With the requisite,appropriate,cautionary,more-work- is needed caveat the authors of a very detailed and elaborate study published in 2014 say that 4-5 one half hour exercise sessions per throughout adulthood will prevent most of the age related loss of the heart's compliance and distensibility .In other words that amount of aerobic exercise will help to prevent the heart chambers from getting too stiff.It would really be nice to think so.
So what is wrong with stiff cardiac muscles ?
Application of the Woody Allen axiom of the pathophysiology of aging tells us that as we get older everything that should be soft gets stiff and everything that should be stiff gets soft.Think lens of eye,arteries and joints to name just a few.
A stiffer left ventricle is not a good thing as far as cardiac function is concerned.
The left ventricle (LV) basically sucks in blood while filling ( diastole) and ejects it during systole.As the heart becomes more stiff, the ventricle fills less easily , less sucking and more push from the atrium.The term diastolic dysfunction refers to this. Diastolic dysfunction (DD) plays a role in a number of heart diseases and some degree of DD is arguably a "normal" process of aging or as the authors of this article imply "sedentary aging".
Researchers the Institute for Exercise and Environmental Medicine in Dallas recruited healthy subjects over age 64 and screened them for histories of lifetime exercise habits and divided them into four group of about 25 per group.There were sedentary folks with no more than one exercise session per week , those with 2-3 session per week (causal exercisers), those with 4-5 sessions per week, labelled "committed" and the competitive group who trained 6-7 times per week and took part in races. (See here for full text of article) (This group lead by DR. B Levine from Southwestern Medical School has published a number of articles on general topic of cardiac function changes with aging and diastolic dysfunction. )
Extensive physiological tests were done including some involving right sided cardiac catherterization to measure the pulmonary capillary wedge (PCW) pressure. (I am still amazed that they found 100 healthy people who agreed to let some one put a catheter in their pulmonary artery for non-therapeutic reasons). PCW pressure is believed to be a reasonably accurate measure of the pressure in the left atrium which reflects left ventricular pressure , and elevation of which is a measure of LV failure.By infusing saline IV they were able to obtain curves relating the LV volume at the end of diastole with PCW pressure providing an indicator of LV compliance and distensibility.
The committed exercisers' values for these measures of ventricular compliance were very close to those of the competitive exercisers and definitely better than the sedentary and casual exerciser group as were values for other measures such as maximal oxygen uptake. This data ( shown in their "Central Illustration",p 1263 constitutes the major evidence for their thesis regarding how much exercise one has to do to maintain some semblance of LV distensibility. The more exercise the less stiffness but what the casual exercisers did was not enough.
Decrease in LV compliance and distensibility characterize heart failure with preserved ejection fraction (HFpEF). Other work by these same authors have shown similar pressure volume relationships in patients diagnosed with HFpEF as those seen in the sedentary and casual exerciser groups.They argue that sedentary aging "sets the stage for this increasingly recognized form of heart failure" It should be noted that heart failure with preserved EF might more correctly be named HF with preserved EF at rest. The EF does not increase normally with exercise in HFpEF and exercise intolerance is a major feature.
How the stage is set is unclear. Studies of exercise programs in patients with heart failure show improvement in exercise capacity but do not show improved values for various tests of diastolic function or ,for that matter-ejection fraction. So the improvement seems to occur in the muscles with increased capacity to extract oxygen for muscle function. Here the oxygen uptake would improve while cardiac output may not -they are able to exercise more because their muscles are better able to extract the oxygen from their limited cardiac output.Remember the Fick equation ( V02=CO X A-V 02 difference).
There is more to ventricular filling than ventricular compliance- how rapidly the heart muscle can relax following the ejection or systolic phase of the cardiac cycle is important. One aspect of relaxation can be measured by the IVRT ( isovolumic relaxation time) ,This can be measured by the time between aortic valve closure and mitral valve opening. The IVRT and the IRCT ( isovolumic contraction time) both increase as a function of age and are apparently not favorably influenced by life long aerobic exercise.
I have a high school friend who quoted one of his football coaches who was fond of saying "you are only as young as your legs".So some threshold value of regular aerobic exercise may serve to keep the ventricles from getting too stiff while exercise after the onset of HFpEF may still help but this time by making the legs a little younger.