Age-related changes in vasomotor reflex control of calf venous capacitance response to lower body negative pressure in humans

The present study was performed to test the hypothesis that calf venous capacitance would be reduced by mild gravitational stress through a vasomotor reflex in humans, and this response could be diminished with advancing age. Nine young (31 +/- 1 years, mean +/- SE) and 9 elderly (69 +/- 1 years) healthy males were exposed to a lower body negative pressure (LBNP) of 15 mmHg. Venous occlusion plethysmography was used to measure calf venous capacitance and calf blood flow. Muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerve along with cardiovascular variables. It was found that baseline MSNA was higher [21 +/- 4 (mean +/- SE) vs. 37 +/- 5 bursts x min(-1), young vs. elderly; p < 0.05] and calf venous capacitance was lower (1.71 +/- 0.12 vs. 1.44 +/- 0.10, ml x 100 ml(-1), young vs. elderly; p < 0.05) in the elderly group. At 15 mmHg-LBNP, heart rate and mean arterial pressure both remained unchanged, MSNA was enhanced, and calf blood flow was reduced in all subjects. Calf venous capacitance during LBNP decreased in the young, but did not change in the elderly. A significant negative correlation between percent changes in MSNA and percent changes in calf venous capacitance existed in the young group (y = 20.171x-11.863, r = 20.682; p = 0.0432), but disappeared in the elderly group. The ratio of percent changes in calf venous capacitance to percent changes in MSNA was markedly lower in the elderly (p < 0.01). In conclusion, these results substantiate our hypothesis that calf venous capacitance is reduced by mild LBNP through the vasomotor reflex, and this response is diminished in the elderly.     

Skeletal muscle StO<Subscript>2</Subscript> kinetics are slowed during low work rate calf exercise in peripheral arterial disease

The time course of muscle oxygen desaturation (StO₂ kinetics) following exercise onset reflects the dynamic interaction between muscle blood flow and muscle oxygen consumption. In patients with peripheral arterial disease (PAD), muscle StO₂ kinetics are slowed during walking exercise; potentially reflecting altered muscle oxygen consumption relative to blood flow. This study evaluated whether StO₂ kinetics measured using near infrared spectroscopy (NIRS) would be slowed in PAD during low work rate calf exercise compared with healthy subjects under conditions in which blood flow did not differ. Eight subjects with PAD and eight controls performed 3 min of calf exercise at 5, 10, 30, and 50% of maximal voluntary contraction (MVC). Calf blood flow responses were measured by plethysmography. Power outputs were similar between groups for all work rates. In PAD, the time constants of StO₂ kinetics were significantly slower than controls during 5% MVC (13.5 ± 1.7 vs. 6.9 ± 1.2 s, P < 0.05) and 10% MVC work rates (14.5 ± 2.7 vs. 6.8 ± 1.1 s, P < 0.05). Blood flow assessed when exercise was interrupted after 30 s did not differ between PAD and control subjects at these work rates. In contrast, the StO₂ time constants were not different between groups during 30 and 50% MVC work rates, where blood flow responses in PAD subjects were lower as compared with controls. Thus in PAD, the slowed StO₂ kinetic responses under conditions of unimpaired calf blood flow reflect slowed muscle oxygen consumption in PAD skeletal muscle during low work rate plantar flexion exercise as compared with healthy skeletal muscle.     

Middle cerebral artery blood velocity,arterial diameter and muscle sympathetic nerve activity during post-exercise muscle ischaemia

