40g Casein Build Lean Muscle Overnight: 27% Elevated MPS Even W/Out Training (30% W/ Ex) - And That in 70-Y+ Olds!

40g Casein Build Lean Muscle Overnight: 27% Elevated MPS Even W/Out Training (30% W/ Ex) - And That in 70-Y+ Olds!

build muscle casein dairy dairy protein elderly high protein pre-bed prebed protein protein supplements sarcopenia sleep

Pre-bed protein (meal or shake) is always a good idea, no matter if you're young or old, if you work out in the PM or not - you don't want to miss the increased overnight protein synthesis.

Gaining muscle over night? No news! You will probably remember the two previous articles on "pre-bed protein ingestion", i.e. "12-Week Study: 25g Bed-Time Protein Almost Doubles Size & Increases Strength Gains" (read it) and "3.2kg of Lean Mass Over Night W/ 40g of Slow Digesting Protein 30min Before Bed!? Over One Year, a Positive Nitrogen Balance and +20% FSR Could Make It Happen!" (read it), but still! With this being the first study to show that even (on average) 71-year-olds can "build muscle overnight" with nothing but 40g of casein being ingested ~30 minutes before they went to bed, it is probably the most impressive of the previously referenced studies.

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There is, allegedly, no long-term data (=actual gains) such as the increase in lean mass after 6-12 weeks, but with this study, which was actually designed to test the hypothesis that...

"[...] that physical activity can augment the impact of presleep protein ingestion on overnight muscle protein synthesis [in] 23 older men (71 6 1 y) who ingested 40 g casein protein intrinsically labeled with L-[1-13C]-phenylalanine and L-[1-13C]-leucine before going to sleep with (PRO+EX8; n = 11) or without (PRO; n = 12) a bout of physical activity being performed earlier in the evening" (Holwerda. 2016),

the study results (that were, by the way, only marginally in line with the scientists hypothesis from the previously cited introduction) exceed my personal expectations, significantly.

Figure 1: Overnight myofibrillar protein FSRs after PRO+EX (n = 11) or PRO (n = 12) presleep treatment in older men as calculated with L-[ring-2H5]-phenylalanine (A) or L-[1-13C]-leucine (B) as tracer. Values are means 6 SEMs. Data were analyzed with an unpaired Student s t test. *Different from PRO, P , 0.01. FSR, fractional synthetic rate; PRO, 40 g protein in rested state; PRO+EX, 40 g protein after resistance-type exercise (Holwerda. 2016)

Before we start discussing the results, though, let's take a look at what the authors of the study actually did: After their subjects had ingested the 40g of labelled casein (I cannot tell if that was micellar casein, but I can tell you that the scientists got it on the free market and that it was produced by Dr. Oetker, Germans and countrymen of the Dutch scientists will know the company), the authors measured the subjects' overnight protein digestion and absorption kinetics and myofibrillar protein synthesis rates by combining primed, continuous infusions of L-[ring-2H5]-phenylalanine, L-[1-13C]-leucine, and L-[ring-2H2]-tyrosine with the ingestion of intrinsically labeled casein protein.

Suggested Read for everyone w/ parents and grandparents: Creatine Will Protect Grandpa's Muscle Even if He Doesn't Train!? More Reasons "E-veryone" Could Take Creatine | more

What did the workouts look like? As you may have gathered by now only the PRO+EX group worked out before going to sleep at the lab. Here's what they did (keep in mind: the average age was 70 years!): "The physical activity protocol consisted of 60 min of moderate-intensity, lower-body, resistance-type exercise. After 15 min of self-paced cycling at 100 W with a cadence of 60–80 rpm, subjects performed 6 sets of 10 repetitions on the horizontal leg press machine (Technogym BV) and 6 sets of 10 repetitions on the leg extension machine (Technogym BV). The first 2 sets of both exercises were performed at 55% and 65% 1RM, respectively, and sets 3–6 were performed at 75% 1RM. Subjects were allowed to rest for 2 min between all sets" (Holwerda. 2016).

