6x1 Min HIIT Before Lifting Shed Extra Fat, Don't Impair 'ur Gainz | Daily AM/PM Training = ZERO Gainz | Alcohol W/Out Acute Effect on Workout Recovery of Trained Women

While alcohol doesn't impair the regeneration and doing HIIT before weights leaves women's gains unchanged while potentially boosting their fat loss, training twice a day, every day appears to be a good idea only for those who are afraid that they could become "too muscular".

Not every study is worth being discussed at length in an article of its own. This is why I've come up with the "Short News" or "Research Updates" - articles like the one at hand in which I address 3-5 studies very briefly. Mostly to give you an idea of the results and make sure that you can say "Yo, I've read about that study, bro" at the gym, when someone tells you: "You know, man, there's that new study showing that alcohol does not exacerbate the inflammatory response to exercise, bro!"

Ok, that was a joke. I hope your real reason to read the following elaborations is to make sure that the way you train is in line with what works according to the latest research - doing HIIT before lifting to shed extra fat without impairing your gains, for example.

Read about exercise- and nutrition-related studies in the SuppVersity Short News

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• Women who HIIT it hard don't risk their weight training gains and may lose extra body fat -- While we do have corresponding evidence from studies in male subjects, it was, until now, not clear, whether doing HIIT and resistance training concurrently would have the same effects in premenopausal women like the sixteen 26–40 year-old ladies who were randomly assigned into two groups that performed either resistance (RT), alone, or concomitant (CT) training in a recent study in the European Journal of Applied Physiology (Gentil 2017). Here's how the authors describe their experimental approach to the question:

  "Both groups performed the same RT program; however, CT performed additional high-intensity interval training (HIIT) on a bicycle ergometer before RT. The study lasted 8 weeks and the participants were tested for ten repetition maximum (10RM) load in elbow flexion (barbell biceps curl) and knee extension exercises pre- and post-intervention. RT was performed with 10–12 repetitions to self-determined repetition maximum in the first four weeks and then progressed to 8–10. During CT, HIIT was performed before RT with six 1-min bouts at 7–8 of perceived subjective exertion (RPE) and then progressed to eight bouts at 9–10 RPE" (Gentil 2017).

  The researchers' analysis of the data revealed significant increases in upper and lower body strength for both the RT and CT groups.

  

  Figure 1: Rel. changes in markers of body fat (waist and sum of three skinfold measurements) on the left and individual strength gains of the knee extensors on the right (Gentil 2017).

  More specifically, the ladies' biceps barbell curl 10RM load increased from 12.9 ± 3.2 kg to 14 ± 1.5 kg in CT (p < 0.05) and from 13 ± 1.8 kg to 15.9 ± 2.5 kg in RT (p < 0.05), with no significant between-groups differences. Knee extension 10RM increase from 31.9 ± 11.6 kg to 37.5 ± 8.5 kg for CT (p < 0.05) and from 30.6 ± 8.6 kg to 41.2 ± 7.4 kg for RT (p < 0.05).
  
  Accordingly, the authors are right to conclude that - within the limits of their study - performing HIIT on a cycle ergometer before resistance training does not seem to impair muscle strength increases in the knee extensors or elbow flexors of pre-menopausal women. This information should be considered when prescribing exercise sessions, since both activities may be combined without negative effects in muscle strength.
• Two-a-days would probably completely impair your gains -- While it is only a rodent study, Junya Takegaki's recent paper (2017) clearly indicates that resting only 8h between workouts blunts the hypertrophy response to exercise.
  
  In the study, male Sprague-Dawley rats were randomly assigned into three groups: resistance-trained with 18 bouts at an interval of 72h (72H), 24h (24H), and 8h (8H). The resistance exercise consisted of 50 repetitions of maximal isometric contraction of the gastrocnemius muscle. The right gastrocnemius muscle was used as trained muscle, and the left was used as internal control. The muscle contraction was induced by transcutaneous electrical stimulation under anesthesia. Muscle samples were collected 48h after the final exercise session and kept frozen until analysis.

