More data on lifelong exercisers-this time from Ball State

Scott Trappe and colleagues (1) from Ball State Human Performance lab  studied 7 women and 21 men all in their 70's who were lifelong ( fifty years or more) exercisers and compared them to elderly,apparently healthy sedentary  subjects and to heathy young exercisers (average age 25)

The lifelong exercisers exercised 5 days/week with a weekly hourly total of 7 hours. for the past 52 =/- 1 years.

Maximal oxygen uptake was measured on a maximal cycle test and muscles biopsy done to determine a "muscle aerobic profile" (MAP for short). MAP refers to the degree of capillarization and metabolic enzymes eg. Citrate synthase,B-HAD and glycogen phosphorylase  were determined by muscle biopsy in the lateral thigh.

While the MAP was the same as in the young exercising controls the 02 max  of course was not .The set of long time exercising women was small, but rounding up women who have exercisers for fifty years is no small feat.

Comparing the 02 max in young women,exercisers and elderly control women we find: 44,26 and 18 .

The authors conclude : " the data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than the more central aspects of the cardiovascular system."

The authors mention the fragility index and quote that the value for men is 17.5 ml/kilo/ min and make their educated guess about what it is for women giving 14 ml/kilo/min as the value. I am not sure why women would have a lower number since the index is corrected for weight. Folks fortunate to have values well above those numbers are said to have more physiologic reserve to withstand and survive various homeostasis challenges whose frequency is a function of age.

This index should not be confused with another fragility index which gives an indicator of how robust are the results of a clinical trial.See here for more on that.  (A clinical trial would have an FI of 1 if the hypothetical movement of one patient from the success column to the failure column would make the study no longer statistically significant ( at the p of 0.05 level)

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1) Gries,J et al Cardiovascular and skeletal muscle health with lifelong exercise
JAP 125: 16736 2018 (full text available on line)

In the long run ( or ride) do runners wear out sooner than cyclists?

 Tim Noakes, the MD, PhD exercise physiologist from South Africa has suggested that perhaps many years of running and the gravity assisted  pounding might accelerate the aging process at least as regards muscles and tendons.

If that is the case, might a comparison of the decrement in performance over time between long time runners and long time cyclists be useful  tend to confirm or deny that hypothesis.

Noakes and colleagues made that comparison (see here) and things look better for the cyclists.

We knew all along who would be the collateral damage from the "war" on opioids

This NYT article puts faces on those who bear the collateral damage. No satisfaction from "I told you so" here

Anyone remember "Cure sometimes,treat often,comfort always."

All cases of LBBB do not have the same ventricular contraction pattern or same response to CRT

The block in left bundle branch block (LBBB)-and this can apply to right bundle as well-may not be actually in the left bundle branch, as least as it has been traditionally described.And  the "block" may not mean complete disruption of the electrical cardiac system perhaps just a delay.Further amazingly, at least sometimes,electrical stimulation of the His Bundle can "fix" LBBB obtaining a normal QRS complex.

The traditional text book electrical  anatomical pathway is from sa node to av node to His bundle and then a division into  left and right bundle branches and then to branching purkinje fibers out to the myocardium.

Anatomical work at least as early as 1971 and physiological studies in 1977-1978 demonstrated in both the canine and human heart that the right and left bundles were actually anatomically distinct within the bundle of His.This was described as longitudinal dissociation.

It has been known at least as early as 1978 that stimulation of the his bundle can normalize the ekg pattern of LBBB and RBBB,Presumably-according to the longitudinal dissociation model - in these situations the lesion or block in the bundle  branch was in the His bundle and that stimulation distal to the lesions resulted in a normal ekg.

In other words the left and right bundles are organized longitudinally and separate within the His Bundle.So a lesion in the His bundle could cause LBBB and could be corrected by stimulation distal to the block.

The work done in the 1970s did not really apply to clinical situations  until  cardiac resynchronization (CRT) was proven effective in the treatment of heart failure in the 1990s.  About 30% of patients did not seem to respond to CRT and it was soon realized that the presence of LBBB was a favorable prognostic factor and that , in a sense it was  the impaired electrical conduction system which was the culprit that caused  mechanical dyssynchrony that could markedly impair cardiac function and in some after a variable lag period  lead to disadvantageous cardiac hypertrophy, chamber enlargement and remodeling and heart failure

Further it has been suggested ( Strauss et al ) that the  traditional ekg criteria for LBBB need to be replaced with critieria that make the diagnosis much more specific  and therefore useful in predicting response  from CRT.The QRS duration should be 0.14 seconds for men and 0.13 for women and there should be a double humped QRS either in lead i and AVL or V5 and V6 ( i.e. 2 contiguous leads) .Using the old criteria,according to Strauss, lead to overdiagnosis of true LBBB and included patients who actually had LVH ( left ventricular hypertrophy) and left anterior hemiblock). It was suggested   that patients with "true "LBBB" by EKG are the ones who are likely to benefit from cardiac resynchronization therapy (CRT).

