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Monday, October 10, 2016

Exercise capacity of octogenarians and age related decline in exercise capacity

A great source for information about the exercise capacity of octogenarians is a 2013 article by Scott Trappe and co-authors.( Trappe,S et al , New records in aerobic power among octogenarian lifelong endurance athletes. JAAP, vol 114, no 1, 3-10.) See here.

The authors studied 9 life long and still competitively active  elite endurance athletes and compared their aerobic capacity as well as myocellular markers of oxidative metabolism with 6 age matched healthy non exercisers.

The V02 max (maximal oxygen uptake ) in the group of athletes was 38 plus/minus 2.1 ml/kilo/minute versus 21 plus minus 1 for the sedentary group. The authors reviewed other published data on aerobic capacity in untrained 80 year olds and found:

1) In 195 men  the average V02max was 21 plus/minus 4
2) In  269 women the average V02max was 18 plus/minus 4

These values are comparable to Trappe's non-exercising  subjects while his athletes  were said to have the highest values reported in a group of octogenarians.(There are some individual case reports with value this high and higher-see below)

Having monitored several hundred stress tests using the Bruce protocol I find it helpful to put these 02max values in that context.

The Bruce protocol has 3 minutes stages and after each the treadmill pace and inclination increase:

Stage I 1.7 mph 10% grade using 5 METS  and requiring 17.5 ml 02/kilo/mi

Stage II 2.5 mph 12%                    7 METs                          24.5

Stage III 3.4 mph 14%                    9 METS                        31.5

Stage IV    4,2    mph 16%               13 METS                        45

Stage V    5 mph  18%                     15 Mets                          52

Stage VI     5,5 mph   20%               18 METS                       68

A MET is the resting oxygen uptake of 3.5 ml 02/kilo/min.

Based on these values many or maybe most of the male non athlete   octogenarians would complete Stage I while a number  of the females might not  not.Most of Trappe/s athletes would complete Stage 111 .

One of Trappe 's'subjects was 91 years old , a former Olympic champion  ( ok he is not an octogenarian)  has an amazing  aerobic capacity of 36! He should complete stage 3 and into stage 4.

Using time estimates from Tim Noakes book (footnote 1   ) you can guesstimate  running and marathon times from aerobic capacity or  at least get a estimate of the aerobic capacity that is required to run at a given speed. An  02 capacity of 30-32 would be required to complete the 26.2 marathon in about 5.5 hours.

Ed Whitlock, dob 1931, was the first man to run a marathon in less than 3 hours at age 70 .At age 73 he ran a 2:54 marathon.It probably takes a 02 Max of 60 to run a sub three hour marathon.

There are real life 80 year  people who complete marathons. For example, 4 men all aged 80 finished the Houston Marathon in times ranging from 4:23 to 5:40  in 2016 .The winner in this group probably has a 02 max of about 40 ( using the table from footnote 1).Also there were three 80 year olds who completed the NY City Marathon in 2016 with times ranging from 5:03 to 5:37.

In 2011 Ed Whitlock at age 80 ran the Toronto Marathon in 3:15corresponding to a 02 uptake of 50-53. This is  comparable to the report by Trive Karlsen who measured the max 02 uptake on an 80 year old Norwegian at 50 and claimed a world record for an 80 year old.See here. There are  a few other octogenarians who have run a sub-four hour marathon, Ed Benham ran 3:48 at age 82. and Harold Willson who did 3:58 at age 80 . These are times  probably requiring an 02 Max of around 40.

(See addendum below for update on Ed Whitlock)

In regard to the non superathlete  male octogenarians , their average 21 ml/kilo/min aerobic capacity should allow them to be able to walk at a fifteen minute per mile pace  ( which is a fairly brisk walking  pace) which probably requires about 17 ml  02/kilo/min as does playing double tennis, doing light yard work ,etc. and a lot more than whittling on the park bench.Finishing Stage II suggests adequate 02 capacity to run a fifteen mile. (Walking a fifteen minute mile requires about 70% as much 02 uptake as does running a mile.)

It seems more than reasonable to assume that these octogenarian marathon finishers has in their youth 02 max values just as impressive for their ages then as they are now and likely could have run a marathon in less than 2 1/2 hours.

The conventional thinking is that from about age 45 to age 70 a persons aerobic capacity declines somewhere between 5% and 10 % per decade. Some studies have shown and other studies have presented contradictory evidence  that those who continuously train aerobically  have a lower rate of decline. ( Personal note-A rough calculation based on my marathon times suggest that my decline was slightly over the 10% per decade number)

Some of subjects in the non athletic group had V02 max value approaching the range that have been proposed as a threshold value for independent living(18 ml/kilo/min) and as a threshold for disability assessment ( 15 ml/kilo/min) refs 2 and 3

The lower the 02 max, the higher percentage of it is used  for the typical  activities of everyday life leading to fatigue and predisposition to inactivity and deconditoning. Further the increased oxygen consumption  attendant to trauma , acute illness and surgery may push someone with a 18 -20 02 max over into the disabled category .

addendum: 10/19/2016- Ed Whitlock, now 85 years old, finished a marathon In Toronto in 3 hours and 56 minutes -over a half hour quicker than the previous record for that age for the marathon.