As the results in Figures 1-2 clearly indicate, the relatively high amount of protein ingested before sleep was

• normally digested and absorbed, with 54% ± 2% of the protein-derived amino acids appearing in the circulation throughout overnight sleep, and
• significantly boosted the overnight myofibrillar protein synthesis rates

In that, the increase in MPS was +31% (0.058% ± 0.002%/h compared with 0.044% ± 0.003%/h; P < 0.01; based on L-[ring-2H5]-phenylalanine) with exercise and at least +27% (0.074% ± 0.004%/h compared with 0.058% ± 0.003%/h; P < 0.01; based on L-[1-13C]-leucine) without exercise.

Figure 2: Eventually, it's the net balance that counts and this is where training provided a non-significant, but potentially still relevant difference (see Figure 3 for tracer incorporation) in the elderly subjects of the study at hand (Holwerda. 2016).

Accordingly, more dietary protein-derived amino acids were eventually incorporated into de novo myofibrillar protein (~new muscle mass) during overnight sleep in the PRO+EX than in PRO treatment (0.042 ± 0.002 compared with 0.033 ± 0.002 mole percent excess; P < 0.05).

This difference between the actual amount of the traced amino acids that ended up in the muscle, was not just statistically significant (see Figure 3, in bottom line). The 10% vs. 20% difference between the PRO and the PRO-EX group is also of potential practical relevance as it increased from - over weeks the muscle gains in the PRO-EX group can thus be expected to be significantly larger. Damas et al. (2016) have, after all, been able to show only recently that the (logical) correlation between acute increases in protein synthesis and lean muscle gains that has previously been doubted does exist - if you account for muscle damage (which is reduced after 1-3 weeks of training).

Figure 3: The incorporation of traced aminos shows that the advantage of working out before sleep may matter.

Bottom line: While working out pre-bed may be best, Holwerda et al. have proven that granny & grandpa will unquestionably benefit from consuming 40g of slow-digesting casein protein (probably micellar casein) 30 minutes before going to bed - "post-workout", or not.

With additional exercise, the net protein accrual, i.e. the actually relevant difference between the amount of amino acids that is eventually incorporated into the muscle and not broken down will be 20% higher (Figure 3), though - a stat. sign. and potentially relevant difference, neither your grand parents, nor you should miss. So what? Train - hit the weights at 2-5 (max!) times a week and inspire the rest of your family to do the same | Comment on Facebook!

References:

• Damas, Felipe, et al. "Resistance training‐induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage." The Journal of physiology (2016). Read the SuppVersity article about this study.
• Holwerda. "Physical Activity Performed in the Evening Increases the Overnight Muscle Protein Synthetic Response to Presleep Protein Ingestion in Older Men." First published June 8, 2016, doi: 10.3945/​jn.116.230086 J. Nutr. jn230086.

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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Caffeine Resis- tance - Does It Even Exist?

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.

GABA - An Effective Sleep Aid W/ GH Boosting Effects that Works Within 30 Minutes - Only 100 mg Pre-Bed Will Suffice

GABA - An Effective Sleep Aid W/ GH Boosting Effects that Works Within 30 Minutes - Only 100 mg Pre-Bed Will Suffice

gaba health sleep

Spinach and beans, two good sources of dietary GABA - 42 µg/g in spinach, 25 µg/g in beans (Oh. 2003)

You may remember my previous article about GABA and the accompanying discussion I had with my friend Carl Lanore on Super Human Radio in 2013 (learn more); and if you do, you will probably also remember that I have mentioned that some people have a paradoxical reaction to GABA.

Instead of getting tired, they get wired. Whether that's related to the likewise previously discussed effects on glucose management and a potential stress response to hypo-glycemia is not clear and I have to admit: The latest GABA study does not provide an answer to this question either.

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What Yamatsu's study does provide, however, is very good evidence that γ-aminobutyric acid (GABA) acts as a potent sleep aid in the average Japanese... about as average as the ten subjects (average age: 37.7±11.5, age range: 24-57, 6 male subjects and 4 female subjects), who were suspected to have small sleep disorders but were not patients, that participated in this study.

Yamatsu et al. used a randomized, single-blind, placebo-controlled, crossover-design, according to which the ten subjects were randomly divided into two groups of five people each (group 1 and group 2). The main study consisted of two intake periods (1 week each) and a wash out period (1 week) between the intake periods. During the first intake period, subjects in groups 1 and 2 took GABA and the placebo, respectively, 30 min before going to bed everyday for a week. During the second intake period, the treatments were exchanged between groups (i.e. subjects in group 1 and group 2 took the placebo and GABA, respectively).

