June 26, 2013
Dietary Supplements for Strength & Power Athletes

The following was presented by Eric Rawson at the 2013 ACSM Conference.  It is my pleasure to share it with you.

1.) Creatine monohydrate 

Doses: 0.3 g/kg/day for 5 days or 0.03 g/kg/day for 30 days is sufficient to increase the concentration of creatine by 20-25%.  

Washout period: 6 weeks is usually recommended

Performance factor: Increase performance of high intensity exercise of durations less than 30 seconds

Safety profile: Excellent

2.) Beta-alanine

Doses: 3-6g for 4-8 weeks can elicit 40-50% increases.  Acts as a buffer

Washout period: 10-15 weeks

Performance factor: Good for H.I.I.T. or sprinting. High intensity exercise (1-6min duration).  Overall 2.58% increase in performance

Safety profile: Safe but may cause a niacin flush (paresthesia)

3.) Sodium Bicarbonate (NaHCO3)

Doses: 300mg/kg taken 1-3 hours pre-exercise can act as an extracellular buffer

 Washout period: None.  Some suggest as a chronic dietary supplement.

Performance factor: 1-2% increase in body mass.  Increase in high intensity exercise (1-5min). Shown previously to take 0.8s off of a 1 min race.  

4.) Protein

Dose: 0.4 g/kg/hour of exercise (Milk is the best bang for your buck)  1.6-1.7 g/kg/day. 

5.) Water

I think it also important to not neglect your carbohydrates.  In exercises lasting 30 seconds to 1 minute, a lot of people think that most of the energy is coming from creatine.  In actuality, 10% is coming from creatine whereas 47-60% is coming from carbohydrate stores.  1.2 g/kg/hour of carbohydrates post-exercise is sufficient for muscle glycogen resynthesis. 

April 17, 2013
Breakfast skipping compared to high protein breakfast: effect of appetite control in girls.

Are you a girl who regularly skips breakfast? Read on because this well-controlled study is for you.

Introduction:  Breakfast skipping is strongly associated with a greater chance of weight gain.  Furthermore, this trend is also linked to poorer food choices.  Higher protein meals are becoming more popular as a way to improve satiety and appetite control. The purpose of this study was to examine if it is better to skip breakfast or eat one higher in protein in regards to appetite control throughout the remainder of the day.

Methods:  Twenty overweight or obese girls between the age of 15-20 who normally skip breakfast were recruited for this study.  They were tracked for 7 consecutive days and randomized to one of 3 groups: breakfast skipping (BS), a normal cereal meal for breakfast (NP), or a high-protein breakfast (HP) consisting of beef and eggs for breakfast.  Breakfast and lunch were controlled but the rest of the day they were free to eat as much as they wanted. 

Results:  

  • NP & HP led to a 60% reduction in daily hunger.
  • HP lead to a greater increase in total fullness.
  • NP & HP led to a 30% reduction in daily desire to eat.
  • HP breakfast but not the others suppressed an important hunger stimulating hormone (ghrelin) by 20%.
  • HP breakfast but not the others increased an important satiety-stimulating hormone (PYY) by 250%.
  • BS & NP led to greater evening snacking than HP.

Discussion/Conclusion:  A small breakfast of merely 350kcal led to reductions in perceived hunger, the desire to eat, and prospective food consumption.  In addition, it also increased fullness.  What is even more interesting is that the high-protein breakfast group had additional benefits of a reduction in the hunger-stimulating hormone ghrelin, increases in PYY (a hormone that makes you feel fuller), and decreases in evening snacking, particularly of high-fat foods.  The authors note that a limitation of this study was that the breakfast skipping group and the high-protein group had similar total amounts of calories consumed during the day.  Although this study looked at 1-week of food consumption, it is not certain if eating a high-protein meal for longer periods of time (a year or more) would prevent weight gain.  

My input:  The most obvious inferences that the authors draw come from the simple fact that the breakfast skipping group is fasted.  Of course, their perceived hunger/fulness, desire to eat, and prospective food consumption will be higher in the morning because they just woke up.  I think the most powerful part of the study came from the blood draws and the actual measurable physiological significance that a high-protein breakfast did decrease a hormone responsible for making you want to eat and increase a hormone that tells your brain that you are full.That is what truly stands out as powerful rather than all the other results based solely on questionnaires.  For that reason, I’d suggest trying out the high-protein diet over your standard cereal-based breakfast and seeing how it works with your own feelings of satiety throughout the day.

