Physiological unloading of cardiopulmonary mechanoreceptors by posture changes does not influence the pressor response to isometric exercise in healthy humans

Summary In recent studies in humans the role of cardiopulmonary baroreflexes in modulating the cardiovascular responses to isometric exercise (somatic pressor reflex) has been investigated by performing static hand-grip exercise during deactivation of cardiopulmonary receptors produced by low levels of lower body negative pressure; however, findings from these studies have not been consistent. The purpose of this study was to investigate whether a more physiological unloading stimulus of cardiopulmonary baroreceptors, obtained by sequentially changing posture, could influence the pressor response to somatic afferent stimulation induced by isometric, exercise. To accomplish this, ten healthy subjects performed a 2-min isometric handgrip (IHG) at 30% maximal voluntary contraction after 10 min of supine rest and, in rapid sequence, after 10 min of sitting and 10 min of standing, at the time when, owing to their transitory nature, the cardiovascular effects, due to arterial baroreceptor intervention should have been minimal. During IHG arterial pressure (BP_a) was continuously and noninvasively measured to quantify accurately the blood pressure response to IHG both in magnitude and time course. Results showed that the pressor response to IHG was not significantly influenced by change in posture, either in magnitude or in time course. The mean arterial pressure increased by 17.4 (SEM 2.5), 18.6 (SEM 1.2) and 17.0 (SEM 1.3) mmHg in supine, sitting and standing [2.3 (SEM 0.3), 2.5 (SEM 0.2) and 2.3 (SEM 0.2) kPa] positions, respectively. Also the heart rate response to IHG was unaffected by change in posture. Most important, the sum of the separate BP_a responses induced by supine IHG and by posture change from supine to sitting (summation of reflexes) was not significantly different from the pressor response observed during sitting IHG (interaction of reflexes). Likewise, the sum of the separate BP_a. responses induced by sitting IHG and by changing postures from sitting to standing was not significantly different from the pressor response to standing IHG. These data indicate that, under physiological conditions, cardiopulmonary baroreflexes do not exert a significant role in modulating the reflex pressor drive from muscles during isometric exercise in healthy humans.     

Reduction in extracellular muscle volume increases heart rate and blood pressure response to isometric exercise

Summary To investigate the effect of local dehydration on heart rate and blood pressure during static exercise, six healthy male subjects performed exercise of the calf muscles with different extracellular volumes of the working muscles. Exercise consisted of 5 min of static calf muscle contractions at about 10% of maximal voluntary contraction. The body position during exercise was identical in all tests, i.e. supine with the knee joint 90° flexed. During a 25-min pre-exercise period three different protocols were employed to manipulate the calf volume. In test A the subjects rested in the exercise position; in test B the body position was the same as in A but calf volumes were increased by venous congestion [cuffs inflated to 10.67 kPa (80 mmHg)]; in test C the calf volumes were decreased by lifting the calves about 40 cm above heart level with the subjects supine. To clamp the changed calf volumes in tests B and C, cuffs were inflated to 300 mmHg 5 min before the onset of exercise. This occlusion was maintained for 1 min after the termination of exercise. Compared to tests A and B, the reduced volume of test C led to significant increases in heart rate and blood pressure during exercise. Oxygen uptake did not exceed resting levels in tests B and C until the cuffs were deflated, indicating that only calf muscles contributed to the neurogenic peripheral drive. It is concluded that extracellular muscle volume plays a significant role in adjusting heart rate and blood pressure during static exercise.     

Effect of graded changes in extracellular muscle volume on cardiovascular drives during static exercise

