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PubMed1992

Sympathetic modulation of blood flow and O2 uptake in rhythmically contracting human forearm muscles.

This study tested the effects of sympathetically mediated changes in blood flow to active muscles on muscle O2 uptake (VO2) in humans. Four minutes of graded (15-80% of maximum voluntary contraction, MVC) rhythmic handgrip exercise were performed. Forearm blood flow (FBF) (plethysmography) and deep vein O2 saturation were measured each minute. Forearm O2 uptake was calculated using the Fick principle. In protocol 1, exercise was performed while supine and again while upright to augment sympathetic outflow to the active muscles. Standing reduced FBF at rest from 3.6 to 2.2 ml.100 ml-1.min-1 (P < 0.05). During light exercise (15-40% MVC) FBF was unaffected by body position. Standing reduced FBF (P < 0.05) from 36.0 to 25.2 ml.100 ml-1.min-1 and forearm VO2 from 38.2 to 28.1 ml.kg-1.min-1 during the final work load. In protocol 2, exercise was performed while supine before and after local anesthetic block of the sympathetic nerves to the forearm. Sympathetic block increased FBF at rest from 3.1 to 8.9 ml.100 ml-1.min-1 (P < 0.05), and FBF was higher during all work loads At 70-80% of MVC sympathetic block increased FBF from 35.4 to 50.7 ml.100 ml-1.min-1 (P < 0.05), and forearm VO2 from 45.5 to 54.2 ml.kg-1.min-1 (P < 0.05). These results suggest that in humans sympathetic nerves modulate blood flow to active muscles during light and heavy rhythmic exercise and that this restraint of flow can limit O2 uptake in muscles performing heavy rhythmic exercise.

Adolescent↗

PubMed1996

Postischemic vasodilation in human forearm is dependent on endothelium-derived nitric oxide.

Although endothelium-derived nitric oxide contributes to basal vascular tone, little is known about its role in regulating blood flow during changes in metabolic supply and demand. We examined the contribution of endothelium-derived nitric oxide to reactive hyperemia in the forearm of 20 normal subjects (12 women, 8 men) aged 27 +/- 4 yr (means +/- SD), using the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA). Forearm ischemia was induced by suprasystolic blood pressure cuff inflation for 5 min, and the subsequent hyperemic flow was recorded for 5 min using venous occlusion strain-gauge plethysmography. The efficacy of nitric oxide blockade was tested by comparing the dose-response relationship to the endothelium-dependent agonist, acetylcholine (3, 10, and 30 mg/min), before and after intra-arterial infusion of up to 2,000 mg/min of L-NMMA. L-NMMA produced a significant downward and rightward shift in the dose-response relationship to acetylcholine and a 39% reduction in response to the maximum dose (P < 0.001). In the presence of L-NMMA, peak hyperemic flow was reduced 16% (26.5 +/- 2.1 to 22.3 +/- 1.5 ml.min-1.100 ml of forearm-1, P < 0.03), and the minimum forearm vascular resistance was increased 22.8% (3.5 +/- 0.3 to 4.3 +/- 0.4 mmHg.ml-1.min.100 ml, P < 0.02). Total hyperemia, calculated from the area under the flow vs. time curve, at 1 and 5 min after cuff release was 17 and 23% less, respectively (13.6 +/- 1.2 vs. 11.3 +/- 1.1 and 31.8 +/- 2.7 vs. 24.6 +/- 1.8 ml/100 ml, P < 0.002), following L-NMMA. These data suggest that endothelium-derived nitric oxide plays a role in both reactive hyperemia and in the maintenance of the hyperemic response following ischemia in the forearm.

Acetylcholine↗

PubMed1998

Exercise-induced muscle injury augments forearm vascular resistance during leg exercise.

