Caffeine, Exercise and Your Sleep: The Link Could be Sign. Different From What You Expect - Sleep Better W/ Caffeine?

Caffeine, Exercise and Your Sleep: The Link Could be Sign. Different From What You Expect - Sleep Better W/ Caffeine?

caffeine coffee ergogenic exercise health sleep sleep duration sleep quality stimulants

Coffee and exercise both effect sleep, but their effects don't simply add up. The study at hand does yet suggest that your preworkout coffee won't ruin your sleep.

I have to admit, the following are not results of peer-reviewed research, but with a 2x2 week design, participants being randomized to exercise (4 workouts per week) or be sedentary and to consume caffeine or placebo prior to exercise or rest, it looks methodologically complex, but sound and, more importantly, interesting enough to make it into the SuppVersity news ... I mean, it's about coffee ;-)

With that being said, the scientists, who were hopefully less biased than I am, required their subjects to refrain from any extra regular physical activity and or coffee / caffeinated beverage consumption outside of the conditioning/treatment sessions, in which they didn't drink coffee, but 350-mL of Gatorade with or without a rel. low dose of 3mg/kg caffeine.

You can learn more about coffee and caffeine at the SuppVersity

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The authors' data analysis involved the usual mixed analysis of variance with treatment (placebo or caffeine) and condition (exercise or sedentary) as between subjects factors. In addition, time as the repeated measure, and the subjects' usual caffeine intake and BMI were included as covariates.

Figure 1: Mean sleep duration (h) in the different arms / phases of the 2x2 week RCT (O'Brien. 2016).

As the data in Figure 1 tells you, the statistical analysis yielded an independent main effect of
condition (sedentary/exercise) on the number of hours the subjects actually slept (this is not "time spent in bed"). In that, it did matter, whether the subjects worked with or without caffeine, but both, the effects of exercise (SED vs. EX | Figure 1), and as those of caffeine (see PLA vs. CAF | Figure 1) are not exactly what you probably expected:

• Effects of exercise - Subjects who exercised in the lab self-reported less time (hours) sleeping [F(1,18) = 4.5, p = 0.049] compared to sedentary. In that, there was a trend for an independent effect of treatment (placebo/caffeine) on hours slept (p = 0.08),
• Effects of caffeine - Subjects who received placebo self-reported less time (hours) sleeping compared those who received caffeine (that was not what you'd expect based on previous evidence). In that, there were no interactions by usual caffeine intake.

Now, one's sleep duration is only one out of several parameters that will determine whether or not you rise and shine refreshed; plus, since all subjects had average sleep times in the "green zone" of 6.5-8h per night, they were all sleeping enough - irrespective of exercise and/or caffeine. The parameter of actual interest is thus the subjects' subjective sleep quality and its relationship to their perceived tiredness in the AM / over 24h, which were both assessed with questionnaires in the study at hand.

Figure 2: Sleep quality and perceived tiredness over the course of the 2x2 week RCT (O'Brien. 2016).

For the former, i.e. the subjects' sleep quality, the data in Figure 2 signifies that here was a significant time x treatment x condition interaction on overall sleep quality [F(11,198) = 1.92; p = 0.038]. In that,  the subjects' sleep quality decreased over time in subjects who exercised compared to condition controls (sedentary). In contrast to what you'd expect, though, it were not the subjects who worked out and consumed caffeine who had the lowest sleep quality, but those "who exercised and received placebo [who] had the lowest overall average sleep quality" (O'Brien. 2016).

