Why did the greatest "ancient marathoner" slow down signficantly in his 70s?

Why did the greatest ancient marathoner of all time slow down so much in the decade of his 70s?

At age 73 Ed Whitlock finished a marathon in 2:54:48. Twenty-five years earlier he ran a marathon in 2:31:23. In a quarter of a century his marathon time decreased by only 23 minutes. See here for the blog Cannute's Efficient Running Site 's tribute to Whitlock.

Whitlock's 02 max was measured at 52.8 ml/kilo/min when he was aged 70 and 11 years later at age 82 a measured Ox max was essentially unchanged ( 54 ml/kilo/min).Yet during this general time period his marathon times decreased signficantly.

A person's maximal oxygen consumption ( 02 Max) decreases with age. The per decade decrement is generally said to be between 5 and 10 Percent. The jury is still out regarding if the rate of decline in endurance athletes is more,less or the same as more sedentary humans. There is good evidence indicating that the rate of decline increases around age 70 and values as high as 15 % percent per year or more have been reported. Assuming the 02 Max measurements are correct, Whitlock's 02 max was essentially unchanged during his running trek through his  70s but his marathon times decreased significantly.

As commented on by Cannute, Whitlock in his 40s was a very good marathoner but was not setting world age marathon records . At age 48 he ran a marathon in 2:31:23- a very good time for age-actually any age- but not the record.  Ye,t by age 70 he was setting marathon records for age and continuing setting records until a few months before his death at age 86.He set the age 85plus marathon record in Toronto clocking in a 3:56:33

So what was his secret? Obviously his genetic endowment included a high 02 max. His marathon times did decrease between age 70 and age 80. He was running sub four hour marathon at 80 plus while running sub 3 hour at 70 plus while his measured 02 max seemed constant over that time period.

Of course there is more to running marathon than 02 max.

Whitlock's training in his 70s and 80 did not follow the current generally accepted marathon training  principles. He did no speed work except in races. In his 70s he is said to  have run up to 3 hours a day , almost every day at a very slow pace, described  by him as a "slow shuffle". He carried the LSD (long slow distances) program to a extreme.

Tim Noakes, noted exercise physiologists and long time endurance athlete, believes that a major reason than marathon times decrease markedly in the decade of their 70s is that most older runners cannot maintain the hours of training necessary to perform well in the marathon  in part because  there are too many minor ( and major injuries), too many aches and pains. The muscles endure better than the "connectors", i.e the structures and tissue connecting the bones to the muscles and joints.

Yet it may be that even in the absence of significant injury or a nagging series of minor injuries and even with high level of training  a human's running speed for distance decreases significantly during the 8th decade of life. (about 25% decrease in marathon running speed for the world's greater old timer marathoner.) One suspect to consider is  muscle loss of "spring function" and the spring function of tendons and the arch of the foot. You figuratively and maybe literally loose the "spring in your step".

Bundle of His Pacing an overnight game changer fifty years in the making may have reached tipping point

Benjamin J. Scherlag,PhD, is credited as the first person to demonstrate an intra cardiac tracing of  His Bundle (HB) electrical activity. In1967, he demonstrated ventricular pacing from the bundle of His.

In 1970, OS Narula and Scherlag demonstrated the feasibility of temporary HB pacing in humans.

 In a 1978  article in Circulation, Scherlag,El-Sherif,Lazzara and others presented clinical and experimental data demonstrating the normalization of bundle branch blocks  ( right and left) with HB pacing.

Thirty years after Narula's work, Deshmukh's 2000 publication reported his experience in placing    permanent His Bundle pacing leads in   18 patients with dilated cardiomyopathy,poorly rate controlled atrial fibrillation and narrow QRS complexes who  underwent AV node  ablation. He  later published a larger series with 3 1/2 year follow-up on patients with supra-Hisian AV block.Although results were encouraging, the time for more widespread use of HB pacing has not yet quite arrived. The procedure was thought  to be  too challenging and  commercially designed equipment which would facilitate the procedure was not yet available .

 It required   a separate mapping catheter and higher pacing thresholds and it was not clear  exactly what subset of patients would be benefited by this method to a degree greater than obtained by the simpler apical right ventricular pacing in regard to which data suggesting the harmful effect of RV pacing were not yet fully appreciated. So HB pacing was not perceived as being ready for prime time.

From 2006 through 2012 work from Kronborg from Denmark and Zanon and others from Italy   strengthened the case for more widespread application of HB pacing.In 2011 Zanon reported the experience from  multi-institutional data using the Medtronic Select Secure system describing 307 patients implanted in the His zone with 87 having direct HB pacing and 220 with indirect or "Para-Hissian" pacing.