The purpose of the present investigation was to examine the effect of exercise-induced muscle injury on hemodynamic responses during exercise. Ten subjects performed unilateral isometric knee extensions (IKE) at 30% of preinjury maximum voluntary contraction to fatigue and for 3 min before and 48 h after muscle injury. Muscle injury was elicited by performing 8 sets of 10 repetitions of eccentric muscle actions of the knee extensor muscles (i.e., quadriceps muscles) by lowering a weight equivalent to 75% of eccentric maximum load. Exercise time to fatigue for IKE at 30% of maximum voluntary contraction in the injured leg was significantly decreased from preinjury to postinjury IKE (257 +/- 21 to 203 +/- 23 s; n = 10), but was unchanged in the control leg (244 +/- 16 to 254 +/- 20 s; n = 7). With the use of a 10-cm visual analog scale, ratings of muscle soreness in the injured leg increased from 0 to 5. 1 +/- 0.7 cm (P < 0.001) but were not changed in the control leg (0 both times). Both heart rate and mean arterial pressure responses to exercise were unchanged following muscle injury. Forearm blood flow and forearm vascular resistance were not different at rest and during the first minute of exercise before and after muscle injury. However, after muscle injury, forearm blood flow was significantly lower and forearm vascular resistance was significantly higher (P < 0.03) during the second and third minutes of exercise. There were no significant changes in any variables with the contralateral control leg. In four subjects, resting magnetic resonance images demonstrated a 23% greater relative cross-sectional area of the knee extensor muscles with an elevated transverse relaxation time in the injured versus control leg. The results indicate that forearm vascular resistance is augmented during isometric knee extension following muscle injury of the knee extensor muscles. The data suggest that muscle injury alters vascular control to non-exercising skeletal muscle during exercise.

Adult↗

PubMed1999

Relative contribution of vasodilator prostanoids and NO to metabolic vasodilation in the human forearm.

Although many factors are thought to contribute to the regulation of metabolic vasodilation in skeletal muscle vasculature, recent interest has focused on the role of the endothelium. We examined the relative roles of nitric oxide (NO) and of vasodilator prostanoids in the control of metabolically induced functional hyperemia in the forearm of humans. In 43 healthy volunteers [24 +/- 5 (SD) yr] we assessed resting and functional hyperemic blood flow (FHBF) in response to 2 min of isotonic forearm exercise before and after inhibition of NO and/or vasodilator prostanoid production with intra-arterial NG-monomethyl-L-arginine (L-NMMA, 2 mg/min) and aspirin (ASA, 3 mg/min), respectively. Blood flow was measured using venous occlusion plethysmography. L-NMMA and ASA decreased resting forearm blood flow by 42% (P < 0.0001) and 23% (P < 0.0001), respectively, whereas infusion of ASA followed by L-NMMA reduced flow by a further 24% (P < 0.05). L-NMMA reduced peak FHBF by 18% [from 13.9 +/- 1.0 to 11.4 +/- 1.1 (SE) ml. 100 ml forearm-1. min-1, P = 0.003] and the volume "repaid" after 1 and 5 min by 25% (8.9 +/- 0.7 vs. 6.7 +/- 0.7 ml/100 ml, P < 0.0001) and 37% (26.6 +/- 1.8 vs. 16.8 +/- 1.6 ml/100 ml, P < 0.0001). ASA similarly reduced peak FHBF by 19% (from 14.5 +/- 1.1 to 11.8 +/- 0.9. 100 ml forearm-1. min-1, P < 0.001) and the volume repaid after 1 and 5 min by 14% (7.5 +/- 0. 6 vs. 6.4 +/- 0.6 ml/100 ml, P = 0.0001) and 20% (21.2 +/- 1.5 vs. 16.9 +/- 1.5 ml/100 ml, P < 0.0001), respectively. The coinfusion of ASA and L-NMMA did not decrease FHBF to a greater extent than either agent alone. These data suggest that endothelium-derived NO and vasodilator prostanoids contribute to resting blood flow and metabolic vasodilation in skeletal muscle vasculature in healthy humans. Although these vasodilator mechanisms operate in parallel in exercise-induced hyperemia, they appear not to be additive. Other mechanisms must also be operative in metabolic vasodilation.

