Arterial blood pressure and carotid baroreflex function during arm and combined arm and leg exercise in humans

AIM: During arm cranking (A) blood pressure is higher than during combined arm and leg exercise (A + L), while the carotid baroreflex (CBR) is suggested to reset to control a higher blood pressure in direct relation to work intensity and the engaged muscle mass. METHOD: This study evaluated the function of the CBR by using neck pressure and neck suction during upright A, L and A + L in 12 subjects and, in order to evaluate a potential influence of the central blood volume on the CBR, also during supine A in five subjects. Exercise intensities for A and L were planned to elicit a heart rate response of c. 100 and 120 beats min(-1), respectively, in the upright position and both workloads were maintained during A + L and supine A. RESULTS: The CBR operating point, corresponding to the pre-stimulus blood pressure, was 88 +/- 6 mmHg (mean +/- SE) at rest. During upright A, L and A + L and supine A it increased to 109 +/- 9, 95 +/- 7, 103 +/- 7 and 104 +/- 4 mmHg, respectively, and it was thus higher during upright A than during A + L and supine A (P < 0.05). In addition, the CBR threshold and saturation pressures, corresponding to the minimum and maximum carotid sinus pressure, respectively, were higher during upright A than during supine A, A + L, L and at rest (P < 0.05) with no significant change in the maximal reflex gain. CONCLUSION: These findings demonstrate that during combined arm and leg and exercise in the upright position the CBR resets to a lower blood pressure than during arm cranking likely because the central blood volume is enhanced by the muscle pump of the legs.     

Increases in central blood volume modulate carotid baroreflex resetting during dynamic exercise in humans

We sought to determine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated by changes in central blood volume (CBV). CBV was increased during exercise by altering: (1) subject posture (supine versus upright) and (2) pedal frequency (80 versus 60 revolutions min⁻¹ (r.p.m.)); while oxygen uptake (     ) was kept constant. Eight male subjects performed three exercise trials: upright cycling at 60 r.p.m. (control); supine cycling at 60 r.p.m. (SupEX) and upright cycling at 80 r.p.m. to enhance the muscle pump (80EX). During each condition, carotid baroreflex (CBR) function was determined using the rapid neck pressure (NP) and neck suction (NS) protocol. Although mean arterial pressure (MAP) was significantly elevated from rest (88 ± 2 mmHg) during all exercise conditions ( P < 0.001), the increase in MAP was lower during SupEX (94 ± 2 mmHg) and 80EX (95 ± 2 mmHg) compared with control (105 ± 2 mmHg, P < 0.05). Importantly, the blood pressure responses to NP and NS were maintained around these changed operating points of MAP. However, in comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and leftward when CBV was increased during SupEX and 80EX. These alterations in CBR resetting occurred without any differences in     or heart rate between the exercise conditions. Thus, increasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced increases in MAP and CBR resetting. These findings suggest that changes in cardiopulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.     

Effects of rhythmic muscle compression on arterial blood pressure at rest and during dynamic exercise in humans.

This study was designed to examine the hypothesis that a rhythmic mechanical compression of muscles would affect systemic blood pressure regulation at rest and during dynamic exercise in humans. We measured the changes in mean arterial pressure (MAP) occurring (a) at rest with pulsed (350 ms pulses at 50 pulses min(-1)) or static compression (50 and 100 mmHg) of leg muscles with or without upper thigh occlusion, and (b) during 12-min supine bicycle exercise (75 W, 50 r.p.m.) with or without pulsed compression (50, 100, 150 mmHg) of the legs in synchrony with the thigh extensor muscle contraction. At rest with thigh occlusion, MAP increased by 4-8 mmHg during static leg compression, and by 5-9 mmHg during pulsed leg compression. This suggests that at rest pulsed leg compression elicits a reflex pressor response of similar magnitude to that evoked by static compression. During dynamic exercise without leg compression, MAP (having risen initially) gradually declined, but imposition of graded pulsed leg compression prevented this decline, the MAP values being significantly higher than those recorded without pulsed leg compression by 7-10 mmHg. These results suggest that the rhythmic increase in intramuscular pressure that occurs during dynamic exercise evokes a pressor response in humans.     

