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

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.

Transient Responses of the Hepatic Lipidome to Acute Exercise Bouts in Mice

“…After HIIE the PUFA content in liver DAG rose to approach this value of PUFA expected from the diet, which may be caused by an exercise-induced release of dietary fatty acids that were stored in adipose tissue. Furthermore, while discussing the impacts of exercise on hepatic lipids, it should be noted that the most substantial impacts were following HIIE, which is an exercise approach that exhibits particularly potent impacts upon health and metabolism (17,25,(31)(32)(33)(34)(35)(36). The remodeling of PUFA content in DAG occurred after HIIE but not CE, and the response of TAG concentration was enhanced following HIIE in comparison to CE.…”

Mechanisms underlying the impact of exercise training in pulmonary arterial hypertension

“…In the majority of the studies, exercise training showed beneficial effects on cardiac remodelling [34,[36][37][38][40][41][42][43][44][45][46]48]. Still, others reported no improvement [47,49] or aggravation [50].…”

Hipertensión arterial pulmonar: el entrenamiento físico como complemento de la terapia farmacológica

“…En lo que respecta a HAP, a la fecha solo se han investigado los efectos del HIIT en modelos animales, destacando el estudio realizado por Brown MB en ratas con HAP leve 30 . En dicho trabajo, se investigó la respuesta al HIIT en comparación con el ejercicio aeróbico continuo, durante 6 semanas de entrenamiento.…”