During exercise the transcranial Doppler determined mean blood velocity (V_mean) increases in the middle cerebral artery (MCA) and reflects cerebral blood flow when the diameter at the site of investigation remains constant. Sympathetic activation could induce MCA vasoconstriction and in turn elevate V_mean at an unchanged cerebral blood flow. In 12 volunteers we evaluated whether V_mean relates to muscle sympathetic nerve activity (MSNA) in the peroneal nerve during rhythmic handgrip and post-exercise muscle ischaemia (PEMI). The luminal diameter of the dorsalis pedis artery (AD) was taken to reflect the MSNA influence on a peripheral artery. Rhythmic handgrip increased heart rate (HR) from 74 ± 20 to 92 ± 21 beats min^?1 and mean arterial pressure (MAP) from 87 ± 7 to 105 ± 9 mmHg (mean ± SD; P < 0.05). During PEMI, HR returned to pre-exercise levels while MAP remained elevated (101 ± 9 mmHg). During handgrip contralateral MCA V_mean increased from 65 ± 10 to 75 ± 13 cm s^?1 and this was more than on the ipsilateral side (from 63 ± 10 to 68 ± 10 cm s^?1; P < 0.05). On both sides of the brain V_mean returned to baseline during PEMI. MSNA did not increase significantly during handgrip (from 56 ± 24 to 116 ± 39 units) but the elevation became statistically significant during PEMI (135 ± 86 units, P < 0.05), while AD did not change. Taken together, during exercise and PEMI, V_mean changed independent of an elevation of MSNA by more than 140% and the dorsalis pedis artery diameter was stable. The results provide no evidence for a vasoconstrictive influence of sympathetic nerve activity on medium size arteries of the limbs and the brain during rhythmic handgrip and post-exercise muscle ischaemia.     

Changes in muscle sympathetic nerve activity and calf blood flow during static handgrip exercise

Summary To test the function of sympathetic vascoconstrictor nerves on blood flow in resting limbs during static muscle contraction, muscle sympathetic nerve activity (MSNA) to the leg muscle was recorded from the tibial nerve microneurographically before, during and after 2 min of static handgrip (SHG). Simultaneously, calf blood flow (CBF) was measured by strain gauge plethysmography. An increase in MSNA, a decrease in CBF and an increase in calf vascular resistance (CVR) in the same resting limb occurred concomitantly during SHG. However, the increase in CVR was blunted in the second minute of handgrip when MSNA was still increasing. The results indicated that the decrease of CBF during SHG reflects the increase in MSNA, while the dissociation between MSNA and CVR at the later period of SHG may be related to metabolic change produced by the vasoconstriction.     

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure

Jacobsen , T. N., Nielsen , H. V., Kassis , E. & Amtorp o S. 1992. Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure. Acta Physiol Scand 144 , 247–252. Received 8 March 1991, accepted 7 Novcmber 1991. ISSN 0001–6772. Department of Cardiology, Gentofte Hospital, University of Copenhagen, Denmark Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [¹³³Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at —10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 ± 2% (mean ± SEM) and in skeletal muscle by 16 ± l%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 ± 3% in subcutaneous tissue and of 30 ± 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.     

Skeletal muscle and skin as targets for powerful homeostatic vasomotor baroreflexes in humans during prolonged circulatory stress: a study on the innervated and nerve blocked forearm

Flow (vascular resistance) was followed in the innervated and axillary nerve blocked arm during prolonged low to high and barely tolerated circulatory stress [15–85 mmHg LBNP (lower body negative pressure) for 10min; room temperature 24.8–25.7 ^oC]. With intact innervation LBNP caused initial graded and potent forearm vasoconstriction. At low LBNP, however, there was soon significant and maintained partial (50%) abolition of the early response. At high LBNP, the initial striking vasoconstriction remained constant throughout 10 min of pronounced circulatory stress [marked tachycardia; fall in systolic pressure but mean arterial pressure (MAP) normal]. Flow decreased in steady state by 15 + 4, 38 + 5, 63 + 2 and by pronounced 78 + 3 % at 15, 40, 70, and 85 mmHg LBNP (resistance raised 27±7, 78+16, 192+18, and 387±55% above control), alterations ascribed to constriction in both muscle and skin. Comparison of LBNP responses with intact and blocked innervation revealed that the vasoconstriction was neurogenic with little or no humoral contribution. The overall observations show that under normal comfortable (thermoneutral) conditions the resistance vessels in muscle and skin, with haemodynamically important large tissue mass and great tolerance to even drastic and prolonged ischaemia, indeed are important targets in the homeostatic sympathetic control, especially when cardiovascular homeostasis is challenged by marked stress with urgent need for strong, maintained compensatory vasoconstriction. The study also demonstrated > three-fold (4.1 +0.5 to 13.1 + 1.9 ml min^-1 100 ml^-1) forearm flow increases upon blockade of resting nervous vasoconstrictor tone. It thus appears that the sympathetic nerves not only can elicit prominent and maintained baroreflex limb vasoconstriction but also that, in humans, reflex inhibition of resting tone might allow surprisingly large resistance decline.     