Adult↗

PubMed2000

Venous emptying mediates a transient vasodilation in the human forearm.

We tested the hypothesis that venous emptying serves as a stimulus for vasodilation in the human forearm. We compared the forearm blood flow (FBF; pulsed Doppler mean blood velocity and echo Doppler brachial artery diameter) response to temporary elevation of a resting forearm from below to above heart level when venous volume was allowed to drain versus when venous drainage was prevented by inflation of an upper arm cuff to approximately 30 mmHg. Arm elevation resulted in a rapid reduction in venous volume and pressure. Cuff inflation just before elevation effectively prevented these changes. FBF was briefly reduced by approximately 16% following arm elevation. A transient (86%) increase in blood flow began by approximately 5 s of arm elevation and peaked by 8 s, indicating a vasodilation. This response was completely abolished by preventing venous emptying. Arterial inflow below heart level was markedly elevated by 343% following brief (4 s) forearm elevation. This hyperemia was minor when venous emptying during forearm elevation had been prevented. We conclude that venous emptying serves as a stimulus for a transient (within 10 s) vasodilation in vivo. This vasodilation can substantially elevate arterial inflow.

Adult↗

PubMed2001

Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation.

The identity of endothelium-dependent hyperpolarizing factor (EDHF) in the human circulation remains controversial. We investigated whether EDHF contributes to endothelium-dependent vasomotion in the forearm microvasculature by studying the effect of K+ and miconazole, an inhibitor of cytochrome P-450, on the response to bradykinin in healthy human subjects. Study drugs were infused intra-arterially, and forearm blood flow was measured using strain-gauge plethysmography. Infusion of KCl (0.33 mmol/min) into the brachial artery caused baseline vasodilation and inhibited the vasodilator response to bradykinin, but not to sodium nitroprusside. Thus the incremental vasodilation induced by bradykinin was reduced from 14.3 +/- 2 to 7.1 +/- 2 ml x min(-1) x 100 g(-1) (P < 0.001) after KCl infusion. A similar inhibition of the bradykinin (P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl. Miconazole (0.125 mg/min) did not inhibit endothelium-dependent or -independent responses to ACh and sodium nitroprusside, respectively. However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and NG-monomethyl-L-arginine, the forearm blood flow response to bradykinin (P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole. Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF. In the human forearm microvasculature, EDHF appears to be a cytochrome P-450 derivative, possibly an epoxyeicosatrienoic acid.

Administration, Oral↗

PubMed1979

Responses of forearm blood flow to graded leg exercise in man.

To test whether the cutaneous vascular responses to exercise are influenced by the level of work, three strategies were followed. In each, forearm blood flow and esophageal temperature were measured throughout. In part I, the forearm blood flow-internal temperature relationships from separate sessions of steady-state exercise at different loads were compared. In part II, work load was varied between 50 and 150 W. Work load was raised or lowered 50 W every 5 min over 60-75 min. The third strategy was to examine the immediate change in forearm blood flow accompanying rapid, large increments or decrements in work load. The results do not support a graded response of the cutaneous circulation to exercise. In both the first and second protocols above, the relationship of forearm blood flow to internal temperature was not measurably altered by work load. Multiple linear regression analysis failed to reveal a consistent role for work load in part II. In the third protocol, there was no consistent or sustained response to an abrupt change in work load. Thus over the range of work loads used in this study there appears to be no major role for the level of work in the regulation of forearm skin blood flow other than through the effect on internal temperature.

Adult↗

PubMed1980

Control of forearm venous volume during exercise and body heating.