Summary The effects of graded changes in peripheral extracellular volume on heart rate and blood pressure during isometric exercise were studied in 12 healthy male subjects. Each subject performed four calf ergometer tests with each calf. In all tests, static plantar flexion of one foot was performed in a supine body position with the knee joint flexed to 90°. After a pre-exercise period of 18 min, during which the calf volume was manipulated, the subjects had to counteract a spring force of 120 N for 8 min. In the pre-exercise period the peripheral extracellular volume of the calf muscle to be tested was manipulated in four ways. Test 1: 15 min of rest in the exercise position. During the last 3.5 min, the calf volume was increased by venous congestion [80 mmHg (10.67 kPa) applied to the distal part of the thigh by pneumatic cuff]. Test 2: the same protocol as in test 1 but with 7.5-min venous congestion. Test 3: 15 min of venous congestion. Test 4: the calf volume was decreased by a negative hydrostatic pressure for 15 min (calf raised about 40 cm above heart level). To clamp the changed calf volume, the thigh cuff was rapidely inflated to 300 mmHg (40.0 kPa) at the end of the volume manipulation and the subjects remained resting for a further 3 min. In test 4, the leg of the subject was passively brought into the exercise position. The occlusion was maintained until 2 min after exercise. The calf volume manipulation led to changes ranging from +105 ml (test 3) to –134 ml (test 4) as measured by water displacement plethysmography. The blood pressure response to exercise was inversely related to the calf volume changes while the heart rate response during exercise showed no clearcut relationship to the pretreatments.     

Exercise capacity in young adults with hypertension and systolic blood pressure difference between right arm and leg after repair of coarctation of the aorta

Coarctation of the aorta represents 5–7% of congenital heart defects. Symptoms and prognosis depend on the degree of stenosis, age at surgery, surgical method and the presence of other heart defects. Postoperative complications are hypertension, restenosis and an abnormal blood pressure response during exercise. This study includes 41 patients, 15–40 years old, operated in the period 1975–1996. All were exercised on a treadmill until maximal oxygen consumption was achieved. Blood pressure was measured in the right arm and leg before and immediately after exercise, and in the right arm during exercise. Oxygen consumption was monitored and we defined an aerobic phase, an isocapnic buffering phase and a hypocapnic hyperventilation phase. The resting systolic blood pressure correlates with the resting systolic blood pressure difference between right arm and leg. A resting systolic blood pressure difference between the right arm and leg of 0.13 kPa (1 mmHg) to 2.67 kPa (20 mmHg) corresponds with a slight increase in resting systolic blood pressure. This rise in blood pressure increases the aerobic phase of the exercise test, helping the patients to achieve higher maximal oxygen consumption. A resting systolic blood pressure difference of more than 2.67 kPa (20 mmHg) corresponds with severe hypertension and causes reduction in the aerobic phase and maximal oxygen consumption. Resting systolic blood pressure and resting systolic blood pressure difference between the right arm and leg are not indicators for blood pressure response during exercise. Exercise testing is important to reveal exercise-induced hypertension and to monitor changes in transition from aerobic to anaerobic exercise and limitation to exercise capacity.     

Effect of posture on body temperature of young men in cold air

We studied eight young adult men to see whether a supine posture caused a fall in body core temperature in the cold, as it does in thermoneutral conditions. In air at 31°C (thermoneutral), a supine posture for 3 h reduced mean aural, gastric, oesophageal and rectal temperatures by 0.2–0.4°C, compared to upright and increased femoral artery blood flow from 278 (SEM 42) ml · min⁻¹ whilst upright to 437 (SEM 42) ml·min⁻¹ whilst supine. In cold air (8°C) the supine posture failed to reduce these temperature differences significantly, or to increase femoral blood flow; it reduced heart rate, and increased arterial systolic and pulse pressures adjusted to carotid sinus level, less than in thermoneutral conditions. However, the behaviour of core temperature at the four sites was significantly nonuniform between the two postures in the cold, mainly because the supine posture tended to reduce rectal temperature. It may have done so by reducing heat production in the muscles of the pelvis, since it reduced overall metabolic rate from 105 (SEM 8) to 87 (SEM 4) W · m⁻² in the cold. In other respects the results indicated that posture ceased to have an important effect on body core temperatures during cold stress.     