Vasoconstriction in active calf persists after discontinuation of combined exercise with high-intensity elbow flexion

The present study aimed to determine whether vasoconstriction in active calf occurring during combined exercise diminished or persisted when added low- and high-intensity elbow flexion exercise ceased and single leg exercise continued. Six active women (mean age, 21.2 years) participated in this study. During 10-min plantar flexion exercise at 10% of maximum voluntary contraction (MVC), elbow flexion exercise at 10% MVC was added over the 3rd and 4th min. Calf blood flow did not change significantly upon superimposition and cessation of this elbow flexion exercise. However, when elbow flexion exercise at 50% MVC was added during the 7th and 8th min, calf blood flow above the resting value (2.23±0.23 mL 100 mL^-1 min^-1) decreased significantly (P<0.05) from 6.72±0.87 (6th min) to 5.14±1.36 mL 100 mL^-1 min^-1 after 2 min of combined exercise and was accompanied by a similar change in the non-exercising calf blood flow value. The vascular conductance of the exercising calf decreased significantly (P<0.01) from 6.48±1.08 (6th min) to 3.11±1.27 mL 100 mL^-1 min^-1 mmHg^-1 at the end of the 2nd min of combined plantar flexion exercise with elbow flexion exercise at 50% MVC. After elbow flexion exercise at 50% MVC was discontinued and plantar flexion exercise at 10% MVC alone was performed, the vascular conductance in the exercising calf remained significantly low for the next 2 min. These results indicate that the vasoconstriction induced by adding high-intensity arm exercise is persistent, suggesting a major contribution of metabo-receptor-mediated vasoconstriction rather than central command- and mechano-receptor-mediated vasoconstriction.     

Heterogeneous oxygenation in nonexercising triceps surae muscle during contralateral isometric exercise

To test whether changes in oxygenation of a resting skeletal muscle, evoked by a static contraction in a contralateral muscle, is uniform within a given skeletal muscle, we used near-infrared spectroscopy (NIRS). Seven subjects performed 2 min static knee extension exercise at 30% of maximal voluntary contraction. Changes in oxygenated hemoglobin (HbO₂) were monitored using multiple-channel NIRS (40 channels, 13 sources and 12 detectors) attached on the contralateral nonexercising triceps surae muscle. Changes in HbO₂ were expressed as a percentage of total labile signals. To characterize the distribution of changes in HbO₂, channels were compared between their positions on the triceps surae muscle, and represented as ‘proximal versus distal’ and ‘lateral versus medial’ portions. During static muscle contraction, the averaged changes in HbO₂ of all channels were correlated with those in calf blood flow (plethysmography; R ²=0.188, P<0.05) and with calf vascular conductance (R ²=0.146, P<0.05). HbO₂ did not differ significantly between the lateral and medial portions of the triceps surae muscle. In contrast, the decrease of HbO₂ in the proximal portion of the muscle was greater than that of the distal portion (P<0.05). These results indicate that the changes in oxygenation of a resting muscle, evoked by static contraction of the contralateral muscle, are heterogeneous.     

Limb neurovascular control during altered otolithic input in humans

Head-down rotation (HDR), which activates the vestibulosympathetic reflex, increases leg muscle sympathetic nerve activity (MSNA) and produces calf vasoconstriction with no change in either cardiac output or arterial blood pressure. Based on animal studies, it was hypothesized that differential control of arm and leg MSNA explains why HDR does not alter arterial blood pressure. Fifteen healthy subjects were studied. Heart rate, arterial blood pressure, forearm and calf blood flow, and leg MSNA responses were measured during HDR in these subjects. Simultaneous recordings of arm and leg MSNA were obtained from five of the subjects. Forearm and calf blood flow, vascular conductances, and vascular resistances were similar before HDR, as were arm and leg MSNA. HDR elicited similar significant increases in leg (Δ6 ± 1 bursts min⁻¹; 59 ± 16 % from baseline) and arm MSNA (Δ5 ± 1 bursts min⁻¹; 80 ± 28 % from baseline). HDR significantly decreased calf (−19 ± 2 %) and forearm vascular conductance (−12 ± 2 %) and significantly increased calf (25 ± 4 %) and forearm vascular resistance (15 ± 2 %), with ∼60 % greater vasoconstriction in the calf than in the forearm. Arterial blood pressure and heart rate were not altered by HDR. These results indicate that there is no differential control of MSNA in the arm and leg during altered feedback from the otolith organs in humans, but that greater vasoconstriction occurs in the calf than in the forearm. These findings indicate that vasodilatation occurs in other vascular bed(s) to account for the lack of increase in arterial blood pressure during HDR.     

