What are the arc (s?) of the normal aging heart ( the sedentary ageing heart and the exercising aging heart)
One of the stories told by physiologists and cardiologists regarding the age related downhill course of cardiac function is something like this.
One way to simplify cardiac function is to consider the two parts of the cardiac cycle,1) contraction and ejection of blood and 2) relaxation and the refilling of the ventricle.
There are data indicating that the first signs of an impending problems are seen in the filling phase ie. diastole.From extensive echocardiographic and invasive physiologic measurements in humans the following sequence can be sketched out and penciled in.
First, there is impaired relaxation following by decreased elastic recoil and later diminished compliance ( which is to say increased stiffness) and then -at least according to work from the.IEEM group- remodeling of hearts with thicker walls and smaller ventricular volumes).Simply put a sedentary ageing lifestyle leads to a small stiff heart and long time endurance exercise leads to a larger more easily filled heart.The contractile function of the heart is well preserved with ageing , at least as indicated by measurement of the resting ejection fraction.( increasing stroke volume with exercise is another matter.)
This is largely consistent with the mainstream echocardiographic model which proposes a predictable,progressive process beginning with impaired relaxation,followed by decreased compliance and ultimately- as a compensation- elevated filling pressures.This model describes three phases of diastolic dysfunction indentifiable by combination of echo findings believed to reflect how well or poorly blood flows into the ventricles from the atrium. This model recognizes that the various indices ( e.g E/A ratio, IVRT,maximal E wave velocity and the time constant of isovolumic pressure decay (Tau) change with age so that what would be abnormal in a 20 year old is normal in a 75 year old.It is thought that that filling pressure can be estimated by use of this model. NOTE-see end note 1 for reference to data that challenges the mainstream model by in part providing data that cardiac cath measurements of left sided pressures do not regularly correspond with the three echo defined stages of diastolic dysfunction)
Now we look at what I have labelled as the "Dallas or IEEM theory" of cardiac ageing. see end note 2
A series of articles from the University of Texas Southwestern Medical School and the IEEM have provided extensive invasive and noninvasive data regarding cardiac function at various ages and the effect of longtime endurance exercise versus sedentary ageing on cardiac structure and function.
Levine et al first demonstrated that lifelong endurance athletes ( 25 years or more of running a lot) had left ventricular compliance virtually identical to those of sedentary 20-30 years olds. Then they compared ventricular compliance in four groups of 25 each of people who exercised at various levels over a 25 years period. These were all subjects over the age of 64 and were screened to excluded pre-existing heart disease.Group 1 was sedentary people who exercised no more than one session per week. Group 2 were labelled "causal exercisers" and exercised 2-3 times per week. Group 3 (Labelled as committed exercisers}worked out 4-5 times per week and the "competitive" group trained 6-7 times per week and regularly raced.The racers had the most elastic or compliant ventricles while group 3 was "very close" in terms of ventricular compliance while groups 1 and 2 has significantly stiffer hearts.Note: while exercise seemed to help maintain compliance , long time endurance exercise did not mitigate the age related loss of ventricular relaxation-as measured by the isovolumic relaxation time (ivrt) which is the time from aortic valve closure to mitral value opening.
Next, Levine studied a group of 70 year old subjects and an vigorous exercise program was unsuccessful in improving the reduced compliance observed in that group. Next another study demonstrated that middle age subjects with a year long exercise program ( that involved in part high intensity interval training) were able to increase their ventricular compliance.This implies that past some point in time you cannot improve LV compliance with endurance training with some interval training but middle age may not be too late.
In another article Levine said that exercise in the range of that performed by the "committed exerciser" might be adequate.
My main question in this regard is "how much exercise "is sufficient to maintain a healthy compliant left ventricle." Levine's amazingly compliant (pun intended) subjects not only stuck with program for a full year but after the first 6 months participated in a hig intensity interval program using the demanding 4X4 workout program that involves 4 minutes of exercise at 95% of maximal heart rate followed by 4 minutes of rest done four times.
End note 1. Grant et al (Grant A, Grading diastolic function by echocardiography:hemodynamic validation of existing guidelines.Cardiovascular Ultrasound 2015 513 :28) compared echocardiography results with left heart catherization data in 460 patients.The data demonstrated that there were no differences in regard to left ventricular pressures between patients with normal diastolic function and those with grade 1 or 2 diastolic dysfunction but there were differences between normal and grade 3 diastolic dysfunction in patients with reduced ejection fraction.In those patients with preserved EF, there is no statistical difference between normal and any grade of diastolic dysfunction. (see figure 5 of their article which graphically illustrates the lack of the "predictable, progressive process "which characterizes the current paradigm.)If the detection of elevated LV pressures which generally correlates with exertional shortness of breath is in part the goal of echo studies of diastolic function it appears to not be reached based on Grant's data.
end note 2. Dr Ben Levine is the director of the Institute for Exercise and Enviromental Medicine (IEEM) housed at the Texas Health Presbyterian Hospital Dallas and professor at University of Medicine Southwestern. His group have done a series of comprehensive physiological studies on subjects recruited from the Dallas Heart Study, a population based sample of 6100 subjects in Dallas .
