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

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

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 14, 2012
Low to moderate sugar-sweetened beverage consumption impairs glucose tolerance and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial.

Continuing with sugar month, here is a decent study looking at practical consumption of sugar-sweetened beverages (SSBs).  By practical, I mean amounts that are equivalent to how much one would consume on average/day.  That is the main appeal here. 

Introduction:  The aim of this study was to investigate the effect of five different SSBs containing fructose, glucose, and sucrose, in amounts likely to be consumed in everyday life and over a limited period, on lipid and glucose metabolism with an emphasis on LDL particle size and inflammatory makers in healthy young men.  Wow, that was a long sentence.

Methods:  As to not be bias, my last post was all with women subjects, now this one is all with normal weight men, 29 of them age 25-50.  The protocol was a randomized crossover of 6 different groups; medium fructose, sucrose and glucose (40 g/day), high fructose, sucrose, and glucose (80 g/day).  Converted in liters, the amount of sugar was 66.5 g/L for the medium drinks and 133.5 g/L for the high drinks and these were consumed with the three main meals of the day for there weeks with a 4-week washout period before entering another group.

Results:  Waist-to-hip ratio was significantly higher in all interventions containing fructose, a significantly higher percentage body fat in the high fructose intervention than in the high glucose, and finally a significantly higher waist circumference in the high sucrose compared to the high glucose group.  LDL particle size decreased significantly only after the high fructose and high sucrose interventions.  A marker for inflammation, hs-CRP, increased significantly after all interventions but the highest after high fructose ingestion.  Comparing the first intervention to the final, there was a significant increase in waist-to-hip ratio and in fasting glucose.

Discussion/Conlusion:  The real intriguing finding of this study was that even with moderate (just 6.5% of subjects daily energy intake) consumption of SSBs everyday for only 3 weeks, adverse effects existed in regards to LDL particle size and distribution, waist-to-hip ratio, fasting glucose, and inflammatory markers.

My input:  The researchers state it best with the main limitation in the study; the actual amount of sugar used was analogous to everyday ingestion; however, the sugar composition itself was not.  When you drink soda or other sweetened beverages, they are always a mix of sugars (fructose or glucose) and not solely one like in this study.  Therefore, the group that would be closest to real-life scenarios would be the sucrose group.  However, this limitation can be downplayed by the fact that it is important for researchers to understand how one sugar reacts in the body over a period of time.  The waist-to-hip ratio difference was small, but it is still significant nonetheless. Three weeks is a short period of time, and it would be interesting to see if waist circumference would increase more after a longer intervention.  Although, they did reach significant differences from baseline in other negative health factors as well.  I hope this has you rethinking those sugary drinks, especially if it is an everyday habit.


Aeberli et al Am J Clin Nutr. 2011 Aug;94(2):479-85

January 12, 2012
Long-term dietary compensation for added sugar: effects of supplementary sucrose drinks over a 4-week period.

First article for sugar month.  I’m not a fan of this study but the reason I’m posting it is because the subjects are 133 normal weight women and the primary audience of this blog are in fact, women.  The other draw is following these volunteers for a month, which I give a lot of credit to because working with humans is a difficult task, although, truly rewarding (I vouch for that).

Introduction:  This can be summed in one sentence, does consuming sugar (sucrose) make you hungry or feel full?

Design & Methods:  The women were divided into two groups; a group that consumed a soda with the sucrose or a group that consumed a soda with the artificial sweetener, aspartame.  Participants were informed to drink these at 4 different time points spread throughout the day starting at 11 in the morning and finishing at 8 at night.  Half of the subjects were blinded as to which drink they received.

Results:  For the sucrose group, energy intake was higher at week 1 and 4 than from the start, but did not significantly differ from weeks 1-4.  This increase was approximately half the energy content of the drink.  The opposite is true with weeks 1 and 4 compared to the start for the aspartame group; however, this was only marginal.  Weeks 1-4 still showed no difference in energy intake.  Carbohydrate intake increased approximately half the amount in the sucrose group while in the aspartame group it remained constant.  That is to say, subjects that received sucrose proportionately decreased their voluntary carbohydrate intake elsewhere in the diet.  The group that received the sucrose drink also decreased their protein and fat consumption as well.  Finally, more women who were given the sucrose drink gained more weight (2kg) during the study than those who received the aspartame although this trend was non-significant.