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‐ (ΔHbO₂) and deoxy‐haemoglobin (ΔHb) 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 (P_ETCO ₂) increased from 45 (42–48) to 48 (46–58) mmHg with a reduction of only 1% in the arterial haemoglobin O₂ saturation (S_aO ₂). During control exercise (normal breathing resistance), muscle and brain ΔHbO₂ were not different from the resting levels, and only the leg muscle ΔHb increased (4 (–2–10) μM , P < 0.05). Moderate resistive breathing increased ΔHbO₂ of the intercostal and vastus lateralis muscles to 6 ± (–5–14) and 1 (–7–9) μM (P < 0.05), respectively, while muscle ΔHb was not affected. Cerebral ΔHbO₂ and ΔHb became elevated to 6 (1–15) and 1 (–1–6) μM 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.     

The effect of arm training on thermoregulatory responses and calf volume during upper body exercise

Purpose

The smaller muscle mass of the upper body compared to the lower body may elicit a smaller thermoregulatory stimulus during exercise and thus produce novel training-induced thermoregulatory adaptations. Therefore, the principal aim of the study was to examine the effect of arm training on thermoregulatory responses during submaximal exercise.

Methods

Thirteen healthy male participants (Mean ± SD age 27.8 ± 5.0 years, body mass 74.8 ± 9.5 kg) took part in 8 weeks of arm crank ergometry training. Thermoregulatory and calf blood flow responses were measured during 30 min of arm cranking at 60 % peak power (W _peak) pre-, and post-training and post-training at the same absolute intensity as pre-training. Core temperature and skin temperatures were measured, along with heat flow at the calf, thigh, upper arm and chest. Calf blood flow using venous occlusion plethysmography was performed pre- and post-exercise and calf volume was determined during exercise.

Results

The upper body training reduced aural temperature (0.1 ± 0.3 °C) and heat storage (0.3 ± 0.2 J g^?1) at a given power output as a result of increased whole body sweating and heat flow. Arm crank training produced a smaller change in calf volume post-training at the same absolute exercise intensity (?1.2 ± 0.8 % compared to ?2.2 ± 0.9 % pre-training; P < 0.05) suggesting reduced leg vasoconstriction.

Conclusion

Training improved the main markers of aerobic fitness. However, the results of this study suggest arm crank training additionally elicits physiological responses specific to the lower body which may aid thermoregulation.     

Melatonin attenuates the sympathetic nerve responses to orthostatic stress in humans

Previous studies have suggested that melatonin alters sympathetic outflow in humans. The purpose of the present study was to determine in humans the effect of melatonin on sympathetic nerve activity and arterial blood pressure during orthostatic stress. Fifty minutes after receiving a 3 mg tablet of melatonin or placebo (different days), muscle sympathetic nerve activity (MSNA), arterial blood pressure, heart rate, forearm blood flow and thoracic impedance were measured for 10 min at rest and during 5 min of lower body negative pressure (LBNP) at -10 and -40 mmHg ( n = 11). During LBNP, MSNA responses were attenuated after melatonin at both -10 and -40 mmHg ( P < 0.03). Specifically, during the placebo trial, MSNA increased by 33 ± 8 and 251 ± 70 % during -10 and -40 mmHg, respectively, but increased by only 8 ± 7 and 111 ± 35 % during -10 and -40 mmHg with melatonin, respectively. However, arterial blood pressure and forearm vascular resistance responses were unchanged by melatonin during LBNP. MSNA responses were not affected by melatonin during an isometric handgrip test (30 % maximum voluntary contraction) and a cold pressor test. Plasma melatonin concentration was measured at 25 min intervals for 125 min in six subjects. Melatonin concentration was 14 ± 11 pg ml⁻¹ before ingestion and was significantly increased at each time point (peaking at 75 min; 1830 ± 848 pg ml⁻¹). These findings indicate that in humans, a high concentration of melatonin can attenuate the reflex sympathetic increases that occur in response to orthostatic stress. These alterations appear to be mediated by melatonin-induced changes to the baroreflexes.     

