Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans

1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Time Course ◽  
Forearm Blood Flow ◽  
Voluntary Contraction ◽  
Double Blind ◽  
Rate Of Increase ◽  
Forearm Exercise ◽  
Blind Manner ◽  
Exercise In Humans

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.

scholarly journals Acute dietary nitrate supplementation does not augment submaximal forearm exercise hyperemia in healthy young men

2015 ◽  
Vol 40 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Jin-Kwang Kim ◽  
David J. Moore ◽  
David G. Maurer ◽  
Daniel B. Kim-Shapiro ◽  
Swati Basu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Young Men ◽  
Evidence Base ◽  
Beetroot Juice ◽  
Double Blind ◽  
Brachial Artery Diameter ◽  
Dietary Nitrate ◽  
Nitrate Supplementation ◽  
Forearm Exercise

Despite the popularity of dietary nitrate supplementation and the growing evidence base of its potential ergogenic and vascular health benefits, there is no direct information about its effects on exercising limb blood flow in humans. We hypothesized that acute dietary nitrate supplementation from beetroot juice would augment the increases in forearm blood flow, as well as the progressive dilation of the brachial artery, during graded handgrip exercise in healthy young men. In a randomized, double-blind, placebo-controlled crossover study, 12 young (22 ± 2 years) healthy men consumed a beetroot juice (140 mL Beet-It Sport, James White Juice Company) that provided 12.9 mmol (0.8 g) of nitrate or placebo (nitrate-depleted Beet-It Sport) on 2 study visits. At 3 h postconsumption, brachial artery diameter, flow, and blood velocity were measured (Doppler ultrasound) at rest and during 6 exercise intensities. Nitrate supplementation raised plasma nitrate (19.5-fold) and nitrite (1.6-fold) concentrations, and lowered resting arterial pulse wave velocity (PWV) versus placebo (all p < 0.05), indicating absorption, conversion, and a biological effect of this supplement. The supplement-associated lowering of PWV was also negatively correlated with plasma nitrite (r = –0.72, p = 0.0127). Despite these systemic effects, nitrate supplementation had no effect on brachial artery diameter, flow, or shear rates at rest (all p ≥ 0.28) or during any exercise workload (all p ≥ 0.18). These findings suggest that acute dietary nitrate supplementation favorably modifies arterial PWV, but does not augment blood flow or brachial artery vasodilation during nonfatiguing forearm exercise in healthy young men.

Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery

1997 ◽  
Vol 273 (5) ◽  
pp. H2388-H2395 ◽  
Author(s):  
J. K. Shoemaker ◽  
J. R. Halliwill ◽  
R. L. Hughson ◽  
M. J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Brachial Artery ◽  
Time Course ◽  
Forearm Blood Flow ◽  
Brachial Artery Diameter ◽  
Cholinergic Mechanism ◽  
Pulsed Doppler Ultrasound ◽  
Exercise Onset ◽  
Drug Treatments

The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + N G-monomethyl-l-arginine (l-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by ∼71% ( P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine +l-NMMA. Both drug conditions reduced FBF during exercise by ∼10% compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + l-NMMA. Total FBF during 5 min of recovery was reduced with atropine +l-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise.

Evidence for sympatholysis at the onset of forearm exercise

2002 ◽  
Vol 93 (2) ◽  
pp. 555-560 ◽  
Author(s):  
Darren S. DeLorey ◽  
Simon S. Wang ◽  
J. Kevin Shoemaker
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Voluntary Contraction ◽  
Dependent Manner ◽  
Vascular Conductance ◽  
Exercise Hyperemia ◽  
Forearm Vascular Conductance ◽  
Forearm Exercise ◽  
Handgrip Contractions

