Showing posts with label more. Show all posts
Showing posts with label more. Show all posts

Friday, April 29, 2016

Foods Not Macros Isoenergetic Breakfast With Identical Macronutrient Content More Satieting With Eggs vs Flakes Plus Omega 3 Microbiome Obesity Interactions

Eggs or Flakes? Not 30% vs. 25% protein! A brief reminder of the fact that the stuff you eat is still food.
I am not quite sure when or why this happened, but I know that more and more people are thinking in terms of "macros" instead of foods. What I do know, though, is that the recent publication of studies from the Pennington Biomedical Research Center at the Louisiana State University System (Bayham. 2014) and an ostensibly unrelated study that was conducted by researchers from the Alimentary Pharmabiotic Centre, Biosciences Institute in Cork and scientists working at the local university and the University of Pittsburgh School of Medicine (Patterson. 2014) confirms - once again (!) - how futile this ignorant approach to nutrition actually is.

Eggs vs. cereals - not the best example, but...

In that, I am well aware that the "battle" between an egg- and a cereal-based breakfast in the Patterson study is not exactly a good model of whats currently going on in the health and fitness community. With cereals being labeled as "the devil" (its always nice to be "anti", isnt it?), no one would after all consider having ...
  • One-and-a-half cup of Special K® RTE cereal, 200 ml Silk® original soymilk, one slice of Natural Grain “Wheat n’ Fiber”® bread, 13 g of butter, and 10 g of sugar-free strawberry jam (CG)
... for breakfast. In view of the fact that the same can be said for the calorie- and mocronutrient matched "high quality protein" breakfast, i.e.
  • Two scrambled eggs, 120 mL skim milk, two slices of Holsum® thin white  bread, 5 g of butter, and 18 g of Smuckers® strawberry jam
... I still believe that the consequences of "breaking the fast" (learn why I am calling breakfast thus in "Breakfast or Breaking the Fast" | read more) with eggs vs. Special K are still relevant to the previously introduced context. And if you know that the acetylated form of ghrelin and PYY are "satiety hormones", it does not take a rocket scientists to interpret the data in Figure 1.
Figure 1: Level(s) of "satiety hormones" after the different breakfasts (Bayham. 2014)
What is difficult to tell, though, is whether the increased satiety after the egg breakfast would actually lead to a reduced intake at the subsequent meal.
  • On an individual basis, i.e. on just one of the two eating occasions, the higher levels of acetylated ghrelin and PYY did not suppress the 20 healthy overweight or obese subjects energy intake during the subsequent lunch
  • For day 1 and day 7, together, on the other hand, the 64kcal the egg eaters consumed less than the cereal eaters did reach statistical significance.
If we throw overboard all the things we (believe) we know about the fallacy of calorie counting, this would translate into a ~448kcal difference for one week and a whopping difference of 23,360kcal for a year, which should shed ~3.3kg of body fat a year.
7000kcal for 1kg of body fat? I know that this is a naive miscalculation, but it should suffice to demonstrate that the protein quality (remember the amount of protein in both breakfast conditions was identical) counts and two eggs (vs. Kellogs Special K) can make the difference between slow, but continuous weight gain on the one and weight stability (or more) on the other hand.
Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in todays science mash-up here at the SuppVersity could answer. What it can tell you though, is that protein and obviously carbohydrates, where even Mr. Average Joe thinks in terms of "low GI" = good and "high GI" = bad carbs, these days, is by no means the only food component, where unspecifically counting macros is not going to cut it (or get you cut, if thats what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what youre thinking right now, but lets be honest, isnt that a bit narrow-minded?  It sure is and still, the results Ellaine Petterson and her Irish and American colleagues present in their most recent paper demonstrate quite clearly that the ingestion of fish and flax seed oil has pretty unique effects that go beyond its ability to increase the tissue concentrations of DHA to levels way beyond what youd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.
Increased lipid oxidation in athletes w/ low dose fish oil (Filaire. 2010)
The health benefits of omega-3s: The often-cited evidence of the benefits of high omega-3 levels in the cells is by far not so conclusive as the laypress and supplement producers would have it. Danthi et al. have shown only recently that fish consumption, but not the omega-3 content of your cells is a reliable predictor of cognitive performance in the elderly. Associations between heart health, mortality, etc. and cellular omega-3 levels could thus be mediated by the whole food source of those omega-3s, i.e. fish consumption, and not by their mere presence in the cells, as well.
In addition it lead to an increase in the relative abundance of bifidobacteria, a gut tenant that has been linked to all sorts of beneficial health effects, but has recently been outshadowed by various strains of lactobacilli (0.95% vs. more than 2% in all other groups), which - and this is an important information - were the lowest in the rodents who were kept on diets with 45% of the energy from fish and flaxseed oils.