Local heat application to the leg reduces muscle sympathetic nerve activity in human

The study was designed to assess the effects of local heat (LH) application on postganglionic muscle sympathetic nerve activity (MSNA) measured by microneurography in healthy men. In the first protocol, MSNA of the left peroneal nerve, blood pressure (BP), heart rate (HR), and skin temperature of the shin (TSK) were recorded in nine men. In the second protocol, leg blood flow (LBF) was measured in the same subjects by strain-gauge plethysmography. In both protocols, after 10 min of rest in the supine position, a heated hydrocollator pack was applied to the shin and anterior foot for 15 min and recovery was monitored over a period of 20 min. TSK gradually increased from 31.7 ± 0.1 to 41.9 ± 0.5°C (mean ± SEM) during LH. No subject complained of pain, and BP and HR remained constant. The MSNA burst rate (16.1 ± 2.1 beats/min) during the control period decreased significantly (P < 0.05) to 72.0 ± 2.3% during LH. Total MSNA also decreased to 59.2 ± 2.6% (P < 0.05) during LH, but both immediately returned to baseline at recovery. In contrast, LBF in the left leg significantly and immediately increased (P < 0.05) after LH application and remained significantly elevated until the end of the recovery period. These results suggest that: (1) LH application significantly attenuates MSNA without any changes in HR and BP. (2) Other factors in addition to MSNA seem to control regional blood flow in the lower extremity during LH.     

Vascular adaptations to low-load resistance training with and without blood flow restriction

Purpose

To examine the effects of low-load knee extensor training to fatigue with and without blood flow restriction (BFR) on calf vascular conductance, calf venous compliance, and peripheral arterial stiffness in middle-aged individuals.

Methods

Eleven men (55 ± 8 years) and five post-menopausal women (57 ± 5 years) completed 6 weeks of unilateral knee extensor training with one limb exercising with BFR (BFR limb) and the contralateral limb exercising without BFR (free flow, FF limb). Before and after the training, femoral pulse wave velocity (PWV), calf blood flow (normalized as conductance), and calf venous compliance were measured in each limb.

Results

PWV increased following training in both limbs (main effect of time, p = 0.036; BFR limb 8.9 ± 0.8 vs. 9.5 ± 0.9 m/s, FF limb 9.0 ± 1.2 vs. 9.0 ± 1.1; Pre vs. Post). Calf blood flow increased (p = 0.026) in the FF limb (25.0 ± 7.0 vs. 31.8 ± 12.0 flow/mmHg; Pre vs. Post) but did not change (p = 0.831) in the BFR limb (29.1 ± 11.3 vs. 28.7 ± 11.5 flow/mmHg; Pre vs. Post). Calf venous compliance did not change in either limb following training.

Conclusions

These results suggest low-load BFR resistance training to fatigue elicits small increases in peripheral arterial stiffness without eliciting concomitant changes in venous compliance. In addition, unlike low-load knee extensor training without BFR, training with BFR did not enhance calf blood flow.     