Leidy et al Am J Clin Nutr. 2013 Apr;97(4):677-88

November 28, 2012
Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women.

This one is for the night-eaters. The ones who find themselves diving into some snacks before bed.  You know who you are.  Did you know they actually consider this a syndrome though?

Introduction:  Night eating syndrome is classified as a delay in the circadian timing for food intake which can alter metabolism and eventually lead to obesity.  This syndrome is diagnosed as ingesting a quarter of your total energy for the day after an evening meal up to three times per week.  The aim of this study was to see how two weeks of snacking either during the day or at night, without changing meal frequency, would alter energy metabolism in lean young women.

Methods:  13 lean healthy women were recruited with 7 of them being randomly assigned to the snacking during the day group (10:00am) and the other 6 to the snacking at night group (11:00pm).  After the two weeks, their energy expenditure and substrate utilization were measured in a whole-room respiratory chamber for one day.  The snack consisted of merely 200kcal.  Breakfast, lunch, and dinner were given at 9:00am, 2:00pm, and 7:00pm for each group during the two weeks.

Results:

During the afternoon, the group that snacked at night had a significantly higher RQ (using more carbohydrates instead of lipids for energy) and significantly lower fat oxidation.  There was a small decrease in 24-hour fat oxidation with the group that snacked at night but this was not statistically significant.  LDL cholesterol levels significantly increased as well in the group that snacked at night.

My input:  A major strength of this study was the strict control of meal frequency during the two weeks.  However, the groups were small and likely underpowered when it came to statistical significance, particularly with the slight decrease in 24-hour fat oxidation which could have been significant had they recruited more volunteers.  Regardless, this study shows the importance of nutrient timing and how eating at specific hours of the day can alter our metabolism due to the hormones naturally controlled by circadian rhythms at those hours.  It is a necessity for the nutritional science field to step away from calories in versus calories out and start looking more towards nutrient timing at different hours of the day under different conditions (rest versus pre/post-exercise).

Hibi et al Am J Physiol Regul Integr Comp Physiol. 2012 Nov 21

September 17, 2012
Nutritional regulation of muscle protein synthesis with resistance exercise: strategies to enhance anabolism.

Maximize your muscle protein synthesis after weight training, bros.  I’ll highlight for you a recent review, which the scientist nerds can read entirely for free here, from Dr. Stuart M. Phillips.  I encourage you to take the time to read this one.

Introuction:  When scientists talk about muscle protein synthesis they are referring to accruing muscle proteins in an overall net positive balance.  That is to say, taking the most basic form of proteins, amino acids, and eventually creating structural muscle (aka hypertrophy).  Normally, this is done by adding to already existing contractile machinery of the muscle cells.  Researchers suggest that muscle protein synthesis (MPS for now on) is controlled by certain factors including dose, food source, and timing.  Let’s see what Dr. Phillips has to say about each of these areas.

"The anabolic window" -Timing

It’s like the holy grail of muscle growth for bros.  ”You can’t miss the window or you ruined the entire workout.”  Well, that’s a bit exaggerated.  Phillips states that, "It is now unequivocal that immediate post-exercise amino acid provision is an effective nutrition based strategy to enhance MPS above rates observed with exercise alone.”  Early post-exercise ingestion of amino acids or protein comes from studies that showed that exercise induced increases in rates of MPS are greatest right after exercise; approximately 100-150% above basal rates.  However, it may not be that big of a deal if you miss this window.  If you look at the figure below, the increase in MPS is in fact greater after exercise but can remain elevated for up to 48 hours.  Phillips suggests that consuming protein during these later times as well can be just as beneficial as ingesting protein directly after exercise.


MPS after resistance exercise

More importantly, Philips discusses the importance of actual exercise intensity and how it relates to muscle failure.  This is in lines with a study I touched upon in the past.  Looking at yet again another figure below, you can see that groups that take resistance exercise to failure, regardless if they’re using heavy load and low volume, or a light load and high volume had an enhanced amino acid sensitivity to muscle protein synthesis.  Let me say that again, IRREGARDLESS OF HOW MUCH WEIGHT YOU USE, as long as you are taking the muscle to failure, you will increase your rates of muscle protein synthesis more than loads not till failure. 

