Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

2005 ◽  
Vol 98 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
Jay T. Williams ◽  
Mollie P. Pricher ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Causal Link ◽  
Skeletal Muscle Blood Flow ◽  
Leg Blood Flow ◽  
Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

Autonomic control of skeletal muscle blood flow at the onset of exercise

1999 ◽  
Vol 277 (5) ◽  
pp. H1872-H1877 ◽  
Author(s):  
John B. Buckwalter ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Ganglionic Blockade

The purpose of this study was to determine whether the autonomic nervous system is involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries. Before treadmill exercise at 3 miles/h, 0% grade, hexamethonium (10 mg/kg) and atropine (0.2 mg/kg) or saline was infused intravenously. Ganglionic blockade increased resting heart rate from 87 ± 5 to 145 ± 8 beats/min ( P < 0.01) and reduced mean arterial pressure from 100 ± 4 to 88 ± 5 mmHg ( P < 0.01). During steady-state exercise, heart rate was unaffected by ganglionic blockade (from 145 ± 8 to 152 ± 5 beats/min), whereas mean arterial pressure was reduced (from 115 ± 4 to 72 ± 4 mmHg; P < 0.01). Immediate and rapid increases in iliac blood flow and conductance occurred with initiation of exercise with or without ganglionic blockade. Statistical analyses of hindlimb conductance at 5-s intervals over the first 30 s of exercise revealed a statistically significant difference between the control and ganglionic blockade conditions at 20, 25, and 30 s ( P < 0.01) but not at 5, 10, and 15 s of exercise. Hindlimb conductance at 1 min of exercise was 9.21 ± 0.68 and 11.82 ± 1.32 ml ⋅ min−1 ⋅ mmHg−1for the control and ganglionic blockade conditions, respectively. Because ganglionic blockade did not affect the initial rise in iliac conductance, we concluded that the autonomic nervous system is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs. Autonomic control of skeletal muscle blood flow during exercise is manifested through vasoconstriction and not vasodilation.

Reliability of NIRS Derived Measurements of Skeletal Muscle Blood Flow and Oxygen Consumption During Exercise

2016 ◽  
Vol 48 ◽  
pp. 1031
Author(s):  
Adam A. Lucero ◽  
Gifty Addae ◽  
Wayne Lawrence ◽  
Beemnet Neway ◽  
Daniel Credeur ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow

scholarly journals α-Adrenergic receptor regulation of skeletal muscle blood flow during exercise in heart failure patients with reduced ejection fraction

2019 ◽  
Vol 316 (5) ◽  
pp. R512-R524 ◽  
Author(s):  
Zachary Barrett-O’Keefe ◽  
Joshua F. Lee ◽  
Stephen J. Ives ◽  
Joel D. Trinity ◽  
Melissa A. H. Witman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Ejection Fraction ◽  
Adrenergic Receptor ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Reduced Ejection Fraction ◽  
Leg Blood Flow ◽  
Related Increase

Patients suffering from heart failure with reduced ejection fraction (HFrEF) experience impaired limb blood flow during exercise, which may be due to a disease-related increase in α-adrenergic receptor vasoconstriction. Thus, in eight patients with HFrEF (63 ± 4 yr) and eight well-matched controls (63 ± 2 yr), we examined changes in leg blood flow (Doppler ultrasound) during intra-arterial infusion of phenylephrine (PE; an α1-adrenergic receptor agonist) and phentolamine (Phen; a nonspecific α-adrenergic receptor antagonist) at rest and during dynamic single-leg knee-extensor exercise (0, 5, and 10 W). At rest, the PE-induced reduction in blood flow was significantly attenuated in patients with HFrEF (−15 ± 7%) compared with controls (−36 ± 5%). During exercise, the controls exhibited a blunted reduction in blood flow induced by PE (−12 ± 4, −10 ± 4, and −9 ± 2% at 0, 5, and 10 W, respectively) compared with rest, while the PE-induced change in blood flow was unchanged compared with rest in the HFrEF group (−8 ± 5, −10 ± 3, and −14 ± 3%, respectively). Phen administration increased leg blood flow to a greater extent in the HFrEF group at rest (+178 ± 34% vs. +114 ± 28%, HFrEF vs. control) and during exercise (36 ± 6, 37 ± 7, and 39 ± 6% vs. 13 ± 3, 14 ± 1, and 8 ± 3% at 0, 5, and 10 W, respectively, in HFrEF vs. control). Together, these findings imply that a HFrEF-related increase in α-adrenergic vasoconstriction restrains exercising skeletal muscle blood flow, potentially contributing to diminished exercise capacity in this population.