Subjects ate ice to cool sufficiently to constrict the superficial forearm veins. After ice-eating, esophageal temperature (Tes) recovered from local cooling in 10-15 min, and thereafter reflected body core temperature. Eight skin temperatures (Tsk) were measured, and a weighted mean (Tsk) computed. The left wrist was suspended 5-6 in. above shoulder level, and left forearm skin temperature was maintained at 35 degrees C with a controlled-temperature air stream. Forearm venous volume (FVV) w-s the volume difference between the forearm drained by gravity and the forearm congested by a pneumatic cuff inflated to 32 Torr. Subjects were warmed either by storage of resting metabolic heat or by cycle exercise at 40-45% of maximal O2 consumption. Exercise experiments were conducted in ambient temperatures of 15, 25, and 35 degrees C, and resting experiments in 25 and 35 degrees C. FVV rose linearly with Tes, but during exercise FVV was lower than at the same Tes and Tsk during rest, and the difference was greater at high Tsk and FVV. Our data fit the equation FVV-FVV0 = (a1 Tes + a2 Tsk - b).[1 - phi (W).(Tsk - T-sk0)], where phi (W) is a function of exercise, and phi (W) = 0 at rest.

Adult↗

PubMed1986

Differential effects of lower body negative pressure on forearm and calf blood flow.

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.

Adult↗

PubMed1989

Vascular responses in forearm and calf to contralateral static exercises.

Ten normal subjects performed a 90-s isometric exercise [20, 30, and 40% of maximal voluntary contraction (MVC) of the flexor muscle of the right index finger or quadriceps muscle of the right leg. Contralateral forearm and calf blood flows (strain gauge plethysmography) and arterial blood pressure (auscultation) were measured simultaneously. Each exercise caused a decrease in forearm vascular resistance and a progressive increase in calf resistance. These changes were greatest with the 40% MVC. With finger exercise at 20 and 40% MVC, the percentage decreases in forearm vascular resistance from control were 12.3 and 22.7%, respectively (P less than 0.01). Similar decreases (9.5 and 24.9%, respectively; P less than 0.01) were noted with exercise of the quadriceps muscle. By contrast, the corresponding increases in calf vascular resistance were greater (P less than 0.01) with quadriceps exercise (13.3 and 55.4%, respectively) than with finger exercise (6.0 and 36.0%). Arrest of the circulation to the exercising muscles just before the exercise ended caused an abrupt increase in forearm vascular resistance and a decrease in calf resistance. These studies provide further evidence of the heterogeneity of responses of forearm and calf resistance vessels to certain cardiovascular stimuli.

Adult↗

PubMed1995

Effect of aging on beta 2-adrenergic receptor-stimulated flux of K+, PO4, FFA, and glycerol in human forearms.

beta-Adrenergic responses have been shown to decline with aging, particularly in the cardiovascular system. We infused terbutaline, a selective beta 2-adrenoceptor agonist, into the brachial artery of 10 young (mean age 25 yr, range 22-31 yr) and 9 elderly (mean age 73 yr, range 68-81 yr) healthy subjects to examine its effects on nutrient flux. Forearm K+, PO4, free fatty acid (FFA), and glycerol uptake were determined by measurement of forearm blood flow (using dye dilution) and brachial arterial and deep venous plasma substrate concentrations. Elderly subjects were less sensitive to terbutaline-mediated increases in forearm blood flow, net fluxes of K+, and glycerol but not net fluxes of FFA or PO4. The mean fitted slopes of each parameter vs. the log of the terbutaline concentration, a measure of forearm beta-adrenergic sensitivity, for young and elderly groups were 4.9 +/- 1.7 (SD) vs. 2.4 +/- 2.3 for forearm blood flow (P < 0.05), 0.84 +/- 0.46 vs. 0.43 +/- 0.37 for K+ net flux (P < 0.05), -157 +/- 113 vs. -26 +/- 26 for glycerol net flux (P < 0.01), -336 +/- 429 vs. -44 +/- 457 for FFA net flux (P = 0.11), and 0.31 +/- 0.24 vs. 0.18 +/- 0.16 for PO4 net flux (P = 0.14). Terbutaline promoted net uptake of K+ into skeletal muscle less well in the elderly, although net PO4 flux was similar in the two groups. Terbutaline-stimulated vasodilation and net glycerol efflux but not FFA efflux were impaired with aging. These data demonstrate that heterogeneous changes in beta-adrenergic responses occur with aging.