Keep in mind that you can train successfully twice a day with ample rest btw. training days

Nine Short Workouts (AM+PM) p. Week Yield Extra Strength, Size and Performance Gains Compared to Volume Matched 3-Day Split, All Differences are Non-Significant, Though | If not Done Everyday AM+PM Works

Two-A-Day Training - That's Bogus, Right? No - Increased Fat Oxidation in Endurance, 2.4x Higher Max. Volume, 2.6x Higher Time to Exhaustion in Resistance Training Study | Two-a-Day & HIIT

• Said analysis showed that the rodents' gastrocnemius wet weight was increased in 72H and 24H, but not in 8H. Similarly, the mitochondrial content was increased in 72H and 24H, but not in 8H.
  
  Against that background, it is interesting to note that the same protein ubiquitination was observed in all groups, and the ubiquitination was increased with shortening of training interval. In other words: human studies will also have to measure real gains, not protein expressions to assess the effect of different training frequency.
• Postworkout alcohol consumption ain't a problem for women -- You will remember that, in men, alcohol can actually increase the testosterone response to exercise (I discussed that in a 2013 article). What it does in women was, until now, not clear. Accordingly, scientists from the University of North Texas and the Louisiana State University conducted a study to investigate the effect of acute alcohol consumption on muscular performance recovery, assessed by maximal torque production, and on inflammatory capacity, assessed by lipopolysaccharide (LPS)-stimulated cytokine production, following muscle-damaging resistance exercise in women.

  "Thirteen recreationally resistance-trained women completed two identical exercise bouts (300 maximal single-leg eccentric leg extensions) followed by alcohol (1.09 g ethanol kg−1 fat-free body mass) or placebo ingestion. Blood was collected before (PRE), and 5 (5 h-POST), 24 (24 h-POST), and 48 (48 h-POST) hours after exercise and analyzed for LPS-stimulated cytokine production (TNF-α, IL-1β, IL-6, and IL-8 and IL-10). Maximal torque production (concentric, eccentric, isometric) was measured for each leg at PRE, 24 h-POST, and 48 h-POST" (Levitt 2017).

  The scientists found that exercise per se increased the LPS-stimulated production of TNF-α (%change from PRE: 5 h-POST 109%; 24 h-POST 49%; 48 h-POST 40%) and decreased LPS-stimulated production of IL-8 (5 h-POST −40%; 24 h-POST −50%; 48 h-POST: −43%) and IL-10 (5 h-POST: −37%; 24 h-POST −32%; 48 h-POST −31%). Consuming alcohol after exercise, however, did not affect this response.
  

  

  Figure 3: LPS-stimulated concentrations of IL-10 (a), IL-8 (b), TNF-α (c), and IL-6 (d) normalized to the pre-exercise (PRE) concentrations at 5 h after exercise (5 h-POST), 24 h after exercise (24 h-POST), and 48 h after exercise (48 h-POST). Asterisk time point means significantly (p < 0.05) different from PRE, dollar symbol time point mean significantly different from 5 h-POST, hash symbol time point mean significantly different from 24 h-POST. Mean ± SE (Levitt 2017).

  Regardless of drink condition, concentric, eccentric, and isometric torque produced by the exercised leg were lower at 24 h-POST (concentric 106 ± 6 Nm, eccentric 144 ± 9 Nm, isometric 128 ± 8 Nm; M ± SE) compared to PRE (concentric 127 ± 7 Nm, eccentric 175 ± 11 Nm, isometric 148 ± 8 Nm). Eccentric torque production was partially recovered and isometric torque production was fully recovered by 48 h-POST.
  
  Only a fool would assume that this implies that you can drink every day and still make the same gains and get the same health benefits from exercise as an alcohol-abstainer. What the study at hand does prove, however, is that the occasional cocktail ain't going to ruin what you've been working so hard for in the gym.

Review the January '17 Research Update | more

Bottom line: That's it for today, come back for another installment of the short news when there's more newsworthy resistance training or nutrition research that's interesting, yet not important enough to devote an independent SuppVersity article on its analysis | Comment!

Ah... and in case you haven't done that already, I highly suggest you subscribe to the news updates on facebook.com/SuppVersity and/or twitter.com/SuppVersity, respectively, to stay up-to-date.

