4. WHAT HAPPENS TO OUR PACEMAKER AS WE
AGE?
How do older sinoatrial node cells set a slower pace?
“Decreased pacemaker activity of sinoatrial node myocytes contributes to the
age-dependent decline in maximum heart rate”
Methods: ECG; autonomic blockade; perforated-patch current-clamp recordings
Major findings:
1. There is an age-dependent decrease in the spontaneous excitability of sinoatrial
myocytes (SAMs) which contributes to the correlated decline in intrinsic heart rate
(iHR) and maximal heart rate (mHR).
2. There are a few parameters of the pacemaker action potential that affect the
age-dependent decrease in spontaneous excitability, iHR, and mHR: maximum
diastolic potential and diastolic depolarization.
3. Age-dependent changes in membrane current channels
affect action potential waveform in a way that lowers
SAM firing rate, there by lowering iHR and mHR.
An action potential is the movement of an electrical chemical across a cell membrane, which makes the cell do something. That current can also move to surrounding cells, telling them to do something. In the sinoatrial node, the cells are called sinoatrialmyocytes that something that action potentials cause as they run through sinoatrialmyocytes is a heartbeat. Action potentials that propagate from the sinoatrial node cascade throughout the heart, causing cardiac muscle to contract, and thereby regulating heart rate. The heart rate is read by sensors and that waveform readout of electrical activity in the heart is generated.So what’s regulating the sinoatrial node? Well, the kind of action potential of the sinoatrial node is unique, and self-propagating…meaning the SA node keeps its own beat going. It has an intrinsic heart rate of 100 beats per minute. That means that if you take away the effects that hormones, neurotransmitters, and activity have on heart rate, the SA node would keep a steady pace all on its own, beating a hundred times every minute. You would say that the sinoatrial node has an intrinsic heart rate of 100 beats per minute.Now, the SA node is connected with nerves, through which the autonomic nervous system affects heart rate. There are two types of nerve endings on cells in the SA node: sympathetic (which make the heart go faster) and parasympathetic (which make the heart beat at a slower rate).
High concentration of Calcium inside muscle cells will catalyze muscle contraction, and generate a heart beat.So when Ca+ enters the cell, it moves the cell closer to having an action potential. This is the process of depolarization.Muscle cells cannot contract for sustained periods of time, and so cardiac muscles beats with a pulse.The time in between beats is called the pacemaker potential—the time when the cell deactivates itself off, by closing it’s doors to Calcium in a process called repolarization…getting itself back down to a resting potential.Once it has relaxed and reached its maximally low potential, it does a “funny” thing—literally what scientists call the “funny current”.It’s the inherent, intrinsically caused turn around in membrane potential—and the turn around point is called the maximum diastolic potential.It’s the point where the heart keeps itself beating. That’s why these cells in the sinoatrial node are nicknamed, pacemaker cells. The physiological mechanisms that regulate this pacemaking activity remain pretty mysterious.
Research done at University of Colorado in Denver by a team lead by Eric Larson and Joshua St Clair. They experimented with mice with a whole range of ages—the equivalent of studying humans aged roughly 17 to 90 years old). They were investigating why the heart beat slows with age, looking particularly for age-dependent changes in the mechanisms of the pacemaking.In order to observe and measure the iHR—the true pacemaker activity—the Denver team employed a common method called autonomic blockade: administering drugs that block the messages from the nervous system that tell the heart to beat faster or slower.By reading activity from individual cells in the SA node, they could tell… Spontaneous excitability is that turn-around moment when the heart gets itself going again. 2. The turn-around takes longer the older we get.3. Lower currency densities means fewer places on the cell membrane to let in the chemicals that push a cell towards an action potential. Which means it will take longer to move enough current into the cell in order make the turn-around towards another heart beat.**Still working on this concept of current densities, and why age makes a difference. I get the concept but the data isn’t legible to me yet.These findings illustrate how changes in membrane currents might lead to slower heart rate, but the ‘why’ is still funny business.
Looking at this regardless of labels…just using it to visualize the timelapse and waveform.Imagine the top waveform represents the iHR of a young heart, and the bottom waveform is the iHR of an aged heart.Because the pacemaker potential of the aged heart takes longer, there will be fewer action potentials per minute—which translates to fewer BPM.This further signifies a slower maximum heart rate, which has implications for older people’s cardiorespiratory capacity and thereby their independence.The greater resolution with which we understand how the heartbeat and rate is generated, the better we can design medical interventions, whether they be drugs or artificial pacemakers.