What may come as a surprise is that this decline in sleep quality had no effect on the subjects' perceived tiredness (Figure 2, right), which showed a main effect of time for ‘Body Feels Tired’ [F(11, 154) = 2.1; p = 0.026], but no treatment (placebo/caffeine) or condition (sedentary/exercise) interactions - which is unquestionably odd. About as odd, as the misleading statement that "[p]oorest sleep quality ratings associated with caffeine and exercise" (O'Brien. 2016) from the scientists' own summary of the results. Now, don't get me wrong. This statement is correct, but only if we are talking about the individual effects of exercise / sedentary and caffeine / placebo, on their own. The way O'Brien et al. phrased it, does however appear to suggest that the subjects' sleep was worst during the exercise + caffeine trials... Now, that, in turn, is what you probably expected the study to show, but another brief glance at the data in Figure 2 (left) confirms: caffeine did not mess with the subjects' sleep quality. In fact, the group with the most stable sleep quality are the sedentary coffee drinkers . eventually, you could thus argue that they had the best sleep quality!

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Bottom line: As the authors point out, "[e]xercise and caffeine did not have the hypothesized results on sleep quality and duration" (O'Brien. 2016). Instead of improving the sleep quality of the subjects, as it has been observed previously in both, middle-aged and older adults (Yang. 2012) and young healthy sleepers (Flausino. 2012), exercise clearly reduced the young subjects' sleep quality in the study at hand. As O'Brien et al. point out, this may have been a function of the novelty of the exercise and subsequent "physical discomfort that disrupted sleep quality and duration" of the previously untrained subjects in the study at hand, so that the results would change over time / be different if the study had used trained individuals.

Another important subject characteristic that may have "messed" with the results were the sujects' individual habitual caffeine consumption (100mg/day on average). Even though their habitual intakes were low, the fact that caffeine did not, as it did in previous studies, per se mess with the subjects' sleep quality, but rather improved it, could, as O'Brien et al. suggest, be due to "[w]ithdrawal reversal" of which the scientist argue that it appears to be "the primary action mechanism of caffeine [in the study at hand]" (O'Brien. 2016). Practically speaking, this would mean that "[r]eversing [the] negative state [of being on caffeine withdrawal] through caffeine administration improved [not decreased the subjects'] sleep quality and duration" (O'Brien. 2016 | my emphasis). How realistic this assumption is does yet appear questionable, with std. deviations of <50mg/day, the subjects don't seem to be caffeine junkies and with a dosage of only 3mg/kg per day (all subjects were normal weight, so that's probably in the 200-300mg range) switching from a caffeine to a no-caffeine group in the 2nd of the 2x2 week phases doesn't appear to be likely to induce significant "caffeine withdrawal", either. I am thus doubly curious to see the (hopefully) full dataset, when this intriguing study is eventually published (also because the the caption of Figure 1 in the "FT" says that there was no interaction with habitual caffeine intake for sleep duration, at least). In the mean time, I'd suggest you simply listen to your body. The effects of exercise and caffeine on one's sleep are, after all, just as so many things, highly individual | Comment!

References:

• O’Brien, E, et al. "Caffeine and Exercise Affect Sleep Duration, Quality and Perceived Tiredness." Department of Exercise and Nutrition Sciences---University at Buffalo, Buffalo, NY (Poster presentation).
• Yang, Pei-Yu, et al. "Exercise training improves sleep quality in middle-aged and older adults with sleep problems: a systematic review." Journal of physiotherapy 58.3 (2012): 157-163.

2-aminoisoheptane aka DMHA or Octadrine, a Legit DMAA Successor? Structure, Effects & Sides Suggest: "Maybe"

2-aminoisoheptane aka DMHA or Octadrine, a Legit DMAA Successor? Structure, Effects & Sides Suggest: "Maybe"

cognitive performance DMAA DMHA fat burner health lose fat performance preworkout PWO stimulant stimulants

DMHA is rather a stim than a fat burner. But I guess it will be marketed as both.

If you are following the supplement market closely, you will have seen the first products with a new stimulant on the shelves. 2-aminoisoheptane or DMHA - a supposedly worthy successor to DMAA aka "geranamine" (the stuff in the old Jacked3D) with unquestionable structural similarities to the original banned stimulant and a questionable efficacy and safety profile. With two other non-OTC agents that have been (ab)used to lose body fat for decades, namely ephedrine and clenbuterol, DMHA, which is also called octadrine and correctly labeled "2-amino-6-methylheptane" shares a history as an asthma agent (Monroe. 1947).