 1.Table 2.3 page 66, Forth Edition of "Lore of Running " Tim Noakes

2 Jackson, AS et al Effect of lifestyle and aging on the longitudinal change in respiratory fitness. Arch Int Med. 2009,169 ,1781

3 Putz, C et al  Incremental shuttle and six minute waking tests in the assessment of functional capacity.in Chronic Heart Failure.Can J Cardiol 2008 24 (2) 131-134

Thursday, October 06, 2016

Exercise intensity and risk of atrial fibrillation-a possible gender specific effect

Dr, S, Moharty  et al have presented a meta-analysis on the relationship between exercise level and risk of atrial fibrillation (AF). In what is the largest data analysis to date on this topic they found that  women's risk of AF is reduced at all levels of exercise while in men low and moderate levels of exercise seem protective risk of AF increases at the highest levels.

The term coined by Jim Manzi,( ref 5)  high causal density, seems appropriate in regard to the etiology of AF. Both inactivity and allegedly " too much exercise" both increase the risk of AF as do aging,obesity, alcohol , hypertension ,  perhaps pericardial fat deposition. and apparently being too tall as well as a number of other putative risk factors.The trick is to figure out what is "too much". Moharty's paper suggests there may be  no "too much" for women ,at least they did not demonstrate a threshold, a claim  which I believe has not been made before.

Reviewing 22 studies (665,750 subjects) they found:

1) In men moderate exercise was protective ,OR .72 , while vigorous exercise increased AF risk with an OR of 3.30 (1.97--4.63). When the authors excluded some small case control studies that had very wide confidence intervals the estimated  risk level was reduced but not eliminated to OR of 2.45 ( 1.1-3.8)

2 )In women moderate exercise was protective with an OR or 0.91 while vigorous exercise seemed even better with an OR of  0.72. So for them more was better without limit?

Previous studies were conflicting with some showing in men the so called J or U shaped curve while others claimed greater physical activity was associated with a lower risk of AF. i.e. a continuing downsloping risk curve as exercise levels increase. Moharty's study indicates that in women the curve is continuously down sloping and supported the existence of a  U-shaped curve in men.

 Intensity levels of exercise in most (all?) of the studies is at best a "coarse grain" indication. Some  of the exercise levels were based on the subjects' declaration of  their exercise level. In Anderson's study of cross country skier exercise  level was defined as finishing one race versus those who finished 5 or more. In some trials AF was self reported, in others AF was  physician confirmed. Often exercise level reflects duration of exercise per week with no consideration of level of intensity of exercise and  some times quantified by number of endurance events completed usually without consideration of intensity, i.e completion times.

The effect of men's age on risk of AF at various exercise levels is also a consideration. At least it seemed to be in Aizer's paper. This was an analysis of AF in men in a post hoc analysis of the randomized aspirin study as part of the Physicians health study. (Ref 1) The only increased AF  risk was shown in men less than age fifty at the highest self reported exercise level.Suggested non-causal explanations for this include survivor effect and the increased risk of so called lone-AF in otherwise healthy runners  usually in a younger or middle aged man 

Another study presented data that suggested increased risk of AF in younger but not older men. This study  by Nikola Drca from Sweden  was a long term followup of 44,000 men with retrospective estimates of their exercise levels. Those 30 year olds who exercised more than 5 hours per week has an increased RR (1.19) but that was not the case for fifty year olds.  Again, could this be a survivor effect or a high number of so-called lone parasympathetic AF in the younger runners? Here we have the relative risk of less than 2, a topic I have ranted about before. An age differential effect was not mentioned in Moharty's paper.

Being the pattern seeking story telling creatures that people are ( ref 4) there are bound to be speculations as to why/how this purported  gender difference could occur. Here is one such such speculation found in a 2011 article by Wilhelm ( ref 3). The authors compared male and female non elite runners and found that the men has subtle changes in diastolic function, slightly large left atria ,changes in heart rate variability and higher BP during exercise, a constellation of findings arguably making male runners, holding training levels constant, more at risk for AF and in fact 4 of the 70 men  studies did have episodes of paroxysmal AF.

How to determine where moderate ends and excessive begins either with group data on for an individual is the problem.

1. Aizer,a et al. Atrial fibrillation is association with different levels of exercise at different ages in men. Heart 2014;100, 1037-1042.

2.Drca, N Atrial fibrillation is associated with different levels of physical activity at different ages in men. Heart, 2014 ,100 (13), p 1037

3. Wilhelm, M et al.Gender Differences of atrial and ventricular remodeling and autonomic tone in non elite athletes.American Coll cardio nov15,2011, vol 108, pg 1489

4."Humans are pattern seeking story telling creatures and are quite adept at telling stories about patterns whether they are true or not.: Usually attributed to  Michael Sherma.The phrase became a theme for Ed Lemer, UCLA economist, in his Book "Macroeconomic Patterns and Stories.

5."Uncontrolled:The surprising payoff of trial-and-error" Jim Manzi ,2012 Basic Books

Wednesday, September 07, 2016

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

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 as the sedentary group-this was measured by the relaxation time (IVRT) of the left ventricle.