However, results from Denmark and Pittsburgh by Dr. Niels Risum (2) indicated that the sine qua non of "true" LBBB is not necessarily the EKG pattern but rather the mechanical activation pattern ( basically delayed left ventricular activation )which they described in terms of 2D strain echocardiography and that  neither the supposedly specific Strauss criteria nor the traditional criteria   always would  indicate which patients would have that contraction pattern and  would therefore be more likely respond to CRT.See end note # 1for Risum criteria:

Risum and colleagues content that all patients with LBBB diagnosed on EKG do not have delayed left ventricular activation which correspond to their criteria for "classic" LBBB activation pattern.

Risum's work offers an explanation for  at least some of the widely quoted 30% CRT poor response rate .Interestingly, as early as 1979 several different patterns of septal movement were described on echocardiogram in LBBB.( Fujii et al )

Their data demonstrated that during a 4 year follow-up 40% of patients without the classic pattern had an adverse event (combined end point of death,need for LVAD,or heart transplant) versus 14 % in the group with the classic pattern.So since it is not 100% versus 0 % the presence or absence of Risum's classic pattern does not explain all cases of CRT failure.



 It would not be expected, on mechanistic grounds, for Bi-Ventricular pacing to improve cardiac output in patients with right bundle branch block since in RBBB the electrical activation and the contraction pattern of the left ventricle would not be abnormal.There is considerable clinical data that CRT results in RBBB are definitely worse than in LBBB; However, there may be an exception.

Rosenbaum described an RBBB pattern in which there is left axis deviation and broad slurred r waves in I and Avl which was termed LBBB masquerading as RBBB in which an argument has been made that Bi-V pacing might be on benefit.(1)


1)Auriccho, A Does Cardiac Resynchronization therapy have a role in patients with right bundle branch block.irc. Arrhymia Electrophysiol 2014 pg 532

2)Risum,N et al, Identification of typical left bundle branch block contraction by strain echocardiography is additive to electrocardiography in prediction of long term outcomes after cardiac resynchronization therapy. Journal American College of Cardioogy  2015 vol 66 no 6 pg 632

3)Fujii, J K, et al  mode and cross sectional echocardiographic study of left ventricular wall motions in complete left bundle branch block. Brit Heart Journal 1979 42 (3) 255

end note 1
Risum 2d strain echo criteria:
1)early shortening of at least one segment of the septal wall atnd early stretching of at least one segment of the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure

Lone Left bundle branch block and increased afterload -bad combination

I have commented before on functional impairment associated with LBBB. See here.

J Aalen and colleagues  (1) see here demonstrated that  cardiac output in asymptomatic patients with isolated LBBB is very sensitive to afterload as  in elevated arterial pressure as would also occur with strenuous exercise.  (Full text is available on line,)

Dr Aalan studied the effect of increasing afterload on left ventricular ejection fraction (LVEF) in 11 asymptomatic patients with isolated ( or lone) LBBB. Afterload was increased not by exercise by increasing blood pressure (increase of 38 +/-12 mm Hg) by pneumatic extremity constrictors and handgrip exercise .

The controls subjects decreased their LVEF from 60 to 54 while the LBBB patients decreased their LVEF from 56 to 42. The increased heart rate and after load accentuated the effect of the left ventricular dyssynchronous contraction which consists of early septal contraction with bulging of the lateral left ventricular wall and delayed lateral wall contraction and bulging of the septum. In LBBB both the IVCT and the IVRT are increased, i.e slowed contraction and prolonged relaxation.

The severity of cardiac functional impairment is not reflected by the resting LVEF. Most studies have indicated at most a mild decrease. On a personal note, when I developed a LBBB my decrease in running speed was by about 20% -close to the 25% decrease in LVEF note in Aalan's paper. (decrease from a fairly comfortable 12 minute mile run  to a difficult 15 minute mile with unusual calf discomfort)

I received 2 comments on the blog post mentioned in the first paragraph from readers indicating their exercise history after LBBB onset was similar to mine.

Lone LBBB is often considered asymptomatic and  often is at rest.  A person not doing strenuous exercise would likely not notice any problem and probably for that reason many texts describe LBBB as asymptomatic. For example, Mayo Clinic Patient website -" in most people BBB does not cause symptoms " and Up to Date "LBBB can also be seen in  asymptomatic patients with structurally normal hearts."(Both accessed on 2/6/19) The key here is "with structurally normal hearts". Patients with already reduced EFs may experience significant worsening of exercise ability with onset of LBBB.

1) Aalen J  et al Afterload hypersensitivity in patients with left bundle branch block . Jan, 2018 JACC Cardiovas imaging.