ARTERIAL PRESSURE AND SKELETAL MUSCLE BLOOD FLOW IN SWINE DURING MAXIMAL AND SUPRAMAXIMAL EXERCISE.

1989 ◽  
Vol 21 (Supplement) ◽  
pp. S85
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
C. Duan ◽  
T. C. Ong ◽  
M. T. Jones ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Supramaximal Exercise ◽  
Skeletal Muscle Blood Flow

Rapid vasoregulatory mechanisms in exercising human skeletal muscle: dynamic response to repeated changes in contraction intensity

2006 ◽  
Vol 291 (3) ◽  
pp. H1065-H1073 ◽  
Author(s):  
Anna M. Rogers ◽  
Natasha R. Saunders ◽  
Kyra E. Pyke ◽  
Michael E. Tschakovsky
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Exercise Intensity ◽  
Time Course ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Relaxation Phase

We tested the hypothesis that vasoregulatory mechanisms exist in humans that can rapidly adjust muscle blood flow to repeated increases and decreases in exercise intensity. Six men and seven women (age, 24.4 ± 1.3 yr) performed continuous dynamic forearm handgrip contractions (1- to 2-s contraction-to-relaxation duty cycle) during repeated step increases and decreases in contraction intensity. Three step change oscillation protocols were examined: Slow (7 contractions per contraction intensity × 10 steps); Fast (2 contractions per contraction intensity × 15 steps); and Very Fast (1 contraction per contraction intensity × 15 steps). Forearm blood flow (FBF; Doppler and echo ultrasonography), heart rate (ECG), and mean arterial pressure (arterial tonometry) were examined for the equivalent of a cardiac cycle during each relaxation phase (FBFrelax). Mean arterial pressure and heart rate did not change during repeated step changes ( P = 0.352 and P = 0.190). For both Slow and Fast conditions, relaxation phase FBFrelax adjusted immediately and repeatedly to both increases and decreases in contraction intensity, and the magnitude and time course of FBFrelax changes were virtually identical. For the Very Fast condition, FBFrelax increased with the first contraction and thereafter slowly increased over the course of repeated contraction intensity oscillations. We conclude that vasoregulatory mechanisms exist in human skeletal muscle that are capable of rapidly and repeatedly adjusting muscle blood flow with ongoing step changes in contraction intensity. Importantly, they demonstrate symmetry in response magnitude and time course with increasing versus decreasing contraction intensity but cannot adjust to very fast exercise intensity oscillations.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

Effects of training on reproductive tissue blood flow in exercising pregnant rats

1990 ◽  
Vol 69 (6) ◽  
pp. 2097-2103 ◽  
Author(s):  
M. T. Jones ◽  
K. I. Norton ◽  
D. R. Dengel ◽  
R. B. Armstrong
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Muscle Blood Flow ◽  
Fetal Weight ◽  
Tissue Blood Flow ◽  
Pregnant Rats ◽  
Acute Bout ◽  
Skeletal Muscle Blood Flow