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 some of his data was non 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 pathways. 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"


 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

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.

Wednesday, August 03, 2016

New high school football season advice-don't let your babies grow up to be defensive backs

 Extracted from an article  from AANS regarding traumatic brain injury (TBI) data from 2012:

Defensive backs in American football are at the greatest risk for both fatal head injury and serous cervical spine injury.:

"The majority of catastrophic injuries occur while playing defensive football. In 2012, two players were on defense and one was in a weight lifting session. Since 1977, 228 players with permanent cervical cord injuries were on the defensive side of the ball and 55 were on the offensive side with 44 unknown. Defensive backs were involved with 34.6 percent of the permanent cervical cord injuries followed by member of the kick-off team at 9.2 percent and linebackers at 9.5 percent."

Spending even a small amount of time watching high school,college and professional football on TV makes it seem obvious that the vast majority of high impact collisions occur in the defensive zone involving defensive backs and either runners or receivers and on kickoffs.Quarterbacks receive many hits with the helmets impacting the ground and have a significant risk of concussion but apparently have  lower risk of fatal injury or injury leading to permanent disability.Offensive and defensive  linemen may receive more sub-concussive head blows over a game or a season and whatever the long term consequences of that may be  seem less likely to regularly  be involved in high impact collisions and therefore less at risk for serious brain or cervical spine injury. There is a reason for ambulances to be  parked near the playing field of high school football games attesting to the cognitive dissonance of some of  the  parents cheering them on.The EMTs are not on site to help manage sprained ankles.

Don't let your babies grow up to be defensive backs.

Notice: This is a lightly edited and altered version of an earlier commentary on this blog. As  I see high school kids  on the practice field in early August in Texas with heat indices pushing 105 my antipathy to high school and youth football  flares again.

Monday, August 01, 2016

Another football season begins, what do we know about sports related head trauma

What do we know about head trauma in high school and college football?

Mild Traumatic Brain Injury ( mTBI) encompasses the clinical entity of concussion. Concussion is defined as a trauma induced alteration of mental status with or without loss of consciousness.

Considerable research has been published regarding concussion and recently  research has been published about the multiple blows to the head that occur in all levels of football in  the absence of a recognized concussion. These "sub-concussive blows" have become the target for various types of brain imaging and cognitive function testing and the results have raised concern about the long term effects on the brains of highs school and college players.

 Some of what we know is :

1.While conventional MRIs and CTs in concussed high school and college football players are normal , Diffusion Tensor Imaging (DTI) and functional MRI have shown abnormal findings some of which may persist for weeks or months. Additionally subtle impairments of verbal memory and other cognitive tests have been reported in concussion cases persisting past the time during which the player has any symptoms.The long term significance of these finding is not known.

2.Similar imaging findings and cognitive testing results are being reported in high school and college players after a season of participation in football even thought the players had no reported concussive event.

3.We know that football helmets do not prevent concussions.

4.We know that at least  some  college level contact sport athletes decades later show abnormal white matter by Diffusion tensor imaging and lowered test results on cognitive testing but again we don't know if these changes are a predictor of later symptoms of CTE.

 Some of  what we don't know is :

1.We do not know what pathological changes underlie the imaging findings. Do the scan results indicate transient damage and tissue repair without likely long term sequelae? Is there a recognizable subset of these players with these findings who if  they continue to be exposed to multiple head blows over many years will develop Chronic Traumatic encephalopathy (CTE)? How can those who may be destined to develop CTE be distinguished from the vast majority of players who never will  have those problems

From  the wide range of head hit exposures in those NFL players who have been diagnosed with CTE the obvious implication is that there must be a fairly wide range of thresholds. There are reports of NFL players with as little as five years of play showing  typical pathological findings at autopsy. Further there has been at least one case of a college player diagnosed with CTE.

2.the long term cognitive changing on various tests  and brain imaging abnormalities have been   demonstrated  in  contact sport athletes in college and high school who did not experience a concussion.

 After the last high school football season ending there were reports of 13 fatalities.   This is about average for the years following the meaningful changes made in the rules and the instruction of techniques of blocking and less dangerous ways to tackle. Better helmets probably prevent skull fractures but not concussions.Can you imagine the outcry if high school boys were forced to take part in an activity that results in deaths each year?

See here for details  of some  of those deaths. Tragically it seems that two were due to heat stroke, all were not due to head injury.In reading over the cases it seems reasonable to designate two of the deaths to the second hit syndrome.

You see the same parents who carefully made sure their kids did not ride tricycles without  wearing helmets are some of the same ones watching and yelling at Friday night football games and probably do not see the irony  of common practice of there being an ambulance at the stadium. If their son is the victim of the second hit syndrome, probably an ambulance won't help.

Note: Much of this posting is a rewrite of another commentary from last year which I shamelessly re-post  now with only  a few additions  because this topic is one I obviously feel strongly about .I used to really enjoy watching professional and college football on tv now I only occasionally watch  just to sample the action to notice obvious head trauma. Professional players increasingly are able to make some effort at an informed decision to play with considerations of the risk to their brains, high school kids and younger much less so.