Non‐invasive and quantitative evaluation of peripheral vascular resistances in rats by combined NMR measurements of perfusion and blood pressure using ASL and dynamic angiography

The in vivo determination of peripheral vascular resistances (VR) is crucial for the assessment of arteriolar function. It requires simultaneous determination of organ perfusion (F) and arterial blood pressure (BP). A fully non‐invasive method was developed to measure systolic and diastolic BP in the caudal artery of rats based on dynamic NMR angiography. A good agreement was found between the NMR approach and the gold standard techniques (linear regression slope = 0.98, R² = 0.96). This method and the ASL‐MRI measurement of skeletal muscle perfusion were combined into one single NMR experiment to quantitatively evaluate the local vascular resistances in the calf muscle of anaesthetized rats, in vivo and non‐invasively 1) at rest: VR = 7.0 ± 1.0 mmHg·min 100 g·ml^?1, F = 13 ± 3 ml min^?1.100 g^?1 and mean BP (MBP) = 88 ± 10 mmHg; 2) under vasodilator challenge (milrinone): VR = 3.7 ± 1.1 mmHg min.100 g ml^?1, F = 21 ± 4 ml min^?1.100 g^?1 and MBP = 75 ± 14 mmHg; 3) under vasopressor challenge (norepinephrine): VR = 9.8 ± 1.2 mmHg min 100 g ml^?1, F = 14 ± 3 ml min^?1.100 g^?1 and MBP = 137 ± 2 mmHg. Copyright © 2009 John Wiley & Sons, Ltd.     

Effect of lower body negative pressure upon local regulation of blood flow in human subcutaneous tissue

Local regulation of subcutaneous blood flow in the forearm was studied during lower body negative pressure (LBNP) in 7 young healthy male subjects in supine position. Blood flow was measured on the forearm by the local ¹³³Xe washout technique. LBNP of -40 and -60 mmHg induced a decrease in the ¹³³Xe washout rate of 34 and 50% respectively. This response to LBNP could be blocked by proximal nervous blockade indicating that the vasoconstriction observed was due to a central sympathetic reflex mechanism. The vasoconstrictor response to increase in venous transmural pressure induced by lowering the arm (veno-arteriolar reflex mechanism) could not be demonstrated during 40 mmHg LBNP. The abolishment of this reflex is most likely due to centrally elicited increase in sympathetic activity as a normal veno-arteriolar reflex was elicited following proximal nervous blockade.     

Effect of arm-cranking on leg blood flow and noradrenaline spillover during leg exercise in man

Controversy exists whether recruitment of a large muscle mass in dynamic exercise may outstrip the pumping capacity of the heart and require neurogenic vasoconstriction in exercising muscle to prevent a fall in arterial blood pressure. To elucidate this question, seven healthy young men cycled for 70 minutes at a work load of 5540%VO_2max. At 30 to 50 minutes, arm cranking was added and total work load increased to (mean ± SE) 82 ± 4% of Vo_2max. During leg exercise, leg blood flow average 6.15 4.511 minutes^-1, mean arterial blood pressure 137 ± 4 mmHg and leg conductance 42.3 ± 2.2 ml minutes^-1 mmHg^-1. When arm cranking was added to leg cycling, leg blood flow did not change significantly, mean arterial blood pressure increased transiently to 147 ± 5 mmHg and leg vascular conductance decreased transiently to 33.5 ± 3.1 ml minutes^-1 mmHg^-1. Furthermore, arm cranking doubled leg noradrenaline spillover. When arm cranking was discontinued and leg cycling continued, leg blood flow was unchanged but mean arterial blood pressure decreased to values significantly below those measured in the first leg exercise period. Furthermore, leg vascular conductance increased transiently, and noradrenaline spillover decreased towards values measured during the first leg exercise period. It is concluded that addition of arm cranking to leg cycling increases leg noradrenaline spillover and decreases leg vascular conductance but leg blood flow remains unchanged because of a simultaneous increase in mean arterial blood pressure. The decrease in leg vascular conductance observed when arm cranking increased mean arterial blood pressure could be regarded more as a measure to prevent overperfusion than a measure to maintain arterial blood pressure.     

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CV_drift) during cycling. Twelve healthy males (23.4 ± 0.5 years, mean ± SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CV_drift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (ΔSV = −16.2 ± 2.0 and −17.1 ± 1.0 ml beat⁻¹; ΔHR = 18.3 ± 2.0 and 17.5 ± 3.0 beats min⁻¹ for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO₂ rebreathing) was 14.7 ± 0.3 l min⁻¹ and 15.0 ± 0.3 l min⁻¹, and mean arterial pressure was 100.0 ± 1.0 mmHg and 96.7 ± 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 ± 1.2% and 11.0 ± 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 ± 0.8 (AU) for 40 rpm and 53.0 ± 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CV_drift during cycling, at least under the present experimental conditions.     

