Arm Blood Flow Research Articles

Comparing Cardiovascular Responses Between Upper Body Negative Pressure and Lower Body Negative Pressure

PURPOSE: LBNP stimulation distal to the iliac crest pulls blood to the legs resulting in a drop in blood pressure. In healthy individuals this is followed by a compensatory baroreflex-mediated increase in sympathetic nervous system activity resulting in global vasoconstriction and increased heart rate in order to recover blood pressure. LBNP is a relatively simple, inexpensive, and efficient method to reliably reproduce baroreflex responses and is therefore often employed as a research tool. Previous research utilizing LBNP is limited to the lower body, thus it is unknown as to whether responses to negative pressure vary based on the part of the body exposed to the stimulus. The aim of this investigation was to compare the cardiovascular responses to negative pressure when applied to the upper and lower limb. METHODS: Healthy participants performed a series of protocols to compare the cardiovascular responses to upper body negative pressure (UBNP) and LBNP. A volumetric edema gauge was first used to quantify the volume of the whole arm (distal to the acromion process) and then match an equal volume of participant’s leg to determine the depth of the leg. In a random order participants then placed their whole left arm (WA), whole leg (WL) (distal to the pubic tubercle) or a portion of the left leg that is volume-matched to the arm (VML) into the NP chamber. Once the limb was sealed in the chamber the subjects remained at rest for 5 minutes to collect baseline data. Following baseline each limb was subject to 5 minutes of -60 mmHg negative pressure. Heart rate (HR), mean arterial pressure (MAP) and brachial artery blood flow (BBF) in the control arm were measured continuously throughout each protocol. RESULTS: Relative to baseline, BBF during the WA, WL, and VML conditions decreased during the negative pressure by 21.2 ml/min, 41.8 ml/min, and 9.9 ml/min, respectively. HR during the WA and WL conditions decreased by 2.2 bpm and 1.2 bpm, respectively, however HR increased during the negative pressure during the VML condition by 2.0 bpm. During the negative pressure MAP increased during the WA condition by 2.4 mmHg and decreased during the WL and VML conditions by 0.9 mmHg and 3.0 mmHg, respectively. CONCLUSIONS: These data indicate that the cardiovascular responses to UBNP and LBNP are different and it is not simply due to a function of limb volume. Proximity of negative pressure relative to the baroreceptors may also have an impact.

The Effect of N‐acetylcysteine on Peripheral Hemodynamics and Fatigue during Exercise

We hypothesized that oral N‐acetylcysteine (NAC) would lead to higher exercising arm blood flow and a delayed onset of peripheral fatigue. Thus far, three healthy men have completed constant power handgrip exercise tests at 80% peak power to exhaustion. Subjects orally consumed either placebo (PLA) or NAC (70mg/kg) 60 min before exercise. Brachial artery blood flow (BABF) was measured via Doppler ultrasound and flexor digitorum superficialis oxygenation characteristics were measured via near infrared spectroscopy. Peripheral and central fatigue were assessed via potentiated doublet twitch force (Qtw), MVC, and voluntary activation (%VA). The mean time to exhaustion was similar (p=0.83) with NAC (368.8±37.5s) and PLA (353.9±90.9s). Mean resting BABF was similar (p=0.68) with NAC (92.7±12.0mL/min) and PLA (112.3±37.2mL/min). Mean peak exercising BABF was similar (p=0.77) between NAC (550.5±73.1mL/min) and PLA (527.5±94.3mL/min). Mean deoxy‐[Hb+Mb] was not different between NAC and PLA from rest to exercise (p=0.63). Mean total‐[Hb+Mb] was similar (p=0.08) between NAC and PLA at rest (NAC: 101.6±2.2 µM; PLA: 90.8±1.8 µM) and during exercise. % change in MVC from pre to post exercise was not different (p=0.18) between NAC (‐43.9±16.6%) and PLA (‐32.5±13.2%). % change from pre to post exercise in Qtw was similar (p=0.29) with NAC (‐34.6±20.4%) and with PLA (24.8±18.6%). Change (%) from pre to post exercise in %VA was less (p=0.019) with NAC (‐8.0±8.9%) than PLA (‐13.8±9.0%). These preliminary data suggest NAC does not affect exercising BA blood flow, but may increase microvascular hematocrit at rest and during exercise. Also, NAC may reduce central fatigue during exercise.

Influence of exercise intensity on respiratory muscle fatigue and brachial artery blood flow during cycling exercise.

