HMB Supplementation Also Works in Trained Subjects

While the positive effect of HMB on body composition and strength in untrained subjects is not controversial, the case doesn’t seem so for trained subject but not for lack of positive data!

Key points: 

1. Studies lasting 6 weeks or less are too short to show positive results from HMB in trained subjects. 

2. Studies lasting more than 6 weeks can show positive results. 

3.Positive results also depend of training intensity, volume and supervision.

Strength Training, Bone Mineral Density and Growth in Adolescents

Does strength training impair growth in adolescents? If you think so you are falling into an old myth.

It has been known for decades that junior competitive weightlifters have an increased bone mineral density (BMC) well above the age-matched controls' mean (1). The effect of this type exercise appears to overcome any race or age-related BMC differences (1).

A Look Into Anabolic Steroid Use In Bodybuilding, Physique and Wellness Competitors

A new study looked into the practices of IFBB competitors. Six (four male and two female) bodybuilders (IFBB) and their coaches were directly interviewed for this study(1).


2 male Bodybuilders in the same category.
2 Men’s Physique competitors belonging to the same category.
2 women competing in different Wellness categories.

BCAAs and Insulin Resistance in Vegans

BCAA supplementation may not be suitable to vegans. These are some main points from a recent  preliminary study comparing vegans to omnivores supplementing with 15 g (women) or 20 g (men) of BCAA daily for 3 months:

New Protein Requirements for Bodybuilders

A new study sought to assess protein requirements at the whole-body level using the IAAO technique in trained subjects.


The RDA for protein is established at 0.8g/kg as the minimum protein intake to offset protein deficiency (net nitrogen losses) for 97.5% of the healthy population above 19 years (1). Believe it or not, the RDA was even deemed appropriate for healthy adults undertaking resistance or endurance exercise (2).

The RDA represents the estimated average requirement plus 2 standard deviations (3), determined from selected nitrogen-balance studies of which very few were performed in older individuals (4,5).

Nitrogen balance studies suffer from several methodologic concerns (6-10). In addition to the impractical need for repeated 7- to 10-d adaptation periods necessary to produce accurate NB data for each of the several protein intakes needed to determine the requirement (6), the use of a linear regression line with a greater residual error for analyzing nonlinear data is not a good fit for either NB or oxidation data (6,8,11).

There is also an over- or underestimation of nitrogen intake and excretion, respectively (6,12). Furthermore, NB may be achievable at low protein intakes for the brief study durations often used because of more efficient amino acid (AA) utilization, reduced turnover rates, and/or accommodation (6,13,14,15).

Better methods such as the indicator amino acid oxidation (IAAO) technique show that the RDA underestimated protein needs by 30-50% (16,17,18). The IAAO technique identifies the plateau in AA oxidation that corresponds to the maximum rate of whole-body protein synthesis.

When dietary protein is inadequate the oxidation of all AAs, including the indicator AA, will be substantial (6). With increasing dietary protein oxidation of the indicator AA will decrease because more AAs are being incorporated into body protein, and once the dietary requirement is met there is no further change in the oxidation of the indicator AA and the resulting ‘‘breakpoint’’ is thought to be the requirement (6,10).

Isotope tracer methodology is considered to be a far more accurate technique, and the IAAO technique was considered an acceptable method to assess protein requirements back in 2005 (6,19).

A protein intake of 0.93-1.2 g/kg/day, exceeding the current requirement by as much as 50%, was unveiled in men using the using the indicator amino acid oxidation technique (18). The results were comparable with those estimated by the application of a biphase linear regression model to the data from nitrogen balance studies (0.91 and 1.0 g/kg/d) (18). 

Nevertheless, the few available NB studies on bodybuilders are quite variable, and even very positive NB (3.8–20 g/d) with protein intakes of 1.8–2.7 g/kg/d observed in men engaged in a rigorous strength-training (ST) program do not result in the expected fat-free mass (FFM) accrual (3,6,19,20). For example, a positive NB (12–20 g N/d) at a protein intake of 2.8g/kg should produce 300–500 g lean mass gain/d, however this was not observed (20).

