Finding the Causes of the Fall in Maximum Heart Rate With Age

Every detrimental change that occurs with aging is directly caused by some collection of cellular mechanisms, but that is only the second to last link in the chain. The deeper cause is an accumulation of unrepaired molecular damage, spiraling outward to create that chain of changes, reactions, and forms of secondary damage. While the list of fundamental damage that causes aging is enumerated and well understood, the final proximate cause of an age-related condition can be challenging to identify and understand - our biology is very complex indeed. You might look at the amount of work and funding that has gone into Alzheimer's research, for example, and the decades it has taken to make any sort of meaningful progress there. Sometimes an immediate cause can turn out to be fairly clear and localized, however, given sufficiently advanced tools for investigation:

[Researchers] have new insight into the age-old question of why maximum heart rate (maxHR) decreases with age. This decrease in maxHR not only limits the performance of aging athletes but it is also a leading cause for nursing home admittance for otherwise-healthy elderly individuals who no longer have the physical capacity required for independent living.

One of the reasons for the age-dependent reduction in maximum heart rate is that aging depresses the spontaneous electrical activity of the heart's natural pacemaker, the sinoatrial node. "I utilized a method to record ECGs from conscious mice and found that maximum heart rate was slower in older mice, just as it is in older people. This result wasn't unexpected. But what was completely new was that the slower maxHR was because the individual pacemaker cells - called sinoatrial myocytes, or 'SAMs' - from old mice just couldn't beat as fast as SAMs from young mice."

The slower beating rate was due to a limited set of changes in the action potential waveform, the electrical signal that is generated by the cells. The changes were caused by altered behavior of some ion channels in the membranes of the older cells. Like most initial discoveries in basic science, this study opens many more questions and avenues for further research. But the significance of the study is that it raises the possibility that sinoatrial ion channels and the signaling molecules that regulate them could be novel targets for drugs to slow the loss of aerobic capacity with age.

Link: http://www.eurekalert.org/pub_releases/2013-10/uocd-wdm101113.php

Comments

I wonder if this also explains the decline in maximum brain rate.

Posted by: Carl at October 15th, 2013 2:05 PM

There is perhaps little or no decline in maximal heart rate in healthy people; my own was still 184 @ 72 (before the side-effects of chemo for cancer kicked in). There is evidence from other research of healthy old people with similar results.

I thus suspect that lowered maximal heart rate is a side-effect of sub-optimal health rather than inherent with ageing.

Posted by: Ian at October 21st, 2013 5:23 AM

There appears to be a trade-off here. With aging, L-type calcium channel current density declines in the heart and increases in the brain's dopaminergic neurons. Blocking the L-type channels with a 'dipine-class drug protects and rejuvenates the dopaminergic neurons but decreases maximum heart rate.

http://www.ncbi.nlm.nih.gov/pubmed/24128759

http://www.ncbi.nlm.nih.gov/pubmed/17884683

Posted by: Krillin at October 24th, 2013 4:42 PM

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