During high intensity exercise, both respiratory muscle fatigue and cardiovascular reflexes occur; however, it is not known how inactive limb blood flow is influenced. The purpose of this study was to determine the influence of moderate and high exercise intensity on respiratory muscle fatigue and inactive limb muscle and cutaneous blood flow during exercise. Twelve men cycled at 70 and 85 % [Formula: see text] for 20 min. Subjects also performed a second 85 % [Formula: see text] test after ingesting 1,800 mg of N-acetylcysteine (NAC), which has been shown to reduce respiratory muscle fatigue (RMF). Maximum inspiratory pressures (P Imax), brachial artery blood flow (BABF), cutaneous vascular conductance (CVC), and mean arterial pressure were measured at rest and during exercise. Significant RMF occurred with 85 % [Formula: see text] (P Imax, -12.8 ± 9.8 %), but not with 70 % [Formula: see text] (P Imax, -5.0 ± 5.9 %). BABF and BA vascular conductance were significantly lower at end exercise of the 85 % [Formula: see text] test compared to the 70 % [Formula: see text] test. CVC during exercise was not different (p > 0.05) between trials. With NAC, RMF was reduced (p < 0.05) and BABF was significantly higher (~30 %) compared to 85 % [Formula: see text] (p < 0.05). These data suggest that heavy whole-body exercise at 85 % [Formula: see text] leads to RMF, decreases in inactive arm blood flow, and vascular conductance, but not cutaneous blood flow.

Low‐intensity training increases peak arm VO2 by enhancing both convective and diffusive O2 delivery

It is an ongoing discussion the extent to which oxygen delivery and oxygen extraction contribute to an increased muscle oxygen uptake during dynamic exercise. It has been proposed that local muscle factors including the capillary bed and mitochondrial oxidative capacity play a large role in prolonged low-intensity training of a small muscle group when the cardiac output capacity is not directly limiting. The purpose of this study was to investigate the relative roles of circulatory and muscle metabolic mechanisms by which prolonged low-intensity exercise training alters regional muscle VO2 . In nine healthy volunteers (seven males, two females), haemodynamic and metabolic responses to incremental arm cycling were measured by the Fick method and biopsy of the deltoid and triceps muscles before and after 42 days of skiing for 6 h day(-1) at 60% max heart rate. Peak pulmonary VO2 during arm crank was unchanged after training (2.38 ± 0.19 vs. 2.18 ± 0.2 L min(-1) pre-training) yet arm VO2 (1.04 ± 0.08 vs. 0.83 ± 0.1 L min(1) , P < 0.05) and power output (137 ± 9 vs. 114 ± 10 Watts) were increased along with a higher arm blood flow (7.9 ± 0.5 vs. 6.8 ± 0.6 L min(-1) , P < 0.05) and expanded muscle capillary volume (76 ± 7 vs. 62 ± 4 mL, P < 0.05). Muscle O2 diffusion capacity (16.2 ± 1 vs. 12.5 ± 0.9 mL min(-1) mHg(-1) , P < 0.05) and O2 extraction (68 ± 1 vs. 62 ± 1%, P < 0.05) were enhanced at a similar mean capillary transit time (569 ± 43 vs. 564 ± 31 ms) and P50 (35.8 ± 0.7 vs. 35 ± 0.8), whereas mitochondrial O2 flux capacity was unchanged (147 ± 6 mL kg min(-1) vs. 146 ± 8 mL kg min(-1) ). The mechanisms underlying the increase in peak arm VO2 with prolonged low-intensity training in previously untrained subjects are an increased convective O2 delivery specifically to the muscles of the arm combined with a larger capillary-muscle surface area that enhance diffusional O2 conductance, with no apparent role of mitochondrial respiratory capacity.

Increased leg blood flow and improved femoral artery shear patterns in metabolic syndrome after a diet and exercise programme

