Evidence map›Paper›PMID 30911900›Full record

ArticleThe journal of physiological sciences : JPS2019

Strength training attenuates post-infarct cardiac dysfunction and remodeling.

Michael A Garza, Emily A Wason, Justin R Cruger, Eunhee Chung, John Q Zhang

Open access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Molecular mechanisms of exercise contributing to tissue regeneration.Signal transduction and targeted therapy · 2022
    Review
  8. Review
  9. Article
  10. Article
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  12. Article
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  15. Article
  16. Morphological and clinical aspects of acute postmyocardial remodeling in patients with pre-existing hypertrophy.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

5 authors at 1 institution in 1 country.

Michael A GarzaLaboratory of Cardiovascular Research, Department of Health, Kinesiology, and Nutrition, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX, 78249, USA.
Emily A WasonLaboratory of Cardiovascular Research, Department of Health, Kinesiology, and Nutrition, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX, 78249, USA.
Justin R CrugerLaboratory of Cardiovascular Research, Department of Health, Kinesiology, and Nutrition, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX, 78249, USA.
Eunhee ChungLaboratory of Cardiovascular Research, Department of Health, Kinesiology, and Nutrition, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX, 78249, USA.
John Q ZhangLaboratory of Cardiovascular Research, Department of Health, Kinesiology, and Nutrition, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX, 78249, USA. john.zhang@utsa.edu.ORCID http://orcid.org/0000-0001-6206-2598
The University of Texas at San Antonio · US

Funding

University of Texas at San Antonio Faculty Research Award
6 · The paper itself

Abstract

Post-myocardial infarction (MI) exercise has been employed to improve cardiac function. However, most studies have focused on endurance training (Et). Although Et has been reported to preserve cardiac function, evidence suggests that Et increases left ventricle (LV) interior dimensions as a result of albumin-induced plasma expansion. In contrast, strength training (St) induces concentric cardiac hypertrophy and improved cardiac function without causing ventricular dilation. Therefore, the purpose of this study was to investigate the effects of St on cardiac function and remodeling in rats with MI. MI was surgically induced in 7-week-old rats via ligation of the coronary artery. Survivors were assigned to two experimental groups, MI-Sed (No exercise; n = 9), MI-St (St; n = 10), with a Sham group (no MI, no St; n = 9). MI-St rats began training 1-week post-MI by climbing a ladder with weights for 10 weeks. Echocardiographic measurements were performed prior to, and following exercise training, while in vivo LV hemodynamic analysis was conducted at the end of the experimental period. Our data revealed that St induced shortening of the LV end-diastolic dimension in the MI-St group compared with the MI-Sed group (P < 0.05). The peak velocities of contraction (+ dP/dt max) and relaxation (- dP/dt max) were significantly greater in the MI-St group than the MI-Sed group (P < 0.05). These training effects contributed to the improved fractional shortening (%FS). Our results demonstrate that St may be beneficial for post-MI by attenuating LV dilation and concomitant cardiac dysfunction associated with MI.

Indexed as

AnimalsCoronary VesselsHeartHemodynamicsMaleMyocardial InfarctionMyocardiumPhysical Conditioning, AnimalRatsRats, Sprague-DawleyResistance TrainingVentricular Function, LeftCardiac functionMyocardial infarctionRatsStrength training

Identifiers

PMID30911900
PMCPMC10717786
OpenAlexW2936595370

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.