Reference:

• Gentil, P., de Lira, C.A.B., Filho, S.G.C. et al. "High intensity interval training does not impair strength gains in response to resistance training in premenopausal women." Eur J Appl Physiol (2017) 117: 1257. doi:10.1007/s00421-017-3614-0
• Levitt, D.E., Luk, HY., Duplanty, A.A. et al. "Effect of alcohol after muscle-damaging resistance exercise on muscular performance recovery and inflammatory capacity in women." Eur J Appl Physiol (2017) 117: 1195. doi:10.1007/s00421-017-3606-0
• Takegaki, Junya, et al. "Resistance training with short interval does not induce skeletal muscle hypertrophy in rats." The FASEB Journal 31.1 Supplement (2017): 1021-15.

Cutting Carbs After PM HIIT Workouts Will Make You Cross the Finish Line Before Anyone Else: 3% Faster Time Trial, 9% More Power and Twice as Much Fat Mass Lost in 7 Days

Don't be a fool. Simply eating no carbs in the PM is not going to yield the same results. It's all about timing it correctly with your workouts... workouts? Yes, bad  news: you got to get off the couch, bro; workout daily: one light, one HIIT day.

I've written about the adaptational response to "training low", i.e. doing endurance training on a low carbohydrate diet previously. In January, this year, for example, I have reported the results of a study from the French National Institute of Sport that showed that strategically cutting carbs in the PM and thus "sleeping low" will trigger game-changing Performance gains in only 3 weeks (read the article).

Now, the scientists go one better: In their latest study, Laurie-Anne Marquet and colleagues investigated the effect on an even shorter timescale - a timescale that is short enough to consider "sleeping low" as a possible  pre-competition strategy... well, assuming that it would work its performance-enhancing magic within as little as the 7 days, during which the subjects' in Marquet's study followed the "no carbs after your workout" (="sleep low" | SL) prescription the researchers copied from their own previously discussed study.

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Overall, 21 endurance-trained male cyclists (mind the typo about the # in the abstract of the original study, in case you read it; the summary says 11, not 21, which is the correct number) volunteered to participate in the study. All were healthy, aged between 18 and 40 years, and training at least 12 h/week, having at least 3 years of prior training. Their mean (±SD) age was 31.2 ± 7.1 years, their mean body mass was 71.1 ± 5.6 kg, their mean maximal oxygen consumption (VO2max) was 64.2 ± 6.0 mL/min/kg, and their mean maximal aerobic power (MAP, W) was 342 ± 38.3 W.

To isolate the effects of the dietary / carbohydrate modulating intervention, the subjects who trained
according to their habitual training program, initially (1st week) ate according to their usual dietary habits, documenting their food intake via a daily food diary. These diaries were then compared to the prescribed carbohydrate pattern in the 2nd week, which set their CHO intake at 6 g/kg per day.

Figure 1: Graphical overview of the study design; CHO: carbohydrates; HIT: high‐intensity training session; LIT: light intensity training session; SL: Sleep‐Low; CON: Control; MAP: Maximal aerobic power (Marquet. 2016).

After the dietary standardization and the pre-test at the end of this period, the subjects were randomly assigned to two different groups undertaking the same one-week training program.

The study used pre-bed protein shakes, a strategy to build muscle.

Nightly protein shakes, glycogen depletion and lean muscle mass: In contrast to what some people may expect, the no-carbs before bed strategy did not lead to measurable decreases in lean mass. Whether and to which extent that was a result of the protein shake both groups consumed before bed cannot be answered without doing another study. What I can tell you based on previous research, however, is that this, i.e. having a protein shake "before" (not necessarily right before) bed, is a very promising strategy to maximize net protein retention (see "12-Week Study: 25g Bed-Time Protein Almost Doubles Size & Increases Strength Gains" | more).

The built-in and significant difference between the group can be found in the nutritional guidelines according to which all subjects consumed the same amount of 6g/kg CHO, in total, but periodized their carbohydrate intake differently over the day. Specifically,...

• the control group trained with a high CHO availability (control group, CON group, n = 9) with an even spread of CHO intake over the day and between training sessions,
• the "sleep low" (SL) group (n = 12 | mind the typo in the scientist' abstract) trained with a CHO intake that was periodized within the various days in a way that no CHO was consumed between the high-intensity interval training sessions (HIIT) held

Practically speaking: The subjects in the "sleep low" group were thus doing truly fasted or, rather, glycogen depleted low-intensity cardio in the morning of each of three of the six otherwise identical workout days.

Figure 2: 20km cylcling times and mean power output in pre- and post-test (Marquet. 2016).

