Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-week exercise training. Twenty-one healthy individuals performed 12-week high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training programme to assess ventricular structure, function and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 bpm, 'stress echocardiography'). Fifteen individuals completed training (22.0±2.4y, 10 male). Hypoxic exercise training increased RV size, including diameter and area (all p<0.05). With exception of an increase in RV fractional area change (p=0.03), RV function did not change post-training (all p>0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training (p<0.05). No adaptation in LV structure, function or mechanics were observed (all p>0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography (r=-0.67, P=0.01) inversely correlated with adaptation in RV basal diameter following 12-week training. In conclusion, 12-week high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals.

Acute exercise-induced changes in cardiac function relates to right ventricular remodeling following 12-weeks hypoxic exercise training

Fornasiero, Alessandro;
2021-01-01

Abstract

Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-week exercise training. Twenty-one healthy individuals performed 12-week high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training programme to assess ventricular structure, function and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 bpm, 'stress echocardiography'). Fifteen individuals completed training (22.0±2.4y, 10 male). Hypoxic exercise training increased RV size, including diameter and area (all p<0.05). With exception of an increase in RV fractional area change (p=0.03), RV function did not change post-training (all p>0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training (p<0.05). No adaptation in LV structure, function or mechanics were observed (all p>0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography (r=-0.67, P=0.01) inversely correlated with adaptation in RV basal diameter following 12-week training. In conclusion, 12-week high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals.
2021
athlete's heart
echocardiography
endurance exercise
hypoxia
speckle tracking echocardiography
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/1044694
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 1
  • ???jsp.display-item.citation.isi??? 1
social impact