Altered vascular shear profiles may contribute to the development of atherosclerosis. Physical activity promotes anti-atherogenic shear patterns, resulting in reduced cardiovascular disease risk. Adults with metabolic syndrome (MetSyn) are at increased risk of developing atherosclerosis and cardiovascular disease. Thus, we hypothesized that conduit artery antegrade shear rate (ASR) would increase and retrograde shear rate (RSR) and oscillatory shear indices (OSI) would decrease in MetSyn patients (n = 16, 51 ± 2 years) after participation in a diet and exercise programme (DEP). Blood flow (Doppler ultrasound, brachial and femoral arteries) was measured, and shear rates were calculated in MetSyn patients before and after 12 weeks of DEP participation. In addition, plasma samples were collected to measure atherogenic markers. Diet and exercise programme participation increased resting leg blood flow and femoral artery ASR (P ≤ 0·05), and tended to decrease OSI (P = 0·09); RSR did not change (P>0·05). No changes in resting arm blood flow or ASR were observed (P>0·05), and both RSR and OSI increased after participation (P≤0·05). DEP participation reduced plasma vascular cell adhesion molecule(VCAM)-1 (P = 0·03), with a trend for reduced intercellular cell adhesion molecule(ICAM)-1 (P = 0·09) (i.e. atherogenic markers). Modest changes in diet and physical activity result in limb-specific improvements in vascular shear profiles and reduced systemic markers of atherosclerotic risk in MetSyn patients. These data provide novel physiologic insight into adaptations that may limit the progression of atherosclerosis in patients with MetSyn.

Metabolic and mechanical involvement of arms and legs in simulated double pole skiing

We evaluated arm and leg work rate and metabolism during double pole ergometer skiing. Thermodilution arm and leg blood flow was determined together with the arterial to venous difference for oxygen, while the work rate was assessed in eight male recreational skiers [24 (SD 7) years]. When work rate increased from 82 (SE 4) to 117 (7) W, leg power increased by 43% (enhanced vertical force and displacement of the body). The elbow angle tended to increase [from 71 (11.3)° to 75 (10.9)°; P = 0.07] and arm oxygen uptake increased by 20 (5)% [from 0.65 (0.07) to 0.78 (0.08) L/min; P < 0.05] because two-arm blood flow increased [from 5.4 (0.6) to 6.3 (0.7) L/min; P < 0.05] with no significant change in oxygen extraction [from 59 (2.3)% to 60 (1.9)%] accompanied with net arm lactate and potassium release. In contrast, two-leg blood flow [from 5.8 (0.5) to 8.0 (0.5) L/min] and oxygen extraction [from 67 (1.3)% to 75 (1.5)%] increased (P < 0.05), resulting in a 53 (8)% increase in leg oxygen uptake [from 0.82 (0.06) to 1.24 (0.07) L/min; P < 0.05]. In conclusion, during double poling on an ergometer, arm muscle metabolism and work rate increase only marginally and an increase in work intensity is covered mainly by the leg muscles.

Effect of short-term heat acclimation on endurance time and skin blood flow in trained athletes

BackgroundTo examine whether short-term, ie, five daily sessions, vigorous dynamic cycling exercise and heat exposure could achieve heat acclimation in trained athletes and the effect of heat acclimation on cutaneous blood flow in the active and nonactive limb.MethodsFourteen male badminton and table tennis athletes (age = 19.6 ± 1.2 years) were randomized into a heat acclimation (EXP, n = 7) or nonheat acclimation (CON, n = 7) group. For 5 consecutive days, the EXP group was trained using an upright leg cycle ergometer in a hot environment (38.4°C ± 0.4°C), while the CON group trained in a thermoneutral environment (24.1°C ± 0.3°C). For both groups, the training intensity and duration increased from a work rate of 10% below ventilatory threshold (VT) and 25 minutes per session on day 1, to 10% above VT and 45 minutes per session on day 5. Subjects performed two incremental leg cycle exercise tests to exhaustion at baseline and post-training in both hot and thermoneutral conditions. Study outcome measurements include: maximum oxygen uptake (VO2max); exercise heart rate (HR); O2 pulse; exercise time to exhaustion (tmax); skin blood flow in the upper arm (SkBFa) and quadriceps (SkBFq); and mean skin (Tsk).ResultsThe significant heat-acclimated outcome measurements obtained during high-intensity leg cycling exercise in the high ambient environment are: (1) 56%–100% reduction in cutaneous blood flow to the active limbs during leg cycling exercise; (2) 28% drop in cutaneous blood flow in nonactive limbs at peak work rate; (3) 5%–10% reduction in heart rate (HR); (4) 10% increase in maximal O2 pulse; and (5) 6.6% increase in tmax.ConclusionHeat acclimation can be achieved with five sessions of high-intensity cycling exercise in the heat in trained athletes, and redistribution of cutaneous blood flow in the skin and exercising muscle, and enhanced cardiovascular adaptations provide the heat-acclimated athletes with the capability to increase their endurance time in the hot environment.

