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Is the new professionalism and ACP's new ethics really just about following guidelines?

The Charter ( Medical Professionalism in the New Millennium.A Physician's Charter) did not deal with just the important relationship of ...

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.

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 bets 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). 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. 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

Friday, September 02, 2016

Health care with other people's money- what could be wrong with that?

Paying for health care with other people's money-what could possibly go wrong?

Dr. Paul Hsieh answers the question posed in the title in a commentary in Forbes. See here.

He outlines four important ominous consequences of basing health care on spending other people's money.

  This excellent article should be read in its entirety but let me briefly  comment on the first in the list.

"Doctors will be increasingly expected to save money for the system  ."

This is already happening.Various medical professional organizations are re-writing traditional medical ethics, pushing the fiduciary duty of the physician to the patients into the memory hole and substituting the bogus concept of the physician as a steward of society's medical resources which at least one physician's organization (the ABIM Foundation) has strangely linked to social justice. I have ranted about this before but the caravan rolls on and increasingly  the rhetoric  in various medical forums emphasizes saving money for the system. It seems that the medical professional elite would have us believe that the road to social justice is for physicians to follow guidelines, which may not be designed for patient benefit alone but also for cost containment for the third party payers.

The medicine of the collective is replacing the medicine of the individual. This is being promoted in part by what I have called the progressive medical elite who, to a frightening degree, seem to occupy the leadership positions in many influential medical organizations . Their unspoken mantra is that medical care is too complex and too important to be left to the individual patient and his physician. Wise leaders with ideas need to be in charge. Of course, it is promoted by the third party payers, private and public who may well consider the medical professional  elite in this ethical paradigm shift as useful idiots.

 The third party payers and the professional medical elite have attempted to turn traditional medical ethics around so that the fiduciary duty to the patient is somehow replaced by an ethical duty to save money and the whole flim-flam activity is sprinkled with non sequiturs  about social justice. Social justice is typically taken to mean redistribution and if cost to the system is reduced it is difficult to see wherein the redistribution lies if everyone gets less.Everyone, of course, except the third party payers.

  In regard to private property the owners have the incentive to be a "good steward" of theirresources.You have to ask what is the incentive of physicians to act as stewards of a mythical  collectively owned resource? 

The notion of "the system" [in regard to medical care] while a rhetorically useful notion for a certain agenda, is basically fallaciously  aggregating elements that do not belong together. In short, there is no system for health care just as there is no car delivery system or a home building system. It makes no sense to speak of the situation in which someone buys a new car as a cost to the car supply system or a person buying a home as a cost to the home supply system.All of these are transactions in which there are buyers and sellers and exchanges take  place.Mr Jones gets a CT  of  the abdomen.. This is not a cost to any system. It is a cost to Jones and/or his insurance company while to the providers of care it is a payment. One person's cost is another person's income.To call this a cost to a system is nonsense.Unless all the health care is provided, operated and owned by  a single entity, usually the government., then the services provided  could be considered  a cost to the system.

Who gains from acceptance of this bogus notion of physicians as stewards of some mythical collectively owned medical resources? The third party payers for whom the gain is obvious and the medical elite progressives who stand to gain from their position of prestige  as experts and rule makers  and the rest of us,physicians and patients,  lose.

So, in summary there is no medical care system to which a cost is charged with every medical care transaction and secondly the physician as steward concept is completely contradictory to the traditional role of the physician as the fiduciary agent of the patient .

Thursday, September 01, 2016

What is going on with the price of the Epipen?

 Scott Alexander on his blog Slate Star Codex offers this insightful explanation of what is going on with the price of the Epipen and why are there not cheaper substitutes available in the US. Actually Alexander tells us this is one.See here.

John Goodman tells a similar story here.

 I have never actually used an Epipen but in an ill planned effort to dispose of an out of date pen I managed to drive the needle through my thumb.