Adult↗

PubMed2001

beta-Receptor agonist activity of phenylephrine in the human forearm.

Phenylephrine is generally regarded as a "pure" alpha(1)-agonist. However, after treatment of the forearm with the alpha-adrenergic-blocking drug phentolamine, brachial artery infusion of phenylephrine can cause transient forearm vasodilation. To determine whether this response was beta-receptor mediated, phenylephrine, phentolamine, and propranolol were infused into the brachial arteries of six healthy volunteers. Forearm vascular conductance (FVC) was also calculated and expressed as arbitrary units (units). Infusion of phenylephrine by itself (0.5 microg. dl forearm volume(-1). min(-1)) caused a sustained decrease (P < 0.05) in FVC from 3.5 +/- 0.7 to 0.9 +/- 0.2 units (P < 0.05). Infusion of the alpha-blocker phentolamine increased (P < 0.05) baseline FVC to 5.7 +/- 1.3 units. Subsequent infusion of phenylephrine after alpha-blockade caused FVC to increase (P < 0.05) for ~1 min from 5.7 +/- 1.3 to a peak of 13.1 +/- 1.8 units. Propranolol had no effect on baseline flow, and subsequent phenylephrine infusion after alpha- and beta-blockade caused a small, but significant, sustained decrease in FVC from 5.1 +/- 1.0 to 3.6 +/- 0.8 units. There were no systemic effects from the infusions, and saline infusion at the same rate (1-2 ml/min) had no forearm vasoconstrictor or dilator effects. These data indicate that in humans phenylephrine can exert transient beta(2)-vasodilator activity when its predominant alpha-constrictor effects are blocked.

Adrenergic alpha-Agonists↗

PubMed2003

Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise.

The purpose of this study was to test the hypothesis that sympathetic vasoconstriction is rapidly blunted at the onset of forearm exercise. Nine healthy subjects performed 5 min of moderate dynamic forearm handgrip exercise during -60 mmHg lower body negative pressure (LBNP) vs. without (control). Beat-by-beat forearm blood flow (Doppler ultrasound), arterial blood pressure (finger photoplethysmograph), and heart rate were collected. LBNP elevated resting heart rate by approximately 45%. Mean arterial blood pressure was not significantly changed (P = 0.196), but diastolic blood pressure was elevated by approximately 10% and pulse pressure was reduced by approximately 20%. At rest, there was a 30% reduction in forearm vascular conductance (FVC) during LBNP (P = 0.004). The initial rapid increase in FVC with exercise onset reached a plateau between 10 and 20 s of 126.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in control vs. only 101.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in LBNP (main effect of condition, P = 0.003). This difference was quickly abolished during the second, slower phase of adaptation in forearm vascular tone to steady state. These data are consistent with a rapid onset of functional sympatholysis, in which local substances released with the onset of muscle contractions impair sympathetic neural vasoconstrictor effectiveness.

Adult↗

PubMed2005

Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia.

In 11 healthy volunteers, we evaluated, in a double-blind crossover study, whether the vasodilation that follows isometric contraction is mediated by prostaglandins (PGs) and/or is O2 dependent. Subjects performed isometric handgrip for 2 min at 60% maximal voluntary contraction (MVC), after pretreatment with placebo or aspirin (600 mg orally), when breathing air or 40% O2. Forearm blood flow was measured in the dominant forearm by venous occlusion plethysmography. Arterial blood pressure was also recorded, allowing calculation of forearm vascular conductance (FVC; forearm blood flow/arterial blood pressure). During air breathing, aspirin significantly reduced the increase in FVC that followed contraction at 60% MVC: from a baseline of 0.09 +/- 0.011 [mean +/- SE, conductance units (CU)], the peak value was reduced from 0.24 +/- 0.03 to 0.14 +/- 0.01 CU. Breathing 40% O2 similarly reduced the increase in FVC relative to that evoked when breathing air; the peak value was 0.24 +/- 0.03 vs. 0.15 +/- 0.02 CU. However, after aspirin, breathing 40% O2 had no further effect on the contraction-evoked increase in FVC (the peak value was 0.15 +/- 0.02 vs. 0.16 +/- 0.02 CU). Thus the present study indicates that prostaglandins make a substantial contribution to the peak of the vasodilation that follows isometric contraction of forearm muscles at 60% MVC. Given that hyperoxia similarly reduced the vasodilation and attenuated the effect of aspirin, we propose that the stimulus for prostaglandin synthesis and release is hypoxia of the endothelium.

