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September 28, 2020International Heart JournalOpen Access

Role of Exercise on Alleviating Pressure Overload-Induced Left Ventricular Dysfunction and Remodeling via AMPK-Dependent Autophagy Activation

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Key result

Four weeks of moderate-intensity treadmill exercise significantly improved left ventricular ejection fraction (74.90% vs 58.89%, p<0.01) and alleviated cardiac dysfunction in rats with pressure overload-induced hypertrophy.

Why the study?

Cardiac hypertrophy is a major risk factor leading to maladaptive remodeling and heart failure, prompting investigation into the cardioprotective function and mechanisms of exercise.

Does moderate-intensity treadmill exercise improve cardiac function and remodeling in rats with pressure overload-induced left ventricular hypertrophy?

Population

Rats undergoing transverse aortic constriction (TAC) or sham operation

Comparison

Sham control vs TAC control vs TAC plus exercise vs TAC plus exercise and 3-MA vs TAC plus exercise and Compound C

Design

Randomized preclinical animal study

Follow-up

4 weeks

Authors

ZMZhichao MaJQJie QiLGLi Gao

Discussion

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Member takes

Overview

Hypothesis-generating for exercise in pressure-overload remodeling; extends AMPK-autophagy mechanism but leaves clinical translation open.

Structured PICO

Does moderate-intensity treadmill exercise improve cardiac function and remodeling in rats with pressure overload-induced left ventricular hypertrophy?

P
Population
50 10-week-old female Wistar rats subjected to transverse aortic constriction to induce left ventricular hypertrophy, followed for 4 weeks of exercise training.
I
Intervention
4 weeks of moderate-intensity treadmill exercise
C
Comparator
Sedentary TAC rats, sham-operated rats, and exercise + inhibitors (3-MA or Compound C)
O
Outcome
Cardiac function (measured via echocardiography), interstitial fibrosis, and apoptosissurrogate

Main Result

Absolute Event Rate: 74.9% vs 58.89%

p-value: p=<0.01

Treadmill exercise alleviates pressure overload-induced left ventricular dysfunction and remodeling in rats through an AMPK-dependent autophagy mechanism.

Limitations

  • The duration of treadmill training was only 4 weeks, which may not be long enough to further aggravate myocardial hypertrophy or fully evaluate long-term remodeling.

Cite This Study

Ma et al. (2020) studied Transverse aortic constriction (TAC)-induced left ventricular hypertrophy (n=50). Moderate-intensity treadmill exercise vs. Transverse aortic constriction without exercise (TC group) was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.01). Four weeks of moderate-intensity treadmill exercise significantly improved left ventricular ejection fraction (74.90% vs 58.89%, p<0.01) and alleviated cardiac dysfunction in rats with pressure overload-induced hypertrophy.

synapsesocial.com/papers/6a98f4aab3d4f622baf0ccc3https://doi.org/10.1536/ihj.19-443
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Downregulation of survival signalling pathways and increased apoptosis in the transition of pressure overload‐induced cardiac hypertrophy to heart failure2009 · 79 citations
  2. 2Structural and functional alterations in heart and skeletal muscle following severe TAC in mice: impact of moderate exercise training2021 · 12 citations
  3. 3Exercise-preconditioning attenuates TAC-induced cardiac hypertrophy and myocardial injury through activating NRF22025 · 12 citations
  4. 4AMP Activated Protein Kinase-α2 Deficiency Exacerbates Pressure-Overload–Induced Left Ventricular Hypertrophy and Dysfunction in Mice2008 · 187 citations
  5. 5Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats2018 · 31 citations