Effects of rhythmic muscle compression on arterial blood pressure at rest and during dynamic exercise in humans

This study was designed to examine the hypothesis that a rhythmic mechanical compression of muscles would affect systemic blood pressure regulation at rest and during dynamic exercise in humans. We measured the changes in mean arterial pressure (MAP) occurring (a) at rest with pulsed (350 ms pulses at 50 pulses min^–1) or static compression (50 and 100 mmHg) of leg muscles with or without upper thigh occlusion, and (b) during 12‐min supine bicycle exercise (75 W, 50 r.p.m.) with or without pulsed compression (50, 100, 150 mmHg) of the legs in synchrony with the thigh extensor muscle contraction. At rest with thigh occlusion, MAP increased by 4–8 mmHg during static leg compression, and by 5–9 mmHg during pulsed leg compression. This suggests that at rest pulsed leg compression elicits a reflex pressor response of similar magnitude to that evoked by static compression. During dynamic exercise without leg compression, MAP (having risen initially) gradually declined, but imposition of graded pulsed leg compression prevented this decline, the MAP values being significantly higher than those recorded without pulsed leg compression by 7–10 mmHg. These results suggest that the rhythmic increase in intramuscular pressure that occurs during dynamic exercise evokes a pressor response in humans.     

Atrial natriuretic peptide response to physical exercise is inhibited by an antagonist of the opioid receptors

It was been shown that physical exercise increases plasma atrial natriuretic peptide (ANP) level. This effect was attributed to the hemodynamic changes of exercise which could increase atrial volume and result in ANP secretion. On the other hand, it was evidenced that morphine and opiate peptides greatly stimulate ANP release. To evaluate to what extent the endogenous opioid secretion during exercise induces the ANP release, six healthy volunteers male trained subjects were submitted to two maximal exercise tests with and without (placebo) opiate receptors blockade by naltrexone (50 mg per os). Blood samples were drawn before (rest) and after maximal exercise in order to measure by radioimmunological methods human atrial natriuretic peptide (alpha-h-ANP), beta-endorphin, plasma aldosterone (ALD), plasma renin activity (PRA) and corticotrophin (ACTH). Expired gas was collected during exercise to measure oxygen consumption. Subjects reached the same value of maximal oxygen consumption (VO2 max) at the end of exercise whatever treatment. Plasma ANP level at rest decreases slightly after administration of naltrexone (32.8 +/- 6.3 pg/ml with placebo versus 21.3 +/- 4.6 pg/ml with naltrexone) but the response to physical exercise was significantly reduced by naltrexone (73.3 +/- 14.9 pg/ml with placebo versus 46.9 +/- 8.6 pg/ml with naltrexone) (p less than 0.05). There was no statistical difference according to the treatment between the plasma levels of beta-endorphin, PRA and ACTH at rest as well as at the end of a maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibition of KATP channel activity augments baroreflex-mediated vasoconstriction in exercising human skeletal muscle

In the present investigation we examined the role of ATP-sensitive potassium (K_ATP) channel activity in modulating carotid baroreflex (CBR)-induced vasoconstriction in the vasculature of the leg. The CBR control of mean arterial pressure (MAP) and leg vascular conductance (LVC) was determined in seven subjects (25 ± 1 years, mean ± s.e.m. ) using the variable-pressure neck collar technique at rest and during one-legged knee extension exercise. The oral ingestion of glyburide (5 mg) did not change mean arterial pressure (MAP) at rest (86 versus 89 mmHg, P > 0.05), but did appear to increase MAP during exercise (87 versus 92 mmHg, P = 0.053). However, the CBR–MAP function curves were similar at rest before and after glyburide ingestion. The CBR-mediated decrease in LVC observed at rest (∼39%) was attenuated during exercise in the exercising leg (∼15%, P < 0.05). Oral glyburide ingestion partially restored CBR-mediated vasoconstriction in the exercising leg (∼40% restoration, P < 0.05) compared to control exercise. These findings indicate that K_ATP channel activity modulates sympathetic vasoconstriction in humans and may prove to be an important mechanism by which functional sympatholysis operates in humans during exercise.     

Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.     

