Evidence map›Paper›PMID 23429876›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

Mechanical effects of muscle contraction increase intravascular ATP draining quiescent and active skeletal muscle in humans.

Anne R Crecelius, Brett S Kirby, Jennifer C Richards, Frank A Dinenno

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.2field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
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  4. KThe Journal of physiology · 2020
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  13. Single passive leg movement assessment of vascular function: contribution of nitric oxide.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
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  19. KIR channel activation contributes to onset and steady-state exercise hyperemia in humans.American journal of physiology. Heart and circulatory physiology · 2014
    Article
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

4 authors at 1 institution in 1 country.

Anne R CreceliusHuman Cardiovascular Physiology Laboratory, Department of Health and Exercise Science, Vascular Physiology Research Group, Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA.
Brett S Kirby
Jennifer C Richards
Frank A Dinenno
Colorado State University · US

Funding

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 HL087952NHLBI NIH HHS HL102720NHLBI NIH HHS R21 HL102720
6 · The paper itself

Abstract

Intravascular adenosine triphosphate (ATP) evokes vasodilation and is implicated in the regulation of skeletal muscle blood flow during exercise. Mechanical stresses to erythrocytes and endothelial cells stimulate ATP release in vitro. How mechanical effects of muscle contractions contribute to increased plasma ATP during exercise is largely unexplored. We tested the hypothesis that simulated mechanical effects of muscle contractions increase [ATP](venous) and ATP effluent in vivo, independent of changes in tissue metabolic demand, and further increase plasma ATP when superimposed with mild-intensity exercise. In young healthy adults, we measured forearm blood flow (FBF) (Doppler ultrasound) and plasma [ATP](v) (luciferin-luciferase assay), then calculated forearm ATP effluent (FBF×[ATP](v)) during rhythmic forearm compressions (RFC) via a blood pressure cuff at three graded pressures (50, 100, and 200 mmHg; Protocol 1; n = 10) and during RFC at 100 mmHg, 5% maximal voluntary contraction rhythmic handgrip exercise (RHG), and combined RFC + RHG (Protocol 2; n = 10). [ATP](v) increased from rest with each cuff pressure (range 144-161 vs. 64 ± 13 nmol/l), and ATP effluent was graded with pressure. In Protocol 2, [ATP](v) increased in each condition compared with rest (RFC: 123 ± 33; RHG: 51 ± 9; RFC + RHG: 96 ± 23 vs. Mean Rest: 42 ± 4 nmol/l; P < 0.05), and ATP effluent was greatest with RFC + RHG (RFC: 5.3 ± 1.4; RHG: 5.3 ± 1.1; RFC + RHG: 11.6 ± 2.7 vs. Mean Rest: 1.2 ± 0.1 nmol/min; P < 0.05). We conclude that the mechanical effects of muscle contraction can 1) independently elevate intravascular ATP draining quiescent skeletal muscle without changes in local metabolism and 2) further augment intravascular ATP during mild exercise associated with increases in metabolism and local deoxygenation; therefore, it is likely one stimulus for increasing intravascular ATP during exercise in humans.

Indexed as

Muscle ContractionAdenosine TriphosphateBiomechanical PhenomenaBlood Flow VelocityBlood Gas AnalysisFemaleForearmHand StrengthHemodynamicsHumansMaleMuscle, SkeletalRegional Blood FlowTime FactorsUltrasonography, DopplerUp-RegulationAdenosine Triphosphate

Identifiers

PMID23429876
PMCPMC3633434
OpenAlexW2164775995

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.