Against that background, it is all-the-more surprising that the subjects saw both: significant reductions in their time-trial times (-3.32%) and improvements in their average power production during the workouts (+9.17%). What is not surprising is that the data in Figure 1 indicates that these power improvements occurred specifically in the latter part of the workout, i.e. when the glycogen stores are running out and the training effect from training low in the AM shows.

Table 1: Rating perception of effort (RPE) during the 20 km cycling time-trial every 5 km (Marquet. 2016).

In contrast to what you would expect, the scientists did not detect a significant difference between group and pre and post tests for the substrate oxidation, markers of lipid oxidation and stress markers - or, more specifically there was ...

• no decrease in CHO oxidation in the SL group and 
• no increase in FAT oxidation in the SL group
• no increased cellular damage in form of lipid oxidation, and
• no significant difference in the subjects' stress response (plasma catecholamines),

... in the high-performing "sleep low" aka "SL" group. Now, there's a (small) catch, though, that should be mentioned in spite of the lack of statistical significance: the scientists observed a small increase in the subjects' rate of perceived exertion during the light AM sessions (+13%), as well as the post-intervention time trial (+10%) in the "sleep low" group. Moreover, the last-mentioned increase is more or less identical to the increase in average power production during the post-test on day 7. Accordingly, it is questionable if one should call this already non-significant effect a "catch", at all.

Brad Schoenfeld's 2014 "Fasted Cardio"-study falsifies the myth of superior long-term (4 week) fat loss in non-glycogen-depleted non-athletes on a moderate energy deficit (more). It does not exclude, however, that the glycogen-depleted subjects of the study at hand could see increased fat loss in the short or long term.

"And the subjects got ripped, right?" Not exactly. While the statement from the headline is 100% accurate, the total fat loss was (and this is not surprising in view of the study duration) marginal: statistically significant −395 ± 491 g in the SL and statistically non-significant −151 ± 363 g in the control group.

The reason that it is still worth mentioning is that previous studies suggested that doing AM cardio on empty would not increase fat loss (even over longer periods of time). So, how can we consolidate these conflicting results? Well, while further research appears necessary, I could imagine that both, the advanced training status of the subjects' in the study at hand and the fact that they were actually glycogen-depleted and not, as the subjects' in Schoenfeld's seminal paper (Schoenfeld. 2014), "only fasted", so that, if anything, their liver glycogen may have been lowered | Comment!

References:

• Marquet, Laurie-Anne, et al. "Periodization of Carbohydrate Intake: Short-Term Effect on Performance." Nutrients 8.12 (2016): 755.
• Schoenfeld, Brad, et al. "Body composition changes associated with fasted versus non-fasted aerobic exercise." Journal of the International Society of Sports Nutrition 11.54 (2014). Previously discussed, here!

Not Getting into Ketosis? Try Plain Old Caffeine to Double Your AM Ketone Levels Regardless of High CHO Breakfast

Neither a ketogenic breakfast nor buttered coffee were necessary to double the subjects' ketone production.

Ok, I have to admit that the breakfast that was served in the latest study from the Research Center on Aging, Sherbrooke, CIUSSS de l’Estrie – CHUS and the Department of Pharmacology & Physiology, Université de Sherbrooke in Canada (Vandenberghe. 2016) is not exactly what anyone would recommend to people who are trying to get into full ketosis. This, however, does not make the scientists' observation that the addition of 3mg/kg and 5mg/kg of caffeine in form of cheap caffeine pills from the pharmacy will almost (moderate dose) and more than (high dose) double the subjects' ketone production, does not make the latest study from Camille Vandenberghe's lab less interesting.

You can learn more about coffee and caffeine at the SuppVersity

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Caffeine Resis- tance - Does It Even Exist?

But, let's tackle things one by one: With ketogenic diets getting more and more attention in mainstream dietary research, it is not exactly surprising to see a study that uses the potential therapeutic effects of ketones on aging-induced cognitive impairments in Alzheimer’s disease as a point of departure for their investigation of caffeine "as a potential ketogenic agent" (Vandenberghe. 2016) - or I guess whe should say "ketogenic facilitator".

Owing to its actions on  lipolysis/ lipid oxidation, the scientists expected that caffeine co-ingestion with breakfast would be ketogenic in healthy adult subjects. To test this hypothesis, the authors recruited a group of healthy adults (BMI 24kg/m² | previous daily caffeine intake < 300mg/day!) to evaluate their individual and average response to the acute ingestion of...