High vs low load

Protein source


Let it be noted that whey, egg albumin, soy, casein, and beef have all been shown scientifically to be able to stimulate MPS.  However, the Philips group has shown in the past that whey and milk can increase MPS greater than soy products following resistance exercise (this could be due to differences in amino acid profiles and/or digestion kinetics).  Why is whey fast-digesting and casein slow-digesting?  Every one knows that or will tell you that but do they even have an explanation why?  Phillips drops a knowledge bomb with one sentence, Whey protein is acid soluble and is associated with a very rapid, large, but transient increase in postprandial amino acid availability,  while casein coagulates and precipitates when exposed to stomach acid and the resultant dairy curd is slowly released from the stomach resulting in a much more moderate but sustained rise in plasma amino acids.”  I love knowledge bombs.

Dose

It is still accepted that in young healthy individuals, approximately 20-25g (which corresponds to approximately 8-10g of essential amino acids) of a rapid digesting protein source (whey or milk) can help maximize stimulation of MPS after resistance exercise. 


There you have it.  Now, I’m off to eat some beef.

March 5, 2012
Early Stage Subcutaneous Adipose Tissue Remodeling

How would you like to be in a study where they fatten you up for 2 months?  Well, this group recruited volunteers just for that and have provided a significant advancement in what is known about adipose tissue structural changes during the first several weeks of weight gain.

Introduction:  The purpose was to examine molecular changes in adipose tissue structure after 2 months of an overfeeding protocol. 

Methods:  Forty-four healthy males were recruited and told to increase their daily caloric consumption to excess of 760 kcal/day.  To accomplish this, they added 100 grams of cheese, 20 grams of butter, and 40 grams of almonds to their usual diet.  Fat biopsies were taken at 2 weeks and again at the end of the 2 months.

Results:  MRI revealed a significant increase in abdominal tissue volume both for subcutaneous and visceral.  No changes in mean adipocyte (fat cell) surface size or number.  There was a significant increase in the density of capillary vessels.  As you would expect, there was an increase in the number of genes related to fatty acid and lipid biosynthesis.  There was also an upregulation in genes involved in formation of the extracellular matrix and angiogenesis (the creation of blood vessels).

Discussion/Conclusion:  Although there was an increase in genes responsible for storing excess fat, there was not yet a significant increase in size or number of fat cells.  Interestingly, there was an upregulation in capillary density and genes involved in creating more blood vessels to supply the adipocytes.  This could also be a reason why the extracellular matrix was remodeled to create space during initial weight gain.

My input:  There were also some other important molecular pathways that were downregulated in this study but for sake of boring you I decided to leave those out.  I think the main important finding in this study is the disovery of genes involved in creating new blood vessels for the fat cells.  It makes sense if you think about it, that an increase in adipose tissue would demand a larger supply of blood.  Therefore, it is necessary to increase the amount of vessels perfusing the cells.  This group did well in not only showing this in gene arrays but also in histological staining from the fat biopsies.   Another article from a different group found similar results in that the adipose tissue of obese and insulin resistant subjects had larger vessels but fewer capillaries when compared to lean subjects.  I would not be surprised to see pharmaceutical studies in the near future aiming at trying to reduce the amount of blood vessels as a way to amerilorate adiposity.  After that, I would not be surprised if that is soon the next gimmick in supplement companies’ “fat burners”/thermogenic products.

Alligier et al  J Clin Endocrinol Metab. 2012 Feb;97(2):E183-92.

February 29, 2012
TRAINING ADAPTATIONS BY TIMED NUTRITION : RECENT KNOWLEDGE AND PRACTICAL APPLICATIONS FOR OLYMPIC SPORTS

Great, great, great video.  John Hawley is a big time name in exercise metabolism research as well as a good friend of our lab.  He came to visit us a few months back on a tour of speaking throughout Europe.  I got to spend two days with him and I must tell you I gained a month’s worth of knowledge in those two days. If you’re an endurance athlete, you need to watch this.

I’ve been spending a lot of time finishing a manuscript for publication and the head of our lab put me on a new project so that is why I haven’t been posting much.  There are some good articles saved in my drafts right now that I’ll post later this week.  For now, take some time out of your day, enjoy this video, and most importantly, learn something that will help you with your fitness endeavors.  

February 10, 2012
The Toxicity of Sugar: You’ll want to read this one.

Last April, there was a very popular article published in the New York Times about how sugar is toxic to the body.  Although it is not entirely scientifically sound, it is still a well written piece, stemming from the original, and hugely popular, video from Dr. Robert Lustig posted on YouTube back in 2009.