The effect of augmented sympathetic outflow on forearm vascular conductance after single handgrip contractions of graded intensity was examined to determine whether sympatholysis occurs early in exercise ( n = 7). While supine, subjects performed contractions that were 1 s in duration and 15, 30, and 60% of maximal voluntary contraction (MVC) in intensity. The contractions were repeated during control and lower body negative pressure (LBNP) (−40 mmHg) sessions. Forearm blood flow (FBF; Doppler ultrasound) and mean arterial pressure were measured continuously for 30 s before and 60 s after the single contractions. Vascular conductance (VC) was calculated. Total postcontraction blood flow increased in an exercise intensity-dependent manner. Compared with control, LBNP caused a reduction in baseline and postexercise FBF ( P < 0.05), VC ( P < 0.01), as well as total excess flow ( P < 0.01). Specifically, during LBNP, baseline FBF and VC were reduced by 29 and 34% of control, respectively ( P < 0.05). After the 15% MVC contraction, peak VC during LBNP was reduced by a magnitude similar to that during baseline (i.e., ∼30%), but it was only reduced by 15% during both the 30 and 60% MVC trials ( P < 0.01). It was concluded that the stimuli for exercise hyperemia during moderate and heavy, but not mild, handgrip exercise intensities, diminish the vasoconstrictor effects of LBNP. Furthermore, these data demonstrate that this sympatholysis occurs early in exercise.

scholarly journals α-Adrenergic control of blood flow during exercise: effect of sex and menstrual phase

2010 ◽  
Vol 109 (5) ◽  
pp. 1360-1368 ◽  
Author(s):  
Jacqueline K. Limberg ◽  
Marlowe W. Eldridge ◽  
Lester T. Proctor ◽  
Joshua J. Sebranek ◽  
William G. Schrage
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Voluntary Contraction ◽  
Follicular Phase ◽  
Menstrual Phase ◽  
Vascular Control ◽  
Adrenergic Control ◽  
Exercise Effect ◽  
Early Follicular Phase ◽  
Forearm Exercise

Sex differences exist in autonomic control of the cardiovascular system. This study was designed to directly test sex or female menstrual phase-related differences in α-adrenergic control of blood flow during exercise. We hypothesized that women would exhibit reduced α-adrenergic vasoconstriction compared with men during exercise; in addition, women would constrict less during the early luteal than the early follicular phase of the female menses. Young men ( n = 10) were studied once and women ( n = 9) studied twice, once during the early follicular phase and once during the early luteal phase of female menses. We measured forearm blood flow (FBF; Doppler ultrasound of the brachial artery) during rest and steady-state dynamic exercise (15 and 30% of maximal voluntary contraction, 20 contractions/min). A brachial artery catheter was inserted for the local administration of α-adrenergic agonists [phenylephrine (PE; α1) or clonidine (CL; α2)]. Blood flow responses to exercise [forearm vascular conductance (FVC)] were similar between all groups. At rest, infusion of PE or CL decreased FVC in all groups (40–60% reduction). Vasoconstriction to PE was abolished in all groups at 15 and 30% exercise intensity. Vasoconstriction to CL was reduced at 15% and abolished at 30% intensity in all groups; women had less CL-induced constriction during the early luteal than early follicular phase ( P < 0.017, 15% intensity). These results indicate that vasodilator responses to forearm exercise are comparable between men and women and are achieved through similar paths of α-adrenergic vascular control at moderate intensities; this control may differ at low intensities specific to the female menstrual phase.

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

2001 ◽  
Vol 90 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Maureen J. MacDonald ◽  
Heather L. Naylor ◽  
Michael E. Tschakovsky ◽  
Richard L. Hughson
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Exercise Bout ◽  
Handgrip Exercise ◽  
Acid Base ◽  
Rate Of Increase ◽  
Forearm Exercise

We used an exercise paradigm with repeated bouts of heavy forearm exercise to test the hypothesis that alterations in local acid-base environment that remain after the first exercise result in greater blood flow and O2 delivery at the onset of the second bout of exercise. Two bouts of handgrip exercise at 75% peak workload were performed for 5 min, separated by 5 min of recovery. We continuously measured blood flow using Doppler ultrasound and sampled venous blood for O2 content, Pco 2, pH, and lactate and potassium concentrations, and we calculated muscle O2uptake (V˙o 2). Forearm blood flow was elevated before the second exercise compared with the first and remained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was not different at 5 min. Arteriovenous O2 content difference was lower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 ml O2/dl) and higher by 30 s of exercise (11.2 ± 0.7 vs. 10.8 ± 0.7 ml O2/dl, P < 0.05). Muscle V˙o 2was unchanged before the start of exercise but was elevated during the first 30 s of the transition to the second exercise bout (26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood Pco 2, pH, and lactate concentration were consistent with reduced reliance on anaerobic glycolysis at the onset of the second exercise bout. These data show that limitations of muscle blood flow can restrict the adaptation of oxidative metabolism at the onset of heavy muscular exertion.