Sympathetic activation increases NO release from eNOS but neither eNOS nor nNOS play an essential role in exercise hyperemia in the human forearm

Nitric oxide (NO) release from endothelial NO synthase (eNOS) and/or neuronal NO synthase (nNOS) could be modulated by sympathetic nerve activity and contribute to increased blood flow after exercise. We examined the effects of brachial-arterial infusion of the nNOS selective inhibitor S-methyl-l-thiocitrulline (SMTC) and the nonselective NOS inhibitor N(G)-monomethyl-l-arginine (l-NMMA) on forearm arm blood flow at rest, during sympathetic activation by lower body negative pressure, and during lower body negative pressure immediately after handgrip exercise. Reduction in forearm blood flow by lower body negative pressure during infusion of SMTC was not significantly different from that during vehicle (-28.5 ± 4.02 vs. -34.1 ± 2.96%, respectively; P = 0.32; n = 8). However, l-NMMA augmented the reduction in forearm blood flow by lower body negative pressure (-44.2 ± 3.53 vs. -23.4 ± 5.71%; n = 8; P < 0.01). When lower body negative pressure was continued after handgrip exercise, there was no significant effect of either l-NMMA or SMTC on forearm blood flow immediately after low-intensity exercise (P = 0.91 and P = 0.44 for l-NMMA vs. saline and SMTC vs. saline, respectively; each n = 10) or high-intensity exercise (P = 0.46 and P = 0.68 for l-NMMA vs. saline and SMTC vs. saline, respectively; each n = 10). These results suggest that sympathetic activation increases NO release from eNOS, attenuating vasoconstriction. Dysfunction of eNOS could augment vasoconstrictor and blood pressure responses to sympathetic activation. However, neither eNOS nor nNOS plays an essential role in postexercise hyperaemia, even in the presence of increased sympathetic activation.

Ursodeoxycholic Acid in Patients With Chronic Heart Failure: A Double-Blind, Randomized, Placebo-Controlled, Crossover Trial

This study sought to assess the effects of ursodeoxycholic acid (UDCA) on endothelial function and inflammatory markers in patients with chronic heart failure (CHF). Endothelial dysfunction is commonly observed in patients with CHF, and it contributes to the limitation in exercise capacity that accompanies this condition. Bacterial lipopolysaccharide may trigger proinflammatory cytokine release and promote further endothelial dysfunction. UDCA, a bile acid used in the treatment of cholestatic liver disease, has anti-inflammatory and cytoprotective properties and may contribute to the formation of mixed micelles around lipopolysaccharide. These properties may help to improve peripheral blood flow in patients with CHF. We performed a prospective, single-center, double-blind, randomized, placebo-controlled crossover study of UDCA in 17 clinically stable male patients with CHF (New York Heart Association functional class II/III, left ventricular ejection fraction <45%). Patients received in random order 500 mg UDCA twice daily for 4 weeks and placebo for another 4 weeks. The primary endpoint was post-ischemic peak peripheral arm blood flow as assessed by strain-gauge plethysmography. Sixteen patients completed the study. UDCA was well tolerated in all patients. Compared with placebo, UDCA improved peak post-ischemic blood flow in the arm (+18%, p = 0.038), and a trend for improved peak post-ischemic blood flow in the leg was found (+17%, p = 0.079). Liver function improved: compared with placebo, levels of γ-glutamyl transferase, aspartate transaminase, and soluble tumor necrosis factor α receptor 1 were lower after treatment with UDCA than after placebo (all p < 0.05). There was no change in 6-min walk test or New York Heart Association functional class, and levels of tumor necrosis factor α and interleukin-6 were unchanged or increased compared with placebo. UDCA is well tolerated in patients with CHF. UDCA improves peripheral blood flow and is associated with improved markers of liver function.

Reduced endothelial function in the skin in Southeast Asians compared to Caucasians