Plasma levels of atrial natriuretic peptide are raised in essential hypertension during low and high sodium intake

Summary Plasma levels of -human atrial natriuretic peptide (hANP) were measured in 17 patients with primary hypertension (11 females, 6 males, aged 22–61; blood pressure systolic 154±7 mmHg, diastolic 92±4 mmHg) and in 9 normotensive controls (4 males, 5 females, aged 20–71; blood pressure systolic 117±4 mmHg, diastolic 76±2 mmHg) during unrestricted sodium diet, at the 4th day of a low sodium intake (40–60 mEq/day) and at the 6th day of sodium loading (280–320 mEq/day) both after an overnight rest and after 4 h of upright posture. In the controls, plasma levels of hANP at 8:00 a.m. were lowered from 73±11 to 49±7 pg/ml during low sodium diet and increased to 128±37 pg/ml after high salt intake. Plasma ANP levels were significantly lower after 4 h of upright posture during unrestricted, low and high sodium intake. In the hypertensive group, plasma ANP levels were elevated during unrestricted diet (203±43 pg/ml), during the low sodium period (139±31 pg/ml), and after high sodium intake (267±63 pg/ml) compared to the controls. All levels were lowered by upright posture. The absolute decrease was more pronounced compared to the normotensives, the relative decline was similar in both groups. In the hypertensives, plasma ANP levels significantly correlate with systolic and diastolic blood pressure (r=0.468,r=0.448,P<0.05) and with urinary aldosterone during unrestricted diet (r=0.536,P<0.05). There was an inverse correlation between plasma ANP levels and plasma renin concentration during low and high sodium intake (r=–0.469,r=–0.496,P<0.05).These studies demonstrate raised circulating plasma ANP levels in patients with essential hypertension. The modulation of ANP by different sodium intake and by upright posture is maintained similar to the changes in plasma ANP in normotensive controls. Raised ANP levels in the hypertensives are correlated with low renin secretion and high aldosterone excretion. High ANP levels, therefore, might indicate sodium retention in essential hypertension.Abbreviation ANP atrial natriuretic peptide Supported by a grant from Ministerium für Wissenschaft und Forschung, NRW     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

Summary The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean ±SEM showed that the ANF plasma level decreased significantly (p<0.05) from 32.5±4 to 28±6 pg · ml⁻¹ after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60±13.6 pg · ml⁻¹ and 53±13 pg · ml⁻¹): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

Role of adenosine in exercise-induced human skeletal muscle vasodilatation

The role of adenosine in exercise-induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline-induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one-legged, knee-extensor exercise at approximately 48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (FaBF) by approximately 20%, i.e. from 3.6 +/- 0.5 to 2.9 +/- 0.5 L min(-1), and leg vascular conductance (VC) from 33.4 +/- 9.1 to 27.7 +/- 8.5 mL min-1 mmHg-1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) FaBF from 0.3 +/- 0.03 L min(-1) to a 15-fold peak elevation (P < 0.05) at 4.1 +/- 0.5 L min(-1). Continuous infusion of adenosine at rest and during one-legged exercise at approximately 62% of peak power output increased (P < 0.05) FaBF dose-dependently to level off (P = ns) at 8.3 +/- 1.0 and 8.2 +/- 1.4 L min(-1), respectively. One-legged exercise alone increased (P < 0.05) FaBF to 4.7 +/- 1.7 L min(-1). Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least approximately 20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Impact of age on critical closing pressure of the cerebral circulation during dynamic exercise in humans

Limited information is available regarding cerebral vascular responses to dynamic exercise in older adults. We examined the influence of age on exercise-induced changes in the critical closing pressure (CCP) of the cerebral vasculature. Twelve young and twelve older subjects performed two bouts of steady-state cycling at low and moderate intensities (30 and 50% heart rate reserve). Mean arterial pressure (MAP), middle cerebral artery blood velocity (MCA V) and partial pressure of end-tidal carbon dioxide ( ) were measured. The CCP was estimated by linear extrapolation of pairs of systolic and diastolic blood pressure and MCA V waveforms. Exercise-induced increases in MAP were greater in older subjects (P < 0.01), while mean MCA V (MCA V(mean)) responses to exercise were similar between groups (P = 0.59). The CCP was elevated from rest during low- and moderate-intensity exercise in both groups (moderate exercise: young, +13 ± 2 mmHg and older, +22 ± 2 mmHg; P < 0.01), with the older subjects exhibiting greater increases in CCP during both exercise intensities (moderate exercise: young, +43 ± 9% rest versus older, +153 ± 45% rest; P = 0.04). In contrast, cerebral vascular conductance index (MCA V(mean)/MAP; CVCi) was only decreased during moderate exercise in older subjects (P < 0.01) and CVCi was not altered from rest in young subjects during low- or moderate-intensity cycling. No age-group differences were observed in at rest or during two intensities of exercise (P = 0.40). These data demonstrate that older subjects exhibit larger exercise-induced increases in CCP and decreases in CVCi. Thus, ageing is associated with greater increases in cerebral vascular tone during low- and moderate-intensity dynamic exercise.     