Whether or not, the negative effects of fish oil on the lactobacillacea count in the guts of the lab animals is also partly responsible for the more or less disappointing effects the fish and flax seed diet had on the body composition (Figure 2) of the wild-type C57BL/6J male mice (21 d old) in the study at hand is questionable.
Figure 2: Body composition analysis at the end of the study (Patterson. 2014)
Its not impossible, though. A brief glance at the insulin levels and leptin levels in Figure 3 reveals that neither of them looks anyway close to what someone whos religiously taking his fish oil caps on a daily basis would be expecting. In the end, it is thus not really that surprising that only the palm oil diet group ended up with an inferior lean-to-fat mass ratio of 1.17 (vs. 1.33 in the omega-3 group).
Figure 3: Changes (%) in relevant metabolic markers in response to the different diets (Patterson. 2014)
The results of the study at hand, i.e. the effects on body composition (Figure 2), as well as blood glucose and lipid metabolism (Figure 3) are thus clearly not in line with the ubiquitously placated message that "fish oil is good for you" - a message, the indoctrinated average supplement junkie will still discern from the abstract of the study:
"[...] Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem." (Petterson. 2014).
Neither the "loss" of lactobacilli, nor the - if anything - negative effects of the high omega-3 diet on the lean-to-fat-mass ratio and the amount of insulin thats floating around in the rodents blood are mentioned in said abstract.


Fat = Diabetes - A FAT Mistake?
If you go take a look at the actual study data, we are thus left with the question, whether the purported benefits of having high amounts of omega-3 fatty acids in our cells (see red info box a couple of paragraphs above) are real enough (or really enough - whatever you prefer) to discard the fact that the study at hand would actually suggest that olive and not fish + flaxseed oil should be your go-to source of dietary fat on a high fat diet.

Moreover, if we abandon any paradigmatic believes, we would even have to concede that - within the current context, i.e. a rodent study and a diet with protein contents of only 19.2% (low fat) and 23% (high fat), the low fat mix of 1.25% of palm, 1.25% olive, 1.25% safflower oil, 0.625% fish and 0.625% flaxseed oil the rodents in the starch and sucrose groups received is superior to any of the high fat variants.

You may say that this is "rodent shit" (and it is, because this is what the scientists analyzed to access the SFCA metabolism of the mice) and a mere coincidence, but wouldnt you agree that this oil mix looks a little too much like the mixture youd get on a low-to-moderate fat diet with olive oil as a staple for everything, where you add oils, palm and safflower oil from processed foods on your cheat days and fish oil / omega-3s from your once or twice a week serving of salmon... ?
Enough of the speculations, though: What I actually wanted was to remind you of the fact that youre still eating food not proteins, carbohydrates and fats and that there are physiological performance-, health- and longevity related, as well as psychological downsides, I can only hint at in the info-box to the right, to any form of "as long as it fits my macros" ignorance.
References: 
  • Bayham, Brooke E., et al. "A Randomized Trial to Manipulate the Quality Instead of Quantity of Dietary Proteins to Influence the Markers of Satiety." Journal of Diabetes and its Complications (2014).
  • Filaire, Edith, et al. "Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes." International journal of sport nutrition 20.6 (2010): 496.
  • Danthiir, Vanessa, et al. "Cognitive Performance in Older Adults Is Inversely Associated with Fish Consumption but Not Erythrocyte Membrane n–3 Fatty Acids." The Journal of nutrition (2014): jn-113.
  • Patterson, E., et al. "Impact of dietary fatty acids on metabolic activity and host intestinal microbiota composition in C57BL/6J mice." The British journal of nutrition (2014): 1-13.


