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

Author:

Brown Mary Beth1,Neves Evandro2,Long Gary1,Graber Jeremy1,Gladish Brett1,Wiseman Andrew1,Owens Matthew1,Fisher Amanda J.1,Presson Robert G.3,Petrache Irina45,Kline Jeffrey2,Lahm Tim45

Affiliation:

1. Department of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana;

2. Department of Emergency Medicine, Indiana University School of Medicine, Indianapolis, Indiana;

3. Department of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana;

4. Department of Pulmonary and Critical Care, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and

5. Richard L. Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana

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.

Funder

American Heart Association Midwest Affiliates- Scientis Development Grant

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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