Mixed venous blood temperature response to exercise in heart failure patients treated with short-term vasodilators

Deep-body or core temperature decreases during exercise in patients with heart failure, primarily due to the circulatory inadequacies associated with the pathophysiology of this condition. Vasodilators are commonly used to treat patients suffering from heart failure because these drugs improve total cardiac output and blood-flow to the regional circulations. In heart failure patients, the core temperature response to exercise should also be affected if the circulation is improved by vasodilators. Patients with severe heart failure were studied at rest and during upright bicycle exercise before, and after, short-term treatment with vasodilators (2-minoxidil, 3-hydralazine, 5-captopril). Their heart rate increased significantly (P less than 0.05) from rest to exercise before (87 +/- 15 109 +/- 14 beats/min), and after 89 +/- 13- 112 +/- 15 beats/min) vasodilators, but there was no drug-related affect on these changes. Mean arterial and pulmonary capillary wedge pressures were significantly (P less than 0.05) decreased at rest and after the administration of vasodilators (mean arterial pressure 88 +/- 7 mmHg before; 77 +/- 8 mmHg after; pulmonary capillary wedge pressure 25 +/- 8 mmHg before, 19 +/- 9 mmHg after). During exercise, the increases in mean arterial and pulmonary capillary wedge pressures were not significantly different from the before vasodilator values (mean arterial pressure 92 +/- 14 mmHg before, 87 +/- 14 mmHg after; pulmonary capillary wedge pressure 31 +/- 11 mmHg before, 29 +/- 11 mmHg after). Vasodilators increased cardiac output significantly (P less than 0.05) at rest (3.1 +/- 0.6 litre/min to 4.1 +/- 1.1 litre/m) and during exercise (4.8 +/- .2 litre/min-5.6 +/- 1.7 litre/min). The core temperature (mixed venous blood temperature) decreased significantly (P less than 0.05) during exercise from 37.04 +/- 0.62 degrees C to 36.65 +/- 0.65 degrees C, before treatment with vasodilators. After administration of vasodilators, resting core temperature was not significantly different (36.95 +/- 0.54 degrees C) and still decreased significantly (P less than 0.05) during exercise to 36.73 +/- 0.53 degrees C. This decrease was significantly (P less than 0.05) different from the core temperature response before the administration of vasodilators. We conclude that heart failure patients, treated with short-term vasodilators, have an attenuation of the core temperature response that typically occurs during exercise. This change in the core temperature response is the result of the vasodilator-induced improvement in circulation.     

Altered sensitivity to and clearance of propranolol in men of Chinese descent as compared with American whites

To determine whether the pharmacokinetics and pharmacodynamics of beta-blockade differ among racial groups, we gave 10 men of Chinese descent and 10 American white men 10, 20, 40, and 80 mg of propranolol every eight hours; the dosages were given in random order, and each dose was given for one day. The degree of beta-blockade was measured as the reduction in the heart rate and blood pressure in the supine and upright positions and during treadmill exercise testing. The Chinese subjects had at least a twofold greater sensitivity to the beta-blocking effects of propranolol than the white subjects, as indicated by the mean (+/- SEM) plasma concentrations producing a 20 percent reduction in the heart rate in both the supine position (197 +/- 31 vs. 536 +/- 58 nmol per liter; P less than 0.05) and the upright position (131 +/- 27 vs. 343 +/- 39 nmol per liter; P less than 0.05) and after exercise testing (96 +/- 12 vs. 185 +/- 23 nmol per liter; P less than 0.05). In addition, the Chinese subjects had much greater sensitivity to the hypotensive effects of propranolol, as shown by the concentrations that reduced blood pressure by 10 percent in the supine position (73 +/- 5 vs. 748 +/- 7 nmol per liter; P less than 0.01) and in the upright position (89 +/- 5 vs. 401 +/- 6 nmol per liter; P less than 0.01). No difference in beta-receptor density or affinity of lymphocytes was found between the groups. The Chinese group had a 45 percent higher free fraction of propranolol in plasma, which may have contributed to the increased drug effect but cannot explain it entirely. This group metabolized propranolol more rapidly than the white group, which resulted in a 76 percent higher clearance of an oral dose (3740 +/- 737 vs. 2125 +/- 214 ml per minute; P less than 0.05) because of increased metabolism through multiple metabolic pathways. We conclude that Chinese men have greater sensitivity than white men to the effects of propranolol on heart rate and blood pressure. Decreased protein binding may be responsible in part, but most of the effect remains to be explained.     