Stable isotope identified 4 different states of protein metabolism studies (6,14,15,21,22):
1) ‘‘protein deficiency,’’ defined as the maximal reduction in protein synthesis to all but the essential organs;
2) ‘‘accommodation,’’ in which balance is achieved via a decrease in physiologic relevant processes;
3) ‘‘adaptation,’’ in which optimal growth, interorgan AA exchange, and immune function are present; and
4) ‘‘excess,’’ which is characterized by AA oxidization for energy and nitrogen excretion via urea, resulting in no further stimulation of protein synthesis (15).

Regardless of age, when protein intakes near the current RDA are combined with Strength training, accommodation results through increased nitrogen utilization efficiency and lower whole-body protein synthesis rates rather than adaptation (6,19,21,23).

Current dietary protein recommendation for bodybuilders varies widely, from the RDA of 0.85g/kg/d (16) to as much as 2.0 g/kg/d (24).

During exercise there is an increase in aminoacid oxidation (1-5% of the total energetic cost of exercise), increased catabolism and increased muscle protein synthesis (25,26,27). Under-recovery is also another concern (25,28).

Protein requirements for bodybuilders in nontraining days

A new study sought to assess protein requirements at the whole-body level using the IAAO technique, in 8 individuals who had undergone regular bodybuilding training for more than 3 years (6). Subjects had a mean 84kg of body mass, 72.4 kg of LBM, and a fat free mass index of 24.

The Exercise “Spot Reduction” Myth

The “spot reduction” hypothesis states that exercise concentrated on a specific area will result in preferential reduction of the fat deposits in that specific area. For example, abdominal exercises are often promoted as an effective means to reduce abdominal fat and trim the waistline.

However results in scientific literature are mixed, especially old studies.  Spot reduction is generally not considered valid without creating a consistent energy deficit, and even in a caloric deficit it is no guarantee you will burn fat at the exercised region.

In 1956 "spot" reducing was deemed possible (1) but it was only in 1960 that this question was addressed scientifically.

The Epidemiology and Physiology of Sedentary Behavior

Physical inactivity is estimated to account for 6% of global deaths (1), and is associated with risk of Metabolic Syndrome and cancer (2,3,4).

Approximately 100,000 new cases of breast and colon cancer each year are linked to sedentary lifestyles (5). Another study found that taking frequent breaks from sitting is associated with smaller waist circumference and lower levels of C-reactive proteins, both biomarkers associated with elevated risk of some cancers for post-menopausal women (6).

The National Health and Nutrition Examination Survey (7) analyzed data of 4,757 participants and found that even short periods of light activity (standing up and walking for at least a minute) – reduced biomarkers such as large waist circumference, elevated triglyceride levels and increased insulin resistance.

There’s also a risk of heart disease and premature death from any cause increases for those spending more than four hours a day sitting. A study (8) with 4,512 subjects, found a 48% increased risk of all-cause mortality and an approximately 125% increase in risk of cardiovascular events for those spending more than four hours sitting. The risk was found to be independent of other detrimental factors such as smoking, hypertension, BMI, and social class.

Another study from Australia show that prolonged sitting is significantly associated with higher all-cause mortality risk independent of physical activity. From a population study of 222 497 subjects, it was suggest that sitting time sitting was responsible for 6.9% of deaths (9).

Being inactive for more than 23 hours per week had a 64% greater risk of death from cardio vascular disease than being sedentary for less than 11 hours per week (10).  Sitting in one position for too long may develop blood clots, which are estimated to be a cause of death for up to 100,000 people per year (11).

A large Canadian Fitness survey (12) looked at more than 7000 men and nearly 10.000 women over a 12-year period, and the participants ranged from 18 to 90 years. The research found a significant link between time spent seated and mortality, and that being active doesn’t balance out the negative effects.

