Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOREARM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1990

Alteration of baroreflex control of forearm vascular resistance by dietary fatty acids.

The effects of dietary safflower (control, n = 10), borage (n = 9), and fish oil (n = 10), as sources of linoleic, gamma-linolenic, and eicosapentaenoic acid, respectively, at a dose of 4.5 ml/day for 4 wk, on cardiovascular responses to lower body negative pressure (LBNP) were studied in normotensive humans in a randomized, double-blind design. Pre- and postsupplementation, subjects were exposed to 5 min of -10 and -40 mmHg LBNP. Blood pressure (BP), heart rate (HR), forearm blood flow (FBF), forearm vascular resistance (FVR), and plasma norepinephrine (PNE) were measured at each level. Subjects were then exposed to a cold-pressor test, isometric handgrip, and forearm ischemia. At pretest, LBNP reduced BP and FBF and increased HR and FVR in all groups. After diets, the PNE and vasoconstrictor responses to -40 mmHg LBNP, as well as the reflex vasodilation on its cessation, were significantly augmented by borage oil. No diet differences were observed in the HR responses to LBNP or in the responses to the other tasks, with the exception that fish oil increased FBF after forearm ischemia. These data indicate that borage oil augments the arterial baroreflex control of vascular resistance. The vasodilatory effects of fish oil may be mediated via local mechanisms.

Adult↗
PubMed1990

Influence of the renin-angiotensin system on human forearm blood flow.

Although angiotensin II is a potent vasoconstrictor agent in all tissues, including the human forearm, equivocal effects on forearm blood flow (FBF) have been found after angiotensin blockade. In 13 healthy Na(+)-depleted subjects FBF was measured by the 133Xe washout technique; subcutaneous and muscle blood flows were determined separately. FBF was measured during supine rest, after the arm was lowered, and during lower body negative pressure (LBNP). The measurements were repeated during intra-arterial saralasin infusion in six subjects and after intravenous administration of enalapril in seven subjects. FBF decreased and forearm vascular resistance (FVR) increased during arm lowering and LBNP, as the result of local and central adrenergic reflexes, respectively. We observed similar FBF and FVR values after both saralasin and enalapril, except for a decrease in FVR at rest after enalapril. It is concluded that, in the human forearm, angiotensin II is not necessary for sympathetic vasoconstrictor reflexes but may, through a central effect, have some influence on arteriolar tone at rest.

Adult↗
PubMed1991

Leg exercise conditioning increases peak forearm blood flow.

To examine whether forearm vascular adaptations could occur after upright-leg exercise training, the reactive hyperemic blood flow after 10 min of forearm circulatory arrest (RHBF10) was studied. RHBF10 was examined in seven subjects before, at 2 wk, and after the completion of 4 wk of bicycle ergometer training. Maximal O2 consumption (VO2max) for leg ergometer work increased 13% (P less than 0.05) over 4 wk. Over that period of time RHBF10 in the forearm increased 50% (P less than 0.05), with a reciprocal drop in minimum vascular resistance. Resting heart rate decreased 15% (P less than 0.05) during the same period. Changes in RHBF10 and VO2max were noted after 2 wk of training. Mean arterial pressure did not change. We conclude that vascular adaptations can occur in the forearm muscle beds, even though the training regimen is designed to condition the lower extremities.

Adult↗
PubMed1992

Hypohydration affects forearm vascular conductance independent of heart rate during exercise.

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.

Adult↗
PubMed1993

Lactate kinetics in resting and exercising forearms during moderate-intensity supine leg exercise.

Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P < 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.

Adult↗
PubMed1993

Hypoxic potentiation of the ventilatory response to dynamic forearm exercise.

The slope of the relationship between ventilation (VI) and O2 consumption, as derived in progressive-intensity exercise tests, is increased markedly by systemic hypoxia. The mechanisms underlying the hypoxic potentiation of the ventilatory response to exercise have not been established, partly because several factors that can increase respiratory drive (e.g., metabolic rate, cardiac output, circulating catecholamine levels) change significantly and simultaneously under these conditions. In an effort to avoid these confounding changes, we sought to determine whether hypoxia potentiates the ventilatory response to dynamic forearm exercise in humans. Forearm exercise increased the O2 consumption by only 80-90 ml/min; nevertheless, hypoxia resulted in a significant potentiation of VI that was mediated by a marked increase in breathing frequency. These observations led us to hypothesize that the hypoxic potentiation of VI is due to an exaggerated stimulation of chemosensitive afferent nerve endings within the exercising muscles ("muscle chemoreceptors"). We tested this hypothesis in separate experiments under conditions of forearm ischemia so that the stimulus to the muscle chemoreceptors in normoxic and hypoxic exercise would be the same. The magnitude of the change in VI evoked by hypoxic ischemic exercise was significantly greater than the sum of the separate changes evoked by normoxic ischemic exercise and hypoxic ischemic rest. We conclude that the combination of dynamic forearm exercise and hypoxia potentiates VI and that this effect is mediated by neural structures that govern respiratory frequency. Moreover the potentiated ventilatory response cannot be attributed to an exaggerated stimulation of intramuscular chemoreceptors.