Leg vascular resistance increases during head-up tilt in paraplegics

Despite loss of centrally mediated sympathetic vasoconstriction to the legs, spinal cord-injured individuals cope surprisingly well with an orthostatic challenge. This study assessed changes in leg vascular resistance following head-up tilt in healthy (C) and in paraplegic (P) individuals. After 10 min of supine rest, subjects were tilted 30° head-up. Mean arterial pressure (MAP) and total peripheral resistance (TPR) increased in C (MAP from 76.7±6.6 mmHg to 80.6±8.2 mmHg; TPR from 1.12±0.26 AU to 1.19±0.31 AU) while both remained unchanged in P. Echo Doppler ultrasound determined red blood cell velocity in the femoral artery, which decreased (P from 18.9±6.2 cm/s to 12.5±4.5 cm/s, P=0.001; C from 16.3±6.2 cm/s to 10.8±5.0 cm/s, P=0.001) and leg vascular resistance, which increased (P from 402±137 AU to 643±274 AU, P=0.001; C from 238±68 AU to 400±122 AU, P=0.003) from supine to upright. The present study shows that independent of supraspinal sympathetic control, humans are able to increase leg vascular resistance and maintain blood pressure during head-up tilt.     

Differences in autonomic modulation of heart rate during arm and leg exercise.

Heart rate (HR) is higher during dynamic arm exercise than during leg exercise at equal oxygen consumption levels, but the physiological background for this difference is not completely understood. The vagally mediated beat-to-beat R-R interval fluctuation decreases until the level of approximately 50% of maximal oxygen consumption during an incremental bicycle exercise, but the vagal responses to arm exercise are not well known. Changes in autonomic modulation of HR were compared during arm and leg exercise by measuring beat-to-beat R-R interval variability from a Poincaré plot normalized for the average R-R interval (SD1n), a measure of vagal activity, in 14 healthy male subjects (age 20 +/- 4 years) who performed graded bicycle and arm cranking tests until exhaustion. Seven of the subjects also performed the dynamic arm and leg tests after beta-adrenergic blockade (propranolol 0.2 mg kg-1 i.v.). More rapid reduction occurred in SD1n during the low-intensity level of dynamic arm exercise than during dynamic leg exercise without beta-blockade (e.g. 11 +/- 6 vs. 20 +/- 10 at the oxygen consumption level of 1.2 l min-1; P < 0.001) and with beta-blockade (e.g. 13 +/- 4 vs. 25 +/- 10 at the level of 1.0 l min-1; P < 0.05), and the mean HR was significantly higher during submaximal arm work than during leg work in both cases (e.g. during beta-blockade 81 +/- 12 vs. 74 +/- 6 beats min-1 at the level of 1.0 l min-1; P < 0.05). These data show that dynamic arm exercise results in more rapid withdrawal of vagal outflow than dynamic leg exercise.     

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 55-60% VO2max. At 30 to 50 minutes, arm cranking was added and total work load increased to (mean +/- SE) 82 +/- 4% of VO2max. During leg exercise, leg blood flow average 6.15 +/- .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.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Endogenous nitric oxide in the control of skeletal muscle oxygen extraction during exercise