Response of the human triceps surae muscle to electrical stimulation during varying levels of blood flow restriction

The changes in muscle force associated with varying degrees of lower-limb ischaemia were investigated. Isometric torque production by the triceps surae muscle was measured during a 5-min continuous train of 2-Hz electrical stimulation in six healthy young adults under different thigh cuff occlusion pressures. The reproducibility of this protocol when performed under complete ischaemia (tested five times over a 2-week period) was assessed as having a coefficient of variation (CV) for fatigue (end/initial force) of [mean (SEM) 12 (1)%; n=5]. This compares favourably with that obtained for maximum voluntary contraction torque [CV 9 (1)%]. In six subjects, triceps surae muscle fatigue was assessed under thigh cuff pressures of 0, 6.7 kPa (50 mmHg, venous occlusion) and 28 kPa (210 mmHg, complete ischaemia), as well as two intermediate levels of occlusion that were established by cuff pressures of 13.4 (0.5) and 20.3 (1.1) kPa [103 (4) and 152 (8) mmHg, respectively]. These corresponded to ankle-brachial pressure indices of 1.3 and 0.8, respectively when subjects were seated, or 0.8 and 0.36 when supine. With undisturbed lower-leg circulation, force potentiated steadily over the 5 min of stimulation such that the final force was 135 (8)% of the initial value. With complete ischaemia, force fell to 47 (2)% of the initial value. Stimulation under thigh occlusion pressures of 6.7, 13.4 and 20.3 kPa elicited intermediate levels of reduction in force, graded according to the increasing restriction of perfusion. The results show that low-force twitch contractions, which themselves do not occlude blood flow, are extremely sensitive to impaired perfusion and may represent a viable alternative to established methods of muscle performance assessment in patients with blood flow insufficiency. Accepted: 5 November 1999     

Haemodynamic and baroreflex responses to whole-body tilting in exercising men before and after 6 weeks of bedrest

We sought to determine whether the cardiovascular deconditioning that occurs in exercising men after prolonged (42 days) bedrest in the head-down tilt (HDT) position is primarily related to mechanical changes in the heart or to an impaired arterial-cardiac-chronotropic baroreflex. Seven subjects were studied before (C, control) and repeatedly after HDT with rapid tilting between the upright and supine positions during steady-state 50-W dynamic leg exercise. Ventricular interdependence was assumed to be an index of cardiac size; it was assessed on the basis of the initial dip of arterial pulse pressure (PP) induced by a sudden tilt from the upright to the supine position (down-tilt). Arterial-cardiac-chronotropic baroreflex sensitivity (ABS) was assessed as the ratio between tilt-induced heart rate transients and the preceding (and reciprocal) transient in arterial pressure. On the first day of recovery, the initial PP dip was −4 (2) mmHg (where 1 mmHg is 0.13 kPa), less than half of the control value; on subsequent recovery days, the initial PP dip was not significantly different from the control value. When tilting from the upright to the supine position, mean ABS ranged from 1.02 to 1.06 bpm/mmHg during three separate control sessions. Tilts in the opposite direction gave lower ABS values because of the more sluggish HR response and ranged from 0.43 to 0.45 bpm/mmHg in the control situations. ABS did not change after HDT. Our results indicate that impairments of the cardiovascular system after long-term bedrest are of haemodynamic rather than baroreflex origin. Accepted: 8 March 2000     

Effects of microgravity on interstitial muscle receptors affecting heart rate and blood pressure during static exercise

Summary Afferent nerve fibers from receptors situated in the interstitium of skeletal muscles can induce cardiovascular reflexes. It has been shown that these interstitial muscle receptors are also sensitive to the local state of hydration: increased heart rates and blood pressure values were seen during dynamic and static exercise after local dehydration on earth. Since weightlessness leads to a persisting fluid loss in the lower part of the body, we hypothesized that leg exercise in space would augment heart rate and blood pressure responses to a similar extent as during local, interstitial dehydration on earth. Initial measurements during weightlessness were obtained in one subject after 6 days of space flight. Heart rate and blood pressure responses to light static foot plantar flexion (18% of maximal voluntary contraction) were recorded in two sessions. To eliminate the influence of muscle perfusion, exercise was performed during a period of arterial occlusion obtained by means of pneumatic cuffs at mid-thigh level. Identical protocols were used in the pre- and postflight controls, which were performed both in the sitting posture and in a –90° tilted sitting posture assumed 30–40 min before arterial occlusion. During weightlessness the exercise responses of heart rate and systolic and diastolic blood pressure closely followed the tracings obtained with the tilted sitting posture on ground. The response amplitudes in these states of reduced lower limb volumes (about 20/min and 20 mmHg, respectively) exceeded the responses in the supine position by a factor of at least 2. Enhancement of cardiovascular reflexes following local fluid losses of skeletal muscles appears to be a general phenomenon that can also be seen during weightlessness.Abbreviations EMG Electromyogram - LBNP Lower body negative pressure - MVC Maximal voluntary contraction     