The purpose of this study were to investigate 1) whether treadmill training would attenuate the reduction in reproductive (RBF) and visceral tissue blood flow (VBF) that occurs during an acute bout of submaximal exercise (EX) in pregnant rats and 2) whether fetal number of fetal weight would be affected by training. One group (T) of female rats trained on a treadmill (10 degrees incline, 30 m/min) for 1 h/day 5 days/wk for 10 wk before becoming pregnant. A second group (UT) was run at the same speed and incline for 10 min/day 5 days/wk for 2 wk. T and UT rats were bred until pregnant. Skeletal muscle blood flow, RBF, and VBF were measured at pre-EX and at 1 and 10 min of EX (10 degrees incline, 30 m/min). No differences were observed before or during exercise between the two groups in RBF and VBF, heart rate, or mean arterial pressure. Both groups experienced decreases in VBF (except liver) and RBF from pre-EX to EX. In most muscles skeletal muscle blood flow increased for both groups from pre-EX to EX. Neither group experienced a change in mean arterial pressure from pre-EX to EX, but heart rate increased significantly for both groups. No differences were observed between groups in fetal number, fetal weight, or fetal resorptions. It was concluded that training does not significantly attenuate the reduction in RBF and VBF in pregnant rats that occurs during an acute bout of submaximal EX and that training does not affect fetal weight or fetal number.

scholarly journals ARTERIAL PRESSURE AND SKELETAL MUSCLE BLOOD FLOW IN SWINE DURING MAXIMAL AND SUPRAMAXIMAL EXERCISE.

1980 ◽  
Vol 21 (Supplement) ◽  
pp. S85
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
C. Duan ◽  
T. C. Ong ◽  
M. T. Jones ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Supramaximal Exercise ◽  
Skeletal Muscle Blood Flow

Abstract 9934: High Mean Arterial Pressure Aggravates Cerebral Hemodynamics After Extracorporeal Resuscitation in Swine

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Hemodynamics ◽  
Reactivity Index ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Standard Map ◽  
Arterial Blood

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)

Biphasic effect of hydrogen peroxide on skeletal muscle arteriolar tone via activation of endothelial and smooth muscle signaling pathways

2004 ◽  
Vol 97 (3) ◽  
pp. 1130-1137 ◽  
Author(s):  
Csongor Csekő ◽  
Zsolt Bagi ◽  
Akos Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Local Regulation ◽  
Prostaglandin H ◽  
Arteriolar Tone

We hypothesized that hydrogen peroxide (H2O2) has a role in the local regulation of skeletal muscle blood flow, thus significantly affecting the myogenic tone of arterioles. In our study, we investigated the effects of exogenous H2O2 on the diameter of isolated, pressurized (at 80 mmHg) rat gracilis skeletal muscle arterioles (diameter of ∼150 μm). Lower concentrations of H2O2 (10−6–3 × 10−5 M) elicited constrictions, whereas higher concentrations of H2O2 (6 × 10−5–3 × 10−4 M), after initial constrictions, caused dilations of arterioles (at 10−4 M H2O2, −19 ± 1% constriction and 66 ± 4% dilation). Endothelium removal reduced both constrictions (to −10 ± 1%) and dilations (to 33 ± 3%) due to H2O2. Constrictions due to H2O2 were completely abolished by indomethacin and the prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist SQ-29548. Dilations due to H2O2 were significantly reduced by inhibition of nitric oxide synthase (to 38 ± 7%) but were unaffected by clotrimazole or sulfaphenazole (inhibitors of cytochrome P-450 enzymes), indomethacin, or SQ-29548. In endothelium-denuded arterioles, clotrimazole had no effect, whereas H2O2-induced dilations were significantly reduced by charybdotoxin plus apamin, inhibitors of Ca2+-activated K+ channels (to 24 ± 3%), the selective blocker of ATP-sensitive K+ channels glybenclamide (to 14 ± 2%), and the nonselective K+-channel inhibitor tetrabutylammonium (to −1 ± 1%). Thus exogenous administration of H2O2 elicits 1) release of PGH2/TxA2 from both endothelium and smooth muscle, 2) release of nitric oxide from the endothelium, and 3) activation of K+ channels, such as Ca2+-activated and ATP-sensitive K+ channels in the smooth muscle resulting in biphasic changes of arteriolar diameter. Because H2O2 at low micromolar concentrations activates several intrinsic mechanisms, we suggest that H2O2 contributes to the local regulation of skeletal muscle blood flow in various physiological and pathophysiological conditions.

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