GABA content of selected uncooked foods (Yamatsu. 2016).

"For two consecutive nights three days prior to each intake period, the subjects went to bed wearing the EEG instrument for adaptation. On the night prior to each intake period, EEG recordings were obtained while the subject was sleeping to serve as the baseline data. EEGs were also collected on the last night of the intake periods. On days that EEGs were recorded, alcohol and drugs, such as cold medicine and hypnotics, were prohibited. In addition, food and drinks, such as coffee, tea, and other items that might affect natural sleep, were also prohibited 2 h before going to bed. Subjects were requested to maintain constant lifestyle patterns regarding their eating habits, exercise, daily work, and so on throughout the study" (Yamatsu. 2016). 

On the day following the EEG measurement, subjects evaluated their sleep with respect to ease of falling asleep, feelings upon awakening, and satisfaction with sleep by using visual analog scores (VAS). Subjects gave high scores if they felt positive effects from the test samples. In addition to VAS,  Pittsburgh Sleep Quality Index (PSQI | Burysee. 1989) was used to evaluate the sleep quality of each subject.

Serum GABA levels over time (Yamatsu. 2016).

How do we know 30 minutes before bed if optimal? In a follow up study, the researchers  were given 100 mL of water with 200 mg of GABA (more for the dose-response (2) vs. the sleep study (1) study), in order to determine the exact plasma GABA kinetics over 60 minutes. What they found is the data in the figure on the left that clearly indicates that the GABA levels and thus probably its effects peak after 30 minutes. Whether this means that your sleep will be the deepest or most recuperative with this timing cannot be guaranteed, though.

And this evaluation yielded quite interesting results: Oral administration of 100 mg of GABA significantly shortened sleep latency by 5.0 min (p=0.020, Fig. 1A, left). The mean value of sleep latency of subjects before GABA administration was approximately 10 min, and their sleep latency after GABA administration was reduced by half.

Figure 1: EEG data and subjective data from the VAS and PSQI test (Yamatsu. 2016). 

The scientists also point out that although there was no significant difference, deep non-REM sleep latency was also shortened in GABA group by 4.1 min (Fig. 1B) and elaborate:

"These results indicate that GABA may help people fall asleep quickly and easily. In other words, GABA exhibited its effect during the early stage of sleep. Besides shortening sleep latency, GABA significantly increased total non-REM sleep time by 2.2% (p=0.040, Fig. 1E). This is favorable because non-REM sleep is a deeper sleep and is thought to rest both the brain and the body. In particular, the time from falling asleep to the first REM sleep, which was in the early stage of sleep and consisted of light and deep non-REM sleep, was longer in the GABA group compared to the placebo (data not shown). This also indicated that GABA was effective, especially during the early stage of sleep" (Yamatsu. 2016). 

The results of sleep evaluation by VAS questionnaires and PSQI are shown in Fig. 1 on the right hand side: Every item of VAS and PSQI was improved in GABA group. For the scientists, that's sufficient evidence that "subjects in the present study felt certain effects after use of GABA".

Now that's cool, but what is even more important than the subjects felt any effect is that their "feelings upon awakening were significantly improved" (p=0.025, Fig. 1A, right | Yamatsu. 2016). This is important, because some drugs used for sleep treatments are so strong that people will feel drowsy and tired on the next morning, in spite of sleeping more than usual. Compared to these drugs, i.e. benzos and co, GABA is thus not just safer and over-the-counter available, it will also leave you less winded on the next AM. Unfortunately, it is questionable, whether GABA strong enough for people with severe sleep disorders - personally, I doubt that.

GABA Supplementation Shown to Improve Glucose Management - Even in Healthy Subjects, There's a Significant Reduction in Glycated Albumin Levels After Only 7 Days on 3x2g GABA per Day | learn more

Bottom line: In view of the previously discussed beneficial effects on growth hormone and glucose management, GABA is an interesting supplement for anyone. Its ability to shorten sleep latency and increase the total non-rapid eye movement (non-REM) sleep time, however makes it even more attractive for people with mild sleep disturbances and people who love to mess with their biorhythm to fine-tune it even further.