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Saturday, April 23, 2016

Study Suggests Frozen Veggies Worse Than Common Wisdom Says Frozen Asparagus Zucchini and Green Beans Lose More Antioxidants During Boiling

Green asparagus from the fridge and  from the market are not created equal - at least not when they finally end up on your plate after a short bath in hot water.
You just have to watch one of the consumer report shows on television to hear it: "Frozen veggies are way better than their reputation would suggest." Actually, here in Germany this sentence has been repeated to soften that Ive even heard people say theyd buy the frozen broccoli because it contained "more vitamins and the other good stuff, you know." And you know what? For some veggies like spinach, for example, this may actually be the case. For others, like broccoli or peas, the nutrient status of the frozen and the raw uncooked vegetable appears to be more or less identical (Favell. 1998). But thats something you cannot say for the green asparagus stems, zucchini and green beans in a recent study from the Università degli Studi di Parma in Italy.
Warning: Dont take this article as an excuse and stop eating veggies completely. The frozen stuff may lose more vitamins, when you boil it, but (a) you can still blanch it and (b) even with significantly reduced antioxidant effects veggies are still among the healthiest things you can eat.
I am not an asparagus expert and can still tell that the cell structure of the Transverse  sections boiled (C - from raw | D - from frozen) is profoundly messed up compared to the raw (A) and blanched (B) variety | legend: c = collenchyma; vp = vascular bundle; p = parenchyma; f = fissure.
In the corresponding experiment, the Italian researchers bought Green asparagus stems (Asparagus officinalis L., var. Grande), zucchini (Cucurbita pepo L., va Quine) and green beans (Phaseolus vulgaris L., var. Giamaica) from a local producer and processed them within 24 hours from harvesting. For each of the veggies four samples were prepared: Raw/uncooked  (R), raw/boiled  (B), blanched (BL) and industrially frozen/boiled (FB)

The raw (ten kilograms of each vegetable), blanched (five kilograms of each vegetable) and industrially frozen  samples  (five  kilograms  of  each  vegetable) had been transported were  transported  to  the  University of  Parma laboratories  under  adequate  refrigerated conditions to avoid the exuberant nutrient loss that occurs upon inadequately slow (re-)freezing.
SuppVersity Suggested Read: " Conventional vs. Organic: Its Not About Getting More, But Getting Less For Your Money. Less Pesticides, Dioxins & Co" | read more if you want to know if the claim "organic is always better" is a similar misconcept as "frozen over fresh".
If you "freeze" your veggies in the freezer compartment of your fridge, this will make the cells blast, so that even before they are cooked, and the nutrients flow out. It is generally assume that the latter would not happen, if the veggies are shock-frosted.
Figure 1: Total antioxidant capacity of green asparagus, zucchini and green beans raw, blanched, boiled and frozen and boiled (Paciulli. 2014); as the data tells you frozen veggies with similar  icy grease on them like you see on the right may not really be a better source of antioxidants than fresh veggies from the farmers or even the supermarket.
If we look at the data in Figure 1, though, it would appear that the cells may have "cracked" already so that they are more susceptible to the subsequent heat assault and the frozen + boiled samples end up having consistently lower total antioxidant (Figure 2) and feric acid reducing capacity than their raw + boiled counterparts.

For a similar reason (nutrient retention), the blanched samples have been cooled immediately after blanching in an ice-water bath for 3 min before they have been transported to the laboratories, where their analysis shows that only the Zucchini lost a small, but significant amount of their total antioxidant activity.
Figure 2: It would be interesting to see if the negative effects of freezing and boiling occur in all vegetables. In view of the fact that previous studies compared raw vs. frozen, but nor raw + cooked vs. frozen + cooked, frozen Broccoli + cooked broccoli could be exactly as "bad" as asparagus, zucchini and green beans.
The thing that is of most practical relevance, tough, is the significant negative effect of freezing + boiling on both, the total antioxidant capacity (Figure 1) and the ferric reducing capacity (Figure 2) of all three vegetables.

The previously "cited" statement that youre better of with the "fresh" frozen veggies is thus probably only right, if you eat them raw. Compared to fresh veggies, the previously frozen asparagus, zucchini and green beans lost almost 11-30% of their antioxidant prowess during the cooking process - and the same may well happen to other veggies, including broccoli, which have been compared in previous studies only on a raw vs. frozen, but not on a cooked vs. frozen + cooked basis. Unless youre afraid that all the good veggies may limit your gains due to their potent anti-oxidant effects, it appears smart to stay away from their frozen varieties.
References:
  • Paciulli, Maria, et al. "Impact of the industrial freezing process on selected vegetables Part I. Structure, texture and antioxidant capacity." Food Research International (2014).


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Monday, April 11, 2016

Want to Design a Killer Workout Reduce the Rest Times and Burn 37 More Energy During Your Workout!