Two important papers from the United States were published in 2015:

A series of 98 HB paced  patients was reported by electrophysiologists from the Geisinger Clinic.
 with a longer follow reported by the same group in 2017.Also Lustgarten reported on a cross over trial comparing Bi-ventricular pacing with HB pacing in patients  receiving Cardiac Resynchronization Therapy (CRT).

Both papers indicated that the procedure was less difficult than previously thought due in part to newer specially designed sheath and leads,required lower pacing thresholds than earlier reports and follow-up data regarding stability of leads was encouraging and left ventricular function improved at least as much brought about by Bi-V pacing. Further the Geisinger data , while not a randomized trial,indicated that long term follow-up showed no decrease in left ventricular function while a parallel group who had the standard right ventricular apical pacing did show  decreased left ventricular function  and a 22% incidence of pacing induced cardiomyopathy was reported.

In EP cardiology, as in most things, there are tradeoffs. The HB paced patients had , in the Geisinger data, twice as many lead revisions after five years( 6.7% vs 3%) and significantly more generator changes when compared with the RV paced group ( 9% vs 1%) . In additional the procedure time was slightly longer as were  fluoroscopy times.

The Geisinger HB registry data was updated and published in 2018.This article was one of  several recent articles describing experiences with HB pacing in a variety of clinical settings and we may have reached a "tipping point" in terms of EP Cardiologist's attitudes re HB pacing.

Francesco Zanon from Rovigo Italy ,an early adaptor of HB pacing, published data on 147 patients referred with a variety of PM indications and various types of bundle branch block. 80 % of patients experienced disappearance of the BBB . 90% of the  patients had effective HB pacing with a mean follow up of five years. He spoke of a "new philosophy of how we pace".

 One of the fathers of electrophysiology, Benjamin Scherlag,has called for a randomized trial comparing HB with BiV pacing for CRT and Dr. Kenneth Ellenbogen has also commented on the need for  RCTs and wrote an editorial suggesting that possibly HB pacing was the Holy Grail of  pacemaker therapy .

age related decline in exercise capacity is not just decrease in 02 max

It has been suggested that the study of the physiology (pathophysiology?) of aging might be informed by the study of aging athletes.

Analyzing information about Ed Whitlock,thought by some to be the greatest "ancient marathoner" ever, may offer some interesting insights.See here for more regarding Whitlock.

02 max measurements were made on Whitlock at age 70 (52.8 ml,/kilo/min)) and age 81 (54ml/kilo/min).

At age 72 he ran a 2:54 marathon and at age 82 his marathon time was 3:41.So his running time decreased significantly from 6.62 minutes per mile to 8.4 minutes per mile.His speed decreased from 9 miles per hour to 7.11 miles per hour, a 20% decrease.  Yet during that same time period his measured maximal oxygen uptake was unchanged. We also know from  published interviews  that his training did not significantly diminish. So what was the cause(s) of his decreased running speed?

The decade of the the 70s is generally said to be one in which the age associated decrease exercise capacity seems to accelerate. and 15 to 20% decrement per ten years have been reported.A reasonable assumption is that a major factor in that decrease is decrease in 02 max. Yet Whitlock's 02 max was unchanged while his running speed decreased in the range typically said to occur in normal humans.

Similar data on other runners have demonstrated that running speed for distance running decreases proportionally greater than the temporal decrease in 02 max.However, in cyclists a different pattern is seen with the 02 max and speed decreasing more proportionately .

It is tempting  to evoke the role of the pounding of the legs in running versus cycling. The long time distance runner and exercise physiologist, Tim Noakes ,has opined about the long term effect of "pounding" on decline in exercise capacity.The constancy of Whitlock's 02 max and the 20% decrease in marathon times from early 70s to early 80 reminds one of the high school coach's aphorism "you are  only as young as your legs".

Could some answers be found in study of titin and its isoforms?Titin (aka connection) is the body's largest protein and is said to act like a spring for muscles, recoiling the sarcomere after it is stretched.

There is a short,stiff isoform ( N2B) as well as other more elastic isofroms ( e.g. N2BA ) . The phosphorylation of titn results in a post translational modification of titin with production of more elastic isoforms. Beta adrenergic stimulation may increase the phosphorylation of titin.

The stiffer ventricular muscles of patients with diastolic heart failure have less of the more elastic titin isoform and more of the shorter stiffer titin isoform.

Titin may or may not play a role -probably more than one factor conspire by a number of mechanisms to cause runners in their seventies to loose much of the "spring in their steps."even if their cardiac output changes little  even though a constant cardiac output over that 10 years period is likely as did  Whitlock very far out on the curve.