Evidence map›Paper›PMID 21885800›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2011

Local control of skeletal muscle blood flow during exercise: influence of available oxygen.

Darren P Casey, Michael J Joyner

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.9field-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

54 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
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  5. Acute dietary nitrate supplementation does not augment submaximal forearm exercise hyperemia in healthy young men.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2015
    Trial
  6. Trial
  7. Vasoconstrictor responsiveness during hyperbaric hyperoxia in contracting human muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2013
    Trial
  8. Article
  9. Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Effects of atmospherically relevant PMFrontiers in public health · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Dynamics of POFrontiers in physiology · 2023
    Article
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  17. Review
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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

2 authors at 1 institution in 1 country.

Darren P CaseyDept. of Anesthesiology, Mayo Clinic, Rochester, MN 55905, USA. casey.darren@mayo.edu
Michael J Joyner
Mayo Clinic · US

Funding

PERFUSION OF ACTIVE MUSCLES--METABOLITES AND NERVESR01HL046493 · NHLBI · MAYO CLINIC ROCHESTER · PI JOYNER, MICHAEL J · 1997 to 2011
$3.7M
Role of Adenosine in Compensatory Dilation During Hypoxic ExerciseF32AR055819 · NIAMS · MAYO CLINIC ROCHESTER · PI CASEY, DARREN PATRICK · 2008 to 2010
$149k
PERFUSION OF ACTIVE MUSCLES: METABOLITES AND NERVESR29HL046493 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI JOYNER, MICHAEL J · 1992 to 1996
–
NHLBI NIH HHS HL-46493NIAMS NIH HHS AR-55819
6 · The paper itself

Abstract

Reductions in oxygen availability (O(2)) by either reduced arterial O(2) content or reduced perfusion pressure can have profound influences on the circulation, including vasodilation in skeletal muscle vascular beds. The purpose of this review is to put into context the present evidence regarding mechanisms responsible for the local control of blood flow during acute systemic hypoxia and/or local hypoperfusion in contracting muscle. The combination of submaximal exercise and hypoxia produces a "compensatory" vasodilation and augmented blood flow in contracting muscles relative to the same level of exercise under normoxic conditions. A similar compensatory vasodilation is observed in response to local reductions in oxygen availability (i.e., hypoperfusion) during normoxic exercise. Available evidence suggests that nitric oxide (NO) contributes to the compensatory dilator response under each of these conditions, whereas adenosine appears to only play a role during hypoperfusion. During systemic hypoxia the NO-mediated component of the compensatory vasodilation is regulated through a β-adrenergic receptor mechanism at low-intensity exercise, while an additional (not yet identified) source of NO is likely to be engaged as exercise intensity increases during hypoxia. Potential candidates for stimulating and/or interacting with NO at higher exercise intensities include prostaglandins and/or ATP. Conversely, prostaglandins do not appear to play a role in the compensatory vasodilation during exercise with hypoperfusion. Taken together, the data for both hypoxia and hypoperfusion suggest NO is important in the compensatory vasodilation seen when oxygen availability is limited. This is important from a basic biological perspective and also has pathophysiological implications for diseases associated with either hypoxia or hypoperfusion.

Indexed as

Adenosine TriphosphateAnimalsBlood Flow VelocityBlood PressureExerciseHumansHyperemiaHypoxiaMuscle ContractionMuscle, SkeletalNitric OxideOxygenPhysical ExertionReflexSympathetic Nervous SystemVasodilationAdenosine TriphosphateNitric OxideOxygen

Identifiers

PMID21885800
PMCPMC3233894
OpenAlexW2100126490

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.