SummaryBackgroundThe reaction of vascular endothelial cells to occlusion and heat in Southeast Asian Indians (SAI) compared to Caucasians (C) has not been studied, although genetic differences are found in endothelial cells between the races.Material/MethodsTen C and Ten SAI (<35 years old) male and female subjects participated. There was no difference in the demographics of the subjects except that the SAI group had been in the United States for 6 months; C was natives to the US. Endothelial function was assessed by the response of the circulation (BF) to local heating and the response to vascular occlusion. The effects of local heat on circulation in the skin on the forearm was assessed by applying heat for 6 minutes at temperatures, 38, 40 and 42°C on 3 separate days. On different days, vascular occlusion was applied for 4 minutes to the same arm and skin blood flow was measured for 2 minutes after occlusion; skin temperature was either 31°C or 42°C.ResultsWhen occlusion was applied at a skin temperature of 31°C, the BF response to occlusion was significantly lower in the SAI cohort compared to C (peak BF C=617±88.2 flux, SAE=284±73 flux). The same effect was seen at skin temperatures of 42°C. The circulatory response to heat was also significantly less in SAI compared to C at each temperature examined (p<0.05)(for temperatures of 38, 40 and 42°C, peak blood flow for C was 374.7±81.2, 551.9±91.3 and 725.9±107 flux respectively and 248.5±86.2, 361.4±104.3 and 455.3±109.7 flux respectively for SAI. (p<0.05).ConclusionsThus there seems to be big differences in these 2 populations in endothelial response to these stressors. The difference may be due to genetic variations between the 2 groups of subjects.

Vildagliptin Improves Endothelium-Dependent Vasodilatation in Type 2 Diabetes

OBJECTIVETo investigate whether the dipeptidyl peptidase-4 inhibitor vildagliptin improves endothelium-dependent vasodilatation in patients with type 2 diabetes.RESEARCH DESIGN AND METHODSSixteen subjects with type 2 diabetes (age 59.8 ± 6.8 years, BMI 29.1 ± 4.8 kg/m2, HbA1c 6.97 ± 0.61) on oral blood glucose–lowering treatment were included. Participants received vildagliptin 50 mg b.i.d. or acarbose 100 mg t.i.d. for four consecutive weeks in a randomized, double-blind, cross-over design. At the end of each treatment period, we measured forearm vasodilator responses to intra-arterially administered acetylcholine (endothelium-dependent vasodilator) and sodium nitroprusside (endothelium-independent vasodilator).RESULTSInfusion of acetylcholine induced a dose-dependent increase in forearm blood flow in the experimental arm, which was higher during vildagliptin (3.1 ± 0.7, 7.9 ± 1.1, and 12.6 ± 1.4 mL ⋅ dL−1 ⋅ min−1 in response to three increasing dosages of acetylcholine) than during acarbose (2.0 ± 0.7, 5.0 ± 1.2, and 11.7 ± 1.6 mL ⋅ dL−1 ⋅ min−1, respectively; P = 0.01 by two-way ANOVA). Treatment with vildagliptin did not significantly change the vascular responses to sodium nitroprusside.CONCLUSIONSFour weeks’ treatment with vildagliptin improves endothelium-dependent vasodilatation in subjects with type 2 diabetes. This observation might have favorable cardiovascular implications.

Effect of cold water immersion on repeated cycling performance and limb blood flow

The purpose of the present study was to compare the effects of cold water immersion (CWI) and active recovery (ACT) on resting limb blood flow, rectal temperature and repeated cycling...

A NOVEL NONINVASIVE IMPEDANCE-BASED TECHNIQUE FOR CENTRAL VENOUS PRESSURE MEASUREMENT

Knowledge of central venous pressure (CVP) is considered valuable in the assessment and treatment of various states of critical illness and injury. We tested a noninvasive means of determining CVP (NICVP) by monitoring upper arm blood flow changes in response to externally applied circumferential pressure to the upper arm veins. Thirty-six patients who were undergoing CVP monitoring as part of their care had NICVP determined and compared with CVP. Volume changes were measured in the upper arm using tetra-polar impedance plethysmography underneath a blood pressure cuff. The cuff was inflated over 5 s to a pressure greater than CVP but less than diastolic arterial pressure. After 45 to 60 s, the cuff was rapidly deflated. Noninvasive CVP was determined as the cuff pressure noted at the maximum derivative of the volume increase under the cuff during deflation. Noninvasive CVP was then compared with invasively measured CVP taken during the same period by Bland-Altman analysis. A total of 108 trials (three per subject) were performed on 36 patients. Mean bias was -0.26 mmHg (95% confidence interval [CI]: -0.67, 0.15). Limits of agreement were -2.7 and 2.2 mmHg with the 95% CI for the lower limit of agreement (-3.4, -2.0 mmHg) and for the upper limit of agreement (1.5, 2.9 mmHg). Correlation between CVP and NICVP was 0.95 (95% CI: 0.93 to 0.97; P < 0.0001). Noninvasive CVP as determined in this study may be a clinically useful substitute for traditional CVP measurement and may offer a tool for early diagnosis and treatment of acute states in which knowledge of CVP would be helpful.