• 2.5 mg/kg caffeine (equiv. to ca. 1.5-3 cups of coffee w/ ~95 mg/cup)
• 5.0 mg/kg caffeine (equiv. to ca. 3-5 cups of coffee w/ ~95 mg/cup)

alongside the afore-hinted-at standardized breakfast that consisted of  two pieces of toast with raspberry jam, a piece of cheese, applesauce and 100 ml of juice - a breakfast that is, with its 85 grams of carbohydrate, only 9.5 g of fat and 14 g of protein, not exactly "ketogenic".

Figure 1: Ketone production and FFA levels in the control and caffeine 2.5 ad 5.0 mg/kg trials (Vandenberghe. 2016).

As you can see in Figure 1, the bolus of caffeine still elevated both, the concentrations of ketone bodies and free fatty acids in the subjects' blood. And what's even more exciting, the ketone advantage became significantly more (not less) pronounced over time (see Figure 2)

Yes, you remember that correctly: High FFA = lower insulin sensitivity - So eventually, you have to be careful with the caffeine for ketones approach if you consume high amounts of carbohydrates and/or are already having issues with glucose management. If that's not you, I'd like to remind you of the beneficial effects of caffeine on glycogen repletion, I discussed in "Post-Workout Coffee Boosts Glycogen Repletion by Up to 30% and May Even Have Sign. Glucose Partitioning Effects" | more.

This is an observation which would suggest that the breakfast coffee could be even more useful for ketogenic dieters who are intermittently fasting, as it would give them a headstart into full-blown ketosis in the time between breakfast and dinner.

Figure 2: Time course of the ketone response in the study subjects according to treatment (Vandenberghe. 2016).

The observation that caffeine enhances lipolysis and increases blood FFA levels, which in turn provide substrates for ketogenesis ad thus stimulate safe and mild ketonemia in healthy adults to a ketone level twice that seen after an overnight fast, has the authors speculate that regular caffeine consumption may be linked to the decreased risk of developing late-life cognitive decline, as it was observed by Panza, et al. only recently in what is one of the latest reviews on this topic, if not primarily, then at least also because of its effect on ketogenesis.

Eventually, we do yet still need evidence that the "trick" works with a ketogenic diet, as well. After all, the relative increase in the study at hand may be huge, the absolute levels of ketones in the blood, on the other hand, are small (compared to eating a 100% ketogenic diet (=nutritional ketosis), where levels will go up to 0.5 - 3.0 mmol/L), but still impressive in view of the fact that the caffeine was consumed with a high carbohydrate (high GI) breakfast.

Bulletproof coffee is a fad, but is it also bad for your blood lipids? Studies suggest that it's at least not the butter that elevates cholesterol | Learn more!

Bottom line: Yes, it's too early to get all-too-excited, but whence we have (a) the studies to evaluate caffeine’s long-term effect on ketonemia and the corresponding impact on brain function during aging, the authors ask for, as well as (b) insights into potential interactions with the composition of the meal it is co-ingested with, and all that confirms what the study at hand suggests, i.e. that caffeine can double the ketone production in healthy individuals, ketogenic dieters would have all-the-more reasons to cherish their large AM pot of coffee (not necessarily with butter, though; after all the trick works without sign. amounts MCTs and even in the presence of ~90g of carbohydrates) | Leave a comment on the SuppVersity Facebook Page!

References:

• Panza, Francesco, et al. "Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: a systematic review." The journal of nutrition, health & aging 19.3 (2015): 313-328.
• Vandenberghe, Camille, et al. "Caffeine intake increases plasma ketones: an acute metabolic study in humans." Canadian Journal of Physiology and Pharmacology (2016) [ahead of print].

Eating 75-100g Fat (M-/PUFA) in the AM Improves Glucose (7-8%), Insulin (40-60%), Trigs (4-16%), GSH & MDA (40-75%)

If we assume that the protein fried eggs with its comparatively low insulinogenicity is not a problem (unlike your whey, for example), avocado and eggs fried in olive oil is the perfect breakfast to replace the liquid test meal used in the study.

