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!

High Dose Caffeine Restores Insulin Sensitivity and Limits Sugar-Induced Total + Visceral Fat Gain . That's in contrast to the still prevalent message that caffeine would ruin your insulin sensitivity | more

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.

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

appetite breakfast exercise fructose health hiking hunger lose fat pre-workout walking

About to go for a walk? Have fructose for breakfast to keep the hunger at bay.

I know very well that fructose is the nutritional boogyman of the 21st century, but avoiding it altogether is about as unwarranted as consuming it by the pound is unhealthy. A recent study from the Department of Health and Physical Education at the Hong Kong Institute of Education and the Department of Sports Science and Physical Education at the Chinese University of Hong Kong does now show a new, hitherto unknown, or at least under-appreciated effect of fructose: The ingestion of a fructose containing, albeit not fructose only (not tested, though) breakfast will significantly reduce the desire to eat that will usually rise sharply after a 60 minute bout of "cardio" training in form of walking at 50% of one's individual VO2max.

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As a SuppVersity reader you will know that low-intensity cardio, much more than HIT or HIIT (learn more), will trigger significant increases in hunger and one's desire to eat. To ameliorate this effect, you could - that's at least what the aforementioned study shows - simply replace part of the starchy or high GI carbs of your breakfast with high fructose fruits and/or other fructose containing food items.... that's at least - as  previously mentioned - what the study at hand suggests; a study in which Hong Kong researchers compared the effects of three isocaloric breakfasts with identical amounts of carbs (1.0 g/kg body weight) from different food sources with different GIs (41, 39, and 72) and fructose contents on the appetite scores of ten healthy young male volunteers (21.7 ± 1.5 yr, 20.9 ± 1.1 kg/m²) who had to rate different aspects of appetite every 30 min during the 2-hr postprandial period after the meal, as well as during the 1-hr recovery period that followed the 1h of brisk walking (46% VO2max) all subjects had do perform 2h after consuming the standardized breakfasts.

"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."

As you can see in Figure 1 the three test-meals initially had very similar effects on the subjects' appetite ratings, i.e. their desire to eat, hunger, fullness, and perceived ability to eat.

Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015).

Only the 25% fructose meal, however, kept the rapid increase (or decrease in the case of fullness) in all four parameters after the 1h of brisk walking (Rec-X in Figure 1) at bay. That's quite an interesting observation, even though one could argue that the study cannot serve as a definite litmus test, because it lacks a post-exercise test-meal where the practical significance of the reduced appetite scores was measured against the reduction in food intake in the fructose group.

But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's  no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).

Irrespective of the previously mentioned methodological short-coming, it is, as the authors highlight, quite striking that "the increased fructose content in LGIF breakfast suppressed the appetite score, compared with isocaloric HGI and LGI breakfast" (Sun. 2015). Previously, scientists often argued that the satiety promoting effect of fructose must be mediated by the lower GI and correspondingly lower insulin spikes as well as reduced glucose excursions after fructose vs. glucose containing meals. The data in Figure 2, however, tells us that neither the insulin spikes (Figure 2, right) nor the glucose excursions (Figure 2, left) differed significantly between the LGI (low GI) and the LGIF (low GI + fructose) meals over the relevant last part of the study period - an observation which does by the way also show us that "[w]hen exercise is included as a co-intervention strategy, the effect of GI on appetite may be highly complex" (Sun. 2015) and in most cases relatively irrelevant.

Figure 2: Glucose and insulin response to the test meals; significant differences were observed for high GI (HGI) compared to the other meals and initially for the fructose meal, where the glucose levels increased slightly more rapidly than in the low GI (LGI) reference meal -  in spite of identical calculated GI values, by the way (Sun. 2015)

Previous studies show that even though exercise exerts the most profound effect on human energy expenditure, it seems that post-exercise energy intake is not affected by exercise itself (Blundell. 1999; Melzer. 2005). In that, a study by Stevenson et al appears to confirm the finding of the study at hand which is that there is no difference relevant appetite scores between HGI and LGI trials during the postprandial period if the time between breakfast and moderate intensity exercise is sufficiently long.

Figure 3: The appetite suppressing effects of fructose preloads in the absence of exercise have been known ever since Rodin's 1990 study on the effects of fructose vs. glucose and water preloads on food intakes (Rodin. 1990).

What's new with the present study, though, is that "eating an LGIF [25% fructose] breakfast resulted in decreased appetite scores compared with HGI breakfast and LGI breakfast [25% non-fructose carbs]" (Sun. 2015). This and the fact that this difference cannot be explained by the usual suspects, i.e. insulin and blood glucose levels leads Sun et al to emphasize that ...

"[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).

In fact, scientists have previously speculated that fructose may affect appetite through slow and incomplete absorption. This effect, however, is eliminated when fructose is consumed with other CHOs (Anderson. 2003). As far as potential mechanisms are concerned, we are thus left with changes in satiety hormones and peptides like ghrelin, cholecystokinin, glucagon-like-peptide-1 and peptide-YY and/or direct or indirect effects on the gut-brain axis as potential mechanisms that would explain the results of Sun's study. Unfortunately, neither of these mechanism was assessed in their study.

Make you choice - cholesterol and regular sugar (left), or fat free and fructose-laden? In the end it all may not even matter. In spite of that, you shouldn't forget that fruit is not the enemy, isolated fructose in drinks is.

So, what's the verdict? I'd like to cite the original conclusion first, before adding my two cents: "It appears that fructose content in, rather than the GI of, a pre-exercise breakfast meals affect subjective appetite score during the recovery period after 1-hr of brisk walking" (Sun. 2015).

There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.

In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!

References:

• Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
• Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
• Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
• Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
• Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
• Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
• Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.