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 865 records · Page 48Linked to original sources
PubMed1991

Potent vasoconstrictor effects and clearance of endothelin in the human forearm.

The vascular effects of endothelin-1 in humans were investigated by infusion into the brachial artery of healthy volunteers. Endothelin-1 (5-500 pmol min-1) evoked potent and long lasting increase in forearm vascular resistance (FVR) and reduction in venous compliance, suggesting constriction of both resistance and capacitance vessels. The threshold for effect on forearm vascular resistance was at a calculated plasma concentration of 614 pmol 1-1. Endothelin-1 was on a molar basis 10-20 times more potent than noradrenaline as constrictor of both resistance and capacitance vessels. The increase in forearm vascular resistance induced by endothelin-1 lasted more than 30 min and that by noradrenaline less than 3 minutes. The endothelin-1-like immunoreactivity collected in the venous effluent during the infusion was 10-26% of the calculated arterial plasma concentration, indicating local removal of endothelin. After the infusion of endothelin-1 the urine concentration of prostacyclin metabolite increased significantly, indicating release of prostacyclin, whereas the concentration of thromboxane metabolite did not increase. It is concluded that endothelin-1 is a highly potent constrictor of human resistance and capacitance vessels, that it causes release of prostacyclin and that circulating endothelin-1 is efficiently removed by the forearm in vivo.

Adult↗
PubMed2005

Effects of handgrip training and intermittent compression of upper arm veins on forearm vessels in patients with end-stage renal failure.

The purpose of our study was to assess the influence of handgrip training and intermittent compression of the upper arm veins on forearm arteries and veins. Eighteen chronic hemodialysis patients performed daily handgrip training for 8 weeks using a rubber ring, together with daily intermittent compression of the upper arm veins by elastic band. The forearm circumference, maximal handgrip strength, and arterial and vein parameters, including endothelium-dependent vasodilatation, were measured at the beginning, and after 4 and 8 weeks (using ultrasound scanning). The maximal handgrip strength and forearm circumference increased significantly. The radial artery diameters were significantly higher after 8 weeks of training (1.89 mm +/- 0.10 at the beginning, 1.95 +/- 0.10 mm after 8 weeks, P = 0.007), and endothelium-dependent vasodilatation was also found to be increased after 4 and 8 weeks of both activities. The venous parameters before tourniquet placement increased significantly after 8 weeks (2.40 +/- 0.16 mm at the beginning, 2.62 +/- 0.17 mm after 8 weeks, P = 0.014), and the venous parameters after tourniquet placement increased significantly after 4 and 8 weeks (3.36 +/- 0.17 mm at the beginning, 3.51 +/- 0.18 mm after 4 weeks, P = 0.009), 3.68 +/- 0.18 mm after 8 weeks, P < 0.001). The distensibility of veins was preserved. Our results showed that handgrip training and intermittent compression of the upper arm veins, performed daily, increase the diameter of forearm arteries and veins and improve endothelium-dependent vasodilatation.

Adolescent↗
PubMed1972

An estimate of adenosine triphosphate release into the venous effluent from exercising human forearm muscle.

1. Human subjects performed a sustained contraction of the forearm muscles for 4 min in the presence of arterial and venous occlusion.2. The contraction was maintained at 5% of the maximum voluntary contraction, a tension during which the muscle blood flow might be expected to increase by about three times (Lind & McNicol, 1967).3. Adenosine triphosphate (ATP) was identified in the venous effluent from occluded exercising forearm, but not in the venous effluent from occluded forearm without exercise.4. The rate of degradation of ATP was assessed in plasma at 37 degrees C, with an estimate of the percentage loss occurring between sampling and testing. This enabled the rate of appearance of ATP in the blood at the time of exercise to be calculated as approximately 7.5-10.5 mug/min (14-20 n-mole/min). These amounts are compared with 16 mug/min that was infused intra-arterially into human forearm to cause a threefold increase in blood flow (Duff, Patterson & Shepherd, 1954).5. It is likely that the ATP detected in the venous effluent has active muscle as the source; if so, then the amounts calculated to be released could satisfy the vasodilator requirements of active skeletal muscle.6. The effects of circulating ATP on respiration and coronary blood flow during exercise is discussed, including the role it may play locally in the production of ischaemic pain.