Adult↗

PubMed1985

Cerebellar nuclear cell activity during antagonist cocontraction and reciprocal inhibition of forearm muscles.

Monkeys were trained to exert a maintained isometric pinch with the thumb and forefinger. This task reliably elicited a simultaneous cocontraction of the forearm muscles. The same monkeys were also taught to insert the open hand into a manipulandum, flex and extend the wrist 35 and 15 degrees, respectively, and maintain an isometric wrist position against a mechanical stop for 1 s. This second task comprised two conditions: a dynamic or movement phase and a static or isometric phase. Movement always involved a wrist displacement of 50 degrees. Although some forearm muscles demonstrated bidirectional activity during the wrist displacement phase, all the wrist and finger muscles were alternatively active in isometric flexion or extension. Of the neurons in the dentate and interposed nuclei that consistently changed discharge during repeated isometric prehension, over 90% (61/67) of the neurons increased activity during this cocontraction of forearm muscles. About 70% (47/67) of these same nuclear cells discharged with a reciprocal pattern of firing during alternating wrist flexion-extension movements. Forty-six neurons had sustained and reciprocal discharge during the maintained isometric wrist postures. No differences were seen between the activity patterns of dentate and interposed cells with respect to either the prehension task or the reciprocal wrist-movement task. The discharge frequency of some dentate and interpositus neurons could be correlated with prehensile force as well as velocity of wrist movement and torque developed by wrist muscles. Correlation coefficients were calculated between nuclear cell discharge and the amplitude of the surface EMGs of the flexors and extensors of the wrist and fingers during the wrist-movement task. Sixteen nuclear cells showed low-order, but reliably positive, correlations with one of the two forearm muscle groups (mean r = 0.33). In contrast, a sample of seven Purkinje cells recorded during the same task demonstrated low-order correlations that were negative in sign (mean r = -0.30) between discharge frequency and one of the two forearm EMGs.

Animals↗

PubMed1989

Volume-pressure analysis of reflex changes in forearm venous function. A method by mental arithmetic stress and radionuclide plethysmography.

Mental arithmetic stress is known to cause forearm arterial dilation, but the venous responses, including possible changes in the volume-pressure relation, have not been defined. Hence, 10 apparently normal subjects, eight men and two women, mean age 46 +/- 9 years, were studied before and during mental arithmetic stress. Changes in forearm venous volume were estimated with 99mTc blood pool scintigraphy. Group variability of this measurement technique was 1.8 +/- 2.3%. A brachial blood pressure cuff was used to obtain venous occluding pressures of 0, 10, 20, and 30 mm Hg. Mental arithmetic stress increased group systolic and diastolic blood pressure from 126 +/- 12 to 152 +/- 20 mm Hg and from 83 +/- 8 to 93 +/- 15 mm Hg, respectively (p less than 0.001). Heart rate increased from a mean of 75 +/- 15 to 85 +/- 17 beats/min (p less than 0.01). There was no evidence of interaction between or nonlinearity of the volume-pressure plots. Linear regression then yielded the equations V = 99.8 + 0.96P before and V = 86.3 + 0.96P during mental arithmetic stress, which represents a 13.5 +/- 1.6% decrease in forearm vascular volume (p less than 0.001). We conclude that 1) a linear relation exists between forearm venous volume and pressure at physiologic pressures before and during mental arithmetic stress; 2) mental arithmetic stress causes forearm venoconstriction; and 3) such venoconstriction takes place by a parallel shift in the volume-pressure relation (i.e., a shift in unstressed venous volume).

