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 very far out on the curve.