The squat may be a power exercise, but trust me, it will also help you to "look good naked"!
I guess it would be hilarious to call the simple insight that cutting the time you rest in-between sets during your squats can turn a regular into a killer workout would be news, right? Well, what about some figures to define "killer" as in one minute rest between sets vs. "regular" as in three minutes rest between sets squats, then? Thats news, right; and we have to thank Nicholas A. Ratamess and his colleagues from the College of New Jersey for these insights.

I mean, huffing and puffing is one thing, but your subjectively perceived level of exhaustion and the very concrete, objectively measured data on the difference in energy expenditure and the contribution of aerobic (fat) and anaerobic (glucose) energy sources during a workout, as they are presented in the paper at hand, are two different animals.
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Apropos animal, you dont necessarily have to be a similar "animal" as the 22-year old subjects of the study at hand with their ~8-year training experience to perform the tightly controlled experimental workout, the researchers describe as follows:
"After BL [baseline] measures, each subject performed a warm-up consisting of 3 minutes of stationary cycling and 2–3 lightto-moderate sets (40–60% of 1RM) of the bench press and squat. Respiratory masks were temporarily removed from each subject during the warm-up to allow subjects to consume water one last time before initiating the protocols.

Find out how to optimally train your legs - The SuppVersity EMG Series - Gluteus, Quads & Co | read more
The protocols consisted of performing 5 sets of the bench press and 5 sets of the back squat for up to 10 repetitions using 75% of their predetermined 1RM. The BP group performed the bench press first, whereas the S group performed the back squat first. For all exercises, resistance remained constant while total numbers of repetitions were recorded. Heart rate and oxygen consumption data were collected during the entire protocol. In addition, a linear position transducer (Tendo Sports Machines, Trencin, Slovak Republic) was attached to the bar to measure power and velocity during each completed repetition."
On each of the three occasions the subjects reported to the lap, a different rest interval was used. With 1-, 2-, and 3-minutes of rest in-between sets, the and a standard 2-minute RI was used in between exercises, the study represents more or less what I see trainees do at the gym on a daily basis, as well... ok, the lazy "I just want to be strong"-10-minutes-of-rest-between-sets-fat-ass was not accordingly represented in the study at hand, but lets be honest, how many of the average trainees do actually fall into this category? I mean, if you ask people why they are going to the gym, they will either lie or tell you that they are there to "look better naked".

"Looking good naked" is a valid training goal, folks - so admit to it!

For most people sculpting their body may be only one of the reasons, but in the end, it usually comes down to this and "health" or "fitness", when youre getting honest answers from gym users.
Figure 2: The amount of energy the trainees expended on bench presses and squats was significantly higher with the 1-min rest periods (17% and 36%, for squats; 8% and 18% for bench presses; data based on Ratamess. 2014)
Against that background, the insight that short rest periods lead to significant increases in energy expenditure is highly relevant (Note: The energy expenditure was calculated by multiplying the total VO2 for the session x 5.05kcal/L). Losing fat is after all number one on the "looking good naked" priority list of most trainees and in spite of the fact that you wont lose any fat without dieting, the 36% higher energy expenditure of the 1min vs. 3min rest time workout could make the difference between ordinary and outstanding fat loss results... in spite of the increase in the respiratory exchange ratio, an indicator of an increased anaerobic contribution to the energy expenditure, by the way!
And what about building muscle? There is insufficient data to draw a firm conclusion, but based on the few hardly comparable studies we have suggest that shorter rest times in the 1-2 minute realm are also associated with a more pronounced growth stimulus (Willardson. 2006; de Salles. 2009) and have either no or a hardly significant, yet positive effect on muscle growth (Ahtianen. 2005; Willardson. 2008). Resting for more than 2 minutes between sets does therefore make sense only if you are training for strength.
Short rest times + 6 Simple Rules of Reasonable Weight Loss = Succes!
Unfortunately, the myth that "burning fat" during exercise was in any way relevant to your weight / fat loss success is as die hard as it is stupid and flawed.

Especially for the leaner folks out there, "burning fat" is absolutely irrelevant. In fact, the whole HIIT research appears to suggest that short intense, highly glycolytic exercise regimen are more suitable to shed body fat for athletic individuals than arduous multiple-hour workouts in the non-existing (!) "fat burning zone".

