We all know caffeine helps exercise performance. Long, short, power, endurance, whatever. I wrote a Jockology column on it for the Globe back in 2008; Gretchen Reynolds had a round-up of the latest research in the New York Times a couple of days ago. So what more is there to say?
Well, if you want to get into the nitty-gritty, there’s a really interesting round-table discussion in the current issue of (wait for it) the Journal of Caffeine Research. It’s freely available online, and it’s not a research paper or a study — it just brings together a bunch of the leading researchers and practitioners in this area from around the world (like Terry Graham from the University of Guelph and Greg Cox from the Australian Institute of Sport) and gets them to air their opinions, thoughts, suspicions and doubts about how and in what contexts caffeine really works.
It turns out things are quite a bit more complicated than you might think. For example, Reynolds in the Times writes:
Caffeine has been proven to increase the number of fatty acids circulating in the bloodstream, which enables people to run or pedal longer (since their muscles can absorb and burn that fat for fuel and save the body’s limited stores of carbohydrates until later in the workout).
However, in the roundtable discussion, Graham disagrees with that statement. In fact, he makes a very broad argument:
I would take the controversial position that the ergogenic effect is not because of an alteration in either blood flow or alteration in delivery of blood-borne metabolites (fuels).
Instead, he believes the evidence points to effects in the muscle itself enhancing contractions, which would explain why it seems to work for virtually every sport. And the others appear to agree.
Interestingly, the editor-in-chief of the journal, Jack James of the National University of Ireland, proposes a totally contrary position. What if the supposed “ergogenic” effects of caffeine are really just due to the fact that, in virtually every study of caffeine, the subjects come to the lab in a state of withdrawal from not having had their usual morning dose? That, apparently, is what the evidence now suggests in studies of caffeine’s mental effects:
What we are talking about here arises from the fact that almost the entire population is exposed to caffeine on a regular basis, and studies show that decrements in psychomotor performance and mood are detectable after as little as 6–8 hours after caffeine was last ingested. Standard double-blind trials involve a brief pre-test period of caffeine abstinence, typically involving overnight abstinence to coincide with usual caffeine consumption patterns. By morning, participants are in the early stages of withdrawal and are experiencing negative withdrawal effects on cognitive performance and mood. When caffeine is then re-ingested under laboratory conditions, participants typically show improvements in performance and mood. However, studies that have controlled for withdrawal effects have repeatedly shown that the observed improvements are due to the reversal of withdrawal effects. That is, for cognitive performance, there is little or no genuine net effect of caffeine over and above reversal of the negative effects caused by caffeine withdrawal. As such, can we be satisfied that this source of confounding has been adequately controlled in studies of physical performance?
It’s an interesting question. There are lots of other interesting nuggets in the discussion, on topics like dosage, responders vs. non-responders, whether habitually consuming caffeine reduces its ergogenic effects (Graham says no), and so on. In all cases, what you realize is that the literature is far less clear than we might have thought. The book on caffeine isn’t quite closed yet after all.