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Gretchen Reynolds has an article in the New York Times about recent research into the origins of “runner’s high,” suggesting that endocannabinoids rather than endorphins might be responsible — in other words, the body’s internal version of marijuana instead of morphine:
But perhaps the most telling experiment was published last year by researchers in France who had bred mice with no functioning endocannabinoid receptors. Mice usually love to run, but the genetically modified animals, given free access to running wheels, ran about half as much as usual.
Reynolds is usually an excellent reporter, but I was a bit disappointed in the lack of context offered in this article. She dismisses the role of endorphins as follows:
Endorphins, however, are composed of relatively large molecules, “which are unable to pass the blood-brain barrier,” said Matthew Hill, a postdoctoral fellow at Rockefeller University in New York. Finding endorphins in the bloodstream after exercise could not, in other words, constitute proof that the substance was having an effect on the mind.
This is true, but German researchers published a study back in 2008 that was very widely reported (including in the Times by Reynolds’s colleague Gina Kolata) that directly measured the increase of endorphins in the brain after a two-hour run. Both Reynolds and Hill are undoubtedly familiar with this study, so it seems disingenuous to pretend that we don’t know anything about the link between exercise and endorphins in the brain.
Ultimately, the runner’s high is such a nebulous, ill-defined thing, meaning different things to different people, that it’s probably a combination of several different effects — endorphins, endocannabinoids, and perhaps other factors, including some straightforward psychological ones. So it seems silly to dismiss the “old” theory in favour of a new one when there’s no reason the two can’t coexist.