The reason I still recommend LISS as a preferable type of cardio training for the advanced trainee with three to four resistance training sessions per week is that all the "high intensity stuff" (dont neglect your strength workouts!) is going to overtax the sympathetic nervous system. The classic light-intensity steady state (LISS) work, on the other hand, offers a welcome parasympathetic stimulus to balance all the intense explosive training youre doing at the gym.
Never train to burn fat! I know this article could create the impression that it would be worth going to the gym to "burn fat", but in the end, the main determinant of fat loss is your diet. If the latter aint in check, all the training is not going to help. So, you better think of your workouts as the tool to control the fat / muscle loss ratio on a diet.
Bottom line: If "looking good naked" is your goal and "losing fat" among your top priorities, the results of the study at hand clearly support the longstanding wisdom that cutting back on your rest times will give you the edge.

You got to be careful, though, without cutting back on your energy intake and following the 6-simple rules of reasonable weight loss, you are not going to be very successful. No matter, if you rest for 1, 2, 3 or 20 minutes - diet and exercise, exercise and diet: If you want to look good naked, the two are simply the front and back of a single coin - you cannot separate them.
References:
  • Ahtianen, Juha P., et al. "Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men." The Journal of Strength & Conditioning Research 19.3 (2005): 572-582.
  • de Salles, Belmiro Freitas, et al. "Rest interval between sets in strength training." Sports Medicine 39.9 (2009): 765-777.
  • Ratamess, Nicolas A., et al. "Acute Oxygen Uptake and Resistance Exercise Performance Using Different Rest Interval Lengths: The Influence of Maximal Aerobic Capacity and Exercise Sequence." Journal of Strength & Conditioning Research 28.7 (2014):1875–1888.
  • Willardson, Jeffrey M. "A brief review: factors affecting the length of the rest interval between resistance exercise sets." The Journal of Strength & Conditioning Research 20.4 (2006): 978-984. 
  • Willardson, Jeffrey M., and Lee N. Burkett. "The effect of different rest intervals between sets on volume components and strength gains." The Journal of Strength & Conditioning Research 22.1 (2008): 146-152.


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Sunday, March 27, 2016

Working Out 45 Min After Dinner Improves Post Meal Blood Glucose Trigs More Effectively Than Working Out Before

Resistance training alone wont make up for a sloppy diet - no matter if you do it before or after meals.
I am not sure how feasible this is going to be for you, but if you are a type II diabetic or anyone concerned about the potential detrimental health effects of the rise in glucose and triglycerides after a meal, working out 45 minutes after dinner is the way to go.

Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are strong risk factors for cardiovascular disease (CVD) in patients with type-2 diabetes. Therefore, scientists expect that interventions that reduce postprandial glucose and TAG concentrations should lower the risk of CVD (Krook. 2003; OGorman. 2008).
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Previous studies have shown that acute exercise typically lowers postprandial glucose and TAG concentrations (Tobin. 2008) in patients with type-2 diabetes, but as Timothy D. Heden et al. point out, there is considerable heterogeneity in the responses with some individuals not experiencing beneficial changes in these risk factors (Gill. 2007; van Dijk. 2012).
"One potential explanation why some patients with type-2 diabetes do not have beneficial changes in postprandial glucose and TAG with acute exercise is because of the timing of the acute exercise session relative to meal consumption. Limited evidence suggests that the timing of aerobic exercise around a meal may be important and might explain why some individuals are exercise “insensitive” or “non responders”." (Heden. 2014) 
The only study to directly compare the effect of pre-meal and post-meal aerobic exercise on postprandial glucose concentrations in patients with type-2 diabetes showed that post-dinner, but not pre-dinner walking, lowered postprandial glucose concentrations (Colberg. 2009).
Figure 1: Previous studies indicate that aerobic workouts after meals have more beneficial effects on the potentially unhealthy increases in glucose or triglycerides (Collberg. 2009)
Although no study has directly examined the effect of exercise timing on postprandial TAG in patients with type-2 diabetes, there is evidence that exercise performed the day prior to a high fat meal has no effect on postprandial TAG responses (Dalgaard. 2004; Gill. 2007), while post-breakfast aerobic exercise reduced the postprandial TAG response (Tobin. 2008). Taken together, it appears that aerobic exercise may have its most powerful effect to lower postprandial glucose and TAG responses when performed after a meal, possibly because of slowed gastric emptying and/or greater skeletal muscle glucose and TAG uptake and utilization at this time.

The question that remained was: Is the same true for resistance training?