There's no debating that increased amounts of free fatty acids in the blood will impair your insulin sensitivity, as they should be there only, when your supply of carbohydrate is running out, AMPK and with it the expression of lypolytic enzymes increase and the triglycerides from your fat stores are broken down into free fatty acids and released into your bloodstream where they can be used by liver, muscle and other organs as an alternative energy source.

Now, the word "alternative" is of paramount importance, here, because you'll find yourself being in (diabetic) trouble if those FFAs pile up on top of high glucose levels. This is what happens with the SAD diet and its high carbohydrate and fat content (and energy!) content.

You can learn more about fat at the SuppVersity

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It's a vicious circle: When the levels FFAs are up, insulin sensitivity goes down (after all, with a normal diet you'd have to burn the fat and spare the precious glucose | Bodne. 1997; Koves. 2008). Since there's more and more glucose spilling in over the portal-vein, though, insulin will keep increasing to a point where it does no longer simply impair, but almost block the oxidation of free fatty acids. Now, without insulin working its glucose shuttling magic, however, the cells begin to starve for glucose and... right, more FFAs are being released, the insulin resistance increases, still hardly more glucose is being shuttled into the cells to restore AMP to ATP and the process continues.

What does all of that have to do with eating more MUFAs and PUFAs to control your glycemia? Well, nothing and everything. First- and most importantly, it should remind you that this is not about eating fat with your carbohydrates. That's exactly not what the latest study from the Hospital Clínico Universitario Valencia in Spain would suggest, even though I bet you will have some idiot already have misinterpret the study in this way "for your" online. Rather than that the study was, as the abstract already tells you, conducted to ...

"[...] evaluate the changes in glycemia, insulinemia, and oxidative stress markers during an oral fat load test in nondiabetic subjects with abdominal obesity and to analyze the association between postprandial oxidative stress markers and postprandial glucose and insulin responses" (Martinez-Hervaz. 2016)

This quote also contains another important information you will have people with an agenda forget to mention: the subjects in whom the fats worked their magic were abdominally obese! Later on we will see why this is relevant and why the same rules won't apply to lean individuals, but for the time being let's firstly take a look at the exact characteristics of the N = 40 (total) subjects in the study in Table 1.

Table 1. General characteristics, fasting lipids and lipoproteins, glucose, insulin and HOMA index values in the studied groups (Martinez-Hervas. 2016); ^a control vs abdominal obesity group (p<0.01).

Even though the discriminating feature, i.e. the characteristic the scientists used to find subjects for the two groups was their waist circumference (>102/88 cm for men and women, respectively vs. <102/88 in the control group), it shouldn't surprise you that the scientists have also observed sign. differences in other anthropometric and metabolic markers such as the BMI, the level of triglycerides, blood lipids and postprandial glucose levels after an oral glucose tolerance test (OGTT | see Table 1).

Is it a problem that the male / female ratio differed? That is difficult to tell. We do know that men and women handle nutrients, esp. fat and carbs slightly differently, but I doubt that the difference between an 11/9 ratio in the control group and a 7/13 ratio in the abdominal obesity group will ruin the results of the study at hand. Nevertheless, this should be addressed in future studies.

After initial testing, the subjects from both groups ingested the same commercial liquid preparation of high-fat meal of long chain triglycerides. The product is called SuperCal and must not be confused with a vitamin D + calcium product with the same name that is being sold on the US market. From a previous European study, I've got some extra-information about its composition, namely that

"[...] 125 ml contains 60 g fat, of which 12 g are saturated, 35.35 g are monounsaturated, and 12.75 g are polyunsaturated. Each 100 ml contains <1 g lauric acid, <1 g myristic acid, 4.8 g palmitic acid, 1.4 g stearic acid, 27.7 g oleic acid, 9.6 g linoleic acid, 1.4 g behenic acid, and 0.5 g lignoceric acid" (Fernández‐Real). 

The detailed fatty acid composition of the SFAs, MUFAs and PUFAs emulsion that was administered at a dosage of 50 g fat per m² of body surface (calculate your body surface if you want to know your individual equivalent dose = result of your calculation in m² x 50g g/m²; e.g. 1.78 m² x 50 g/m² = 89 g of fat) at 8:30 after an overnight fast is not mentioned in the Martinez-Hervas study. What the authors of the study at hand tell us, however is that the likewise relevant ratio ω6/ω3 is > 20/1 - similar to the average diet, by the way; a fact that excludes that this is an omega-3 effect we are seeing, here. Similarly, exercise or previous meals, shouldn't have messed with the results, either. After all, in both groups, only water was permitted during the "eating" or rather "drinking" process, and no physical exercise was undertaken before or during the "fasted" fat loading test in the AM.