Adenosine Triphosphate↗
PubMed1976

Effect of regional alpha- and beta-adrenergic blockade on blood flow in the resting forearm during contralateral isometric handgrip.

In a previous study we have shown that an isometric handgrip is accompanied by a rapid decrease in vascular resistance in the resting (contralateral) forearm, lasting for about 1 min, which in all probability is neurogenic. 2. In the present study the distribution of the vasodilatation was investigated by analysing O2 saturation in a deep vein, draining mainly muscle tissue. Some possible neurogenic mechanisms for the vasodilatation were tested by repeating the handgrip after local beta- and alpha-adrenergic blockade of the resting forearm with propranolol and phentolamine, respectively. 3. Without blockades the forearm vascular resistance decreased and the deep vein O2 saturation increase to similar degrees on contralateral handgrip. Propranolol markedly reduced both the decrease in resistance and the increase in deep vein O2 saturation. Phentolamine did not alter the initial decrease in resistance, but with phentolamine resistance continued to decrease after 1 min. 4. It is concluded that the rapid decrease in vascular resistance in the resting forearm on contralateral handgrip takes place, to a great extent, in muscle. It is mediated by neurogenic beta-adrenergic mechanisms and if the contraction is prolonged it gradually changes to a vasoconstriction mediated by alpha-adrenergic mechanisms.

Adult↗
PubMed1988

Instability in human forearm movements studied with feed-back-controlled electrical stimulation of muscles.

1. Amplitude-modulated electrical stimulation was applied to the elbow flexors and extensors to produce movements of the forearm in normal subjects. The parameters of the modulating (command) signal were set in isometric trials so as to produce equal and opposite background torques, and equal and supportive torque modulations. 2. Bode plots relating forearm movement to command signal (modulating) frequency showed the muscle-load to have a low-pass characteristic similar to that previously described in the cat, and a slightly larger bandwidth than described previously in man. 3. The transduced forearm signals were fed back to provide the command signal to the stimulators via a filter which mimicked the transfer function of muscle spindle primary endings. In effect this replaced the neural part of the reflex arc with an accessible model, but left the muscle-load effector intact. 4. All six subjects developed forearm oscillations (tremor) when the loop gain exceeded a threshold value. The mean tremor frequency at onset was 4.4 Hz, which was similar to that of the equivalent vibration-evoked tremor (previous paper, Prochazka & Trend, 1988). 5. With the linear spindle model, oscillations tended to grow rapidly in amplitude, and the stimuli became painful. The inclusion of a logarithmic limiting element resulted in stable oscillations, without significant alterations in frequency. This allowed us to study the effect on tremor of including analog delays in the loop, mimicking those associated with peripheral nerve transmission and central reflexes. In one subject, loop delays of 0, 20, 40 and 100 ms resulted in tremor at 4.0, 3.6, 3.0 and 2.1 Hz respectively, as quantified by spectral analysis. 6. By considering separately the phase contributions of the different elements of the reflex arc, including delays, it became clear that muscle-load properties were important in setting the upper limit of tremor frequencies which could conceivably be supported by reflexes. 7. The results support the conclusion of the related vibration study (Prochazka & Trend, 1988), that for moderate levels of background co-contraction, the contribution of stretch reflexes to tremor at the elbow should be sought in the 3-5 Hz range. Exaggerated long-latency reflexes would be expected to reduce these baseline frequencies by 1 or 2 Hz.

Adult↗
PubMed2003

Failure of systemic hypoxia to blunt alpha-adrenergic vasoconstriction in the human forearm.