Since resistance exercise (RE) has a more pronounced long(er)-lasting effect on ones metabolism than aerobic training, the researchers from the University of Missouri tested the hypothesis that post-dinner RE, compared to pre-dinner RE, would in fact be more effective at improving two clinically important postprandial risk factors (glucose and 109 TAG) for CVD at a time of day when they are typically highest in obese patients with type-2 diabetes.

The standardized test workout consisted of the following exercises (in this order): leg press, seated calf raises, seated chest flyes, seated back flyes, back extensions, shoulder raises, leg curls, and abdominal crunches. All exercises were performed for three sets (1-2 min rest between sets) of 10-repetitions for each RE. During this session, the first set for each exercise was a warm-up set and the weight used was 50% of the participants 10-RM. After the warm-up set, the weight for the next two sets was the participants previously determined 10-RM.
Figure 2: Postrandial lipid response in the obese type II diabetics (Heden. 2014)
As you can see in Figure 2 the scientists suspicion was right, the postprandial workout (M-RE) had significantly more pronounced beneficial effects on the lipid metabolism of the type II diabetic subjects who consumed a standardized breakfasts (English muffin, cheddar cheese, one large egg, ham, hash brown, ketchup, and apple or orange juice) lunch (white bread, ham, mayonnaise, cheddar cheese, a granola bar, and apple or orange juice) and dinner meals (spaghetti noodles, spaghetti sauce with beef added, garlic bread, a lemon lime flavored soda, and 1.5 g of acetaminophen (to assess gastric emptying)) containing ~50% carbohydrate, 35% fat, and 15% protein.

Similar effects were observed for the insulin and glucose responses (see Figure 3) which were significantly improved and should thus complement the beneficial effects of the reduced triglyceride and very low density lipoprotein (VLDL) levels.
Figure 3: Changes in postprandial insulin and glucose levels (Heden. 2014)
Bottom line: Before we get to the actual interpretation of the result let me briefly point out that it would probably have been at least as effective if the subject had not been fed bull**** like ketchup, mayonnaise, granola bars, and purportedly healthy, but de facto obesogenic fruit juices. The unfortunate truth, however, is that 99% of the type II diabetics still eat like this. For them, the use of resistance training after each meal may be a possible, but unquestionably not practical way to ameliorate the unwanted cardiovascular side effects.

In view of the fact that most diabetics dont work at all, I am 100% convinced that the results of the study at hand have zero practical significance - even I wouldnt go work out after dinner only to lie in bed hungrily, thereafter, And if I did, I would raid the fridge later at night - certainly not a practice thats heart healthier than working out before dinner.

Speaking of which: Working out before dinner would also mean working out after lunch and could thus effectively help the increase in triglycerides and glucose after lunch. Not too bad either, right? | Comment on Facebook!
References:
  • Colberg, Sheri R., et al. "Postprandial walking is better for lowering the glycemic effect of dinner than pre-dinner exercise in type 2 diabetic individuals." Journal of the American Medical Directors Association 10.6 (2009): 394-397. 
  • Dalgaard, Marian, Claus Thomsen, and Kjeld Hermansen. "Effects of one single bout of low-intensity exercise on postprandial lipaemia in type 2 diabetic men." British Journal of Nutrition 92.03 (2004): 469-476.
  • Gill, Jason MR, et al. "Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: heterogeneity of responses." Atherosclerosis 194.1 (2007): 134-143.
  • Heden, Timothy D., et al. "Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes."
    Journal of Applied Physiology (2014). Ahead of print.
  • Krook, Anna, et al. "Reduction of risk factors following lifestyle modification programme in subjects with type 2 (non?insulin dependent) diabetes mellitus." Clinical physiology and functional imaging 23.1 (2003): 21-30.
  • OGorman, Donal J., and Anna Krook. "Exercise and the treatment of diabetes and obesity." Endocrinology and metabolism clinics of North America 37.4 (2008): 887-903.
  • Tobin, L. W. L., Bente Kiens, and Henrik Galbo. "The effect of exercise on postprandial lipidemia in type 2 diabetic patients." European journal of applied physiology 102.3 (2008): 361-370.
  • van Dijk, Jan-Willem, et al. "Exercise and 24-h glycemic control: equal effects for all type 2 diabetic patients?." Medicine and science in sports and exercise (2012).


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Sunday, March 20, 2016

How to Type More than 15 Digits in MS Excel




If you are a regular user of Microsoft Excel then you might be in danger while typing more than 15 digits in a cell. If you type 1111222233334444 then it will be 1111222233334440. Or if you type 25127680876675435 then it will be 25127680876675400. Simply the digits after 15th place will be changed to zeros! Doesnt it seem peculiar? 