A large slice of cardiac output or humble pie for the respiratory muscles?

A large slice of cardiac output or humble pie for the respiratory muscles?

Effect of functional electrostimulation on impaired skin vasodilator responses to local heating in spinal cord injury

Spinal cord injury (SCI) induces vascular adaptations below the level of the lesion, such as impaired cutaneous vasodilation. However, the mechanisms underlying these differences are unclear. The aim of this study is to examine arm and leg cutaneous vascular conductance (CVC) responses to local heating in 17 able-bodied controls (39 +/- 13 yr) and 18 SCI subjects (42 +/- 8 yr). SCI subjects were counterbalanced for functional electrostimulation (FES) cycling exercise (SCI-EX, n = 9) or control (SCI-C, n = 9) and reanalyzed after 8 wk. Arm and leg skin blood flow were measured by laser-Doppler flowmetry during local heating (42 degrees C), resulting in an axon-reflex mediated first peak, nadir, and a primarily nitric oxide-dependent plateau phase. Data were expressed as a percentage of maximal CVC (44 degrees C). CVC responses to local heating in the paralyzed leg, but also in the forearm of SCI subjects, were lower than in able-bodied controls (P < 0.05 and 0.01, respectively). The 8-wk intervention did not change forearm and leg CVC responses to local heating in SCI-C and SCI-EX, but increased femoral artery diameter in SCI-EX (P < 0.05). Interestingly, findings in skin microvessels contrast with conduit arteries, where physical (in)activity contributes to adaptations in SCI. The lower CVC responses in the paralyzed legs might suggest a role for inactivity in SCI, but the presence of impaired CVC responses in the normally active forearm suggests other mechanisms. This is supported by a lack of adaptation in skin microcirculation after FES cycle training. This might relate to the less frequent and smaller magnitude of skin blood flow responses to heat stimuli, compared with controls, than physical inactivity per se.

Effect of cold water immersion on recovery and limb blood flow following high-intensity cycling

Introduction: We recently demonstrated that cold water immersion (CWI) facilitates improved performance recovery following high-intensity cycling compared with hot water immersion and passive recovery. The present study aimed to compare the effect of CWI with active recovery (ACT) on cycling performance. Furthermore, we aimed to investigate the effects of these recovery interventions on resting arm and leg blood flow. Methods: Ten endurance trained male cyclists volunteered to participate (age: 33.4 ± 5.13 years; VO2 peak 66.7 ± 6.1 ml/(kg min)). Subjects underwent two testing sessions (CWI and ACT), which were separated by 7 days, in a random order. At each session subjects initially performed a 30 min bout of high-intensity cycling that included 15 min of steady state cycling followed by a 15 min maximal time-trial. They then completed one of the two recovery interventions: CWI: 15 min full body immersion (excluding head and neck) in cold water (15 °C); ACT: 15 min cycling at 40% peak power. Forty minutes following recovery, subjects repeated the 30 min bout of high-intensity cycling, including the 15 min time-trial. Resting limb blood flow was measured at baseline, following the cycling time-trial and again following the recovery intervention using strain gauge plethysmography. Results/conclusions: Total work during the time trial fell from 493 ± 59 kJ to 484 ± 59 kJ when subjects performed the ACT recovery, whereas time-trial performance was maintained (490 ± 58 to 490 ± 60 kJ) with CWI recovery. Resting blood flow to the arms and legs was elevated immediately after the initial bout of high-intensity cycling; it then decreased to a greater extent following CWI (leg: 72%, arm: 91%) compared with ACT (leg: 40%, arm: 33%). Core temperature was lower following CWI than ACT. These data suggest that the positive influence of CWI as a recovery intervention is associated with a reduction in body temperature and altered limb blood flow.

