I read your new article and there’s one thing I don’t get. The beta Adrenergic receptors reside in the CNS as well as on peripheral tissue. You talk mostly about the central nervous system, in which noradrenaline is the neurotransmitter used by the body. How come that the increased conversion of NA to Adrenaline in the adrenal glands can influence downregulation of receptors in the CNS, when it does not enter the CNS?
I must be getting something wrong. It would be nice if you could help me with that.
Beta-adrenergic receptors are found in a lot of tissues, which is why adrenaline can affect a large number of tissues.
The Beta1 adrenergic receptors are found in the heart, kidneys and adipocytes
The Beta2 adrenergic receptors are found in lungs, vascular smooth muscles, heart, uterus, bladder, adipocytes, muscle, liver, etc.
The Beta2 adrenergic receptors are found in adipocytes, heart, bladder and uterus.
there is a small amount of adrenaline produced in the neurons of the central nervous system
I often refer to beta-adrenergic downregulation/desensitization as “what is often called CNS fatigue”… but also explain that there is no such thing as CNS fatigue. When I say “what is called CNS fatigue” it is implied that it’s not what happens (which I explained in a previous article), but since that’s what its been called for a while I mention it.
The symptoms that we associate with “CNS fatigue” are due to a downregulation of the beta-adrenergic receptors (thus affecting all the tissues mentioned above) and a reduction of dopamine levels (due to the overproduction of adrenaline) and of noradrenaline. The central effects are likely due to dopamine and noradrenaline depletion while the peripheral effects (which has a greater influence on performance) are due to beta receptors downregulation.
The central effects are likely due to dopamine and noradrenaline depletion while the peripheral effects (which has a greater influence on performance) are due to beta receptors downregulation.
Okay, thanks!
That’s interesting, so my assumption that the mood effects are due to receptor desensitization through noradrenaline or through depletion is correct.
I didn’t know the periphery effect was that strong. That’s really good to know.