In a nut shell the concept is that everyone with aging develops some degree of diastolic dysfunction related to impaired relaxation and loss of diastolic suction,Later aging (particularly sedentary ageing) is associated with loss of ventricular compliance ( AKA increased stiffness). A long term endurance exercise program is capable of mitigating the changes in compliance but not the decrement in relaxation and diastolic suction. IEEM's studies further indicate that a sedentary lifestyle may lead to a small stiff heart which may be the precursor to heart failure with preserved ejection fraction (HFpEF) ) and the Dallas group suggest that an appropriate amount of endurance type exercise begun no later than early middle age may play an important role in the prevention of HFpEF.
"Humans are pattern-seeking story -telling animals and we are quite adept at telling stories about patterns, whether they exist or not".Michael Shermer.
End note 3:In 2008, Shermer coined the term "patternicity" -the tendency to find meaningful patterns in meaningless noise. I am not suggesting that the extensive,very carefully done research referenced above is meaningless noise.I just really like the quote but I certainty hope the "Dallas hypothesis" ( my term) is a reasonably accurate approximation of the ways things really are at least sometimes- having spent a lot of time running a lot over the last 40 plus years.
addendum 11/6/18 Several minor editorial changes.
addendum 1/20/18 I realized I had used a erroneous abbreviation for the Institute for Exercise and environmental Medicine referring to it as "EEM"
Tuesday, March 20, 2018
Sunday, March 18, 2018
Mitochondrial function in octogenarian endurance athletes
Scott Trappe from Ball State University and colleagues from the Karolinska Institute studied 9 lifelong endurance athletes 80 years of age or older with 6 healthy 80 years olds who did no regular exercise. Aerobic capacity and muscles biopsies -done to measure levels of oxidative enzymes- were compared between the two groups.
The muscle biopsies showed high levels of citrate synthase and beta hydoxyacyl-Co A dehydrogenase in the athletes said to reflect the oxidative potential of the mitochondria. These values were similar to those from untrained young subjects.
Quoting the authors: " It is important to note that mitochondrial function normally declines with age and this decline does not appear to be reversible with endurance training in sedentary adults greater than 80 yr old or very old animals." This implies that one has to start earlier and maintain some level of regular aerobic exercise to keep your muscle mitochondrial young.
I have commented before on the impressive aerobic capacity of select elite older athletes.see here.Trappe's athletes had measured maximal oxygen uptakes of 38 +/- 1 while the healthy controls averaged 21+/1/ .(O2 max in the range seen in the athletes would roughly correlate to the levels seen in someone able to run a 26.2 marathon in 4 to 4/1/4 hours,A 21 02 Max should allow someone to finish stage 1 of the Bruce treadmill protocol and into the second stage but likely not to completion of Stage 2.)Stage 1 Bruce protocol corresponds to 5 Mets roughly equivalent to walking a 15-16 minute mile and to be able to finish Stage 2 corresponds to 7 Mets roughly equivalent to jogging a 15 minute mile.
Trappe's article is entitled "New Records" but as amazing as these guys were aerobic wise an Englishman transposed to Canada is one rung above on the aerobic scale. Ed Whitlock at age 80 finished the Toronto Marathon in 3 hours and 15 minutes.Using table 2.3 from Tim Noakes's book ,4 th edition The Lore of Running this time would correspond to an estimated V02 Max of 50-55! See end note 1.That value range corresponds to actual 02 max laboratory measurement done on Whitloc at age 70 and again at age 81.
1) Trappe S Et al New Records in aerobic power among octogenarian lifelong endurance athletes.J. Applied Physiology 114.3-10 2013.