Blood flow in the brachial artery increases after intense cycling exercise

During cycling blood flow is redistributed from physically inactive tissues to working leg muscles. It is unknown how long this situation persists after very intense exercise or whether it differs between intense exhausting and non-exhausting exercise. It is also not known to what extent the redistribution differs between different types of non-active tissues. Therefore nine healthy young men cycled first for 2min at 328 W (non-exhausting exercise, mean). Blood velocity in thigh and arm (ultrasound-doppler), perfusion of forearm skin (non-acral skin) and finger tip (acral skin, with arterio-venous anastomoses) were measured for 30min after exercise (laser-doppler). To be able to study vascular resistance and central circulation, blood pressure (Finometer), heart rate (ECG), and stroke volume (ultrasound-doppler) were measured. Thereafter the subjects cycled at the same power to exhaustion (4min), and the measurements were repeated. After both exercises mean blood pressure was unchanged (≤ 80mm Hg) despite increased cardiac output (≥ + 30% vs. pre-exercise). Blood velocity in the brachial artery was higher during the whole recovery period than at rest (p≤0.02; no differences between exercises). Blood perfusion of non-acral skin was unchanged from pre-exercise level after 2min of non-exhausting exercise, but it was twice as high after 4min cycling to exhaustion as at rest (p=0.02). Blood perfusion of acral skin rose after both exercises and did not differ between exhausting and non-exhausting exercise. In conclusion, arm blood flow increases above the pre-exercise level in the recovery period after short-lasting, strenuous exercise.

Rebuttal from Drs. Thijssen and Hopman

POINT-COUNTERPOINTRebuttal from Drs. Thijssen and HopmanPublished Online:01 Sep 2008https://doi.org/10.1152/japplphysiol.90570.2008cMoreSectionsPDF (33 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Reading through Drs. Green, Maiorana, and Cable's argument, we hit on another of Oscar Wilde's wisdoms: “The truth is rarely pure and never simple.”In a series of experiments, Dr. Green and colleagues demonstrated that typical changes in shear pattern, characterized by an increase in retrograde flow, are linked with endothelial NO release in the nonactive regions (4). Although it might be tempting to relate vascular adaptation in inactive regions to alterations in shear pattern, we believe that the truth is not that simple. In nonactive vascular beds during exercise, an enhanced release of vasoconstrictors is present, such as endothelin-1 (5), angiotensin II (7), and vasopressin (8). The actions of these local vasoconstrictors, combined with enhanced activity of the sympathetic nervous system (2), likely outweigh the beneficial effects of NO.The role for shear rate in exercise-induced vascular adaptations is well recognized, but shear rate is not the only factor involved; unfortunately the truth is never simple. Hypoxia, through release of growth factors such as VEGF, importantly contributes to exercise-induced vascular adaptations (6). Notably, hypoxia and VEGF also contribute to the release and homing of circulating bone marrow-derived endothelial progenitor cells (1). These progenitor cells predict the occurrence of cardiovascular events and death (9), possibly through their capability for endothelial repair, arteriogenesis, and angiogenesis. Appreciating a key role for hypoxia in exercise-induced vascular adaptations casts doubt on vascular adaptations in nonactive muscles during exercise where this essential physiological stimulus is absent (3).Interestingly, blood flow and related shear patterns vary markedly among different locations and sizes of arteries at rest and during exercise. The prominent retrograde component in the nonactive brachial artery blood flow pattern is hypothesized to result from an increased downstream vasoconstriction (4). In contrast, arteries supplying highly metabolic tissues (i.e., heart and legs) have marked vasodilation and will therefore not demonstrate this blood flow pattern. Therefore, one may question whether findings in the brachial artery during leg exercise can be extrapolated to the coronary vascular bed, since shear rate as well as other physiological stimuli will be markedly different.Taken together, the central question in this discussion is which stimuli are obligatory, either alone or in combination with others, to result in exercise-induced vascular adaptations in the active and nonactive regions. We enjoyed discussing this topic and hope we presented our arguments in line with Oscar Wilde's “One should always play fairly when one has the winning cards.”REFERENCES1 Asahara T, Murohara T, Sullivan A, Silver M, van der Zee R, Li T, Witzenbichler B, Schatteman G, Isner JM. Isolation of putative progenitor endothelial cells for angiogenesis. Science 275: 964–967, 1997.Crossref | PubMed | ISI | Google Scholar2 Buckwalter JB, Clifford PS. The paradox of sympathetic vasoconstriction in exercising skeletal muscle. Exerc Sport Sci Rev 29: 159–163, 2001.Crossref | PubMed | Google Scholar3 Calbet JA, Gonzalez-Alonso J, Helge JW, Sondergaard H, Munch-Andersen T, Boushel R, Saltin B. Cardiac output and leg and arm blood flow during incremental exercise to exhaustion on the cycle ergometer. J Appl Physiol 103: 969–978, 2007.Link | ISI | Google Scholar4 Green DJ, Bilsborough W, Naylor LH, Reed C, Wright J, O'Driscoll G, Walsh JH. Comparison of forearm blood flow responses to incremental handgrip and cycle ergometer exercise: relative contribution of nitric oxide. J Physiol 562: 617–628, 2005.Crossref | PubMed | ISI | Google Scholar5 Maeda S, Miyauchi T, Sakane M, Saito M, Maki S, Goto K, Matsuda M. Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans? J Appl Physiol 82: 1107–1111, 1997.Link | ISI | Google Scholar6 Prior BM, Yang HT, Terjung RL. What makes vessels grow with exercise training? J Appl Physiol 97: 1119–1128, 2004.Link | ISI | Google Scholar7 Stebbins CL, Symons JD. Role of angiotensin II in hemodynamic responses to dynamic exercise in miniswine. J Appl Physiol 78: 185–190, 1995.Link | ISI | Google Scholar8 Stebbins CL, Symons JD. Vasopressin contributes to the cardiovascular response to dynamic exercise. Am J Physiol Heart Circ Physiol 264: H1701–H1707, 1993.Link | ISI | Google Scholar9 Werner N, Kosiol S, Schiegl T, Ahlers P, Walenta K, Link A, Bohm M, Nickenig G. Circulating endothelial progenitor cells and cardiovascular outcomes. New Engl J Med 353: 999–1007, 2005.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 105Issue 3September 2008Pages 1007-1007 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.90570.2008cHistory Published online 1 September 2008 Published in print 1 September 2008 Metrics