Figure 1: Overview of the rel. levels of glucose, insulin, HOMA-index, trigs, the GSSG/GSH ratio and MDA, a byproducs of lipid oxidation (Martinez-Heras. 2016); levels expressed relative to control at baseline (T = 0), see explanation below

In order to make the data more accessible (compared to the tabular overview of absolute values in thee FT) for you, I've standardized each of the measurable variables to match 100%. This means that all the fasting bars at T = 0h will be at the 100% mark, because they are what the effects of fat loading are compared to. Let's take a look at two examples:

• 

  PUFA Increases Postprandial Thermo-genesis in Women & Beyond - 14% Increase Over MUFA & SFA Sounds Huge, But Does it Matter?

  Insulin: In contrast to what you will see if you co-administer fat and carbohydrates (learn more), the administration of the high MUFA + PUFA fat supplement in the absence of carbohydrates lead to a sign. reduction of the initially 3.8-fold increased insulin levels. Not to normal levels, but at least to 158% (i.e. 1.6-fold elevated) of the fasted value of the lean subjects. Ah, but remember: All that happened with the fat load, alone, and in the absence of CHOs. In the presence of carbs the results would have been much different.
• GSSG/GSH ratio: The effects on the ratio of 'used' glutathione (GSSG) to the amount of the 'fresh' master anti-oxidant (GSH) were quasi the opposite of what the scientists observed for insulin. Here, the abdominally obese group had 2.4x elevated levels to begin with. This tells you that, compared to the normal controls, their anti-oxidant status was a mess. After only 8h, however, their GSSG/GSH ratio had not just declined, it was actually lower than the fasted value of the control group.
  
  And again, likewise similar to the effects on insulin, the control group saw benefits as well, with a 64% decrease in the GSSG/GSH ratio their antioxidant defenses did also benefit from the MUFA + PUFA load in the AM.

For other parameters you will see similar, for many of you probably surprising benefits. Things to keep in mind, though, is that we are talking non diabetic subjects in both groups, even if the abdominally obese subjects had fasting HOMA index values fourth fold higher than controls, higher fasting triglyceridemia and higher fasting oxidative stress markers. If that sounds like you, then the acute ingestion of ~75-120g (depending on your body surface) of fat on empty in the AM, when hyperlipidemia is not that much of an issue, you can benefit from a high MUFA + PUFA fat load as you would find it in an avocado + egg fried in olive oil, for example... or, as the authors of the study at hand have it:

"[O]ur study has demonstrated a significant reduction of postprandial glycemia, insulinemia, c-peptide and oxidative stress markers using an acute oral overload of unsaturated fat. We have found a significant correlation between oxidative stress markers and postprandial lipemia. There is an increase of TG achieving the maximum peak four hours after the beginning of the test. However, although postprandial lipemia has been implicated in the development of insulin resistance and oxidative stress, and despite the increase of TG, there are significant reductions of the HOMA index and oxidative stress markers" (Martinez-Hervas).

Even though you may think otherwise, the authors are also right, when they point out that "[t]he influence of dietary macronutrients in insulin sensitivity is not well known" (ibid.) This is especially true, when we begin mixing proteins, carbohydrates and fats and start to take into consideration that we can have a dozen of types of the three in a single meal.

What about me? I am not abdominally obese, will I benefit, too? If we assume that you deprive yourself of any carbohydrates (and proteins?), you should see the same benefits as the subjects in the control group - those are lower than what we see in the big belly group and may simply be a result of the moderate energy intake (that's < 900kcal before an 8h fast even for many bigger guys), it would appear as if the answer to your rightly asked question would be "Yes, you can benefit, as well." Whether this will also require you to abstain from all, not just insulinogenic dairy proteins, however, will have to be tested in future studies.