End note 1.Rather than considering estimated 02 max from a table we can see actual measured values done on Ed Whitlock on two occasions. From the excellent blog entitled "Canute's efficient Running Site" we learn that just before his 70th birthday Whitlock's measured V02 max was 52.8 and at age 81 it was measured at a physiology lab at McGill to be 54!. Assuming that the difference between 52.8 and 54 was just normal test-retest variation, Whitlock seemed to loose no aerobic capacity over a ten year period. Conventional wisdom and more than a little data indicate that the 70-80 decade is typically a time period in which there is an accelerated decline in 02 max,perhaps twice that of the 10 % per decade decline than is widely quoted. Whitlock did not get the memo.The VDOTvalues that are referenced on Canute's website and found in detail on Jack Daniel's VDOT Running Calculation web site appear to give more realistic estimates of running times that those that I have been using for comparison with exercise testing comparison that those found on Noake's table.
addendum: End note 1 was completely redone after discovering Canute's web site.
The muscle biopsies showed high levels of citrate synthase and beta hydoxyacyl-Co A dehydrogenase in the athletes said to reflect the oxidative potential of the mitochondria. These values were similar to those from untrained young subjects.
Quoting the authors: " It is important to note that mitochondrial function normally declines with age and this decline does not appear to be reversible with endurance training in sedentary adults greater than 80 yr old or very old animals." This implies that one has to start earlier and maintain some level of regular aerobic exercise to keep your muscle mitochondrial young.
I have commented before on the impressive aerobic capacity of select elite older athletes.see here.Trappe's athletes had measured maximal oxygen uptakes of 38 +/- 1 while the healthy controls averaged 21+/1/ .(O2 max in the range seen in the athletes would roughly correlate to the levels seen in someone able to run a 26.2 marathon in 4 to 4/1/4 hours,A 21 02 Max should allow someone to finish stage 1 of the Bruce treadmill protocol and into the second stage but likely not to completion of Stage 2.)Stage 1 Bruce protocol corresponds to 5 Mets roughly equivalent to walking a 15-16 minute mile and to be able to finish Stage 2 corresponds to 7 Mets roughly equivalent to jogging a 15 minute mile.
Trappe's article is entitled "New Records" but as amazing as these guys were aerobic wise an Englishman transposed to Canada is one rung above on the aerobic scale. Ed Whitlock at age 80 finished the Toronto Marathon in 3 hours and 15 minutes.Using table 2.3 from Tim Noakes's book ,4 th edition The Lore of Running this time would correspond to an estimated V02 Max of 50-55! See end note 1.That value range corresponds to actual 02 max laboratory measurement done on Whitloc at age 70 and again at age 81.
1) Trappe S Et al New Records in aerobic power among octogenarian lifelong endurance athletes.J. Applied Physiology 114.3-10 2013.
End note 1.Rather than considering estimated 02 max from a table we can see actual measured values done on Ed Whitlock on two occasions. From the excellent blog entitled "Canute's efficient Running Site" we learn that just before his 70th birthday Whitlock's measured V02 max was 52.8 and at age 81 it was measured at a physiology lab at McGill to be 54!. Assuming that the difference between 52.8 and 54 was just normal test-retest variation, Whitlock seemed to loose no aerobic capacity over a ten year period. Conventional wisdom and more than a little data indicate that the 70-80 decade is typically a time period in which there is an accelerated decline in 02 max,perhaps twice that of the 10 % per decade decline than is widely quoted. Whitlock did not get the memo.The VDOTvalues that are referenced on Canute's website and found in detail on Jack Daniel's VDOT Running Calculation web site appear to give more realistic estimates of running times that those that I have been using for comparison with exercise testing comparison that those found on Noake's table.
addendum: End note 1 was completely redone after discovering Canute's web site.
Tuesday, March 06, 2018
What does reduced ejection fraction in elete athletes mean?
Some NBA players and professional European cyclists (1) have been shown to have reduced cardiac ejection fractions (EF) and some NFL players(2 )have EFs in the lower range of normal.
In regard to the cyclists this observation has , at least in one review, been used to bolster the argument that "too much exercise" is harmful , i.e. support for the "U-Shaped" curve theory."Too much " exercise certainty can be harmful (maybe that is what "too much" means) but reduced resting EF in elite athletes is not proof of that contention.
The "wisdom of the body "may dictate that maintenance of stroke volume a priority and not EF. These athlete have large preloads ( aka end diastolic volumes) so that a smaller percentage can be ejected to maintain the resting stroke volume. These basketball players had a normal increase in stroke volume and EF with exercise as did the NFL players.I believe the exercise EF was not measured in the cyclists.
1.Abergel, E. Serial left ventricular adaptations in world -class professional cyclists.J AM Coll Cardiology July 2004.