Mechanisms of hypotensive effects of a posture change from seated to supine in humans

The hypothesis tested was that the hydrostatic stimulation of carotid baroreceptors is pivotal to decrease mean arterial pressure at heart level during a posture change from seated to supine. In eight males, the cardiovascular responses to a 15‐min posture change from seated to supine were compared with those of water immersion to the xiphoid process and to the neck, respectively. Left atrial diameter and cardiac output (rebreathing) increased similarly during the posture change and water immersion to the xiphoid process and further so during neck immersion. Mean arterial pressure decreased by 12 ± 2 mmHg during the posture change, by 5 ± 1 mmHg during xiphoid immersion, and was unchanged during neck immersion. Arterial pulse pressure increased by 12 ± 3 mmHg during the posture change (P < 0.05) and less during xiphoid and neck immersion by 7 ± 3 mmHg (P < 0.05). Total peripheral vascular resistance decreased similarly during the posture change and neck immersion and slightly less during xiphoid immersion (P < 0.05). In conclusion, the hydrostatic stimulation of carotid baroreceptors combined with some additional increase in arterial pulse pressure, which also stimulates aortic baroreceptors, accounts for more than half of the hypotensive response at heart level to a posture change from seated to supine.     

Reduced sweating threshold during exercise-induced hyperthermia

Two methods have been proposed previously for evaluating thermoregulatory responses to isolated core temperature perturbations. One involves clamping skin temperature at 28°C by water immersion and elevating core temperature by exercise. In the other, core temperature is reduced by central venous infusion of cold fluid while skin temperature is kept constant near 36°C. The sweating-to-shivering temperature range determined using the first protocol is 0.6±0.2°C, but is 1.4±0.6°C using the second. The authors tested the hypothesis that the disparity results from an exercise-induced reduction in the sweating threshold. The sweating threshold was determined three times each in six men, with skin temperature kept constant (36.5–37.0°C) throughout. The first threshold (control) was in response to gradual core hyperthermia that resulted from a skin temperature sufficiently high to prevent dissipation of metabolic heat. The second threshold (exercise) was in response to exercise-induced hyperthermia, and followed a period of core cooling ( 1°C) induced by central venous infusion of cold lactated Ringer's solution. The purpose of the central venous cooling was to reduce core temperature to a level well below the sweating threshold. The third threshold (recovery) again resulted from a skin temperature sufficiently high to prevent dissipation of metabolic heat. The control sweating threshold was 0.7±0.2°C greater than during exercise (P<0.01), but virtually identical to that during recovery. Since the control and recovery thresholds were similar, hyperhydration (necessary in this protocol) appears not to have influenced sweating thresholds. Our results thus indicate that exercise per se reduces the sweating threshold sufficiently to explain reported differences in the sweating-to-shivering range.     

Influence of angiotensin II blockade during exercise in the heat

The effect of the blockade of the renin angiotensin system (RAS) on thermorgulatory, cardiovascular and renal function during moderate exercise in a hot [mean (SEM) 34.4 (0.1)°C] environment was evaluated. Six men and three women cycled at 60% peak oxygen uptake for 45 min following acute administration of a placebo (PLAC) or enalapril (ENAL), an angiotensin converting enzyme inhibitor (ACE-I). Resting mean arterial pressure (MAP) was reduced by ENAL, but the pressor response to exercise was unaffected [MAP = 7.8 (1.4) mmHg for both trials (P > 0.05)]. Peak esophageal temperature [T _es = 38.7 (1.0)°C (PLAC) vs 38.4 (0.2)°C (ENAL)] and mean skin temperatures [ _sk = 36.5 (0.1)°C (PLAC) vs 36.6 (0.1)°C (ENAL)] were similar for both drug treatments during the exercise. Both aldosterone and plasma renin activity (PRA) increased five fold above resting values during exercise; however, only the PRA response [16.7 (3.2) ng angiotensin I (Ang I) · ml^–1 · h^–1 (ENAL) vs 7.4 (1.2) ng Ang I · ml^–1 · h^–1 (PLAC)] was significantly altered by ENAL treatment (P < 0.05). Urine flow, sodium excretion and glomerular filtration rates, determined from creatinine clearance, were similarly reduced following exercise for both ENAL and PLAC treatments. These results suggest acute administration (5 mg) of ACE-I does not impair thermoregulatory, cardiovascular or renal responses during moderate exercise in the heat.     