Adult↗
PubMed1994

Sympathetic nerve activity during prolonged rhythmic forearm exercise.

Exercise is a potent stimulus to activate the sympathetic nervous system. Previous work suggests that metabolite-sensitive muscle afferents are activated near the point of fatigue, and, when activated, they determine the muscle sympathetic nerve activity (MSNA) response to isometric forearm exercise. Yet, studies using a more prolonged rhythmic exercise paradigm suggest that the sympathetic nervous system can be activated in a more graded fashion. The purpose of this study was to determine whether metaboreceptor stimulation would also be responsible for MSNA responses to prolonged rhythmic isotonic forearm exercise. Subjects (n = 16) performed rhythmic isotonic forearm exercise at 25% maximal voluntary contraction for 30 min as we measured MSNA (microneurography). We observed progressive increases in MSNA with a peak increase of 161 units from a baseline value of 180 units. We also performed posthandgrip circulatory arrest (PHG-CA) in nine of these subjects. This maneuver isolates the metaboreceptor contribution to MSNA. During PHG-CA, delta MSNA values were not different from those observed during a freely perfused recovery period (n = 7). We also compared MSNA responses during the rhythmic paradigm with those seen during a static protocol at 40% of maximal voluntary contraction in five subjects. The two types of exercise caused similar increases in MSNA, but only the static paradigm was associated with a sustained MSNA response during PHG-CA. Finally, 31P-nuclear magnetic resonance was used to evaluate muscle metabolic responses during rhythmic and static forearm exercise (n = 6). Static exercise caused muscle acidosis and an increase in H2PO4-, whereas rhythmic exercise had no effect on muscle metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Modification of forearm resistance vessels by exercise training in young men.

The aim of this study was to determine whether a 4-wk handgrip training program would elicit changes in endothelium-dependent and endothelium-independent vasodilatation in resistance vessels of the human forearm. Minimum vascular resistance after a 10-min ischemic stimulus, an index of peak vasodilator capacity, was also determined. Forearm blood flow response to the endothelium-dependent vasodilator methacholine chloride did not change over the 4-wk-intervention period either in the group undertaking training (n = 11) or in control subjects (n = 6). Similarly, the response to sodium nitroprusside was not influenced by the handgrip training program. Peak vasodilator capacity of the trained forearms significantly increased, whereas no change was evident in the untrained limbs. These results suggest that 4 wk of forearm exercise training enhances peak vasodilator capacity of the vasculature without influencing stimulated activity of the nitric oxide dilator system.

Adult↗
PubMed1997

Effects of supplemental oxygen on forearm vasodilation in humans.

Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 +/- 7.9 vs. 47.8 +/- 6.7 ml.min-1.100 ml-1; P < 0.02; vascular resistance 1.7 +/- 0.2 vs. 2.4 +/- 0.4 mmHg.min.100 ml.ml-1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; -30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2 raised minimal resistance (2.3 +/- 0.4 RA; 2.8 +/- 0.5 O2+LBNP+VC, P < 0.04). When O2 alone (experiment 1) was compared with O2+LBNP+VC (experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

Adult↗
PubMed1998

Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction.

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eight adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to approximately 20% maximal voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 120 mmHg for a 1-s period, then released as a simulation of the mechanical effect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscarinic blockade with atropine; and 3) after NO synthase inhibition with NG-monomethyl-L-arginine (L-NMMA) plus atropine. Forearm blood flow (FBF), measured by combined pulsed and echo Doppler ultrasound, was reduced at rest with L-NMMA-atropine compared with the other two conditions. After the single contraction, there were no effects of atropine, but L-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereas L-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation that L-NMMA reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of the hyperemia with exercise. It is unlikely that ACh and NO from the endothelium are involved in the dilator response to a single muscle contraction.

Acetylcholine↗
PubMed2001

Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm.

We tested the hypothesis that increases in forearm blood flow (FBF) during the adaptive phase at the onset of moderate exercise would allow a more rapid increase in muscle O2 uptake (VO2 mus). Fifteen subjects completed forearm exercise in control (Con) and leg occlusion (Occ) conditions. In Occ, exercise of ischemic calf muscles was performed before the onset of forearm exercise to activate the muscle chemoreflex evoking a 25-mmHg increase in mean arterial pressure that was sustained during forearm exercise. Eight subjects who increased FBF during Occ compared with Con in the adaptation phase by >30 ml/min were considered "responders." For the responders, a higher VO2 mus accompanied the higher FBF only during the adaptive phase of the Occ tests, whereas there was no difference in the baseline or steady-state FBF or VO2 mus between Occ and Con. Supplying more blood flow at the onset of exercise allowed a more rapid increase in VO2 mus supporting our hypothesis that, at least for this type of exercise, O2 supply might be limiting.