Our previous studies uncovered an inhibitory effect of nitric oxide (NO) on leg skeletal muscle respiration in dogs at rest. The role of NO in the modulation of O2 consumption and O2 extraction in hindlimb muscle during elevated metabolic states was investigated in chronically instrumented dogs while walking and at three exercise intensities which markedly increased hindlimb blood flow. Walking resulted in increased O2 consumption by 17 +/- 4 mL min-1 and O2 extraction from 24 +/- 1 to 37 +/- 8%, with no alteration in hindlimb blood flow (BFLeg) and vascular resistance (VRLeg). Running at the highest speed (9.1 mph) resulted in an increase in BFLeg from 0.67 +/- 0.05 to 2.2 +/- 0.1 L min-1, a reduction of VRLeg and elevation of hindlimb O2 consumption from 33 +/- 3 to 226 +/- 21 mL min-1 and O2 extraction from 29 +/- 2 to 61 +/- 5%, with a decrease in leg venous PO2 from 38 +/- 1 to 25 +/- 1 mmHg. After nitro-L-arginine (NLA) (35 mg kg-1, i.v.) to inhibit endogenous NO synthesis, walking caused greater increases in hindlimb O2 consumption (29 +/- 5 mL min-1) and O2 extraction (43 +/- 1 to 60 +/- 3%) (both P < 0.05), with no significant change in BFLeg. During running at the highest speed, BFLeg was 1.9 +/- 0.1 L min-1 (P < 0. 05) and VRLeg was higher, accompanied by increases in hindlimb O2 consumption from 49 +/- 7 to 318 +/- 24 mL min-1 and O2 extraction from 41 +/- 2 to 79 +/- 4% (both P < 0.05), with a greater decrease in leg venous PO2 from 33 +/- 1 to 20 +/- 1 mmHg (P < 0.05). Similar results were found for intermediate levels of exercise. Our results indicate that NO modulates hindlimb skeletal muscle O2 extraction and O2 usage whether blood flow increased or not during exercise.     

Assessment of blood pressures and gradients by automated blood pressure device compared to invasive measurements in patients previously operated on for coarctation of the aorta.

The aim of the study was to compare invasive and non-invasive blood pressure measurements and gradients. Twenty-two children and 16 adults previously operated for coarctation of the aorta were included. Invasive blood pressures were recorded proximally and distally close to the former operation site and non-invasive systolic blood pressures were recorded by an automated sphygmomanometer on right arm and leg. The adults were investigated at rest and during supine exercise. The correlation between invasive and non-invasive measurements of proximal blood pressures in adults at rest and children were the following, r = 0.92, SD 7.6 mmHg (n = 16) and r = 0.85, SD 11 mmHg (n = 22) respectively. The corresponding correlation for the distal blood pressures were the following for adults at rest 0.64, SD 11.9 mmHg and in children r = 0.82, SD 9.2 mmHg. During exercise in adults we found a low correlation when comparing invasive and non-invasive proximal and distal blood pressures and a poor correlation regarding the gradients, r = 0.50, SD 16 mmHg, r = 0.45, SD 15.9 mmHg and r = 0.30, SD 22.9 mmHg respectively (n = 16). We also measured the time interval between cessation of exercise and completion of the blood pressure recordings, which gave a mean interval of 73 sec (range 45-115 sec). During that interval the mean fall in the proximal blood pressure was 37 mmHg (range 20-80 mmHg), and the mean fall of the gradient was from 41 mmHg (range 20-76 mmHg) to 23 mmHg (range 6-56 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen uptake kinetics during high-intensity arm and leg exercise

The purpose of the present study was to examine the oxygen uptake kinetics during heavy arm exercise using appropriate modelling techniques, and to compare the responses to those observed during heavy leg exercise at the same relative intensity. We hypothesised that any differences in the response might be related to differences in muscle fibre composition that are known to exist between the upper and lower body musculature. To test this, ten subjects completed several bouts of constant-load cycling and arm cranking exercise at 90% of the mode specific V(O(2)) peak. There was no difference in plasma [lactate] at the end of arm and leg exercise. The time constant of the fast component response was significantly longer in arm exercise compared to leg exercise (mean+/-S.D., 48+/-12 vs. 21+/-5 sec; P < 0.01), while the fast component gain was significantly greater in arm exercise (12.1+/-1.0 vs. 9.2+/-0.5 ml min(-1) W(-1); P < 0.01). The V(O(2)) slow component emerged later in arm exercise (126+/-27 vs. 95+/-20 sec; P < 0.01) and, in relative terms, increased more per unit time (5.5 vs. 4.4% min(-1); P < 0.01). These differences between arm crank and leg cycle exercise are consistent with a greater and/or earlier recruitment of type II muscle fibres during arm crank exercise.