Evidence map›Paper›PMID 23299658›Full record

ReviewReviews in endocrine & metabolic disorders2013

Type 2 diabetes mellitus and exercise impairment.

Jane E B Reusch, Mark Bridenstine, Judith G Regensteiner

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

65 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
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  4. Sildenafil enhances central hemodynamic responses to exercise, but not V̇oJournal of applied physiology (Bethesda, Md. : 1985) · 2019
    Trial
  5. Effects of Physical Activity Intervention on Physical and Cognitive Function in Sedentary Adults With and Without Diabetes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Trial
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  8. [Geriatric aspects of diabetes mellitus (Update 2026)].Wiener klinische Wochenschrift · 2026
    Review
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  13. Association between subclinical right ventricular alterations and aerobic exercise capacity in type 2 diabetes.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2024
    Article
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5 more citing papers are in PubMed but not listed here.

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

3 authors.

Jane E B ReuschDenver VA Medical Center, Clermont Street, Denver, CO 80220, USA. Jane.Reusch@ucdenver.edu
Mark Bridenstine
Judith G Regensteiner

Funding

VRAC and Rho in pulmonary EC proliferationP01HL014985 · UNIVERSITY OF COLORADO DENVER · 1985 to 2005
$10.6M
Translational Pulmonary Vascular Biology ProgramT32HL007171 · UNIVERSITY OF COLORADO DENVER · 1985 to 2025
$2.3M
Transcriptional Regulation of PDGF Receptor AlphaR01DK064741 · UNIVERSITY OF COLORADO DENVER · 2004 to 2005
$597k
CSRD VA I01 CX001532NCATS NIH HHS UL1 TR000154NHLBI NIH HHS P01 HL014985NHLBI NIH HHS T32 HL007171NICHD NIH HHS K12 HD057022NIDDK NIH HHS R01 DK064741
6 · The paper itself

Abstract

Limitations in physical fitness, a consistent finding in individuals with both type I and type 2 diabetes mellitus, correlate strongly with cardiovascular and all-cause mortality. These limitations may significantly contribute to the persistent excess cardiovascular mortality affecting this group. Exercise impairments in VO2 peak and VO2 kinetics manifest early on in diabetes, even with good glycemic control and in the absence of clinically apparent complications. Subclinical cardiac dysfunction is often present but does not fully explain the observed defect in exercise capacity in persons with diabetes. In part, the cardiac limitations are secondary to decreased perfusion with exercise challenge. This is a reversible defect. Similarly, in the skeletal muscle, impairments in nutritive blood flow correlate with slowed (or inefficient) exercise kinetics and decreased exercise capacity. Several correlations highlight the likelihood of endothelial-specific impairments as mediators of exercise dysfunction in diabetes, including insulin resistance, endothelial dysfunction, decreased myocardial perfusion, slowed tissue hemoglobin oxygen saturation, and impairment in mitochondrial function. Both exercise training and therapies targeted at improving insulin sensitivity and endothelial function improve physical fitness in subjects with type 2 diabetes. Optimization of exercise functions in people with diabetes has implications for diabetes prevention and reductions in mortality risk. Understanding the molecular details of endothelial dysfunction in diabetes may provide specific therapeutic targets for the remediation of this defect. Rat models to test this hypothesis are under study.

Indexed as

AnimalsDiabetes Mellitus, Type 2Endothelium, VascularExerciseHumansMuscle, SkeletalPhysical Fitness

Identifiers

PMID23299658
PMCPMC3593997

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.