DMHA will be banned, when this article is a SV Classic and caffeine again the stim of choice

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Aside from the previously cited study by Monroe et al., a study that showed weak, but existing cytoxic effects in cancer cells by Craciunesco et al. from the early 1980s and an old safety study in rodents and guinea pigs by Fellows (1947), which allows us to estimate the "safety range" of the agent at a human equivalent roughly < 400mg (in rodents, the equivalent dose will already trigger tremors and sign. increases in activity), there's unfortunately no scientific evidence to prove that the agent is (a) safe for human consumption and/or (b) even works as it is supposed to.

Whether the active substance in Eskay Oralator inhalants from the 1940s is a legitimate successor to DMAA can thus only be answered based on speculation and information from the first users, as well as the fact that the agent ended up on Rasmussen et al's recently published list of "novel stimulants in supplements" that are supposed ot "substitute for recently successful products based on ephedrine and amphetamine" (Rasmussen. 2015 | see Table 1 #8).

Table 1: Trivial and chemical names of the compounds supplement companies have dug up in articles from the 1940-50s to replace banned substances in their products (Rasmussen. 2015).

So let's look at what we have: The obviously unreliable user feedback is positive and in line with the implications of the fact that DMHA shares the same structural characteristics which allowed DMAA to interact with the trace amine associated receptor 1 and modulate dopamine and norepinephrine by increasing their production and reducing their reuptake.

Figure 1: It is not difficult to see the structural ressamblance of "geranium" or "geranamine" aka "DMAA" (found for ex. in the old "Jack3D") and "octadrine" aka "DMHA" (as it is found in supps like "InfraRed") when you compare the two.

The structural resemblance to DMAA (see Figure 1) is yet not the only thing the two agents with similar acronyms have in common. Another one is the lack of compelling scientific evidence of their efficacy and safety: Just like DMHA now, DMAA had no no real scientific backup when it first appeared on the radar of the average supplement junkie and it still blew many away - in the positive sense of being happy w/ the results,... at least until the stimulant effects wore off and the crash turned the positive into similarly negative feelings.

Remember the craze about tainted charges of DS Craze with more than just dendobrium | read more

Speaking of supplement junkies... in view of the facts that corresponding products are already on the market, we are certainly going to learn relatively soon about the efficacy and safety of this compound from hundreds if not thousand of human guinea pigs on "the boards" (fitness forums).

Don't be one of those guinea pigs that use an untested product of which I am sure it's going to be banned soon based on hearsay only - regardless of what you hear about purported α-2 receptor activity (like yohimbine) or the fact that it supposedly has similar effects as high dose caffeine or DMAA, but without the crash, by the way | Comment!

References:

• Craciunescu, D. G., et al. "Structure-antitumour activity relationships for new platinum complexes." Chemico-biological interactions 42.2 (1982): 153-164.
• Fellows, Edwin J. "The pharmacology of 2-amino-6-methylheptane." Journal of Pharmacology and Experimental Therapeutics 90.4 (1947): 351-358.
• Monroe, Russell R., and Hyman J. Drell. "Oral use of stimulants obtained from inhalers." Journal of the American Medical Association 135.14 (1947): 909-915.
• Rasmussen, Nicolas, and Peter HJ Keizers. "History full circle:‘Novel’sympathomimetics in supplements." Drug Testing and Analysis (2015).
• Thompson, W.F. - Memo, ‘Low CNS Inhaler’, 22 December 1941; R.S. Fox memo, ‘Disposal of Certain Patent Cases’, 22 March 1942; M.T. Rabbitt to Thompson re ‘Chronologic Report on the Study of Normal-Amylmethyl Carbinamine Sulfate’, 7 June 1945. All in the archives of the California Institute of Technology, Gordon Alles papers, box 15, unlabelled folder.