scholarly journals Ascorbic acid increases muscle blood flow during dynamic exercise in older healthy humans

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Brett S Kirby ◽  
Wyatt F Voyles ◽  
Carrie B Simpson ◽  
Rick E Carlson ◽  
William G Schrage ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ascorbic Acid ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Healthy Humans

scholarly journals Nitric oxide, but not vasodilating prostaglandins, contributes to the improvement of exercise hyperemia via ascorbic acid in healthy older adults

2010 ◽  
Vol 299 (5) ◽  
pp. H1633-H1641 ◽  
Author(s):  
Anne R. Crecelius ◽  
Brett S. Kirby ◽  
Wyatt F. Voyles ◽  
Frank A. Dinenno
Keyword(s):  
Nitric Oxide ◽  
Older Adults ◽  
Blood Flow ◽  
Ascorbic Acid ◽  
Steady State ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Healthy Older Adults ◽  
Group 2 ◽  
Group 1

Acute ascorbic acid (AA) administration increases muscle blood flow during dynamic exercise in older adults, and this is associated with improved endothelium-dependent vasodilation. We directly tested the hypothesis that increase in muscle blood flow during AA administration is mediated via endothelium-derived vasodilators nitric oxide (NO) and prostaglandins (PGs). In 14 healthy older adults (64 ± 3 yr), we measured forearm blood flow (FBF; Doppler ultrasound) during rhythmic handgrip exercise at 10% maximum voluntary contraction. After 5-min steady-state exercise with saline, AA was infused via brachial artery catheter for 10 min during continued exercise, and this increased FBF ∼25% from 132 ± 16 to 165 ± 20 ml/min ( P < 0.05). AA was infused for the remainder of the study. Next, subjects performed a 15-min exercise bout in which AA + saline was infused for 5 min, followed by 5 min of the nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine (l-NMMA) and then 5 min of the cyclooxygenase inhibitor ketorolac ( group 1). The order of inhibition was reversed in eight subjects ( group 2). In group 1, independent NOS inhibition reduced steady-state FBF by ∼20% ( P < 0.05), and subsequent PG inhibition had no impact on FBF (Δ 3 ± 5%). Similarly, in group 2, independent PG inhibition had little effect on FBF (Δ −4 ± 4%), whereas subsequent NO inhibition significantly decreased FBF by ∼20% ( P < 0.05). In a subgroup of five subjects, we inhibited NO and PG synthesis before AA administration. In these subjects, there was a minimal nonsignificant improvement in FBF with AA infusion (Δ 7 ± 3%; P = nonsignificant vs. zero). Together, our data indicate that the increase in muscle blood flow during dynamic exercise with acute AA administration in older adults is mediated primarily via an increase in the bioavailability of NO derived from the NOS pathway.

scholarly journals Acute Oral Ingestion of Ascorbic Acid Improves Muscle Blood Flow and Oxygen Consumption During Exercise In Older Healthy Humans

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jennifer C. Richards ◽  
Anne R. Crecelius ◽  
Brett S. Kirby ◽  
Leora J. Garcia ◽  
Dennis Larson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ascorbic Acid ◽  
Oxygen Consumption ◽  
Muscle Blood Flow ◽  
Oral Ingestion ◽  
Healthy Humans

Endothelin-1-mediated vasoconstriction at rest and during dynamic exercise in healthy humans

2007 ◽  
Vol 293 (4) ◽  
pp. H2550-H2556 ◽  
Author(s):  
D. Walter Wray ◽  
Steven K. Nishiyama ◽  
Anthony J. Donato ◽  
Mikael Sander ◽  
Peter D. Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Exercise Intensity ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Dynamic Exercise ◽  
Dependent Manner ◽  
Drug Infusion ◽  
Leg Blood Flow ◽  
Healthy Humans ◽  
Arterial Blood