Forearm blood flow follows work rate during submaximal dynamic forearm exercise independent of sex

2007 ◽  
Vol 103 (6) ◽  
pp. 1950-1957 ◽  
Author(s):  
Joaquin U. Gonzales ◽  
Benjamin C. Thompson ◽  
John R. Thistlethwaite ◽  
Allison J. Harper ◽  
Barry W. Scheuermann
Keyword(s):  
Blood Flow ◽  
Muscle Strength ◽  
Forearm Blood Flow ◽  
Handgrip Strength ◽  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Work Rate ◽  
Metabolic Demand ◽  
Task Failure ◽  
Forearm Exercise

To test the hypothesis that sex influences forearm blood flow (FBF) during exercise, 15 women and 16 men of similar age [women 24.3 ± 4.0 (SD) vs. men 24.9 ± 4.5 yr] but different forearm muscle strength (women 290.7 ± 44.4 vs. men 509.6 ± 97.8 N; P < 0.05) performed dynamic handgrip exercise as the same absolute workload was increased in a ramp function (0.25 W/min). Task failure was defined as the inability to maintain contraction rate. Blood pressure and FBF were measured on separate arms during exercise by auscultation and Doppler ultrasound, respectively. Muscle strength was positively correlated with endurance time ( r = 0.72, P < 0.01) such that women had a shorter time to task failure than men (450.5 ± 113.0 vs. 831.3 ± 272.9 s; P < 0.05). However, the percentage of maximal handgrip strength achieved at task failure was similar between sexes (14% maximum voluntary contraction). FBF was similar between women and men throughout exercise and at task failure (women 13.6 ± 5.3 vs. men 14.5 ± 4.9 ml·min−1·100 ml−1). Mean arterial pressure was lower in women at rest and during exercise; thus calculated forearm vascular conductance (FVC) was higher in women during exercise but similar between sexes at task failure (women 0.13 ± 0.05 vs. men 0.11 ± 0.04 ml·min−1·100 ml−1·mmHg−1). In conclusion, the similar FBF during exercise was achieved by a higher FVC in the presence of a lower MAP in women than men. Still, FBF remained coupled to work rate (and presumably metabolic demand) during exercise irrespective of sex.

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

1998 ◽  
Vol 85 (6) ◽  
pp. 2249-2254 ◽  
Author(s):  
R. W. Brock ◽  
M. E. Tschakovsky ◽  
J. K. Shoemaker ◽  
J. R. Halliwill ◽  
M. J. Joyner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Forearm Blood Flow ◽  
Mechanical Effect ◽  
Voluntary Contraction ◽  
Single Muscle ◽  
Cuff Inflation ◽  
S Period ◽  
Echo Doppler Ultrasound

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 ∼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 N G-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, butl-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereasl-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation thatl-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.

Adenosine contributes to hypoxia-induced forearm vasodilation in humans

1999 ◽  
Vol 87 (6) ◽  
pp. 2218-2224 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Kris Gray ◽  
Michael D. Herr
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Adenosine Receptors ◽  
Forearm Blood Flow ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Normal Subjects ◽  
Local Release ◽  
Forearm Vascular Resistance

In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during acute hypoxia (inspired O210.5%; ∼20 min). In experiment I, aminophylline (50–200 μg ⋅ min−1 ⋅ 100 ml forearm tissue−1) was infused into the brachial artery to block adenosine receptors ( n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery ( n = 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O2 saturation 77 ± 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 ± 6% in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm ( P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm ( P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.