From the slightly sarcastic tone in the last sentence of the previous paragraph, you may already have concluded that I am not going to suggest everyone should supplement GABA: no long-term data, no real need... so you better only consider it, if you have sleep issues | Comment!

References:

• Buysse, Daniel J., et al. "The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research." Psychiatry research 28.2 (1989): 193-213.
• Oh, Suk-Heung, Yeon-Jong Moon, and Chan-Ho Oh. "γ-Aminobutyric acid (GABA) content of selected uncooked foods." Preventive Nutrition and Food Science 8.1 (2003): 75-78.
• Yamatsu, Atsushi, et al. "Effect of oral γ-aminobutyric acid (GABA) administration on sleep and its absorption in humans." Food Science and Biotechnology 25.2 (2016): 547-551.

Two Hours of Extra-Sleep Before Sleep Deprivation Minimize the Performance Decrements Due to 24h Sleep Deprivation

Two Hours of Extra-Sleep Before Sleep Deprivation Minimize the Performance Decrements Due to 24h Sleep Deprivation

health performance sleep sleep deficit sleep deprivation vorschlafen

If you want to practice "vorschlafen" you may have to set your alarm-clock to tell you when to go to bed.

"Vorschlafen" is the German term for getting extra sleep the nights before an event of which you know that it will leave you sleep deprived. Sounds stupid? Well, there are studies which show that increasing sleep duration for around one week may influence cognitive performance during a subsequent sleep loss period, but aside from a study on the accuracy of tennis serves (Schwartz. 2015), their practical significance for athletes is obviously limited. Why? Since your ability to focus during cognitive tasks is - as important as it is - not a reliable marker of exercise performance... or at least a very unreliable one.

Against that background it's good that in a new study from the Université de Lyon, Instead of testing cognitive performance markers such as the attention span of an individual, the researchers set out to "assess the effect of 6 nights of sleep extension on neuromuscular function and motor performance before and after [total sleep deprivation] TSD" (Arnal. 2016).

Learn more about the health effects of correct / messed up circadian rhythms

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Pre-Workout Supps Could Ruin Your Sleep

So what did the scientists do? Well, the subjects, twelve healthy men (age: 32.2 ± 3.9 years, weight: 75.2 ± 6.2 kg, height: 176.9 ± 6.2 cm, body mass index: 23.7 ± 1.7 kg/m², physical activity: < 4 h per week) participated in two counterbalanced experimental conditions (cross-over design):

• extended sleep aka EXT - mean (SE) h = 9.8 (0.1) time in bed and
• habitual sleep aka HAB - mean (SE) h = 8.2 (0.1) time in bed.

The two conditions were seperated by a 6-week washout period. In each condition, subjects performed six nights of either EXT or HAB followed by two days in-laboratory.

Sleep Science Update: New Insights into the Effect of a Lack of Quality Sleep on Glucose Control and Diabesity Risk | more

"Two weeks before the first phase, a familiarization night was spent in the laboratory to avoid any first-night laboratory effects. Moreover, a control week where subjects spent 8 h in bed each night was realized before the first phase to avoid starting the experiment with the subjects in sleep debt. Time in bed during the control week was checked with actigraphy (Actiwatch TM, Cambridge Neurotechnology, Cambridgeshire, UK). The first phase consisted in 5 nights at home (N1 to N5) with sleep recorded by polysomnography. In HAB, subjects were instructed to maintain their habitual sleep time and spend at least 8 h in bed (bedtime between 22:30 and 23:00 and wake up at 07:00).

In EXT, they spent 10 h in bed between 21:00 and 07:00. In both conditions, volunteers maintained a wake time of 07:00 to accustom themselves to the waking time of 07:00 used during the second laboratory phase. Volunteers were allowed to maintain their usual lifestyles but needed to return the polysomnography equipment to the laboratory every morning" (Arnal. 2016).

The second phase was conducted in the laboratory and started at 17:00 after the 5th night at home
(standardized to be on Saturday for everyone for each condition). Subjects were familiarized
with the experimental protocol between 17:00 and 20:00. The day after was considered as the
baseline day during which neuromuscular testing was performed between 17:00 and 20:00 (D0).
Neuromuscular testing was repeated at the same time of day the following day, i.e. after 34-37 h
of continuous wakefulness (D1).