Body position affects the power spectrum of heart rate variability during dynamic exercise

Summary The power spectrum analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in six men in supine (S) and sitting (C) postures at rest and during steady-state cycle exercise at about 14010, 28%, 45%, 67% of the maximal oxygen consumption (% VO_2max). The total power of RRV decreased exponentially as a function of exercise intensity in a similar way in both postures. Three components were recognized in the power spectra: firstly, a high frequency peak (HF), an expression of respiratory arrhythmia, the central frequency (f _central) of which increased in both S and C from a resting value of about 0.26 Hz to 0.42 Hz at 67% VO_2max; secondly, a low frequency peak (LF) related to arterial pressure control, the f _central of which remained constant at 0.1 Hz in C, whereas in S above 28% VO_2max decreased to 0.07 Hz; and thirdly, a very low frequency component (VLF; less than 0.05 Hz, no f _central). The power of the three components (as a percentage of the total power) depended on the body posture and the metabolic demand. HF% at rest was 30.3 (SEM 6.6) % in S and 5.0 (SEM 0.8) % in C. During exercise HF% decreased by about 30% in S and increased to 19.7 (SEM 5.5) % at 28% VO_2max in C. LF% was lower in S than in C at rest [31.6 (SEM 5.7) % vs 44.9 (SEM 6.4) %; P<0.05], remaining constant up to 28% VO_2max. At the highest intenstities it increased to 54.0 (SEM 15.6) % in S whereas in C it decreased to 8.5 (SEM 1.6) %. VLF represented the remaining power and the change was in the opposite direction to LF. The changes in power spectrum distribution of RRV during exercise depended on the intensity and the body posture. In particular, the LF peak showed opposite trends in S and C tasks, thus suggesting a different readjustment of arterial pressure control mechanisms in relation to the blood distribution and peripheral resistances.     

Human temperature regulation during cycling with moderate leg ischaemia

The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2)°C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3)°C) and Absolute (2.4 (0.7)°C) trials, but was substantially lower (P<0.01) in the Relative trial (1.4 (0.8)°C). Ischaemia potentiated (P<0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m^–2 min^–1) compared to the Control trial (13.4 (6.2) g m^–2 min^–1), concomitant with an attenuated (P<0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex.     

The role of posture on the changes in plasma atrial natriuretic factor and arginine vasopressin levels during immersion

Summary In seven healthy male volunteers we investigated changes in plasma atrial natriuretic factor ([ANF]), arginine vasopressin ([AVP]) and plasma volume (PV) during supine immersion. Twenty minutes head-out water immersion in a supine position in a thermo-neutral water bath attenuated the increase in PV induced by 20 min in a supine position in air, but increased the mean plasma [ANF] from 32.0 pg · ml^–1, SEM 5.1 to 53.3 pg · m^–1, SEM 3.6 and decreased the mean plasma [AVP] from 1.4 pg · ml ^–1, SEM 0.1 to 0.9 pg · ml^–1, SEM 0.04. Simultaneously, diuresis and natriuresis increased markedly. During a 20-min control period in the supine posture without immersion, PV, plasma [ANF] and [AVP] remained unaffected while diuresis and natriuresis did not increase to the same extent. These data suggest that an increase in the central blood volume induced by a weak external hydrostatic pressure during supine immersion triggered the changes in plasma [ANF] and [AVP] and that the increase was probably due to a shift of blood volume from peripheral to central vessels. The changes in plasma [ANF] contributed to the changes in natriuresis.     

