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.


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

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?


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.

August 23, 2011
The influence of carbohydrate-protein co-ingestion following endurance exercise on myofibrillar and mitochondrial protein synthesis.

Back to the carbohydrate + protein for post-exercise recovery story.  This time, looking at proteins inside of the muscle.

Introduction:  Studies suggest that adding protein to a carbohydrate recovery drink increases muscle protein synthesis (MPS).  However, no studies have attempted to discover specific protein fractions that contribute to MPS in the muscle and the mitochondria.  Hence, the specific aim of this study was to do just this experiment following a bout of cycling.

Results:  Ingestion of CHO + PRO increased the levels of the amino acids phenylalanine, leucine and threonine by 37, 130 and 58% which peaked 1 hour after exercise whereas in the CHO only group they peaked 30 min after. mTOR phosphorylation (a marker of protein synthesis) was the same post-exercise; however, it increased four hours later with CHO + PRO whereas it decreased at this time with ingestion of just CHO.  Mitochondrial protein synthesis rates were similar for both groups.  As shown in numerous other studies, myofibrillar protein rates (the contractile properties of the muscle) were approximately 35% higher with CHO + PRO than just CHO alone. 

Conclusion:  "We have shown that when protein is co-ingested with carbohydrates after cycling exercise myofibrillar, but not mitochondrial, protein synthesis is increased. It is possible that frequent post-endurance exercise protein ingestion may promote muscle hypertrophy over time.”

My input:  A lot of the other protein fractions that the researchers looked at failed to show any significance between the two groups.  All in all, this is just another study supporting supplementation with a protein post-exercise can create a physiological environment that favors increases in muscle mass.

Breen et al J Physiol. 2011 Aug 15;589(Pt 16):4011-25

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

April 7, 2011
Influence of Ingesting versus Mouth Rinsing a Carbohydrate Solution during a 1-hr Run

Scientists wished to see whether or not rinsing a carbohydrate mouth solution was better at improving performance rather than ingesting it.

Conclusion:  Mouth rinsing, followed by the ingestion of a carbohydrate–electrolyte solution, was associated with increased distance covered during a 1-h running performance test in comparison with mouth rinsing the same solution or mouth rinsing followed by the ingestion of a placebo solution.

My input:  I believe it is too early to suggest simply rinsing your mouth with your favorite sports beverage will help your performance.  Keep ingesting as always but not to the extent you suffer an upset stomach.

Rollo et al MSSE 2011 Mar;43(3):468-75.