Figure 1: Overview of the two phases of the experimental protocol (Arnal. 2016).

With temperature and light control, abstinence exercise, caffeine, tobacco, alcohol and other psychoactive substances 48 hours before and during the laboratory phase and standardized meals and caloric intakes (2600 kcal/day), the scientists sought to limit confounding factors.

Figure 2: The fact that the effect size was individual should not surprise you and could be due to the fact that the extra 2h in bed may not have been spent sleeping in all subjects (Arnal. 2016).

Accordingly, they are quite confident to conclude that the small, but for some of the subjects highly significant inter-treatment difference they observed, namely...

• a longer time to exhaustion in EXT compared to HAB (+3.9 ± 7.7% and +8.1 ± 12.3% at D0 and D1, respectively), as well as 
• a lower rating of perceived exertion during exercise at D2 in the EXT compared to HAB (-7.2 ± 7.5%) group 

triggered these performance benefits, of which the scientists say that it was no induced by blunted central fatigue in response to total sleep deprivation (TSD), but rather a consequence of the beneficial effect the subjects' ratings of perceived exertion in the sleep deprived state.

Figure 3: Rates of perceived exertion before and after total sleep deprivation (Arnal. 2016).

Bottom line: "Vorschlafen" works - at least in some individuals. If you scrutinize the data in Figure 2 and take a look at the average rates of perceived exertion and their large error bars in Figure 3, you will have to admit, though, that a significant effect of sleeping 2h extra before being sleep deprived cannot be guaranteed.

Speaking of sleeping: Since the subjects simply spent 2h extra in bed, we don't know whether those who didn't respond (a) even got 2h extra sleep and whether (b) this extra sleep was quality sleep. Next to potentially existing inter-individual difference in the response to "vorschlafen", methodological shortcomings of the study may thus also explain the heterogeneity of the results | Comment on Facebook!

References:

• Arnal, et al. "Sleep Extension before Sleep Loss: Effects on Performance and Neuromuscular Function." Medicine & Science in Sports & Exercise (2016): Publish Ahead of Print - DOI: 10.1249/MSS.0000000000000925
• Schwartz, Jennifer, and Richard D. Simon. "Sleep extension improves serving accuracy: A study with college varsity tennis players." Physiology & behavior 151 (2015): 541-544.

Sleep Science Update: New Insights into the Effect of a Lack of Quality Sleep on Glucose Control and Diabesity Risk

Sleep Science Update: New Insights into the Effect of a Lack of Quality Sleep on Glucose Control and Diabesity Risk

diabesity diabetes glucose management health insulin insulin resistance obesity on short notice sleep

Blue light is not the only enemy of sleep, but it's the most prevalent one, today.

Personally, I believe that sleep, "a condition of body and mind which typically recurs for several hours every night, in which the nervous system is inactive, the eyes closed, the postural muscles relaxed, and consciousness practically suspended" (that's what Google's "define"-feature will tell you about sleep), is still an under-appreciated determinant of optimal health and performance.

Evidence to support this assertion comes from a series of studies that were presented at the Winter Meeting of the British Nutrition Society on December 8-9, 2015 - a meeting with the telling title: "Roles of sleep and circadian rhythms in the origin and nutritional management of obesity and metabolic disease" (O'Sullivan. 2015).

Learn more about the health effects of correct / messed up circadian rhythms

Sunlight, Bluelight, Backlight and Your Clock

Sunlight a La Carte: "Hack" Your Rhythm

Breaking the Fast to Synchronize the Clock

Fasting (Re-)Sets the Peripheral Clock

Vitamin A & Caffeine Set the Clock

Pre-Workout Supps Could Ruin Your Sleep

• Circadian disruption in shift workers – the effects of insufficient sleep on dietary and lifestyle behaviours (Nea. 2016) - It will not surprise you that shift workers report more sleep problems compared to the general public. Studies estimate that 10–30 % of shift workers suffer from a circadian rhythm disorder known as “shift work disorder”(Gumenyuk. 2012). With their new quantitative study, a team of young researchers from the Dublin Institute of Technology and the University of Ulster provides some insights into the consequences of this problem.
  