Cardiac output and leg and arm blood flow during incremental exercise to exhaustion on the cycle ergometer

To determine central and peripheral hemodynamic responses to upright leg cycling exercise, nine physically active men underwent measurements of arterial blood pressure and gases, as well as femoral and subclavian vein blood flows and gases during incremental exercise to exhaustion (Wmax). Cardiac output (CO) and leg blood flow (BF) increased in parallel with exercise intensity. In contrast, arm BF remained at 0.8 l/min during submaximal exercise, increasing to 1.2 +/- 0.2 l/min at maximal exercise (P < 0.05) when arm O(2) extraction reached 73 +/- 3%. The leg received a greater percentage of the CO with exercise intensity, reaching a value close to 70% at 64% of Wmax, which was maintained until exhaustion. The percentage of CO perfusing the trunk decreased with exercise intensity to 21% at Wmax, i.e., to approximately 5.5 l/min. For a given local Vo(2), leg vascular conductance (VC) was five- to sixfold higher than arm VC, despite marked hemoglobin deoxygenation in the subclavian vein. At peak exercise, arm VC was not significantly different than at rest. Leg Vo(2) represented approximately 84% of the whole body Vo(2) at intensities ranging from 38 to 100% of Wmax. Arm Vo(2) contributed between 7 and 10% to the whole body Vo(2). From 20 to 100% of Wmax, the trunk Vo(2) (including the gluteus muscles) represented between 14 and 15% of the whole body Vo(2). In summary, vasoconstrictor signals efficiently oppose the vasodilatory metabolites in the arms, suggesting that during whole body exercise in the upright position blood flow is differentially regulated in the upper and lower extremities.

Regional differences in glucose clearance: effects of insulin and resistance training on arm and leg glucose clearance in older hypertensive individuals

The purpose of this study was to compare insulin's ability to stimulate glucose uptake in the arm and leg in a group of older hypertensive individuals (n = 13, 66 +/- 2 yr old). We also examined the effect of a 4-mo whole body resistance-training (RT) program on arm and leg glucose clearance (GC) during a hyperinsulinemic-euglycemic clamp. During the hyperinsulinemic-euglycemic clamp, GC was assessed by simultaneous measurement of arm and leg blood flow (BF) and assessment of fractional glucose extraction (GE) in blood samples from the brachial artery, brachial vein, and popliteal vein. At baseline, a significant main effect (arm vs. leg) demonstrated greater GC and BF in the arm than in the leg (P = 0.006 for GC and P = 0.012 for BF). Insulin significantly increased GE, BF, and GC in the arm and leg (main effects: P = 0.0001 for GE, P = 0.0001 for BF, and P = 0.0001 for GC) at baseline. However, the effect of insulin was similar in the arm and leg. After RT, a significant main effect (baseline vs. RT) demonstrated greater GE and GC in the leg (P = 0.024 for GE and P = 0.053 for GE), but not in the arm (P = 0.31 for GE and P = 0.14 for GC). No significant main effect (baseline vs. RT) for BF in the arm or leg was observed after RT. In conclusion, the greater GC in the arm than in the leg at baseline is primarily due to enhanced arm BF. Furthermore, whole body RT appears to increase GC in the leg but not in the arm.