Dr. Lustig publicly proclaims that sugar is indeed toxic to the body as that of tobacco products or alcohol.  This acclimation began with a publication in the American Dietetic Association journal back in 2010 when Dr. Lustig wrote an entire detailed review on fructose having similar properties to ethanol.  In summary, Dr. Lustig states that fructose has deleterious effects on the liver similar to that of ethanol in that it:

  1. Drives de novo lipogenesis, resulting in dyslipidemia, steatosis, and insulin resistance.
  2. Increases the amount of reactive oxygen species which in turn increases the risk for liver cell damage.
  3. Activates reward centers in the brain by blocking leptin and promoting sensations of hunger, which contributes to a positive feedback pathway for continuous ingestion of food, even when you’re not hungry.

Although these consequences of consuming excess sugar are possible, Dr. Lustig also provides two “antidotes” to combat the harmful liver effects from fructose:

  1. Exercise:  which increases hepatic TCA cycle maximal velocity leading to a process of biochemical events that will eventually provide less substrate for the creation of triglycerides.  In addition, improving the activity of mitochondrial proteins involved in promoting insulin sensitivity. 
  2. Fiber:  by reducing glycemic load and rate of carbohydrate absorption, fiber reduces the content of energy from the food the liver has to metabolize which in turn again, reduces triglycerides and improves insulin sensitivity.  Also, fiber is well known to increase satiety which would reduce consumption of more sugar.

Dr. Lustig also adds that although fructose is considered a carbohydrate, it is metabolized more like fat substances.

More recently (as of last week), Dr. Lustig is back at it again, publishing a comment article in Nature where he states some dramatic proposals in regards to fighting the war on increased sugar consumption.  Again he drives home the point that sugar is analogous to consuming alcohol claiming that it is unavoidable in society, toxic, has the potential for abuse and creates a negative impact (metabolic syndrome) on society.  There is even a link between sugar consumption and increases in the likelihood of cancer.  He then proposes that there should be a tax on any processed foods that contain any form of added sugars including soda, juice, sports drinks, and chocolate milk.  Does this seem extreme to you?  Would this really reduce consumption?  Statistical models show that for this to have an impact, companies would have to double the prices of all of these drinks to reduce intake.  Furthermore, Dr. Lustig states that there should be a limit on the availability of these products, such as limiting the hours retail stores are open to sell these products, regulating the location and amount of retail markets, and setting a limit as to who can legally purchase these items.  Yes, that’s right, Dr. Lustig feels you should be at least 17 years old to purchase drinks with added sugar.  

Okay, I understand the detrimental effects of sugar on the body and you’ve seen for the past month numerous studies showing them, but accomplishing all of these does not seem feasible in the U.S.  High-fructose corn syrup (HFCS) is not the sole culprit for the increase in obesity and Type 2 diabetes in the United States.  This notion was stated by John White in an article back in 2008 on the content of HFCS where he goes on to break some common misconceptions about this sweetener and sucrose.  As stated in the first week of sugar month, HFCS has a similar content to that of sucrose; 50% glucose and 50% fructose.  The only real difference is, and the reason of the stigmatic popularity to brand this sweetener as the reason for the obesity epidemic, is that it is cheaper for companies to use in their products.  White states that HFCS is not predictive of the rise in US obesity due to these conclusions:

  1. HFCS has the same sugar composition of other “benign” fructose-glucose sweeteners such as sucrose, honey, and fruit juice concentrates.
  2. Increased caloric intake since 1970 was not due to added sugars (including HFCS) but rather due to increased consumption of all caloric nutrients, especially fats, flour, and cereals
  3. Fructose-glucose sweeteners are all metabolized through similar pathways regardless if you ingest them from fruit, sodas, or fruit drinks.

Therefore, in White’s view, switching back to sucrose instead of HFCS in products would have, “no change in basic metabolism and no changes in the rates of obesity” (since sucrose and HFCS are essentially the same two monosaccharides).  ”The one change that consumers would notice is higher prices as sucrose is substituted for the less-expensive HFCS.”

Tomorrow is the conclusion of sugar month but for now I would like to know what some of you think about this post.  Do you think sugar is truly as toxic as Dr. Lustig states and should we take such drastic actions in limiting the consumption and availability of these sugar additives?