Today I will explain when & why this problem occurs and how you can solve it easily. 


When the Problem Occurs?

The problem occurs when you try to type more than 15 digits in a cell like below: 

####-####-####-####
1234324545679876

But when you press Enter, the output will be 1234324545679870. Excel changes the last digit to a 0. And why someone needs to type more than 15 digits in a cell? It cant be a currency figure. 

Usually when you type a Credit Card/ Debit Card/ BO Account Number you have to type 16 digits. And the calculation of excel doesnt allow you to type more than 15 digits. Thats why it converts the last digits (after 15th place) into zeros.  


Reason

You may ask - why Excel restricts users to type 15 digits in a cell? Im also searching for a satisfactory answer. I found the following reason from Microsoft Support: 

Excel follows the IEEE 754 specification on how to store and calculate floating-point numbers. Excel therefore stores only 15 significant digits in a number, and changes digits after the fifteenth place to zeroes. 

I dont know what does it mean! :) Anyway, I can show you several ways to get rid of this problem . . . 


Solution

There are several ways through which you can avoid this problem. First Id like to show you an easy way:

Method 1: Putting Inverted () Before the Number

When you type more than 15 digits in a cell, just place an inverted comma ( ) before that number. And that mark will not be displayed on the sheet after pressing Enter! Though it will be displayed in the formula bar. Look at the image below: 


I dont know why the inverted mark disappears automatically. But I can explain why the 16th digit doesnt change to 0. Because when you type before a number then Excel doesnt consider this value as Number. It maybe consider the cell as text. Thats why it remains unchanged. 


Method 2: Format the Cell as Text

Maybe the 2nd method is more useful. Before typing more than 16 digits in a cell, you have to format those cells as text. 

You need to select the cells first. Office 2003 users will find the Format Cell options from the Format Menu > Cells > Format Cells. And Office 2007 and 2010 users will get this as below: 


Format Cells Menu in Excel 2010


Format cell window is same in all version of MS Excel. After selecting the cells, you will just need to choose the Text option and then hit OK. Thats it. 

Now you will be able to type more than thousand characters in a single cell! 


Applies to: 

All versions of Microsoft Excel. 


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Friday, March 18, 2016

8g day Citrulline Increase Leg Workout Performance More Reps on Leg Press Hack Squat Leg Ext in Exp Gymrats

The study tested only leg exercises, but you can safely expect increased reps on other exercises, as well.
Citrulline? Yes thats the stuff the supplement industry claims to be a better version of arginine. A "super pump supplement", but not necessarily an ergogenic - in spite of the fact that corresponding evidence from rodent and human studies (Briand. 1992; Pérez-Guisado. 2010; Giannesini. 2011) existed years before the study at hand was published (Wax. 2014).

Benjamin Wax and his colleagues from the Mississippi State University and the Auburn University  investigated the effects of citrulline malate supplementation on lower-body resistance exercise performance, blood lactate, heart rate, and blood pressure.

Based on citrulline malate’s chemical composition and a review of the current literature Wax et al. hypothesized that citrulline malate supplementation would mitigate fatigue occurring to the working muscle; therefore, augmenting resistance training performance.
You can learn more about citrulline at the SuppVersity

Citrulline prevents muscle catablism more than leucine

Arginine & citrulline for blood lipid control

EAA, BCAA, or citrulline for anti-catabolism?

Glutamine not citrulline to heal the gut?

Citrulline to ignite fatty acid oxidataion?

High & low dose arginine ineffec- tive NO boosters
To test their hypothesis the researchers recruited 12 advanced resistance trained male subjects (85kg body weight; <12% body fat; 22.1 ± 1.4 years) and conducted a randomized, counterbalanced, double blind study.

The subjects were randomly assigned to placebo or citrulline malate (8 g; 60 minutes before the workout) groups and then performed repeated bouts of multiple lower body resistance exercise:
"Subjects warmed up on an upright stationary bike (Life Fitness, Brunswick Corporation, Lake Fores, IL) for five minutes, at 60 – 70 revolution/minute with a mass of 3 – 5 kg. Following this warm up, subjects performed two warm up sets (10 repetitions at 90.9 kg and 8 repetitions at 136.4 kg) on the leg press machine. Subjects rested three minutes between sets during the warm up and trial sets.