Naloxone-provoked vaso-vagal response to head-up tilt in men

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg· kg^–1) on cardiovascular responses to 50° head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8–40) to 5 (3–10) min (median and range; (P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) ; P < 0.01 of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats · min^–1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg min 1^–1,P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1 · mint, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats · min^–1 (P < 0.02 compared to control) and MAP remained stable. The episode of hypotensive-bradycardia appeared as mean control HR decreased to 77 (SEM 7)beats · min^–1, TPR to 31.4(SEM 7.7)mmHg · min · 1^–1 and MAP to 60 (SEM 5)mmHg (P < 0.01), and the volunteers were tilted supine. Cardiovascular effects of naloxone on central hypovolaemia included a reduced elevation of HR and blood pressures and provocation of the episode of hypotensive-bradycardia.     

Exercise thermoregulation after 6 h of chair rest, 6° head-down bed-rest,and water immersion deconditioning in men

The purpose was to investigate the mechanism for the excessive exercise hyperthermia following deconditioning (reduction of physical fitness). Rectal (T _re) and mean skin ( ) temperatures and thermoregulatory responses were measured in six men [mean (SD) age, 32 (6) years; mass, 78.26 (5.80) kg; surface area, 1.95 (0.11)m²; maximum oxygen uptake ( ), 48 (6) ml·min^–1·kg^–1; whilst supine in air at dry bulb temperature 23.2 (0.6)°C, relative humidity 31.1 (11.1)% and air speed 5.6 (0.1) m·min^–1] during 70 min of leg cycle exercise [51 (4)% ] in ambulatory control (AC), or following 6 h of chair rest (CR), 6° head-down bed rest (BR), and 20° (WI20) and 80° (WI80) foot-down water immersion [water temperature, 35.0 (0.1)°C]. Compared with the AC exercise T _re [mean (SD) 0.77 (0.13)°C], T _re after CR was 0.83 (0.08)°C (NS), after BR 0.92 (0.13)°C (^*P<0.05), after WI80 0.96 (0.13)°C^*, and after WI20 1.03 (0.09)°C^*. All responded similarly to exercise: they decreased (NS) by 0.5–0.7°C in minutes 4–8 and equilibrated at +0.1 to +0.5°C at 60–70. Skin heat conductance was not different among the five conditions (range = 147–159 kJ·m^–2·h^–1·°C^–1). Results from an intercorrelation matrix suggested that total body sweat rate was more closely related toT _re at 70 min (T _re70) than limb sweat rate or blood flow. Only 36% of the variability inT _re70 could be accounted for by total sweating, and less than 10% from total body dehydration. It would appear that multiple factors are involved which may include change in sensitivity of thermo- and osmoreceptors.     

Heterogeneous blood flow response in the foot on dependency,assessed by laser Doppler perfusion imaging

The exact nature of the decrease in foot skin blood flow seen after a change in posture remains unsettled. This mechanism has previously been examined by non-invasive techniques such as the laser Doppler perfusion monitor (laser Doppler flowmetry). Taking into account the shortcomings of laser Doppler perfusion monitoring when applied to the determination of skin blood flow, which normally shows substantial heterogeneity, we have applied an emerging technology, the laser Doppler perfusion imager (LDPI). This technique provides a more comprehensive picture of the blood flow distribution in the skin, as it maps skin blood flow over a surface area (120×120 mm, 4096 measurement sites). It was used to examine if the reduction in tissue perfusion or the alterations in flow distributions seen after a change in posture (supine to dependency) could be fully explained by an increase in venous pressure (venous stasis of 50 mmHg) or if the data suggest a complementary mechanism. Skin blood flow of the forefoot decreased from 0.60 V (volt) (median) during rest to 0.40 and 0.38 V during venous stasis and dependency, respectively. Although almost identical median values were obtained during stasis and dependency, the flow distributions were different, with a loss of high flow values during venous stasis. Biological zero was 0.24 V. As the LDPI technique readily records skin perfusion during variations in venous stasis and posture, as well as information on flow distribution changes, it appears promising for future application in stimuli-response studies of skin blood flow. The difference in flow distribution seen between increased venous pressure and dependency suggests an additive regulatory mechanism to the veni-vasomotor reflex during a change in posture.     