-Nick

February 8, 2012
Simple but powerful thought for Sugar Month

A day of beverages:

8:00am - Orange juice 8 oz (110 calories)

10:00am - Medium mocha (400 calories)

Noon - Regular cola 20 oz (280 calories)

2:00pm - Some fruit drink 16 oz (230 calories)

5:00pm - Sweet tea 16 oz (200 calories)

8:00pm - Beer 12 oz (150 calories)

Total of 1,370 calories, approximately 65% of your standard daily value. 

January 23, 2012

Continuing with fructose, our focus now shifts towards the effects on the liver.  Some of you might have heard of non-alcoholic fatty liver disease, which is the accumulation of fat inside the liver that eventually leads to inflammation, scarring, and finally, cirrhosis (when the scar tissue replaces the actual liver cells).  Through the mechanisms of storing fat outside of normal fat depots (what we call ectopic fat depositions), scientists believe this creates a milieu of metabolites that eventually leads to insulin resistance and, subsequently, Type 2 Diabetes.  I’ll keep it short this time.

If you look at Figure 1, you can see that ingesting large amounts of fructose (in this case it was equal to 4L of soda/day, yikes) causes an increase in de novo lipogenesis from the liver.  It is also known to increase fasting triglycerides, which this study suggests a correlation between the two.  I know this large amount is not comparable to everyday ingestion for a normal person but nonetheless it shows you the possibility.

The second figure is another study that shows increases in ectopic lipids (IMCL = intramyocellular lipids and IHCL = intrahepatocellular lipids) as well as triglycerides.

In regards to insulin resistance, the third figure from another study actually done here in the department of physiology shows indeed, even fructose overfeeding decreases hepatic insulin sensitivity.

Finally, the last figure is a proposed pathway by Prof. Luc Tappy on how fructose can lead to insulin resistance through several different mechanisms.

Figures adapted with aid of Prof. Luc Tappy MD, PhD

January 18, 2012

 For those who did not see, I received this question last week in regards to artificial sweeteners:

For the first part, there is a fairly recent study looking at the effects of stevia, aspartame (the most popular artificial sweetener found in diet soda), and sucrose on food intake, satiety, and post-prandial glucose and insulin levels.  As you can see in the first figure, aspartame did well indeed cause an increase in insulin after ingestion but I would not consider this a “spike” (clearly it is not as much as sucrose).  The researchers didn’t speculate on this subtle increase but it does show that the artificial sweetener, aspartame, can indeed increase insulin levels but it is worth noting that this is not that high.  As far as energy intake, you can see in the second figure that the three different loads of either stevia, sucrose, or aspartame did not effect hunger levels throughout the day at other meals.  The only difference was total energy intake but this makes sense since aspartame has no calories compared to sucrose.

On to the next part of the question and whether or not artificial sweeteners can increase appetite.  This time we’ll use another artificial sweetener, sucralose, or as you might know it, Splenda.  An article published last year states that sucralose cannot effect hormones responsible for the satiety response (GLP-1, PYY), insulin levels, or appetite.

Furthermore, does the human gut respond the same way to sugar and artificial sweeteners?  Well, in this study, glucose seems to be the driving factor in activating mechanisms for appetite whereas other sugars or artificial sweeteners did not.  The authors state that sweetness per se does not effect secretion of gastric peptides but the sugar must have a structural integrity similar to that of glucose for these effects to exist.

Let’s move on now to the brain, specifically the amygdala (sorry Waterboy), which is a part that can respond to food aromas and the insula, which relates oral sensations with internal states.  This study shows that in fact, artificial sweeteners can affect these two regions of the brain and interrupt brain chemistry for sensing normal sugars such as sucrose.

As far as safety, it is documented scientifically in this review that artificial sweeteners are in fact safe to use. 

Et voilà. In summary, artificial sweeteners will not affect your appetite and therefore you can go back to ordering a large fast food meal (no really, don’t) with that barge of diet softdrink.  As far as the insulin response, I feel a lot of people downplay the ability of the brain in regards to hunger or satiety.  It is similar phenomena as Pavlov’s dogs salivating in anticipation of a meal after they hear the tuning fork.  Even at the smell of food, your gut will release gastric hormones in anticipation of the food that will soon be eaten and digested.  It could be the same response as to why there was a slight increase in insulin to aspartame.  The mind thought something sweet was being consumed when in fact it was not.  I hope this clarified some of the issues and answered the proposed question.

Nick