Evidence map›Paper›PMID 27784688›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

High-intensity interval training, but not continuous training, reverses right ventricular hypertrophy and dysfunction in a rat model of pulmonary hypertension.

Mary Beth Brown, Evandro Neves, Gary Long, Jeremy Graber, Brett Gladish, Andrew Wiseman, Matthew Owens, Amanda J Fisher, Robert G Presson, Irina Petrache and 2 more

Open access · bronzeAbstract readComparative StudyEvaluation Study
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
5.1field-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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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  15. Skeletal muscle blood flow during exercise is reduced in a rat model of pulmonary hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
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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

12 authors at 3 institutions in 1 country.

Mary Beth BrownDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana; brownmb@iu.edu.
Evandro NevesDepartment of Emergency Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Gary LongDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Jeremy GraberDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Brett GladishDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Andrew WisemanDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Matthew OwensDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Amanda J FisherDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana.
Robert G PressonDepartment of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana.
Irina PetracheDepartment of Pulmonary and Critical Care, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and.
Jeffrey KlineDepartment of Emergency Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Tim LahmDepartment of Pulmonary and Critical Care, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and.
Indiana University Health · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Ceramide-induced Lung Destruction in EmphysemaR01HL077328 · NHLBI · NATIONAL JEWISH HEALTH · PI PETRACHE, IRINA · 2006 to 2024
$8.0M
EMAP II, a molecular link of inflammation and apoptosis in pulmonary emphysema.R01HL090950 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAUSS, MATTHIAS, PETRACHE, IRINA · 2008 to 2011
$1.5M
Maximizing benefit and minimizing detriment of exercise for pulmonary hypertensionR15HL121661 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI BROWN, MARY BETH · 2015 to 2015
$455k
Hypoxia-mediated protective estrogen receptor signaling in pulmonary hypertensionI01BX002042 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI Tim Lahm · 2014 to 2026
–
BLRD VA I01 BX002042NHLBI NIH HHS R01 HL077328NHLBI NIH HHS R01 HL090950NHLBI NIH HHS R15 HL121661
6 · The paper itself

Abstract

Exercise is beneficial in pulmonary arterial hypertension (PAH), although studies to date indicate little effect on the elevated pulmonary pressures or maladaptive right ventricle (RV) hypertrophy associated with the disease. For chronic left ventricle failure, high-intensity interval training (HIIT) promotes greater endothelial stimulation and superior benefit than customary continuous exercise training (CExT); however, HIIT has not been tested for PAH. Therefore, here we investigated acute and chronic responses to HIIT vs. CExT in a rat model of monocrotaline (MCT)-induced mild PAH. Six weeks of treadmill training (5 times/wk) were performed, as either 30 min HIIT or 60 min low-intensity CExT. To characterize acute hemodynamic responses to the two approaches, novel recordings of simultaneous pulmonary and systemic pressures during running were obtained at pre- and 2, 4, 6, and 8 wk post-MCT using long-term implantable telemetry. MCT-induced decrement in maximal aerobic capacity was ameliorated by both HIIT and CExT, with less pronounced pulmonary vascular remodeling and no increase in RV inflammation or apoptosis observed. Most importantly, only HIIT lowered RV systolic pressure, RV hypertrophy, and total pulmonary resistance, and prompted higher cardiac index that was complemented by a RV increase in the positive inotrope apelin and reduced fibrosis. HIIT prompted a markedly pulsatile pulmonary pressure during running and was associated with greater lung endothelial nitric oxide synthase after 6 wk. We conclude that HIIT may be superior to CExT for improving hemodynamics and maladaptive RV hypertrophy in PAH. HIIT's superior outcomes may be explained by more favorable pulmonary vascular endothelial adaptation to the pulsatile HIIT stimulus.

Indexed as

AnimalsHigh-Intensity Interval TrainingHypertension, PulmonaryHypertrophy, Right VentricularMalePhysical Conditioning, AnimalPhysical EnduranceRatsRats, Sprague-DawleyTreatment OutcomeVentricular Dysfunction, Rightapelinendothelial nitric oxide synthase

Identifiers

PMID27784688
PMCPMC5504398
OpenAlexW2542729035

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.