α-Adrenergic effects on low-frequency oscillations in blood pressure and R-R intervals during sympathetic activation

The present study was designed to address the contribution of α-adrenergic modulation to the genesis of low-frequency (LF; 0.04-0.15 Hz) oscillations in R-R interval (RRi), blood pressure (BP) and muscle sympathetic nerve activity (MSNA) during different sympathetic stimuli. Blood pressure and RRi were measured continuously in 12 healthy subjects during 5 min periods each of lower body negative pressure (LBNP; -40 mmHg), static handgrip exercise (HG; 20% of maximal force) and postexercise forearm circulatory occlusion (PECO) with and without α-adrenergic blockade by phentolamine. Muscle sympathetic nerve activity was recorded in five subjects during LBNP and in six subjects during HG and PECO. Low-frequency powers and median frequencies of BP, RRi and MSNA were calculated from power spectra. Low-frequency power during LBNP was lower with phentolamine versus without for both BP and RRi oscillations (1.6 ± 0.6 versus 1.2 ± 0.7 ln mmHg(2), P = 0.049; and 6.9 ± 0.8 versus 5.4 ± 0.9 ln ms(2), P = 0.001, respectively). In contrast, the LBNP with phentolamine increased the power of high-frequency oscillations (0.15-0.4 Hz) in BP and MSNA (P < 0.01 for both), which was not observed during saline infusion. Phentolamine also blunted the increases in the LBNP-induced increase in frequency of LF oscillations in BP and RRi. Phentolamine decreased the LF power of RRi during HG (P = 0.015) but induced no other changes in LF powers or frequencies during HG. Phentolamine resulted in decreased frequency of LF oscillations in RRi (P = 0.004) during PECO, and a similar tendency was observed in BP and MSNA. The power of LF oscillation in MSNA did not change during any intervention. We conclude that α-adrenergic modulation contributes to LF oscillations in BP and RRi during baroreceptor unloading (LBNP) but not during static exercise. Also, α-adrenergic modulation partly explains the shift to a higher frequency of LF oscillations during baroreceptor unloading and muscle metaboreflex activation.     

Heart and brain circulation and CO2 in healthy men

Aim: To compare blood flow response to arterial carbon dioxide tension change in the heart and brain of normal elderly men. Methods: Thirteen healthy elderly male volunteers were studied. Hypercapnea was induced by carbon dioxide inhalation and hypocapnea was induced by hyperventilation. Myocardial blood flow [mL min^?1 × (100 g of perfusable tissue)^?1] and cerebral blood flow [mL min^?1 × (100 g of perfusable tissue)^?1] were measured simultaneously at rest, under carbon dioxide gas inhalation and hyperventilation using the combination of two positron emission tomography scanners. Results: Arterial carbon dioxide tension increased significantly during carbon dioxide inhalation (43.1 ± 2.7 mmHg, P < 0.05) and decreased significantly during hyperventilation (29.2 ± 3.4 mmHg, P < 0.01) from baseline (40.2 ± 2.4 mmHg). Myocardial blood flow increased significantly during hypercapnea (88.7 ± 22.4, P < 0.01) from baseline (78.2 ± 12.6), as did the cerebral blood flow (baseline: 39.8 ± 5.3 vs. hypercapnea: 48.4 ± 10.4, P < 0.05). During hypocapnea cerebral blood flow decreased significantly (27.0 ± 6.3, P < 0.01) from baseline as did the myocardial blood flow (55.1 ± 14.6, P < 0.01). However, normalized myocardial blood flow by cardiac workload [100 mL mmHg^?1 × (heart beat)^?1 × (gram of perfusable tissue)^?1] was not changed from baseline (93.4 ± 16.6) during hypercapnea (90.5 ± 14.3) but decreased significantly from baseline during hypocapnea (64.5 ± 18.3, P < 0.01). Conclusion: In normal elderly men, hypocapnea produces similar vasoconstriction both in the heart and brain. Mild hypercapnea increased cerebral blood flow but did not have an additional effect to dilate coronary arteries beyond the expected range in response to an increase in cardiac workload.