Adult↗

PubMed1992

Augmented forearm vasoconstriction during dynamic exercise in healthy older men.

BACKGROUND: We tested the hypothesis that the nonactive limb vasoconstriction evoked during large-muscle dynamic exercise becomes augmented with aging in humans. METHODS AND RESULTS: Sixteen young control subjects (age, 26 +/- 1 year) and twelve older (65 +/- 1 year) healthy men with similar chronic physical activity levels were studied during supine leg cycling exercise. Both peak work load (1,100 +/- 60 versus 1,400 +/- 40 kpm/min) and peak O2 uptake (1.85 +/- 0.10 versus 2.38 +/- 0.07 l/min) were lower in the older men (p < 0.05). There were no differences in the two groups under conditions of quiet supine (basal) rest. During cycling for 5 minutes each at mild, moderate, and heavy submaximal intensities (approximately 45%, 65%, and 85% of peak O2 uptake), the increases in arterial blood pressure generally were similar in the young and older subjects; however, heart rate rose less in the older men (p < 0.05). Whole forearm blood flow (venous occlusion plethysmography) was lower and vascular resistance was higher (approximately 55-90%) in the older men at all loads (p < 0.05), but the steady-state forearm skin blood flow responses (laser Doppler velocimetry) were not different in the two groups. The increases in antecubital venous norepinephrine concentrations were greater in the older men at each work load (p < 0.05), although the plasma epinephrine responses were similar in the two groups. In other studies, 1) peak whole forearm reactive hyperemia and vascular conductance after sustained circulatory arrest (ischemia) were slightly (approximately 20%) but not significantly lower in the older men and 2) the forearm vasoconstrictor and plasma norepinephrine responses to a nonexercise sympathoexcitatory stimulus (limb immersion in ice water) tended to be blunted in the older men. CONCLUSIONS: During brief, submaximal, large-muscle dynamic exercise, healthy older men demonstrate augmented forearm vasoconstriction that is probably caused by greater constriction of skeletal muscle resistance vessels; this appears to be mediated, at least in part, by increased sympathetic outflow. These altered sympathetic vasoconstrictor adjustments do not represent a nonspecific hyperresponsiveness to acute stress with human aging. Finally, the regulation of arterial blood pressure appears to be normal in these healthy older men.

Adult↗

PubMed1989

Forearm blood flow responses of offspring of hypertensives to an extended stress task.

The forearm blood flow and other cardiovascular responses of 10 healthy young men with a parental history of hypertension to an extended laboratory stressor were compared with the responses of 10 age-matched men with normotensive parents. To eliminate the effects of the anticipation of stress on baseline measures, all subjects participated in a separate 1-hour counterbalanced baseline session in which no stress was presented. There were no significant differences between the two groups in resting blood pressure, heart rate, blood volume pulse, forearm blood flow and vascular resistance, and self-report anxiety, although offspring of hypertensive parents exhibited marginally greater (p = 0.08) forearm blood flow at rest. During the stress session, subjects played video games for 1 hour and avoided mild electric shocks depending on performance. Offspring of hypertensive parents exhibited significantly greater heart rate (+19 +/- 6 vs. +3 +/- 2%), forearm blood flow (+52 +/- 14 vs. +9 +/- 4%), and self-report anxiety (+25 +/- 6 vs. +9 +/- 3%) responses to the task. There were no significant group differences in blood pressure response to the task. Significant positive correlations between forearm blood flow and heart rate responses to the task were observed. These findings extend earlier results that suggested healthy young offspring of hypertensive and normotensive parents may exhibit different patterns of hemodynamic response to stress in the absence of differences in resting blood pressure or blood pressure responsiveness to stress.

Adult↗