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The Brain Also Talks to the Heart Using the Language
of "Biochemistry"
The sympathetic nervous system, one of the two divisions of the autonomic
nervous system, as previously noted, is sometimes referred to as the adrenergic
nervous system (meaning having activity like that of adrenalin). This
system has alpha and beta adrenergic components. Neurotransmitters, or
signaling substances, called epinephrine and norepinephrine, activate
the heart's beta adrenergic receptors. Autonomic nerve fibers as well
as your adrenal gland release these neurotransmitters during exercise
and other kinds of stress. These substances travel to the heart cells
through the blood. They deliver the brain's message by binding with special
receptors on the membranes of the heart cells, and set off a chain of
molecular events within these cells that might end with a faster beating
heart, stronger contractions, and faster relaxation between beats. Or,
depending on what neurotransmitter is called upon, the autonomic nervous
system can tell the heart to reverse all these effects and slow down.
We can define the essence of sympathetic nervous system influence on the
heart and blood vessels by examining the results of the following study.
The study compared a young person's cardiovascular performance during
vigorous exercise (when full sympathetic nervous input occurs) with that
measured during vigorous exercise in the presence of a drug that blocked
(or substantially reduced) sympathetic signaling. The drug used is called
a beta blocker, i.e. it blocks the beta adrenergic component of the autonomic
system. You may have heard of this type of drug, as it is used in clinical
medicine in the treatment of cardiovascular diseases (a future article
will address this). Compared to the situation when the beta adrenergic
stimulation was intact, in the presence of the beta-blocking drug the
heart rate during vigorous exercise in the young volunteer did not increase
as much, the heart size dilated, and the usual increase in ejection fraction
was reduced. Does this pattern sound familiar to you? It should if you
have been following this Series, "Aging of Your Heart and Blood Vessels
is Risky".
The effects of the beta blocking drug on the young heart:
1. acute cardiac enlargement during exercise
2. diminished increase in heart rate and
3. reduced ejection fraction
are the characteristics of the exercise response of older persons compared
to younger persons. This response was discussed in Article 3 "How Good
a Pump is Your Older Heart?" In essence, by blocking the beta adrenergic
system of the young volunteer the investigators of this study converted
the cardiovascular performance profile of a young person into one of an
older person! Thus, the essence of the beta adrenergic modulation of heart
function during exercise is to make the heart beat faster and stronger
and to keep its size small. A young heart normally responds in this way
to vigorous exercise. However, aging, even in otherwise healthy persons,
is accompanied by a reduction in the effectiveness of the beta adrenergic
nerve influence on the heart. In other words, the beta adrenergic signaling
which acts in young hearts to accommodate vigorous exercise tends to falter
with age, even in normal healthy people. Why is this? The reduced beta
adrenergic influence on the older heart during exercise could be attributed
to a reduction in the production of the neurotransmitters (norepinephrine
and epinephrine), resulting in reduced delivery of these signaling substances
to "docking sites" on the heart and blood vessel cells. (Docking sites,
called receptors, are areas on cells where specific substances, like biochemicals,
can be accepted, absorbed or passed through.) Alternatively, the age-associated
deficit could be due to a reduced response to these substances by the
older heart and blood vessel cell's docking sites. Which is it? The answer
is that it is a reduced response to the neurotransmitters by the docking
sites on the heart and blood vessel's cells. Is this normal human aging?
What do scientists know about this? Can anything be done to prevent or
delay this age related process? We will discuss some of these issues in
our next article.
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