic ratio when a conscious effort is required, irrespective of the muscle groups engaged. However, the comparatively small reduction in the cerebral metabolic ratio during arm cranking suggests that it is influenced by the exercise paradigm.
Adult↗
Cerebral carbohydrate cost of physical exertion in humans.
Above a certain level of cerebral activation the brain increases its uptake of glucose more than that of O(2), i.e., the cerebral metabolic ratio of O(2)/(glucose + 12 lactate) decreases. This study quantified such surplus brain uptake of carbohydrate relative to O(2) in eight healthy males who performed exhaustive exercise. The arterial-venous differences over the brain for O(2), glucose, and lactate were integrated to calculate the surplus cerebral uptake of glucose equivalents. To evaluate whether the amount of glucose equivalents depends on the time to exhaustion, exercise was also performed with beta(1)-adrenergic blockade by metoprolol. Exhaustive exercise (24.8 +/- 6.1 min; mean +/- SE) decreased the cerebral metabolic ratio from a resting value of 5.6 +/- 0.2 to 3.0 +/- 0.4 (P < 0.05) and led to a surplus uptake of glucose equivalents of 9 +/- 2 mmol. beta(1)-blockade reduced the time to exhaustion (15.8 +/- 1.7 min; P < 0.05), whereas the cerebral metabolic ratio decreased to an equally low level (3.2 +/- 0.3) and the surplus uptake of glucose equivalents was not significantly different (7 +/- 1 mmol; P = 0.08). A time-dependent cerebral surplus uptake of carbohydrate was not substantiated and, consequently, exhaustive exercise involves a brain surplus carbohydrate uptake of a magnitude comparable with its glycogen content.
Adrenergic beta-1 Receptor Antagonists↗