It is now generally accepted that α-adrenoreceptor-mediated vasoconstriction is attenuated during exercise, but the efficacy of nonadrenergic vasoconstrictor pathways during exercise remains unclear. Thus, in eight young (23 ± 1 yr), healthy volunteers, we contrasted changes in leg blood flow (ultrasound Doppler) before and during intra-arterial infusion of the α1-adrenoreceptor agonist phenylephrine (PE) with that of the nonadrenergic endothelin A (ETA)/ETB receptor agonist ET-1. Heart rate, arterial blood pressure, common femoral artery diameter, and mean blood velocity were measured at rest and during knee-extensor exercise at 20%, 40%, and 60% of maximal work rate (WRmax). Drug infusion rates were adjusted for blood flow to maintain comparable doses across all subjects and conditions. At rest, PE infusion (8 ng·ml−1·min−1) provoked a rapid and significant decrease in leg blood flow (−51 ± 3%) within 2.5 min. Resting ET-1 infusion (40 pg·ml−1·min−1) significantly decreased leg blood flow within 5 min, reaching a maximal vasoconstriction (−34 ± 3%) after 25–30 min of continuous infusion. Compared with rest, an exercise intensity-dependent attenuation to PE-mediated vasoconstriction was observed (−18 ± 5%, −7 ± 2%, and −1 ± 3% change in leg blood flow at 20%, 40%, and 60% of WRmax, respectively). Vasoconstriction in response to ET-1 was also blunted in an exercise intensity-dependent manner (−13 ± 3%, −7 ± 4%, and 2 ± 3% change in leg blood flow at 20%, 40%, and 60% of WRmax, respectively). These findings support a significant contribution of ET-1 and α-adrenergic receptors in the regulation of skeletal muscle blood flow in the human leg at rest and suggest a similar, intensity-dependent “lysis” of peripheral ET and α-adrenergic vasoconstriction during dynamic exercise.

scholarly journals Exercise-induced hyperemia is associated with knee extensor fatigability in adults with type 2 diabetes

2019 ◽  
Vol 126 (3) ◽  
pp. 658-667 ◽  
Author(s):  
Jonathon W. Senefeld ◽  
Jacqueline K. Limberg ◽  
Kathleen M. Lukaszewicz ◽  
Sandra K. Hunter
Keyword(s):  
Type 2 Diabetes ◽  
Blood Flow ◽  
Lower Limb ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Dynamic Exercise ◽  
Extensor Muscles ◽  
Exercise Induced

The aim of this study was to compare fatigability, contractile function, and blood flow to the knee extensor muscles after dynamic exercise in patients with type 2 diabetes mellitus (T2DM) and controls. The hypotheses were that patients with T2DM would demonstrate greater fatigability than controls, and greater fatigability would be associated with a lower exercise-induced increase in blood flow and greater impairments in contractile function. Patients with T2DM ( n = 15; 8 men; 62.4 ± 9.0 yr; 30.4 ± 7.7 kg/m2; 7,144 ± 3,294 steps/day) and 15 healthy control subjects (8 men, 58.4 ± 6.9 yr; 28.4 ± 4.6 kg/m2; 7,893 ± 2,323 steps/day) were matched for age, sex, body mass index, and physical activity. Fatigability was quantified as the reduction in knee extensor power during a 6-min dynamic exercise. Before and after exercise, vascular ultrasonography and electrical stimulation were used to assess skeletal muscle blood flow and contractile properties, respectively. Patients with T2DM had greater fatigability (30.0 ± 20.1% vs. 14.6 ± 19.0%, P < 0.001) and lower exercise-induced hyperemia (177 ± 90% vs. 194 ± 79%, P = 0.04) than controls but similar reductions in the electrically evoked twitch amplitude (37.6 ± 24.8% vs. 31.6 ± 30.1%, P = 0.98). Greater fatigability of the knee extensor muscles was associated with postexercise reductions in twitch amplitude ( r = 0.64, P = 0.001) and lesser exercise-induced hyperemia ( r = −0.56, P = 0.009). Patients with T2DM had greater lower-limb fatigability during dynamic exercise, which was associated with reduced contractile function and lower skeletal muscle blood flow. Thus, treatments focused on enhancing perfusion and reversing impairments in contractile function in patients with T2DM may offset lower-limb fatigability and aid in increasing exercise capacity. NEW & NOTEWORTHY Although prior studies compare patients with type 2 diabetes mellitus (T2DM) with lean controls, our study includes controls matched for age, body mass, and physical activity to more closely assess the effects of T2DM. Patients with T2DM demonstrated no impairment in macrovascular endothelial function, evidenced by similar flow-mediated dilation to controls. However, patients with T2DM had greater fatigability and reduced exercise-induced increase in blood flow (hyperemia) after a lower-limb dynamic fatiguing exercise compared with controls.

Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision

2004 ◽  
Vol 97 (1) ◽  
pp. 384-392 ◽  
Author(s):  
Loring B. Rowell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Muscle ◽  
Neural Control ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Site Of Action ◽  
New Vision ◽  
Muscle Chemoreflex

This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows. 1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 3) How important is muscle's mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on cardiac output? 4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

The Effects of Ascorbic Acid Supplementation on Muscle Blood Flow in Aged Rats

2010 ◽  
Vol 42 ◽  
pp. 124-125
Author(s):  
Peter J. Schwagerl ◽  
Steven W. Copp ◽  
Daniel M. Hirai ◽  
Robert T. Davis ◽  
Brian S. Snyder ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ascorbic Acid ◽  
Muscle Blood Flow ◽  
Aged Rats ◽  
Acid Supplementation ◽  
Ascorbic Acid Supplementation

scholarly journals Acute ascorbic acid ingestion increases skeletal muscle blood flow and oxygen consumption via local vasodilation during graded handgrip exercise in older adults

2015 ◽  
Vol 309 (2) ◽  
pp. H360-H368 ◽  
Author(s):  
Jennifer C. Richards ◽  
Anne R. Crecelius ◽  
Dennis G. Larson ◽  
Frank A. Dinenno
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Ascorbic Acid ◽  
Oxygen Consumption ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Forearm Vascular Conductance

Human aging is associated with reduced skeletal muscle perfusion during exercise, which may be a result of impaired endothelium-dependent dilation and/or attenuated ability to blunt sympathetically mediated vasoconstriction. Intra-arterial infusion of ascorbic acid (AA) increases nitric oxide-mediated vasodilation and forearm blood flow (FBF) during handgrip exercise in older adults, yet it remains unknown whether an acute oral dose can similarly improve FBF or enhance the ability to blunt sympathetic vasoconstriction during exercise. We hypothesized that 1) acute oral AA would improve FBF (Doppler ultrasound) and oxygen consumption (V̇o2) via local vasodilation during graded rhythmic handgrip exercise in older adults ( protocol 1), and 2) AA ingestion would not enhance sympatholysis in older adults during handgrip exercise ( protocol 2). In protocol 1 ( n = 8; 65 ± 3 yr), AA did not influence FBF or V̇o2 during rest or 5% maximal voluntary contraction (MVC) exercise, but increased FBF (199 ± 13 vs. 248 ± 16 ml/min and 343 ± 24 vs. 403 ± 33 ml/min; P < 0.05) and V̇o2 (26 ± 2 vs. 34 ± 3 ml/min and 43 ± 4 vs. 50 ± 5 ml/min; P < 0.05) at both 15 and 25% MVC, respectively. The increased FBF was due to elevations in forearm vascular conductance (FVC). In protocol 2 ( n = 10; 63 ± 2 yr), following AA, FBF was similarly elevated during 15% MVC (∼20%); however, vasoconstriction to reflex increases in sympathetic activity during −40 mmHg lower-body negative pressure at rest (ΔFVC: −16 ± 3 vs. −16 ± 2%) or during 15% MVC (ΔFVC: −12 ± 2 vs. −11 ± 4%) was unchanged. Our collective results indicate that acute oral ingestion of AA improves muscle blood flow and V̇o2 during exercise in older adults via local vasodilation.

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