It may thus depend on the food-matrix whether the results of previous studies, most of which clearly indicate that saturated fat will increase in fasting and postprandial insulin resistance would have yielded different results if the meals were administered in the absence of carbohydrates, for example - even though, additional evidence traced these effects back to increased levels of saturated fat in the cells' phospholipids that can alter their phyco-chemical properties and decrease the glucose transporters (while MUFA and PUFA have been shown to do the opposite | Borkman. 1993). Martinez et al. who have not actually tested the effect of SFAs in their studies provide additional evidence in their discussion:

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?" | Learn the answer

"Iggman et al demonstrated in elderly men that palmitic acid, the major saturated fatty acid found in adipose tissue, inversely correlates to insulin sensitivity measured by euglucemic-hyperinsulinemic clamp. However, they also found a positive relation of insulin sensitivity with the content of linoleic acid in adipose tissue (Iggman. 2010). It is in accordance with our results because our commercial liquid preparation of high-fat meal of long chain triglycerides is composed in the majority by linoleic acid (59%). Furthermore, in line with our findings, the replacements of dietary saturated fat by unsaturated fat also improved fasting insulin sensitivity (Vessby. 2001).

Several other studies have demonstrated that unsaturated fat improves fasting and postprandial IR, although the mechanism is largely unknown (Wang. 2015). Moreover the PREDIMED study has recently demonstrated that unsaturated fat can improve fasting insulin sensitivity and prevent the incidence of type 2 diabetes (Salas-Salvadó. 2011).

Another thing the study could not address is the chicken or egg question: After all, you can argue athat the significant reduction in oxidative stress markers the scientists throughout the fat load test could - as a result - have improved the subjects insulin sensitivity, but - at least in theory - it is imaginable that this worked the other way around... by an unknown feedback loop.

Figure 2: Relative in-group reduction in the parameters from Figure 1 from 0h to 8h (Martinez-Hervas); in contrast to the previous figure the one at hand shows the in-group difference, i.e. the change in control at 0 vs 8h, etc.

As you see, there's still lots to be learned about dietary fat out there - including the fact that a "high fat" diet that combines high energy with high fat and high carbohydrate intakes is always detrimental for your health and should no longer be used in studies, unless the goal is to mimic the Western diet (and I beg scientists to then call it what it is, and that's not a "HFD").

Beware of dairy proteins, especially whey, but also casein are highly insolinogenic and may reduce if not reverse the effects of fat loading in the AM on glucose management and inflammation | learn more.

Bottom line: Before you get addicted to the previously suggested avocado + eggs fried in olive oil breakfast, please keep in mind that this is not what the scientists tested. Especially in view of the relatively high protein level in eggs, another study would have to make sure that the latter won't interfere with the benefits... even if that's much less likely for eggs, meat or fish than for the highly insulinogenic dairy proteins.

Furthermore, the study at hand cannot tell us anything about the long-term effects, because it is an acute intervention (not even lasting for 24h, there could have been a rebound at 12h or 24h or with the ingestion of another meal at noon, etc.) that suffers from another methodological problem.

Without a control supplement containing high(er) amounts of saturated fat, the assumption that the results were MUFA + PUFA specific is simply based on the scientists' review of the existing research (see previous elaborations + quotes). And as the scientists add, last- and [f]inally, oxidative stress markers analyzed could be also altered by others players regulating the postprandial state" (Martinez-Hervas. 2016) | Leave a comment, praise or criticism on Facebook!

References:

• Boden, Guenther. "Role of fatty acids in the pathogenesis of insulin resistance and NIDDM." Diabetes 46.1 (1997): 3-10.
• Borkman, Mark, et al. "The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids." New England Journal of Medicine 328.4 (1993): 238-244.
• Fernández‐Real, José M., et al. "Fat overload induces changes in circulating lactoferrin that are associated with postprandial lipemia and oxidative stress in severely obese subjects." Obesity 18.3 (2010): 482-488.
• Iggman, David, et al. "Adipose tissue fatty acids and insulin sensitivity in elderly men." Diabetologia 53.5 (2010): 850-857.
• Koves, Timothy R., et al. "Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance." Cell metabolism 7.1 (2008): 45-56.
• Martinez-Hervas, Sergio, et al. "Unsaturated Oral Fat Load Test Improves Glycemia, Insulinemia and Oxidative Stress Status in Nondiabetic Subjects with Abdominal Obesity." PloS one 11.8 (2016): e0161400.
• Vessby, Bengt, et al. "Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study." Diabetologia 44.3 (2001): 312-319.