While it is true that the majority of athletes will see a
decrease in resting HR (RHR), it is not universal, nor is it
a sign of performance potential. Case in point: Frank
Shorter, known to most as a "pretty good" runner (Olympic
Gold is pretty good) was reported to have a resting HR
around 75 beats/min. That sucks, if he were competing in the
resting HR games.
The important thing to remember about most of the initial
changes in performance (RHR, strength training and even
endurance) is that there is always a neural component. In
this case, at rest, the sympathetic nervous system (SNS-
stimulating) decreases its input, and, more importantly, the
parasympathetic (PNS-relaxing/digestion) increases its input
to the heart. This input is the major reason why RHR
decreases so rapidly after you start training, not an
increase in heart size.
Consequently, congestive heart failure (CHF) heart growth is
completely different from the increase you see with
endurance athletes. Certainly an overly large heart can lead
to electrical problems (ie, arrhythmias), but the growth
seen is not due to muscle growth - defined here as a thicker
muscle, rather, the chambers get larger, while the wall
thickness is largely unchanged. However, the heart muscle
itself does get stronger, and the larger volume allows for
greater filling capacity in the heart and ultimately greater
pumping (per beat) capacity - Stroke volume. In contrast,
CHF growth results in increase muscle tissue in parallel
(ie, the fibers stack and run in parallel), creating very
thick walls. Initially, the heart gets stronger from the
greater work (CHF is a complicated process that increases
the work on the heart, with the heart trying to adapt), but
the thicker walls cause electrical problems, and more
significantly, become difficult to perfuse with blood. As
the diagram shows, the outer tissue gets the O2, but the
inner tissue doesn't and eventually dies. Dead tissue
doesn't conduct impulses and doesn't pump blood. Just like
having big legs with a big gut and big ass makes climbing
hills harder, all that dead tissue doesn't help with the
heart function.
[ + ] O2 ======> [ No ]
[ O2 ][ + ] <====== O2 [ + ] [ + ]
Hope this clears things up.
Chris Harnish, M.S. Coach People Cycle, Inc.
[email protected] (J999w) wrote in message news:<20040316134335.29604.00001645@mb-
m21.aol.com>...
> >>
> >>I worry about what happens to that big 'ol heart if you
> >>stop cycling in old age (>70years) ... like any muscle,
> >>it will get weaker.
> >
> >Teh efficiency of the circulatory system is not just
> >the size of the heart muscle is it? In fact, does a
> >runner doing long slow distance to build his base
> >really make his heart bigger? Certainly new capillaries
> >are created, etc.
> >
> >
> >Gleshna - Multi-Thousandaire
> >
>
> Okay, I've been out of school for a while, but if I
> recall, _one_ of the adaptations of the heart to aerobic
> exercise is to grow larger. I know this is different from
> congestive heart failure where the heart tries to improve
> by getting larger, but remains an inefficient pump no
> matter how big it grows ... but what becomes of that once
> healthy, strong, yet larger than normal heart once you
> age and are no longer active? Does it weaken and become
> too big for it's own good? I would guess in the long run,
> it's going to be a better than average pump until your
> dying day, but is that the case if you stop training when
> you're 50+ ?
>
> Anyone know?
>
> jw milwaukee