Dependence of muscleV˙o 2on blood flow dynamics at onset of forearm exercise

1996 ◽  
Vol 81 (4) ◽  
pp. 1619-1626 ◽  
Author(s):  
R. L. Hughson ◽  
J. K. Shoemaker ◽  
M. E. Tschakovsky ◽  
J. M. Kowalchuk
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Flow Dynamics ◽  
Cross Sectional ◽  
Mean Response Time ◽  
Rate Of Increase ◽  
Blood Flow Dynamics ◽  
Forearm Exercise

Hughson, R. L., J. K. Shoemaker, M. E. Tschakovsky, and J. M. Kowalchuk. Dependence muscle ofV˙o 2on blood flow dynamics at the onset of forearm exercise. J. Appl. Physiol. 81(4): 1619–1626, 1996.—The hypothesis that the rate of increase in muscle O2 uptake (V˙o 2 mus) at the onset of exercise is influenced by muscle blood flow was tested during forearm exercise with the arm either above or below heart level to modify perfusion pressure. Ten young men exercised at a power of ∼2.2 W, and five of these subjects also worked at 1.4 W. Blood flow to the forearm was calculated from the product of blood velocity and cross-sectional area obtained with Doppler techniques. Venous blood was sampled from a deep forearm vein to determine O2 extraction. The rate of increase inV˙o 2 musand blood flow was assessed from the mean response time (MRT), which is the time to achieve ∼63% increase from baseline to steady state. In the arm below heart position during the 2.2-W exercise, blood flow andV˙o 2 musboth increased, with a MRT of ∼30 s. With the arm above the heart at this power, the MRTs for blood flow [79.8 ± 15.7 (SE) s] and V˙o 2 mus(50.2 ± 4.0 s) were both significantly slower. Consistent with these findings were the greater increases in venous plasma lactate concentration over resting values in the above heart position (2.8 ± 0.4 mmol/l) than in the below heart position (0.9 ± 0.2 mmol/l). At the lower power, both blood flow andV˙o 2 musalso increased more rapidly with the arm below compared with above the heart. These data support the hypothesis that changes in blood flow at the onset of exercise have a direct effect on oxidative metabolism through alterations in O2transport.

Action of the endothelin receptor (ETA) antagonist BQ-123 on forearm blood flow in young normotensive subjects

2002 ◽  
Vol 102 (6) ◽  
pp. 661-666 ◽  
Author(s):  
R.C. WIMALASUNDERA ◽  
S.A.McG. THOM ◽  
L. REGAN ◽  
A.D. HUGHES
Keyword(s):  
Blood Flow ◽  
Vascular Tone ◽  
Forearm Blood Flow ◽  
Randomized Study ◽  
Double Blind ◽  
Eta Receptor ◽  
Normotensive Subjects ◽  
Eta Receptor Antagonist ◽  
Forearm Occlusion

Endothelin-1 (ET-1) has been proposed to contribute to the regulation of vascular tone in humans. BQ-123, an ETA receptor antagonist, has also been reported to increase forearm blood flow (FBF) in vivo; however, the efficacy of BQ-123 as an antagonist of ET-1 has not been evaluated in the forearm. The present study investigated the effects of BQ-123 on changes in FBF in response to ET-1 and noradrenaline (NA; norepinephrine), taking into account the possible influence of vasodilator effects of BQ-123 on responses to vasoconstrictors. Six subjects (age 25-34 years) participated in a double-blind randomized study. FBF was measured by forearm occlusion plethysmography. Drugs were infused intra-arterially into the non-dominant arm (study arm) on four separate occasions; the non-infused arm was used as a control. The effects of BQ-123 (50nmol/min for 60min, or 300nmol/min for 5min followed by saline for 55min) were compared with the effects of infusion of sodium nitroprusside (SNP; 12nmol/min for 60min) or saline on vasoconstriction induced by ET-1 (10pmol/min for 7min) and NA (120pmol/min for 7min). Infusion of BQ-123 at either dose did not significantly increase FBF, whereas SNP increased FBF by 134% (P = 0.03). ET-1 significantly reduced FBF, and this effect was almost completely inhibited by both doses of BQ-123, but was unaffected by SNP. NA also reduced FBF, and this action was unaffected by BQ-123 or SNP. The data show that BQ-123 is a selective ET-1 antagonist, but do not confirm a major role for ET-1 in influencing resting forearm vascular tone in young normotensive subjects.

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