Evidence map›Paper›PMID 26023228›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2016

Skeletal muscle vasodilation during systemic hypoxia in humans.

Frank A Dinenno

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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  18. Adrenergic control of skeletal muscle blood flow during chronic hypoxia in healthy males.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Frank A DinennoHuman Cardiovascular Physiology Laboratory, Department of Health and Exercise Science, Center for Cardiovascular Research, Colorado State University, Fort Collins, Colorado frank.dinenno@colostate.edu.
Colorado State University · US

Funding

Exercise Hyperemia in HumansR01HL119337 · NHLBI · MAYO CLINIC ROCHESTER · PI DINENNO, FRANK A, JOYNER, MICHAEL J · 2014 to 2017
$3.0M
Aging, Sleep Apnea, & Vascular Control During Systemic HypoxiaR01HL095573 · NHLBI · COLORADO STATE UNIVERSITY · PI DINENNO, FRANK A · 2010 to 2014
$1.8M
Aging, Endothelial Dysfunction, and ATP-mediated Vasodilation in HumansR21HL087952 · NHLBI · COLORADO STATE UNIVERSITY · PI DINENNO, FRANK A · 2007 to 2008
$404k
Role of circulating ATP and smooth muscle cell hyperpolarization in vascular contR21HL102720 · NHLBI · COLORADO STATE UNIVERSITY · PI DINENNO, FRANK A · 2010 to 2011
$393k
NHLBI NIH HHS HL-087952NHLBI NIH HHS HL-095573NHLBI NIH HHS HL-102720NHLBI NIH HHS HL-119337NHLBI NIH HHS R01 HL119337
6 · The paper itself

Abstract

In humans, the net effect of acute systemic hypoxia in quiescent skeletal muscle is vasodilation despite significant reflex increases in muscle sympathetic vasoconstrictor nerve activity. This vasodilation increases tissue perfusion and oxygen delivery to maintain tissue oxygen consumption. Although several mechanisms may be involved, we recently tested the roles of two endothelial-derived substances during conditions of sympathoadrenal blockade to isolate local vascular control mechanisms: nitric oxide (NO) and prostaglandins (PGs). Our findings indicate that 1) NO normally plays a role in regulating vascular tone during hypoxia independent of the PG pathway; 2) PGs do not normally contribute to vascular tone during hypoxia, however, they do affect vascular tone when NO is inhibited; 3) NO and PGs are not independently obligatory to observe hypoxic vasodilation when assessed as a response from rest to steady-state hypoxia; and 4) combined NO and PG inhibition abolishes hypoxic vasodilation in human skeletal muscle. When the stimulus is exacerbated via combined submaximal rhythmic exercise and systemic hypoxia to cause further red blood cell (RBC) deoxygenation, skeletal muscle blood flow is augmented compared with normoxic exercise via local dilator mechanisms to maintain oxygen delivery to active tissue. Data obtained in a follow-up study indicate that combined NO and PG inhibition during hypoxic exercise blunts augmented vasodilation and hyperemia compared with control (normoxic) conditions by ∼50%; however, in contrast to hypoxia alone, the response is not abolished, suggesting that other local substances are involved. Factors associated with greater RBC deoxygenation such as ATP release, or nitrite reduction to NO, or both likely play a role in regulating this response.

Indexed as

AnimalsExerciseFollow-Up StudiesHumansHypoxiaMuscle, SkeletalNitric OxideProstaglandinsVasodilationNitric OxideProstaglandinsendotheliumerythrocytesoxygenationsympathoadrenal

Identifiers

PMID26023228
PMCPMC4719058
OpenAlexW2283823651

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.