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Wednesday, September 07, 2016

Endurance exercise athletes heart works differently from the untrained but how much is training and how much genetic?

People who do endurance exercise training may re-model their hearts in a way that not surprisingly facilitates exercise but also this may have public health implications in regard to
the increasing incidence and prevalence of diastolic heart failure, more properly labelled as HFpEF(heart failure with preserved ejection fraction.

The exercise physiology party  line had been for years-probably fifty or more- that as one increases his level of exercise, both heart rate  and stroke volume (SV) increase together up to a point. That point is around a heart rate of around 120 or a work load of about 40% of  02Max at which time the SV levels off. The thinking was that at higher heart rates diastolic filling time will become  so limited that SV would flatten out at a relatively low heart rate More recent data indicate that while  that pattern is what happens when the untrained person exercises , a different pattern has been observed in ( at least some) well trained endurance athletes and this difference may be due in part to impressive diastolic function .

The endurance athlete continues to increase the SV to levels higher than the text book limit of a heart rate of 120  and several authors including Gledhill et al ( ref 1 below) showed no plateau to the SV in heart rates up to 200 beat per minute in trained endurance athletes. Their ability to continually  increase stroke volume was attributed to not only enhanced ventricular emptying but to a even greater increase in ventricular filling. The left ventricular ejection time was longer and the diastolic or filling time was shorter. Not only could they push blood out better they could suck blood into the ventricle even  better.

This enhanced ventricular filling make the endurance  trained group better able to use the Frank Starling mechanism. ( Shifting the curve up and to the left) Further the greater blood volume seen in endurance athletes helps maintain adequate filling pressure and end diastolic volume given the shortened filling times that occur with heart approaching 200 beats per minutes. The greater ability to empty out the ventricle leads to a greater recoil from a lower end systolic volume with a greater suction effect enabling better filling.

The athletes were able to , for example, refill the ventricle with each 188 ml stroke volume in 0.1 sec.

Levine and co workers have shown similar patterns of  enhanced diastolic function in older endurance athletes.  (ref 2)

 Gledhill compared young ( average age 22) untrained subjects with a 02 max of about 40 with a trained group with  02 max of 60 plus. ( Group average for  the untrained was 44 versus 68 in the trained). So the trained group has 02 max values typically associated with folks who can run a sub-three hour marathon.  A trained person with a baseline of 44 V02 max  would be expected to be able to run a marathon in under 4.5 hours. (Estimates are from data of Davies and Thompson as depicted in table 2.3 in Noakes' Lore of  Running, 3rd edition.) Obviously Gledhill's endurance trained group  were rather far out on the curve of ability to exercise  and though they trained hard you have to wonder how high was their 02 max before training.

The authors of this and several similar articles hoped to study how fitness levels modify the heart and vascular system response to exercise. However the authors realized that this type of cross-sectional study cannot tease out the effect of  training from the effect of genetic endowment,
Quoting Gledhill:

"It is not possible to state with certainty ,based on these findings, that the difference in cardiac function between endurance trained athletes and normally active individuals is an adaptation to endurance training, a consequence of genetics or a combination of these influences."

 So far all of this seems little more than inside baseball physiology talk but could there be a broader significance ?

A optimistic " maybe" seems to be the view of Dr. Benjamin Levine of Southwestern Medical School (see reference number 3).

Levine's et al showed that there was some preservation of diastolic function-i.e ventricular compliance as measured by echocardiography  (E/a ratio etc) as a function of the amount of long standing aerobic exercise and it seemed proportional to the amount of exercise. Long term exercisers had better compliance ( aka measure of ventricular stiffness) while measurements of "relaxation" decreased in the exercisers to about the same degree with aging  as the sedentary group-this was measured by the relaxation time (IVRT) of the left ventricle.IVRT is the time between closure of the aortic valve and the opening of the mitral valve.

On the other hand, Hirofumi Tanaka et al from Colorado  (see reference 4) concluded that the compliance was not preserved in the long term exercisers ( though I believe  some of his data was not really inconsistent with that hypothesis) while  there was a beneficial modulation of the age associated stiffness in the large elastic arteries ( as measured by the aortic pulse wave velocity)

 Levine ( reference 5) has suggested that the long term endurance exercise ( maybe as "little" as 2-3 hours per per week) can prevent the decrease in left ventricular compliance associated with aging and/or inactivity and perhaps have important implication for prevention of cardiovascular disease ( ie. HFpEF or diastolic heart failure).  While, in my opinion,the evidence for this is a something less than overwhelmingly convincing this  is a  reasonable possibility and it would be very nice to think so, particularly to someone who has done a lot of running over the years.

A mechanism by which exercise may help to maintain  ventricular compliance has been outlined by Hyo-Bum Kwak ( ref 6) on the basis of rat research into apoptosis or programmed cell death and exercise. Myocytes decrease in the aging heart and this is in part thought be due to a mitochondrial-mediated apoptotic pathway. Kwak has shown that exercise training decreased these apoptotic pathways .

 "Reason is, and ought only  to be, the slave of the passions and can never pretend to any other office than to serve and obey them." David Hume "Treatise on Human Nature"circa 1738.


 1.Gledhill, N. et al  Endurance athlete's stroke volume does not plateau:major advantage in diastolic function.Medicine and Science in Sports and exercise,26, pp 1116-1121, 1994

2.Levine, BD et al. Left ventricular pressure volume and Frank-Starling relations in endurance athletes.Circulation 84:1016-1023.1991

3.Prasad,A The Effects of Aging and Physical Activity on Doppler measurements of diastolic function. Am J Cardiol 2007, 99, 1629

4.Tanaka, H Endurance exercise performance in Master's athletes age-associated changes and underlying physiological mechanisms.  J Physiol 586, 2008, 555-58

5.Bhella, P Impact of Lifelong exercise "dose"on left ventricular compliance and distensibility
JACC 641257-1266,2014

6. Kwak,H , Effects of aging and exercise training on apoptosis in the heart. J exer Rehabil 2013 apr 212-219

addendum several additions made to introduction to text-2/4/17

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