# Previous resistance exercise training mitigates progression of right ventricle dysfunction and remodeling in male rats with pulmonary arterial hypertension

**Authors:** Alexandre Martins Oliveira Portes, Anselmo Gomes de Moura, Franciany de Jesus Silva, Luiz Otávio Guimarães‐Ervilha, Maíra Oliveira de Freitas, Leôncio Lopes Soares, Bruna Aparecida Fonseca da Silva, Sebastião Felipe Ferreira Costa, Sara Caco dos Lúcio Generoso, Thiago de Souza Silva, Thainá Iasbik‐Lima, Luciano Bernardes Leite, Mariana Machado Neves, Emily Correna Carlo Reis, Antônio José Natali

PMC · DOI: 10.14814/phy2.70786 · Physiological Reports · 2026-02-23

## TL;DR

Resistance exercise training in rats with pulmonary hypertension helps protect the right ventricle from dysfunction and structural changes.

## Contribution

This study shows that prior resistance exercise training can mitigate right ventricle dysfunction and remodeling in pulmonary arterial hypertension.

## Key findings

- Previous resistance training increased physical effort tolerance and prevented pulmonary artery resistance increase.
- Resistance training improved right ventricle systolic function and myocyte contractility in rats with PAH.
- Exercise inhibited adverse right ventricle remodeling, including hypertrophy and collagen deposition.

## Abstract

This study investigated whether previous resistance exercise training (RT) affects the progression of right ventricular dysfunction and remodeling in rats with severe pulmonary artery hypertension (PAH). Male Wistar rats were submitted to a RT protocol (i.e., ladder‐climbing) for 8 weeks, while controls remained in cages without exercising. Then, exercised rats were randomly divided into trained monocrotaline discontinued (TMD), and trained monocrotaline continued (TMC) groups. Subsequently, they received a single monocrotaline injection (i.e., 60 mg/kg) and the TMD group stopped RT, while the TMC group exercised for an additional 6‐week period. After euthanasia, right ventricle (RV) was dissected and processed for histological and single RV myocyte analyses. Previous RT increased physical effort tolerance, prevented pulmonary artery resistance augment (i.e., AT/ET) and mitigated the reduction in RV systolic function (i.e., TAPSE). RT also lessened impairments in single RV myocyte contractility and intracellular calcium transient (i.e., amplitude, and times to peak and relaxation) in the TMC group only. Moreover, RT inhibited adverse RV remodeling (i.e., hypertrophy and collagen deposition) in both trained groups. In conclusion, previous RT attenuates the progression of RV dysfunction and remodeling in rats with severe monocrotaline‐induced PAH, being the extension of protective effects dependent on the exercise training continuity.

## Linked entities

- **Chemicals:** monocrotaline (PubChem CID 9415)
- **Diseases:** pulmonary arterial hypertension (MONDO:0015924), pulmonary hypertension (MONDO:0005149)

## Full-text entities

- **Genes:** Gatm (glycine amidinotransferase) [NCBI Gene 81660] {aka AT}, Nos3 (nitric oxide synthase 3) [NCBI Gene 24600] {aka eNos}, Ryr2 (ryanodine receptor 2) [NCBI Gene 689560] {aka RYR-2, RyR}, Pln (phospholamban) [NCBI Gene 64672] {aka Plm}
- **Diseases:** TMD (MESH:D000095027), muscle (MESH:D019042), inflammation (MESH:D007249), dyspnea (MESH:D004417), collagen (MESH:D003095), heart failure (MESH:D006333), vasculature (MESH:C565633), hypertensive (MESH:D006973), PAH (MESH:D000081029), RV dysfunction (MESH:C535682), weight loss (MESH:D015431), right ventricular dysfunction (MESH:D018497), hypertrophy (MESH:D006984)
- **Chemicals:** Isoflurane (MESH:D007530), ethanol (MESH:D000431), nitric oxide (MESH:D009569), NaOH (MESH:D012972), CaCl2 (MESH:D002122), phosphate (MESH:D010710), O2 (MESH:D010100), MgCl2 (MESH:D015636), NaCl (MESH:D012965), MCT (MESH:D016686), paraformaldehyde (MESH:C003043), taurine (MESH:D013654), EGTA (MESH:D004533), fura-2 am (MESH:C049925), glucose (MESH:D005947), calcium (MESH:D002118), methacrylate (MESH:D008689), glutaraldehyde (MESH:D005976), KCl (MESH:D011189), HEPES (MESH:D006531), Ca2+ (-), NO (MESH:D009614), creatine (MESH:D003401), oil (MESH:D009821)
- **Species:** Hathewaya histolytica (species) [taxon 1498], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

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## References

64 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929195/full.md

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Source: https://tomesphere.com/paper/PMC12929195