Effects of increased muscle perfusion pressure on responses to dynamic leg exercise in man

Summary Ventilatory, cardiovascular and metabolic functions and work performance were studied in men performing incremental-load dynamic leg exercise until exhaustion.Part I: Responses to supine exercise were investigated in 8 subjects during exposure of the lower body to subatmospheric pressure at –6.67 kPa (–50 mm Hg) (Lower Body Negative Pressure, LBNP). Due to curtailment of stroke volume, cardiac output was reduced by LBNP over a wide range of work intensities, including heavy loads: ventilation, oxygen uptake and blood lactate concentrations increased with work load, but at lower rates than in the control condition.Part II: In 9 subjects, work performance was compared in three conditions: supine exercise with and without LBNP, and upright exercise. Performance in supine exercise was enhanced by LBNP, and was further improved in upright exercise. In supine exercise, the LBNP-induced reduction in blood lactate and enhancement of work performance are attributed to a more efficient muscle blood flow resulting from increased local perfusion pressure. This strongly suggests that the primary limitation of work performance was set by the peripheral circulation in working muscles rather than by cardiac performance. A similar mechanism may, in part, explain why work performance in dynamic leg exercise was greater in the upright than in the supine posture. It is also concluded that supine leg exercise during LBNP is a useful model of upright exercise, with regard to the central circulation and the circulation in working muscles.     

Effect of “Vein Pump” Activation upon Venous Pressure and Blood Flow in Human Subcutaneous Tissue

The effect of “vein pump” activation upon superficial venous pressure and blood flow in human subcutaneous adipose tissue was studied in 6 normals and 2 patients with venous insufficiency. Blood flow in subcutaneous tissue was measured at the lateral malleolus by the local ¹³³Xenon washout technique. with the subject placed in a supine position. During passive lowering of the leg blood flow decreased 50 per cent and total vascular resistance increased 136 per cent. Activation of the vein pump by continuously tipping the foot up and down caused a decrease in venous pressure of 5 mmHg in horizontal position. Venous pressure increased only by 8 mmHg when the leg was lowered during exercise. In this situation blood flow remained constant corresponding to an increase in vascular resistance of 42 per cent. However increasing venous pressure to 28 mmHg by venous stasis in the lowered leg during exercise caused an additional increase in vascular resistance of 82 per cent. In the patients with venous insufficiency exercise did not prevent the decrease in blood flow during lowering of the leg. Hence venous pressure elevation of 25 mmHg or more caused an additional increase in vascular resistance in subcutaneous tissue, “vasoconstrictor response”. It is concluded that this “vasoconstrictor response” depends on a vasoconstrictor impulse transmission from veins to arterioles, veno-arteriolar reflex.     

Reference values for gas exchange during exercise in healthy nonsmoking and smoking men

The gas exchange at rest and during exercise was measured in 50 healthy men, 25 lifelong nonsmokers and 25 smokers, between 20 and 65 years of age. Arterial blood samples were taken and expired air was collected at rest, supine and sitting, and during graded exercise. Prediction formulas for various gas exchange variables were obtained by multiple regression. Optimal conditions for gas transfer were present at light exercise. The arterial oxygen tension (PaO2) remained approximately constant during exercise, although in individual smokers and nonsmokers it decreased by up to 1.8 kPa (13.5 mmHg) between a workload of 50 W and the maximal workload. The lower limit for PaO2 at maximal exercise was about 10.7 kPa (80 mmHg). The alveolo-arterial difference in oxygen tension (PA-aO2) increased considerably with increased workload, from 1.09 +/- 1.05 kPa at 50 W to 3.1 +/- 0.9 kPa at maximal exercise. Ageing and tobacco smoking were associated with a decrease in PaO2 and an increase in PA-aO2 at rest in the supine position, but at maximal exercise neither PaO2 nor PA-aO2 was significantly influenced by age or tobacco smoking. In contrast, the dead space and total ventilation were increased during exercise by ageing and tobacco smoking.