Will a few hours of aerobic exercise per week practiced over along period of time (years) prevent the ventricle from becomes stiff and could the current epidemic of diastolic heart failure be diminished if many people follow that practice. Does sedentary aging resulting in stiff left ventricles play a major role in the increasing numbers of older folks with heart failure (HF). If it does could the sufficient amount of exercise prevent it and what do we mean by "sufficient"?
Echocardiography and other imaging techniques have provided detailed information emphasizing the importance of diastole, the filling process of the ventricle priming the heart pump for systole or ventricular contraction.Indeed a key distinguishing feature of the endurance athlete's heart is its superior filling or diastolic function. The better diastolic function or ventricular filling the better is one's fitness or exercise level.
Knowledge of diastole has lead to a new concept of heart failure, one if which systolic function is said to be normal- at least at rest.Actually less than that is claimed as the systolic function is represented by one test of that function namely the ejection fraction done at rest. This has lead to the notion of "HFpEF" or heart failure with preserved ejection fraction and HFrEF, or heart failure with reduced ejection fraction. HFpEF is said to represent at least half of HF cases and other than exercise training there seems to be little evidence of an effective therapeutic approach. There are several echocardiographic tests used to assess diastolic function: EA ratio. E/E prime ratio,left atrial volume, etc .
Woody Allen's basic axiom of physiology can be paraphrased : as we get older everything that should be soft gets stiff and everything should be stiff gets soft. Aging certainly makes the left ventricle get stiff and the aorta as well.
The group from Dallas having the wealth of patient data available from the Cooper Longevity institute has published several articles claiming that long time endurance athletes are able to maintain a much more compliant left ventricle than matched persons with little on no regular aerobic exercise. Further their data suggest that a group with exercise levels lower than that of the competitive runner group ( about 2-3 hours per week of aerobic exercise) fare almost as well in regard to left ventricular compliance.This suggest that training or exercise far short of running marathon every year or doing the full Iron man type triathlon will suffice.
Ventricular compliance is one factor to consider in regard to diastolic function- another is the relaxation capability and in that regard long term endurance exercise does not mitigate the age related loss of optimal relaxation function. One way to measure relaxation is with the isovolumic relaxation time or.IVRT. This is the time interval after aortic valve closure and mitral valve opening. It is prolonged as humans age and the IVRT was no shorter in the fit group or the super fit group versus the sedentary group in the Dallas articles. .
The heart remodels itself. The remodeling pattern is different in the fit person from that in the sedentary person, the latter described by the Dallas group as a small heart, with concentric remodeling or hypertrophy and impaired filling or impaired diastolic function.
Heart size in this context refers to the volume of ventricle at the end of diastole (end diastolic ventricular volume). Concentric remodeling means no chamber enlargement with ventricular wall thickening. The terms concentric and eccentric dates back at least to the Morganroth hypothesis in 1975 from his cardiac echo study of endurance athletes and resistance training athletes.
As more data was generated it appeared that there is more to it that what Dr. Morganroth suggested. Some data from the Dallas group suggested that in the first year of aerobic training at least some folks develop concentric type changes and only later ( or perhaps with more intense training-long runs and/or high intensity interval training) does the classical runners heart pattern appear. Another study failed to show any concentric hypertrophy after a six month period of weight training.Studies involving rowers and cyclists show a mixed pattern.
Basically,the athlete's heart (at least the endurance athlete's heart) is big (but not in a bad way) muscular and very compliant and can relax quickly so that it can pump large volume of blood rapidly for prolonged periods of time. How much of that picture is genetic and how much is due to long time training is not known Whether levels of exercise equal to or slightly greater than the 2008 party line recommendations will mitigate the current "epidemic" of diastolic heart failure is an attractive hypothesis and one that I would like to believe.
"A man hears what he wants to hears and disregards the rest" - Paul Simon,song "The Boxer",1969
addendum 11/7/17- Several typos corrected along with minor editorial tweaks.
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