Evidence map›Paper›PMID 23887898›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2014

Muscle blood flow, hypoxia, and hypoperfusion.

Michael J Joyner, Darren P Casey

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Prolonged adenosine triphosphate infusion and exercise hyperemia in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2016
    Trial
  5. Trial
  6. Review
  7. The pathophysiology of wild-type transthyretin amyloidosis: implications for exercise intolerance.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Michael J JoynerDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota.
Darren P Casey
Mayo Clinic · USUniversity of Iowa · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
PERFUSION OF ACTIVE MUSCLES--METABOLITES AND NERVESR01HL046493 · NHLBI · MAYO CLINIC ROCHESTER · PI JOYNER, MICHAEL J · 1997 to 2011
$3.7M
PERFUSION OF ACTIVE MUSCLES: METABOLITES AND NERVESR29HL046493 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI JOYNER, MICHAEL J · 1992 to 1996
–
NCATS NIH HHS UL1TR000135-07NHLBI NIH HHS HL-46493
6 · The paper itself

Abstract

Blood flow increases to exercising skeletal muscle, and this increase is driven primarily by vasodilation in the contracting muscles. When oxygen delivery to the contracting muscles is altered by changes in arterial oxygen content, the magnitude of the vasodilator response to exercise changes. It is augmented during hypoxia and blunted during hyperoxia. Because the magnitude of the increased vasodilation during hypoxic exercise tends to keep oxygen delivery to the contracting muscles constant, we have termed this phenomenon "compensatory vasodilation." In a series of studies, we have explored metabolic, endothelial, and neural mechanisms that might contribute to compensatory vasodilation. These include the contribution of vasodilating substances like nitric oxide (NO) and adenosine, along with altered interactions between sympathetic vasoconstriction and metabolic vasodilation. We have also compared the compensatory vasodilator responses to hypoxic exercise with those seen when oxygen delivery to contracting muscles is altered by acute reductions in perfusion pressure. A synthesis of our findings indicate that NO contributes to the compensatory dilator responses during both hypoxia and hypoperfusion, while adenosine appears to contribute only during hypoperfusion. During hypoxia, the NO-mediated component is linked to a β-adrenergic receptor mechanism during lower intensity exercise, while another source of NO is engaged at higher exercise intensities. There are also subtle interactions between α-adrenergic vasoconstriction and metabolic vasodilation that influence the responses to hypoxia, hyperoxia, and hypoperfusion. Together our findings emphasize both the tight linkage of oxygen demand and supply during exercise and the redundant nature of the vasomotor responses to contraction.

Indexed as

ExerciseMuscle ContractionVasodilationAdaptation, PhysiologicalHumansHypoxiaMuscle, SkeletalNitric OxideOxygenOxygen ConsumptionReceptors, AdrenergicRegional Blood FlowSignal TransductionNitric OxideOxygenReceptors, Adrenergicexercisehypoxiaoxygenvasodilation

Identifiers

PMID23887898
PMCPMC3972742
OpenAlexW1984959258

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.