Adult↗
PubMed2005

Selective alpha2-adrenergic properties of dexmedetomidine over clonidine in the human forearm.

We tested the hypothesis that dexmedetomidine (Dex) has greater alpha(2)- vs. alpha(1) selectivity than clonidine and causes more alpha(2)-selective vasoconstriction in the human forearm. After local beta-adrenergic blockade with propranolol, forearm blood flow (plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine (alpha(1)-agonist) were determined in healthy young adults before and after alpha(2)-blockade with yohimbine (n = 10) or alpha(1)-blockade with prazosin (n = 9). Yohimbine had no effect on phenylephrine-mediated vasoconstriction but blunted Dex-mediated vasoconstriction (mean +/- SE: -41 +/- 5 vs. -11 +/- 2%; before vs. after yohimbine) more than clonidine-mediated vasoconstriction (-39 +/- 5 vs. -28 +/- 4%; before vs. after yohimbine) (P < 0.02). Prazosin blunted phenylephrine-mediated vasoconstriction (-39 +/- 4 vs. -8 +/- 2%; before vs. after prazosin) but had similar effects on both Dex- (-30 +/- 4 vs. -39 +/- 6%; before vs. after prazosin) and clonidine-mediated vasoconstriction (-29 +/- 3 vs. -41 +/- 7%; before vs. after prazosin) (P > 0.7). Both Dex and clonidine reduced deep forearm venous norepinephrine concentrations to a similar extent (-59 +/- 12 vs. -55 +/- 10 pg/ml; Dex vs. clonidine, P > 0.6); this effect was abolished by yohimbine and blunted by prazosin. These results suggest that Dex causes more alpha(2)-selective vasoconstriction in the forearm than clonidine. The similar vasoconstrictor responses to both drugs after prazosin might be explained by the presynaptic effects on norepinephrine release.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2005

External compression increases forearm perfusion.

Application of compression stockings to the lower extremities is a widely used therapeutic intervention to improve venous return, but there is little information about the effects of compression on local arterial perfusion. Therefore, we tested the hypothesis that a positive external pressure increases forearm perfusion. The relation of increasing external pressure induced by standardized compression to the arterial inflow and arterial flow reserve of the forearm was critically evaluated in a group of healthy young men (n = 9). Flow was measured with venous occlusion plethysmography after a 10-min application of six different stockings with compression pressure increasing from 13 to 23 mmHg. During compression, the arterial inflow increased significantly from 3.7 +/- 0.85 to 8.8 +/- 2.01 ml.min(-1).100 ml tissue(-1) (P < 0.001) and the arterial flow reserve increased from 17.7 +/- 4.7 to 28.3 +/- 7.0 ml.min(-1).100 ml tissue(-1). The flow increase was persistent after 3 h of constant application of external pressure and also during simultaneous low-intensity hand grip. Similar results obtained with occlusion plethysmography were seen with MRI. During the interventions, forearm temperature was unchanged, and the volunteers reported no discomfort. In conclusion, 1) arterial perfusion of the human forearm increases more than twofold during application of external compression over a pressure range of 13-23 mmHg, and 2) the result is interpreted as an autoregulatory response following the decrease of the vascular transmural pressure gradient.

Adult↗
PubMed2004

Evidence of sustained forearm vasodilatation after brief isocapnic hypoxia.

Healthy subjects exposed to 20 min of hypoxia increase ventilation and muscle sympathetic nerve activity (MSNA). After return to normoxia, although ventilation returns to baseline, MSNA remains elevated for up to an hour. Because forearm vascular resistance is not elevated after hypoxic exposure, we speculated that the increased MSNA might be a compensatory response to sustained release of endogenous vasodilators. We studied the effect of isocapnic hypoxia (mean arterial oxygen saturation 81.6 +/- 4.1%, end-tidal Pco2 44.7 +/- 6.3 Torr) on plethysmographic forearm blood flow (FBF) in eight healthy volunteers while infusing intra-arterial phentolamine to block local alpha-receptors. The dominant arm served as control. Forearm arterial vascular resistance (FVR) was calculated as the mean arterial pressure (MAP)-to-FBF ratio. MAP, heart rate (HR), and FVR were reported at 5-min intervals at baseline, then while infusing phentolamine during room air, isocapnic hypoxia, and recovery. Despite increases in HR during hypoxia, there was no change in MAP throughout the study. By design, FVR decreased during phentolamine infusion. Hypoxia further decreased FVR in both forearms. With continued phentolamine infusion, FVR after termination of the exposure (17.47 +/- 6.3 mmHg x min x ml(-1) x 100 ml of tissue) remained lower than preexposure baseline value (23.05 +/- 8.51 mmHg x min x ml(-1) x 100 ml of tissue; P < 0.05). We conclude that, unmasked by phentolamine, the vasodilation occurring during hypoxia persists for at least 30 min after the stimulus. This vasodilation may contribute to the sustained MSNA rise observed after hypoxia.