Systemic hypoxia in humans evokes forearm vasodilatation despite significant reflex increases in sympathetic vasoconstrictor nerve activity and noradrenaline spillover. We sought to determine whether post-junctional alpha-adrenergic vasoconstrictor responsiveness to endogenous noradrenaline release is blunted during systemic hypoxia. To do so, we conducted a two-part study in healthy young adults. In protocol 1, we measured forearm blood flow (FBF; venous occlusion plethysmography) and calculated the vascular conductance (FVC) responses to brachial artery infusions of two doses of tyramine (evokes endogenous noradrenaline release) in 10 adults during normoxia and mild systemic hypoxia (85 % O2 saturation; pulse oximetry of the earlobe). Systemic hypoxia evoked significant forearm vasodilatation as indicated by the increases in FBF and FVC (approximately 20-23 %; P < 0.05). The low and high doses of tyramine evoked significant reductions in FVC (vasoconstriction) that were similar in magnitude during normoxia (-29 +/- 3 and -53 +/- 4 %) and mild hypoxia (-35 +/- 4 and -58 +/- 3 %; P = 0.33). In protocol 2, forearm vasoconstrictor responses to the high dose of tyramine were determined in eight young adults during normoxia and during graded levels of systemic hypoxia (85, 80 and 75 % O2 saturation). The reductions in FVC were similar during normoxia (-59 +/- 2 %) and the three levels of hypoxia (85 % O2 saturation, -64 +/- 3 %; 80 % O2 saturation, -62 +/- 1 %; 75 % O2 saturation, -61 +/- 3 %; P = 0.37). In both protocols, the tyramine-induced increases in deep venous noradrenaline concentrations were similar during normoxia and all levels of hypoxia. Our results demonstrate that post-junctional alpha-adrenergic receptor vasoconstrictor responsiveness to endogenous noradrenaline release is not blunted during mild-to-moderate systemic hypoxia in healthy humans.

Adult↗
PubMed2004

Local inhibition of nitric oxide and prostaglandins independently reduces forearm exercise hyperaemia in humans.

We tested the hypothesis that inhibition of synthesis of either nitric oxide (NO) or vasodilating prostaglandins (PGs) would not alter exercise hyperaemia significantly, but combined inhibition would synergistically reduce the hyperaemia. Fourteen subjects performed 20 min of moderate rhythmic forearm exercise (10% maximal voluntary contraction). Forearm blood flow (FBF) was measured by Doppler ultrasound. Saline or study drugs were infused (2 ml x min(-1)) into the forearm via a brachial artery catheter to locally inhibit synthesis of NO and PGs during steady state exercise (N(G)-nitro-L-arginine methyl ester (L-NAME), 25 mg over 5 min to inhibit NO synthase (NOS); and ketorolac, 3 mg over 5 min to inhibit cyclooxygenase (COX)). After achieving steady state exercise over 5 min (control), L-NAME was infused for 5 min, followed by 2 min saline, then by a 5 min infusion of ketorolac, and finally by 3 min of saline (n= 7). Drug order was reversed in seven additional subjects, such that single inhibition of NOS or COX was followed by combined inhibition. FBF during exercise decreased to 83 +/- 2% of control exercise (100%) with NOS inhibition, followed by a transient decrease to 68 +/- 2% of control during COX inhibition. However, FBF returned to levels similar to those achieved during NOS inhibition within 2 min (80 +/- 3% of control) and remained stable through the final 3 min of exercise. When COX inhibition was performed first, FBF decreased transiently to 88 +/- 4% of control (P < 0.01), and returned to control saline levels by the end of ketorolac infusion. Addition of L-NAME reduced FBF to 83 +/- 3% of control, and it remained stable through to the end of exercise. Regardless of drug order, FBF was approximately 80% of steady state control exercise (P < 0.01) during the last 30 s of exercise. We conclude that (1). NO provides a significant, consistent contribution to hyperaemia, (2). PGs contribute modestly and transiently, suggesting a redundant signal compensates for the loss of vasodilating PGs, and (3). NO and PG signals appear to contribute independently to forearm exercise hyperaemia.

Adult↗
PubMed2006

A model of stress and strain in the interosseous ligament of the forearm based on fiber network theory.