  As the scientists point out, overall, just 34·3 % of the sample was achieving adequate sleep. A number of factors were associated with insufficient sleep – being male (p < 0·001), being 35–54 years of age (p < 0·001), having adult/child dependents (p < 0·001), working in larger organisations (p = 0·045), working in distribution/logistics, manufacturing or construction (p = 0·005), working night shifts (p = 0·042), and working longer shifts (p = 0·002).
  

  

  Factors that increased the subject's risk of not getting adequate sleep (Nea. 2016).

  Furthermore, the scientists observed that insufficient sleep had an effect on the diet of workers. Those who did not achieve adequate sleep were more likely to skip meals on working days and skipped meals significantly more frequently (p = 0·023).

  "Workers with insufficient sleep were also significantly less likely to consume the recommended 5 portions of fruit and vegetables per day (37·5 % vs 43·3 %, p = 0·045) and were less likely to consume the recommended 3 portions of milk/cheese/yoghurt per day (11·6 % vs 8·1 %, p = 0·050). In addition, those with insufficient sleep had higher prevalence of hypertension (10·2 % vs 5·7 %, p = 0·008) and depression/anxiety (7·3 % vs 3·4 %, p = 0·008)" (Nea. 2016)

  Participants were also questioned how they perceived shift work impacts on various aspects of their lives. Compared to those who achieve adequate sleep, those who had insufficient sleep were significantly more likely to report that shift work had a negative effect on their physical health (p < 0·001), mental health (p = 0·003), family life (p = 0·001), social life (p = 0·046), physical activity levels (p = 0·029) and overall quality of life (p = 0·002). Those with insufficient sleep were also significantly more likely to report that shift work increases how much alcohol they drink (p = 0·041).
• Oral glucose tolerance test results are affected by prior sleep duration: a randomised control crossover trial of normoglycaemic adults (Ellison. 2016) - As Ellison et al. rightly point out, "[o]ral glucose tolerance tests (OGTTs) remain the key clinical tool for assessing glucose control and diagnosing diabetes" (Ellison. 2016). In that, they criticize that "[c]urrent guidelines for administering such tests emphasise the importance of a preceding 8 hour fast (often undertaken overnight) but overlook the potential role that preceding sleeping patterns night might play in glucose control the following day" (ibid.). In view of the number of recent observational and experimental studies, which suggest that poor sleep is associated with an increased risk of diabetes, these tests may very well be messed up by a lack of sleep during the previous 8h fast. The aim of the latest study by scientists from the Sound Asleep Laboratory in Leeds was therefore "to explore the effect of early vs. late bedtimes on OGTT results using a cross-over randomised controlled trial" (ibid.).
  
  To this ends, the authors recruited 40 normoglycemic adults who were, after they had been stratification by self-reported pre-existing sleep patterns (as assessed using the Pittsburgh Sleep Quality Index; PSQI), allocated to either a ‘short’ (2·00am-7·00am) then ‘long’ (10·00pm−7·00am), or a ‘long’ then ‘short’ sleep duration, on two consecutive nights.

  "On each occasion, objective measures of sleep were obtained using the ‘SleepMeister’ application on an iPhone 4, with additional subjective assessments of sleep provided by subsequent completion of a version of the PSQI adapted to generate self-reports of sleep during the preceding night (as opposed to the preceding month). On each of the mornings following ‘short’ or ‘long’ sleep, participants again completed the PSQI and underwent a two-hour 75 g oral glucose tolerance test (OGTT), with blood glucose readings taken at 0, +30, +60, +90 and +120 minutes thereafter using finger-prick tests. Data were analysed using STATA v12. Ethical approval was granted by the University of Leeds REC (Ref:HSLTLM12075)" (Ellison. 2016).

  As it was to be expected, both the ‘SleepMeister’ application and the PSQI recorded significantly later bedtimes (SleepMeister: −19·9; 95 %CI: −20·1,−19·7; PSQI: −19·9; 95 %CI: −20·1,−19·7) and significantly shorter sleep durations (decimal hours: ‘SleepMeister’: −3·8;95 %CI: −4·3,−3·4; PSQI: −3·4; 95 %CI: −3·9,−2·9) following a 2am (vs.10pm) bedtime (i.e. ‘short’ and ‘long’ sleep duration, respectively) - a fact, the scientists consider evidence "that levels of compliance were high" (ibid.).
  