Next, 60% of each subject’s predetermined 1RM was loaded on the leg press machine and the subject completed as many repetitions as possible until failure occurred. This process was completed for 4 additional sets for a total of 5 sets on the leg press. Next, the subjects performed one warm upset (10 repetitions) on the hack squat machine at a mass of 40.9 kg. This warm up set was followed by 5 sets of 60% of their predetermined 1RM to failure. Finally, following one warm up set (10 repetitions at 36.4 kg) on the leg extension, subjects completed 5 sets of 60% of their 1RM to failure." (Wax. 2014)
The rest periods (recovery periods between sets of exercise), exercise order, and number of sets performed were the same for all subjects in this investigation, for sessions 2 and 3. Blood lactate, heart rate, systolic blood pressure, and diastolic blood pressure were determined pre and post exercise.
Practical applications - What the scientists say: "Although citrulline malate supplements are marketed to improve muscle performance via a reduction in lactic acid and ammonia production, the current study does not fully support this assertion. While our investigation did note improved muscle performance occurring during the strength protocol,blood lactate remained indifferent comparing the citrulline malate treatment to the placebo treatment. The known capacity of citrulline malate to increase plasma L-arginine (Hickner. 2006), act as a buffer to lactate and hyperammonemia (Briand. 1992; Giannesini. 2011; Verleye. 1995) remain valid; however, further research is necessary to determine which mechanism may be directly attributed ergogenic effects occurring during resistance training protocols. Finally, specific investigations utilizing training protocols designed to test muscular strength and power are warranted." (Wax. 2014)
The exercise protocol resulted in sequential significant (p < 0.05) decrease in the number of repetitions in all three exercises. However, subjects in the citrulline malate group performed significantly (p < 0.05) higher number of repetitions during all three exercises compared to placebo group.
Figure 1: Wax et al. observed significant increases in maximal leg press, hack squat, and leg extension (not shown) repetitions in response to the ingestion of 8g of citrulline malate 60min before exercise (Wax. 2014)
Blood lactate and heart rate, on the other hand, were significantly increased (p < 0.05) post-exercise in both groups with no significant inter-group differences between citrulline malate and placebo (p > 0.05).
Bottom line: I am not sure, if the study at hand is going to change anyones perspective on citrulline. The "pump" is after all (for whatever reason) still what appears to be most attractive to trainees. The fact that the increased number of reps could translate into increased strength and size gains over time, on the other hand, doesnt appear sexy enough to be marketed as the main benefit of citrulline.

Can citrulline prevent muscle loss, when youre dieting | learn more
Apropos "main effect", there I guess you will remember that citrulline will also affect protein synthesis, right? Ive written about these effects in August last year in my article "Citrulline = The Dieters Amino Acid? Citrulline Maintains Muscle Protein Synthesis & Strength Endurance During Caloric Deficits Better Than Leucine!?" (read more).

So, if you dont consider increased rep numbers sexy enough, you may feel that a reduced muscle breakdown on your next diet may be worth heading over to the bulk supplier of your choice and order a 1kg bag of citrulline malate for 100$ (will last 125 days) - no? Well, honestly, I am not sure if its worth that, either | What do you think?
References:
  • Briand, Joël, et al. "Use of a microbial model for the determination of drug effects on cell metabolism and energetics: Study of citrulline?malate." Biopharmaceutics & drug disposition 13.1 (1992): 1-22.
  • Hickner, Robert C., et al. "L-citrulline reduces time to exhaustion and insulin response to a graded exercise test." Medicine and science in sports and exercise 38.4 (2006): 660-666.
  • Giannesini, Benoît, et al. "Citrulline malate supplementation increases muscle efficiency in rat skeletal muscle." European journal of pharmacology 667.1 (2011): 100-104.
  • Pérez-Guisado, Joaquín, and Philip M. Jakeman. "Citrulline malate enhances athletic anaerobic performance and relieves muscle soreness." The Journal of Strength & Conditioning Research 24.5 (2010): 1215-1222.
  • Verleye, M., et al. "Effects of citrulline malate on bacterial lipopolysaccharide induced endotoxemia in rats." Arzneimittelforschung 45.6 (1995): E712.
  • Wax, Benjamin, et al. "Effects of Supplemental Citrulline Malate Ingestion During Repeated Bouts of Lower-body Exercise in Advanced Weight Lifters." The Journal of Strength & Conditioning Research (2014).


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