Fiber network theory was developed to describe cloth, a thin material with strength in the fiber directions. The interosseous ligament (IOL) of the forearm is a broad, thin ligament with highly aligned fibers. The objectives of this study were to develop a model of the stress and strain distributions in the IOL, based on fiber network theory, to compare the strains from the model with the experimentally measured strains, and to evaluate the force distribution across the ligament fibers from the model. The geometries of the radius, ulna, and IOL were reconstructed from CT scans. Position and orientation of IOL insertion sites and force in the IOL were measured during a forearm compression experiment in pronation, neutral rotation, and supination. An optical image-based technique was used to directly measure strain in two regions of the IOL in neutral rotation. For the network model, the IOL was represented as a parametric ruled three-dimensional surface, with rulings along local fiber directions. Fiber strains were calculated from the deformation field, and fiber stresses were calculated from the strains using average IOL tensile properties from a previous study. The in situ strain in the IOL was assumed uniform and was calculated so that the net force predicted by the network model in neutral rotation matched the experimental result. The net force in the IOL was comparable to experimental results in supination and pronation. The model predicted higher stress and strain in fibers near the elbow in neutral rotation, and higher stresses in fibers near the wrist in supination. Strains in neutral forearm rotation followed the same trends as those measured experimentally. In this study, a model of stress and strain in the IOL utilizing fiber network theory was successfully implemented. The model illustrates variations in the stress and strain distribution in the IOL. This model can be used to show surgeons how different fibers are taut in different forearm rotation positions-this information is important for understanding the biomechanical role of the IOL and for planning an IOL reconstruction.

Adult↗
PubMed2004

Evaluation of physiological standard pressures of the forearm flexor muscles during sport specific ergometry in sport climbers.

BACKGROUND: Chronic exertional compartment syndromes (CECS) are well known in sports medicine. Most commonly affected is the tibialis anterior muscle compartment in runners and walkers. Only a few cases of CECS of the forearm flexor muscles have been reported. OBJECTIVES: To determine pressure levels inside the deep flexor compartment of the forearms during a sport specific stress test. METHOD: Ten healthy, high level climbers were enrolled in a prospective study. All underwent climbing specific ergometry, using a rotating climbing wall (step test, total climbing time 9-15 minutes). Pressure was measured using a slit catheter placed in the deep flexor compartment of the forearm. Pressure, blood lactate, and heart rate were recorded every three minutes and during recovery. RESULTS: In all the subjects, physical exhaustion of the forearms defined the end point of the climbing ergometry. Blood lactate increased with physical stress, reaching a mean of 3.48 mmol/l. Compartment pressure was related to physical stress, exceeding 30 mm Hg in only three subjects. A critical pressure of more than 40 mm Hg was never observed. After the test, the pressure decreased to normal levels within three minutes in seven subjects. The three with higher pressure levels (>30 mm Hg) required a longer time to recover. CONCLUSIONS: For further clinical and therapeutic consequences, an algorithm was derived. Basic pressure below 15 mm Hg and stress pressure below 30 mm Hg as well as pressures during the 15 minute recovery period below 15 mm Hg are physiological. Pressures of 15-30 mm Hg during recovery suggest high risk of CECS, and pressures above 30 mm Hg confirm CECS.

Adolescent↗
PubMed1996

Risk factors, falls, and fracture of the distal forearm in Manchester, UK.

OBJECTIVE: To determine the risk factors associated with fracture of the distal forearm, and to evaluate the influence of falls on these risks. DESIGN: This was a case-control study. SETTING: Manchester, UK. PARTICIPANTS: The cases were 62 white women aged 45-82 years who had sustained a fracture of the distal forearm and had attended local hospitals. Two control groups were studied - 50 women who had fallen onto the hand but had not sustained a fracture (recruited from the same source as those with fracture) and 116 women randomly selected from primary care age and sex registers in the catchment area of the hospitals. Both cases and controls were sent a letter inviting them to take part in the study. Data were collected by questionnaire completed by an interviewer. MAIN RESULTS: Compared with the population control group, those with fracture were more likely to walk at a brisk pace (odds ratio (OR) = 3.5; 95% confidence interval (CI) 1.3, 9.6) though they had undertaken less physical activity at home or work on a daily basis throughout life (OR = 0.4; 95% CI 0.2, 0.9). The risk associated with brisk walking was less marked when the cases were compared with fall controls. Other lifestyle factors including calcium intake, smoking, and alcohol consumption were not associated with fracture. Analysis of gynaecological and hormonal factors suggested that compared with population controls, those with fracture of the distal forearm had had fewer fertile years (OR = 0.4; 95% CI 0.1, 0.9) and were less likely to have used oral contraceptives (OR = 0.3; 95% CI 0.1, 0.9). CONCLUSIONS: The data highlight the need for caution when advising middle aged and elderly subjects about exercise. Such advice should be combined with practical information about the prevention of falls. Hormonal factors seem to be additional determinants of fracture. Other lifestyle interventions seem unlikely to play an important part in preventing distal forearm fracture.