2. Abernethy,WB Echocardiographic characteristics of professional football players.JACC Jan 2003 p 280
3)Engel,D Athletic cardiac remodeling in U.S. professional basket ball players. JAMA Cardiol 2016, (1) 80-87
In regard to the cyclists this observation has , at least in one review, been used to bolster the argument that "too much exercise" is harmful , i.e. support for the "U-Shaped" curve theory."Too much " exercise certainty can be harmful (maybe that is what "too much" means) but reduced resting EF in elite athletes is not proof of that contention.
The "wisdom of the body "may dictate that maintenance of stroke volume a priority and not EF. These athlete have large preloads ( aka end diastolic volumes) so that a smaller percentage can be ejected to maintain the resting stroke volume. These basketball players had a normal increase in stroke volume and EF with exercise as did the NFL players.I believe the exercise EF was not measured in the cyclists.
1.Abergel, E. Serial left ventricular adaptations in world -class professional cyclists.J AM Coll Cardiology July 2004.
Monday, March 05, 2018
Reversing cardiac aging-maybe some but it isn't easy
More about cardiac aging and aerobic exercise from the Institute for Exercise and Environmental Medicine is found the January 2018 issue of Circulation. Howden et al(1) report the results of a two year trial of a vigorous exercise program on various physiological measurements.
They were able to show some improvement in cardiac compliance ( i.e. a decrease in myocardial stiffness) in a group of middle aged,otherwise healthy subjects over a 2 year period but the exercise required was considerably more than frequent brisk walks or slow jogs around the park.Rather , part of the exercise program involved a vigorous high intensity interval program using the "4 by 4 " Norwegian Skier technique twice a week and later in program only once a week.
Dr. Ben Levine, the Director of the Institute, and his team seemed to be able to recruit subjects who would persevere in a demanding exercise program over a 2 year program and to also permit right heart catheterizations which were done to give the investigators an index of compliance of the left ventricle.The bottom line is that they were able to demonstrate a reduction in cardiac stiffness with their exercise program .
This study is the most recent in a series of publications which have demonstrated that there is some level of prolonged endurance exercise that can at least to some degree mitigate the age related loss of cardiac compliance . Previously they had attempted to improve cardiac compliance in older subjects (in their 70's) and were unsuccessful. In this study they hoped they could find a "sweet spot", a time frame in which it was not loo late to reverse the age driven stiffness and they seemed to have , at least to some measurable degree, succeeded .
Levine characterizes the sedentary heart as a "small, stiff heart" versus the endurance athlete's heart as larger,slightly thicker and more compliant.
Levine describes the stages in the aging of the heart :1) loss of relaxation ,2) stiffening ( beginning in middle age), and finally 3) remodeling. The hope is that adequate exercise might mitigate or significantly delay stage 2 which may be the precursor or a prerequisite for heart failure with preserved diastolic function. Years of endurance exercise does not seem to prevent the first phase but Levine's data suggest that exercise may counteract the stiffening and remodeling.
1) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized trial.Circulation,2018 137; (full text available on line without firewall)
They were able to show some improvement in cardiac compliance ( i.e. a decrease in myocardial stiffness) in a group of middle aged,otherwise healthy subjects over a 2 year period but the exercise required was considerably more than frequent brisk walks or slow jogs around the park.Rather , part of the exercise program involved a vigorous high intensity interval program using the "4 by 4 " Norwegian Skier technique twice a week and later in program only once a week.
Dr. Ben Levine, the Director of the Institute, and his team seemed to be able to recruit subjects who would persevere in a demanding exercise program over a 2 year program and to also permit right heart catheterizations which were done to give the investigators an index of compliance of the left ventricle.The bottom line is that they were able to demonstrate a reduction in cardiac stiffness with their exercise program .
This study is the most recent in a series of publications which have demonstrated that there is some level of prolonged endurance exercise that can at least to some degree mitigate the age related loss of cardiac compliance . Previously they had attempted to improve cardiac compliance in older subjects (in their 70's) and were unsuccessful. In this study they hoped they could find a "sweet spot", a time frame in which it was not loo late to reverse the age driven stiffness and they seemed to have , at least to some measurable degree, succeeded .
Levine characterizes the sedentary heart as a "small, stiff heart" versus the endurance athlete's heart as larger,slightly thicker and more compliant.
Levine describes the stages in the aging of the heart :1) loss of relaxation ,2) stiffening ( beginning in middle age), and finally 3) remodeling. The hope is that adequate exercise might mitigate or significantly delay stage 2 which may be the precursor or a prerequisite for heart failure with preserved diastolic function. Years of endurance exercise does not seem to prevent the first phase but Levine's data suggest that exercise may counteract the stiffening and remodeling.
1) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized trial.Circulation,2018 137; (full text available on line without firewall)
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