Discussion:  The researchers state that sugar satiated for the fact that the group that received sucrose reduced the amount of carbohydrates, protein, and fat they consumed daily.  However, there was not a full compensation for the additional sucrose in that the women who received it consumed approximately 800kJ more energy per day, although the drink contained 1800 kJ.  Carbohydrate intake was reduced to about half the amount of carbohydrates found in the sugary drink which therefore could have led to the weight gain.  This weight gain was non-significant and not of clinical concern.

Conclusion/My input:  First, normal weight women compensate for added sucrose in the diet by decreasing their overall food consumption, specifically of carbohydrate.  Second, this cannot be related to individuals who are overweight so one cannot assume adding sucrose-containing drinks to the diet would satiate this group of people. Third, this data supports the notion that people have a better appetite suppressant response to carbohydrates than fat.  Fourth, (just for completion purposes) this study did not affect mood or food choice.

This is one of the first “long-term” studies for following ingestion of sugar in humans the effect on satiety.  I’m not satisfied with the outcomes and design, but it is important to give this some credence for following a group of people this long of time.  In fact, women did decrease the amount of energy consumed daily when drinking the sucrose drink and as I stated before, half of them were blinded and did not even know it was true sucrose and not a diet calorie-free variation.  To conclude, sucrose, for this study, is neither good or bad.

Reid et al Br J Nutr. 2007 Jan;97(1):193-203.

September 21, 2011
New weight loss series.

To the faithful followers,

I get a lot, and I mean a lot, of weight loss questions.  Now when it comes to questions, I do prefer more science based ones but I will answer anything and help you with anything that you desire so don’t be afraid to ask.  Even if you want me to keep it private I will do so.  There are a lot of good science questions that I have been saving to get into details with, but for my followers that want help losing weight and getting into shape I have something special for you for the next four months.

With that said, I am going to soon begin posting about a good friend of mine who gave me permission to use him as “putty in my hands”.  He wants to lose weight and get into shape and he has come to me for advice.  I have not trained anyone since starting my PhD so this is my first one in a long time.  Mostly everyone I train now are older individuals for our study.

This is a good way for all of my followers to see my techniques and see my recommendations for exercise and diet.  Even though this will be specific to my friend, you can still use my methods as a blueprint for your own weight loss endeavors.  Don’t think this means I won’t answer your questions because I will.  I just thought this would be great to add on my blog along with the usual exercise science articles.  Check back soon.  Now all I need is a witty name for the series. Hmmm

Nick

August 10, 2011
Carbohydrates added to protein drink does not increase muscle protein synthesis.

Let’s step away from the molecular stuff for now and go back to some practical studies.  Are you adding carbohydrates to your protein drinks after resistance training hoping for added growth? 

Introduction:  We know that muscle protein accretion occurs when muscle protein synthesis (MPS) is greater than muscle protein breakdown (MPB).  Hyperinsulinemia, induced by adding carbohydrates to your protein drink, is thought to aid in this protein accretion.  So, researchers sought after this to see if it works.

Hypothesis:  Insulin (from the ingestion of carbohydrates) would augment protein-stimulated inhibition of MPB after exercise but not at rest.

Methods:  9 young recreationally active males mean age 23 performed unilateral leg extension testing for each leg for 4 sets of 8-12RM.  The consumption of a protein (25g of whey) or protein+carb (25g whey + 50g maltodextrin) drink was added during this time.

Results/Conclusion:  Addition of carbohydrates to a protein drink does not increase rates of MPS nor does it further inhibit MPB.

My input:  It is a low sample size (9 participants) but it still has enough power to contribute to the field.  It is imperative to note that this study uses the tested dose of whey protein (25 g) that significantly increases markers of protein synthesis necessary for recovery and growth.  Thus, save your extra scoop of whey for the next session because it is simply not needed.  Insulin release in this case did not aid to MPS, but it is also important to note that whey protein can digest so rapidly that it will also cause spikes in insulin, enough to the point of increasing MPS without the addition of carbs.  This is important for people watching their carbohydrate intake for weight loss purposes because data from this study suggests you will not need to add additional carbs to aid in muscle recovery.  In fact, insulin is not entirely necessary for skeletal muscle to uptake the glucose for replenishing lost glycogen stores.  More studies will indeed follow in this area but for now, no further insulin is needed.

Staples et al MSSE 43(7) pp. 1154-1161