Accidental Falls↗
PubMed2001

Forearm vasoreactivity in type 1diabetic subjects.

This study compared forearm vasoreactivity in 15 Type I diabetic subjects with 15 healthy controls. The groups were matched for age, exercise capacity, and the absence of other cardiovascular risk factors. Vasoreactivity was measured using strain gauge plethysmography, at rest, after arterial occlusion (OCC), and following OCC coupled with handgrip exercise (ROCC). Forearm blood flows were significantly elevated between conditions 2.58 +/- 0.37ml/100mltissue at rest to 26.80 +/- 6.56 after OCC and 32.80 +/- 8.26ml/100mltissue following ROCC in Type I diabetic subjects. There were no differences in forearm blood flow between groups for any of the conditions. These data indicate the degree of forearm blood flow is directly related to the intensity of the vasodilatory stimulus. However, our study did not reveal evidence of impaired vasodilatory capacity in Type I diabetic subjects compared to controls in the absence of other risk factors.

Adult↗
PubMed2003

Forearm vascular control during acute hyperglycemia in healthy humans.

The vascular endothelium is a site of pathological changes in patients with diabetes mellitus that may be related to severe chronic hyperglycemia. However, it is unclear whether transient hyperglycemia alters vascular function in an otherwise healthy human forearm. To test the hypothesis that acute, moderate hyperglycemia impairs endothelium-dependent forearm vasodilation, we measured vasodilator responses in 25 healthy volunteers (11 F, 14 M) assigned to one of three protocols. In protocol 1, glucose was varied to mimic a postprandial pattern (i.e., peak glucose approximately 11.1 mmol/l) commonly observed in individuals with impaired glucose tolerance. Protocol 2 involved 6 h of mild hyperglycemia (approximately 7 mmol/l). Protocol 3 involved 6 h of euglycemia. Glucose concentration was maintained with a variable systemic glucose infusion. Insulin concentrations were maintained at approximately 65 pmol/l by means of a somatostatin and "basal" insulin infusion. Glucagon and growth hormone were replaced at basal concentrations. Forearm blood flow (FBF) was calculated from Doppler ultrasound measurements at the brachial artery. In each protocol, FBF dose responses to intrabrachial acetylcholine (ACh) and sodium nitroprusside (NTP) were assessed at baseline and at 60, 180, and 360 min of glucose infusion. Peak endothelium-dependent vasodilator responses to ACh were not diminished by hyperglycemia in any trial. For example, peak responses to ACh during protocol 2 were 307 +/- 47 ml/min at euglycemic baseline and 325 +/- 52, 353 +/- 65, and 370 +/- 70 ml/min during three subsequent hyperglycemic trials (P = 0.46). Peak endothelium-independent responses to NTP infusion were also unaffected. We conclude that acute, moderate hyperglycemia does not cause short-term impairment of endothelial function in the healthy human forearm.

Adaptation, Physiological↗
PubMed1991

Effect of glycemia and nonesterified fatty acids on forearm glucose uptake in normal humans.