  In spite of that, there was no significant effect of sleep duration on fasting blood glucose levels prior to the OGTT after adjustment for sleep duration sequence (i.e. ‘short’ then ‘long’ vs. ‘long’ then ‘short’) and a modest imbalance in gender between the two intervention sequence group.
  

  

  Figure 2: Normal response (=expected response in OGGT, not the actual response of the subjects, because the absolute values are not disclosed in the abstract and an FT is not yet available) vs. calculated response as a consquence of insufficient sleep (normal + difference, rel. difference above bars | Ellison. 2016).

  What did differ, though, were the glucose levels recorded after the ingestion of 75 g glucose, which were consistently higher following a ‘short’ as opposed to a ‘long’ sleep duration, as well as the levels recorded at +60 and +90 minutes, which were likewise significantly higher by 1·18 mmol/l (95 %CI: 0·43,1·92; p = 0·003) and 0·55 mmol/l (95 %CI: 0·05,1·06; p = 0·032), respectively. These results, the scientists say, "indicate that short sleep duration the night before results in an immediate elevation in blood glucose levels the following morning in normoglycaemic adults" (ibid.). That this is a problem, should be obvious, after all it may falsely classify healthy individuals as pre-diabetics. Therefore, "further standardisation of pre-OGTT sleep duration, similar to that for an overnight fast," (ibid.) appears warranted.
• Less Sleep Duration and Poor Sleep Quality Lead to Obesity (Parvaneh. 2016) - In a recent cross-sectional study that was carried out to investigate the association of sleep deprivation and sleep quality with obesity, Malaysian scientists analyzed data from 225 Iranian adults (109 males and 116 females) aged 20–55 years.

  "Heart Questionnaire (SHHQ), International Physical Activity Questionnaire (IPAQ) and a 24-hour dietary recall were interview-administered to evaluate sleep pattern, physical activity and dietary intake of the subjects. Besides, anthropometric also were measured, then subjects were categorized into normal weight and over-weight/obese based on WHO (2000). Sleep duration and sleep quality were assessed based on 2 groups of normal weight and overweight/obese" (Parvaneh. 2016).

  The scientists' analysis of the data revealed that overweight/obese individuals have significantly shorter sleep duration (5·37 ± 1·1 hours) as compared to normal weight subjects (6·54 ± 1·06 hours).
  

  

  Figure 3: Overweight / obesity is linked to sign. sleep problems (Parvaneh. 2016).

  Sleep duration was yet not the parameter the scientists from the National University of Malaysia identified as a major risk factor for obesity - that was a poor sleep quality, which was associated with a 100% increased risk for being overweight or obese (OR: 2·0, 95 % CI: 1·18–3·37, p < 0·05). As a conclusion, the scientists state that "lower sleep quality and sleep duration increase the risk of being overweight and obese" and demand: "[S]trategies for the management of obesity should incorporate consideration on sleeping pattern" (Parvaneh. 2016). These strategies, by the way, may also help people keep their triglyceride levels in check. After all, another study that was presented at the same meeting of the Nutrition Society suggests that a high sleep efficiency shows a strong and negative correlation with triglycrides and another important marker of heart disease risk, the total cholesterol to HDL ratio (Al Khatib. 2016).
• Is insulin resistance associated with light at night in healthy sleep deprived individuals? (AlBreiki. 2016) - The simple answer to this question is "Yes!". The more complex one is that a recent study that was designed to investigate the impact of light and/or endogenous melatonin on plasma hormones and metabolites prior to and after a set meal in healthy sleep deprived subjects found that bright blunts the release of melatonin and the effects of insulin on glucose disposal.
  
  In the study, seventeen healthy participants, 8 females (22·2 years (SD 2·59) BMI 23·62 kg/m2 (SD 2·3)) 9 males (22·8 years (SD 3·5) BMI 23·8 kg/m2 (SD 2·06)) were randomised to a two way cross over design protocol; dim light condition (<5lux) and bright light condition (>500lux), separated by at least seven days.

  

  Melatonin promotes female weight loss - Suggested Read: "Trying to Lose Fat & Get "Toned"? Taking 1-3 mg Melatonin Helps Women Lose 7% Body Fat, Gain 3.5% Lean Mass".