Adult↗
PubMed2004

Evidence for a rapid vasodilatory contribution to immediate hyperemia in rest-to-mild and mild-to-moderate forearm exercise transitions in humans.

Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the present study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition, where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction), rhythmic, dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% maximal voluntary contraction) in each of arm above (condition A) or below (condition B) heart level. Beat-by-beat measures of brachial arterial blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions (condition A: E-E, 52.8 +/- 10.7 vs. R-E, 60.3 +/- 11.7 ml.min(-1).100 mmHg(-1), P = 0.66; condition B: E-E, 43.2 +/- 12.8 vs. R-E, 33.9 +/- 8.2 ml.min(-1).100 mmHg(-1), P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first nine contraction-relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in R-E and E-E transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.

Adaptation, Physiological↗
PubMed2004

[Capillary blood sample for type 2 diabetes screening: fingertip versus forearm].

BACKGROUND AND OBJECTIVE: In Spain, around 50% of diabetic mellitus cases remain undiagnosed. Capillary blood puncture improves the diabetes screening accessibility. New test strips used in the Blood Glucose Monitoring System allow fingertip and forearm punctures yet they create the dilemma on what is the best anatomic place. PATIENTS AND METHOD: We compared fingertip and forearm capillary blood glucose determinations. RESULTS: In a sample of 107 patients, a 110 mg/dl cut-off point for the fingertip and 125 mg/dl for the forearm were more sensitive. Patient's preferences were as follows: 67% indifferent, 28% forearm and 5% fingertip. CONCLUSIONS: In this study, the best anatomic site for puncture depended on the cut-off point used in diabetes screening.

Aged↗
PubMedDate not supplied

Mg(2+)-induced vasodilation in human forearm vasculature is inhibited by N(G)-monomethyl-L-arginine but not by indometacin.

We have investigated the mechanism of the vasodilator action of Mg(2+) in human forearm resistance vasculature. Venous occlusion plethysmography was used to measure vasodilator responses to Mg(2+) infused via the brachial artery in healthy men, and to determine effects on Mg(2+) responses of indometacin (an inhibitor of cyclo-oxygenase) and of N(G)-monomethyl-L-arginine (L-NMMA, an inhibitor of the L-arginine/nitric oxide, L-arg/NO, pathway). Magnesium sulphate infusion (0.05, 0.1, 0.2 mmol x min(-1)) increased plasma Mg(2+) concentration to 1.57+/-0.16 mmol x l(-1) in venous blood from the infused arm at the highest dose. There was a dose-related increase in forearm blood flow in the infused arm to a maximum of 6.37+/-1.37 ml x min(-1) x dl forearm(-1) at the highest dose corresponding to an increase of 159+/-25% in blood flow relative to the non-infused arm. There was no tachyphylaxis during a second infusion following a 21-min recovery period. Indometacin had no effect on vasodilator responses to Mg(2+), whereas L-NMMA inhibited Mg(2+) responses (area under the dose-response curve) by 43+/-6% (p = 0.0003 by repeated-measures ANOVA). Therefore the L-arg/NO pathway is responsible, in part, for the vasodilator action of Mg(2+) in human forearm resistance vasculature.

Adult↗
PubMed1997

The influence of forearm, hand and thumb positions on extensor carpi ulnaris and abductor pollicis longus activity.

The objective of this study was to investigate the influence of forearm, hand and thumb positions on electromyography (EMG) activity of the abductor pollicis longus (APL) and the extensor carpi ulnaris (ECU) muscles. A second objective was to study the role of these muscles in stabilizing the wrist during movements of the thumb. This knowledge is important in clinical assessment and reconstructive surgery. At a constant force of 5 N for the thumb and 20 N for the hand, EMG activity was recorded with intramuscular wire electrodes in isometric and dynamic contractions in different positions and movements in the thumb and the hand. EMG activity of the right hand of 7 subjects was scaled relative to the mean EMG value at maximum voluntary isometric contraction to compare relative muscle activity in the tests. The results show that the position of the forearm does influence activity of the APL, but not of the ECU. The deep part of the APL shows differences in EMG activity between the positions of the forearm in dorsal flexion of the hand and the superficial part of the APL in palmar flexion of the hand. The ECU and the deep part of the APL are very active during movements and isometric contractions of the thumb. It is suggested that these muscles are necessary to stabilize the wrist during movements of the thumb to prevent undesired movements of the hand and the forearm.

Adult↗