The purpose of this study was to examine the effect of physiological plasma nonesterified fatty acid (NEFA) levels on insulin-stimulated forearm and whole body glucose uptake and substrate oxidation during euglycemia and hyperglycemia. Seven healthy men received Intralipid and heparin for 210 min in two studies, with saline as control in two further studies. Insulin (0.05 U.kg-1.h-1) was infused from 60 min, and euglycemia was maintained during lipid (EL) and control (EC) studies, and hyperglycemia was maintained in the other studies (HL and HC). Forearm NEFA uptake was comparable in the lipid studies (+61 +/- 10 and +52 +/- 8 nmol.100 ml forearm-1.min-1, EL and HL) and was suppressed in the controls. With Intralipid, forearm glucose uptake decreased during euglycemia but not during hyperglycemia (+3.85 +/- 0.34 vs. +3.34 +/- 0.25 mumol.100 ml forearm-1.min-1, EC vs. EL, P less than 0.02), with comparable changes in whole body glucose uptake. Glucose oxidation and forearm alanine release decreased with Intralipid at both blood glucose levels, with no significant change in the rates of nonoxidative glucose disposal. These observations support the operation of the glucose-fatty acid cycle at physiological plasma NEFA levels at both blood glucose concentrations, but this was associated with a decrease in peripheral insulin sensitivity only during euglycemia.

Adult↗
PubMed1992

Thermogenic response to epinephrine in the forearm and abdominal subcutaneous adipose tissue.

Whole body energy expenditure, thermogenic and metabolic changes in the forearm, and intercellular glucose concentrations in subcutaneous adipose tissue on the abdomen determined by microdialysis were measured during epinephrine infusion in healthy subjects. After a control period, epinephrine was infused at rates of 0.2 and 0.4 nmol.kg-1 x min-1. Whole body resting energy expenditure was 4.36 +/- 0.56 (SD) kJ/min. Energy expenditure increased to 5.14 +/- 0.74 and 5.46 +/- 0.79 kJ/min, respectively (P < 0.001), during the epinephrine infusions. Respiratory exchange ratio was 0.80 +/- 0.04 in the resting state and did not change. Local forearm oxygen uptake was 3.9 +/- 1.3 mumol.100 g-1 x min-1 in the basal period. During epinephrine infusion, it increased to 5.8 +/- 2.1 (P < 0.03) and 7.5 +/- 2.3 mumol.100 g-1 x min-1 (P < 0.001). Local forearm glucose uptake was 0.160 +/- 0.105 mumol.100 g-1 x min-1 and increased to 0.586 +/- 0.445 and 0.760 +/- 0.534 mumol.100 g-1 x min-1 (P < 0.025). The intercellular glucose concentration in the subcutaneous adipose tissue on the abdomen was equal to the arterial concentration in the basal period but did not increase as much during infusion of epinephrine, indicating glucose uptake in adipose tissue in this condition. If it is assumed that forearm skeletal muscle is representative for the average skeletal muscle, it can be calculated that on average 40% of the enhanced whole body oxygen uptake induced by infusion of epinephrine is taking place in skeletal muscle. It is proposed that adipose tissue may contribute to epinephrine-induced thermogenesis.

Abdomen↗
PubMed1995

A model of skeletal muscle leucine kinetics measured across the human forearm.

We propose a new six-compartment model of intracellular muscle kinetics of leucine and of its transamination product alpha-ketoisocaproic acid (KIC) by combining systemic tracer infusions of [14C]- and [15N]leucine with the arterial-deep venous catheterization of the human forearm. Venous [14C]KIC specific activity (SA) is taken as representative of intracellular [14C]leucine SA, whereas net [15N]leucine disposal is used to calculate leucine inflow and outflow across forearm cell membrane(s). In post-absorptive normal subjects, model-derived rates of intracellular leucine release from and incorporation into protein were approximately 32% (P = 0.03) and approximately 37% greater (P = 0.025), respectively, than those calculated using a conventional arteriovenous approach. Forearm fasting proteolysis exceeded protein synthesis (P < 0.025), whereas leucine oxidation was greater than zero (P < 0.01), suggesting a net negative leucine (i.e., protein) balance. Leucine inflow from blood to cell represented approximately 30% of arterial leucine delivery; therefore approximately 70% of arterial leucine bypassed intracellular metabolism. This model provides a comprehensive description of regional leucine and KIC kinetics and new estimates of protein degradation and synthesis across the human forearm.

Adult↗
PubMed1998

Extreme hyperinsulinemia unmasks insulin's effect to stimulate protein synthesis in the human forearm.

