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After experiencing things like stress, intense exercise, or using drugs such as caffeine and amphetamine, subjects often assume a depressive and lethargic state afterwards, known as a "crash." What is the neuroscience behind it? Could it have to do with the depletion of neurotransmitters such as the catecholamines, or a downregulation of certain receptors in response to the overproduction of such neurotransmitters?

(This question is a remix of a previous question I posted, which was not focused enough)

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  • $\begingroup$ In terms of specifically caffeine, caffeine is an inhibitor of cAMP phosphodiesterase. Your glycogen phosphorylase will be active to a higher level (this also means the glycogen synthase is downregulated!) All the glycogen will clear out of your muscle eventually, and when your caffeine levels fall, all the cellular cAMP will begin to degrade. There's suddenly no glycogen, however, and your muscle cells will pull what they can from the blood to replenish it. Especially combined w/ high sugar intake, the pancreas tends to release too much insulin and clear too much blood sugar. $\endgroup$
    – CKM
    Commented May 18, 2015 at 18:48
  • $\begingroup$ so if your hypothesis accounts for the main symptoms of the crash (that low blood glucose is at fault), adequate nutrition, for example snacking on carbohydrate heavy foods throughout the day but not having large meals, would eliminate the crash? Or, more directly, a glucose clamp would counter the effect completely? $\endgroup$
    – SorcererofDM
    Commented May 18, 2015 at 19:00
  • $\begingroup$ this study indicates that under a hyperinsulinemic-euglycemic clamp, subjects ingesting caffeine has less glucose disposal than subjects ingesting dextrose. $\endgroup$
    – SorcererofDM
    Commented May 18, 2015 at 19:11

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The "crash" effect is typically perceived as a deterioration in affect. With drugs, this deterioration happens as the drug is cleared from blood circulation, particularly cerebral circulation. With the ingestion of amphetamines, there is a brief reuptake of certain neurotransmitters, particularly dopamine and norepinephrine. Amphetamines also temporarily prevent the 'recycling' of said neurotransmitters, so the reuptake effect can last anywhere from 4 to 24 hours. The brain regulates internal homeostasis of mood based on perceived 'high' and 'low' elevations; thus, after an extended elevation in mood, there must be a 'comedown' period, or a deterioration in affect.

Further essential to this idea of homeostasis are the stress hormones, cortisol and adrenaline. Upon release, these hormones may raise blood sugar levels, blood pressure, and/or heart rate. As heart rate increases, the flow of blood goes to the heart, with less going to the brain. This causes the groggy and tired feeling afterwards that might be associated with a 'crash'. Stress hormones also impact the thyroid (which controls how fast the body uses energy, and controls hormonal sensitivity) as well as the central nervous system.

Exercise also leads to increased heart rate, as well as muscle fatigue. However, exercise itself doesn't typically lead to a depressed, lethargic state, as exercise promotes the release of endorphins (which are known to improve general sense of well-being). However, it is not uncommon for some people to experience "endorphin withdrawal" after suddenly stopping excessive exercise, which could mirror the crash that comes from the 'comedown' after drug use.

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