  "Each session started at 18:00 h and finished at 06:00 h the next day. All participants were sleep deprived and semi-recumbent throughout the session. An isocalorific breakfast was consumed at 08:00 h and lunch was timed to be 10 hours before the evening meal. Each participant consumed an evening meal (1066 Kcal, 38 g protein, 104 g CHO, 54 g fat, 7 g fibre) at an individualised time based on estimated melatonin onset. Plasma and saliva samples were collected at specific time intervals to assess glucose, insulin and melatonin levels" (AlBreiki. 2016).

  As previously stated, the bright light reduced the salivary levels of melatonin significantly (p = 0·005). What is more relevant to the research question, however is that it also increased the postprandial glucose and insulin levels significantly compared to dim lights (p = 0·02, p = 0·001) respectively.
  
  

  

  Figure 3: Effect of light intensity on melatonin levels and glucose response of 8 female and 9 male normal-weight normoglycemic subjects to standardized meal consumed at night (AlBreiki. 2016).

  For the scientists this result is not exactly surprising. They had expected that the melatonin release would be suppressed due to the light intensity; that the increase in insulin was not able to compensate for the light-induced increased glucose resistance, however, shows that the ill effects of a  'night-shift-esque' bright light exposure at night on glucose metabolism are more severe than previously thought.

Redeem your sleep dept, now!

Bottom line: Along with studies highlighting the importance of sufficient hours of quality sleep on glucose control in pregnancy (Alghamdi. 2016; Alnaja. 2016) and the "largest study to-date to demonstrate a strong inverse association between late-onset diabetes and poor sleep, even after adjustment for potential confounding factors" (Alfazaw. 2016), the previously discussed studies highlight that sleep hygiene' is as important for your health as "clean eating" (whatever that maybe) and a sufficient amount of light and intense physical activity | Comment on Facebook!

References:

• AlBreiki, et al. "Is insulin resistance associated with light at night in healthy sleep deprived individuals?" Proceedings of the Nutrition Society, 75 (2016). 
• Alfazaw, et al. "Variation in sleep is associated with diagnosis of late-onset diabetes: a cross-sectional analysis of self-reported data from the first wave of ‘Understanding Society’ (the UK Household Longitudinal Study)." Proceedings of the Nutrition Society, 75 (2016). 
• Alghamdi, et al. "Short sleep duration is associated with an increased risk of gestational diabetes: Systematic review and meta-analysis." Proceedings of the Nutrition Society, 75 (2016). 
• Alnaja, et al. "Relationship between sleep quality, sleep duration and glucose control in pregnant women with gestational diabetes." Proceedings of the Nutrition Society, 75 (2016). 
• Al Khatib, et al. "The Sleep-E Study: An on-going cross-sectional study investigating associations of sleep quality and cardio-metabolic risk factors." Proceedings of the Nutrition Society, 75 (2016). 
• DeFronzo, Ralph A. "The triumvirate: β-cell, muscle, liver. A collusion responsible for NIDDM." Diabetes 37.6 (1988): 667-687.
• Ellison, et al. "Oral glucose tolerance test results are affected by prior sleep duration: a randomised control crossover trial of normoglycaemic adults." Proceedings of the Nutrition Society, 75 (2016). 
• Gumenyuk, Valentina, Thomas Roth, and Christopher L. Drake. "Circadian phase, sleepiness, and light exposure assessment in night workers with and without shift work disorder." Chronobiology international 29.7 (2012): 928-936.
• Nea et al. "Circadian disruption in shift workers – the effects of insufficient sleep on dietary and lifestyle behaviours." Proceedings of the Nutrition Society, 75 (2016). 
• O’Sullivan (ed.). "Roles of sleep and circadian rhythms in the origin and nutritional management of obesity and metabolic disease." Proceedings of the Nutrition Society. Volume 75 / Issue OCE1 - Winter Meeting, 8–9 December 2015. Published January 2016: E1-E42.
• Parvaneh, et al. "Less Sleep Duration and Poor Sleep Quality Lead to Obesity." Proceedings of the Nutrition Society, 75 (2016). 
• Peschke, Elmar. "Melatonin, endocrine pancreas and diabetes." Journal of pineal research 44.1 (2008): 26-40.