Insulin clearly stimulates skeletal muscle protein synthesis in vitro. Surprisingly, this effect has been difficult to reproduce in vivo. As in vitro studies have typically used much higher insulin concentrations than in vivo studies, we examined whether these concentration differences could explain the discrepancy between in vitro and in vivo observations. In 14 healthy volunteers, we raised forearm insulin concentrations 1,000-fold above basal levels while maintaining euglycemia for 4 h. Amino acids (AA) were given to either maintain basal arterial (n = 4) or venous plasma (n = 6) AA or increment arterial plasma AA by 100% (n = 4) in the forearm. We measured forearm muscle glucose, lactate, oxygen, phenylalanine balance, and [3H]phenylalanine kinetics at baseline and at 4 h of insulin infusion. Extreme hyperinsulinemia strongly reversed postabsorptive muscle's phenylalanine balance from a net release to an uptake (P < 0.001). This marked anabolic effect resulted from a dramatic stimulation of protein synthesis (P < 0.01) and a modest decline in protein degradation. Furthermore, this effect was seen even when basal arterial or venous aminoacidemia was maintained. With marked hyperinsulinemia, protein synthesis increased further when plasma AA concentrations were also increased (P < 0.05). Forearm blood flow rose at least twofold with the combined insulin and AA infusion (P < 0.01), and this was consistent in all groups. These results demonstrate an effect of high concentrations of insulin to markedly stimulate muscle protein synthesis in vivo in adults, even when AA concentrations are not increased. This is similar to prior in vitro reports but distinct from physiological hyperinsulinemia in vivo where stimulation of protein synthesis does not occur. Therefore, the current findings suggest that the differences in insulin concentrations used in prior studies may largely explain the previously reported discrepancy between insulin action on protein synthesis in adult muscle in vivo vs. in vitro.

Adult↗
PubMed2002

Effect of cardiac pacing on forearm vascular responses and nitric oxide function.

We examined the hypothesis that changes in heart rate at rest influence bioactivity of nitric oxide (NO) in humans by examining forearm blood flow responses during cardiac pacing in six subjects. Peak forearm and mean forearm blood flows across the cardiac cycle were continuously recorded at baseline and during pacing, with the use of high-resolution brachial artery ultrasound and Doppler flow velocity measurement. The brachial artery was cannulated to allow continuous infusion of saline or N(G)-monomethyl-L-arginine (L-NMMA). As heart rate increased, no changes in pulse pressure and mean or peak blood flow were evident. L-NMMA had no effect on brachial artery diameter, velocity, or flows compared with saline infusion. These results contrast with our recent findings that exercise involving the lower body, associated with increases in heart rate and pulse pressure, also increased forearm blood flow, the latter response being diminished by L-NMMA. These data suggest that changes in blood pressure, rather than pulse frequency, may be the stimulus for shear stress-mediated NO release in vivo.

Blood Pressure↗
PubMed2000

Effects of forearm bier block with bretylium on the hemodynamic and metabolic responses to handgrip.

We tested the hypothesis that a reduction in sympathetic tone to exercising forearm muscle would increase blood flow, reduce muscle acidosis, and attenuate reflex responses. Subjects performed a progressive, four-stage rhythmic handgrip protocol before and after forearm bier block with bretylium as forearm blood flow (Doppler) and metabolic (venous effluent metabolite concentration and (31)P-NMR indexes) and autonomic reflex responses (heart rate, blood pressure, and sympathetic nerve traffic) were measured. Bretylium inhibits the release of norepinephrine at the neurovascular junction. Bier block increased blood flow as well as oxygen consumption in the exercising forearm (P < 0.03 and P < 0.02, respectively). However, despite this increase in flow, venous K(+) release and H(+) release were both increased during exercise (P < 0.002 for both indexes). Additionally, minimal muscle pH measured during the first minute of recovery with NMR was lower after bier block (6.41 +/- 0.08 vs. 6.20 +/- 0.06; P < 0.036, simple effects). Meanwhile, reflex effects were unaffected by the bretylium bier block. The results support the conclusion that sympathetic stimulation to muscle during exercise not only limits muscle blood flow but also appears to limit anaerobiosis and H(+) release, presumably through a preferential recruitment of oxidative fibers.

Adult↗