Remodeling of the heart will occur whether you do anything about it or not. What you do about it may determine what type of remodeling you get.
The prototypical remodeling that occurs with a sedentary lifestyle seem very different from that of a long term exerciser.
Studies from the cardiology group at Southwestern Medical School and the Cooper Center Longitudinal Study have described important aspects of the structure and function of the heart in the sedentary and the persistent aerobic exerciser. Higher levels of exercise directly affect heart function and structure in a way different from sedentary aging.
In a study of over 3000 healthy participants at the Cooper Clinic in Dallas, Brinker et al characterized the remodeling patterns of individuals as correlated with their "fitness" levels as determined by their levels of exercise achieved on a treadmill tests.
In a nutshell, the low fit individuals had smaller hearts,concentric remodeling/hypertrophy and poorer diastolic function while the fitter participants demonstrated a pattern of eccentric remolding , larger hearts and normal diastolic function.
Definitions are in order.
Heart size for this purpose, refers to left ventricular volume at the end of diastole( left ventricular end diastolic diameter) typically determined by echocardiography. Concentric remodeling refers to increased wall thickness and normal ventricular mass while concentric hypertrophy means increased LV mass and increased wall thickness.Eccentric remodeling refers to increased LV diastolic volume (hence LV mass)with no significant increase in wall thickness.
The relationship beween LV chamber size and wall thickness is expressed by the relative wall thickness (RWT) and defined as 2 X posterior LV wall thickness/ LV diameter at end of diastole.
Concentric remolding has a RWT of greater the 0.42 while eccentric remodeling is less than 0.42. The range of normal is 0.32 -0.42
The distinction between concentric and eccentric remodeling of the heart dates back to the 1975 "Morganroth hypothesis" which described different stereotypic cardiac adaptations to endurance exercise and strength building or resistance exercise. The idea was that endurance training presents a volume overload while resistance exercise presents a pressure overload. Remember though it is called an hypothesis.Several studies have reexamined the concept and reported that every endurance athlete does not get eccentric hypertrophy and many weight lifters do not have concentric changes.
The diastolic dysfunction , in the Dallas study, was assessed by the ratio e/e' ( e over e prime) where e is the the early diastolic flow through the mitral valve and e prime is movement of the mitral annulus.the ratio giving some measure of left ventricular compliance or stiffness.
The "Dallas hypothesis", my term as far as I know, is that the cardiac phenotype ( structure and function ) of the sedentary heart is a likely precursor of diastolic heart failure. aka heart failure with preserved ejection fraction ( HFpEF) . ( Note this designation is not the same as saying heart failure with preserved systolic function.EF is only one measure of systolic function. Some studies have shown decreased systolic function in HFpEF as measured by speckle echo exams measuring longitudinal strain.)
I have argued before that the lower level of the 2008 recommendation for exercise , while decreasing the overall risk of cardiovascular disease, is not sufficient to prevent heart failure. Exercise at at least twice that level seems to be needed. The minimum recommendation was for 500 ME\T min per week which would translate to 2.5 hours of moderate exercise per week or 1.25 hours of vigorous exercise ( where vigorous is over 7 MET)
The argument is that the reduction is diastolic heart failure risk may be brought about by endurance exercise induced structural changes in the heart and preservation of left ventricular compliance.