The physiology

Prolonged sitting disrupts metabolic health, increases plasma triglyceride levels and decreases levels of high-density lipoprotein cholesterol, increases insulin resistance (3,13)  and affects carbohydrate metabolism (3).

Studies have used radioactive triglyceride tracers to examine metabolic effects of not standing on specialized leg muscles, such as the deep red quadriceps, that are designed for postural support (not all muscles have this same function). These muscles quickly lost more than 75% of their ability to siphon off the fat circulating in the lipoproteins from the bloodstream when incidental contractile activity was reduced. This was related to a 90% to 95% loss of lipoprotein lipase (LPL) activity locally in the most oxidative skeletal muscles in the legs, which are specialized for postural support (14).

In addition, sitting appears to lead to about a 20% reduction in high-density lipoprotein, or good cholesterol, increasing the risk of suffering from a cardiovascular disease (15). Remaining sedentary for more than 24 hours impairs the ability of insulin to uptake glucose, raising the risk of diabetes (16).

“We just aren’t really structured to be sitting for such long periods of time, and when we do that, our body kind of goes into shutdown. If there’s a fountain of youth, it is probably physical activity. So the problem isn’t whether it’s a good idea, the problem is how to get people to do more of it” Dr. Toni Yancey.

Sitting trains the body to do nothing and leads to physiological adaptations that reduce functionality.

Non-exercise activity thermogenesis (NEAT)

Sedentary behavior must be reduced, particularly reducing the long, uninterrupted bouts of inactivity. One method is engaging in non-exercise activity thermogenesis (NEAT).

Nonexercise activity thermogenesis (NEAT) is the energy expended for everything that is not sleeping, eating, or sports-like exercise. It includes the energy expended walking to work, typing, performing yard work, undertaking agricultural tasks, and fidgeting (17).

In 2005 Levine et al (18) published detailed results of his analysis of metabolism. Levine tracked food consumption and every activity using motion tracking underwear, he measured their body postures and movements every half-second for 10 days. Those who didn’t gain weight moved more than others, while eating the same, due to a difference of minus 2 hours sitting each day on average. The study suggested that “adopting the NEAT-enhanced behaviors of lean counterparts, might expend an additional 350 calories (kcal) per day.”

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1. World Health Organization. Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks. Geneva, Switzerland:WHOPress; 2009.
2. Proper KI, Singh AS, van Mechelen W, Chinapaw MJM. Sedentary behaviors and health outcomes among adults: a systematic review of prospective studies. Am J Prev Med. 2011;40(2):174-182.
3. Tremblay MS, Colley RC, Saunders TJ, Healy GN, Owen N. Physiological and health implications of a sedentary lifestyle. Appl Physiol Nutr Metab. 2010;35(6):725-740
4. Grøntved A, Hu FB. Television viewing and risk of type 2 diabetes, cardiovascular disease, and all-cause mortality: a meta-analysis. JAMA. 2011;305(23): 2448-2455.
5. Research presented in November, 2011 at the American Institute for Cancer Research's (AICR) annual conference.  The AICR presented data suggesting that about 100,000 new cases of breast cancer and colon cancer per year can be associated with physical inactivity.
6. Christine M. Friedenreich, Heather K. Neilson. Inflammatory Marker Changes in a Yearlong Randomized Exercise Intervention Trial among Postmenopausal Women. Cancer Prev Res (Phila). 2012 Jan;5(1):98-108.
7. Genevieve N. Healy Charles E. Matthews, David W. Dunstan, Elisabeth A.H. Winkler, Neville Owen. Sedentary time and cardio-metabolic biomarkers in US adults: NHANES 2003–06. Eur Heart J. 2011 Mar; 32(5):590-7.
8. Emmanuel Stamatakis, Mark Hamer, David W. Dunstan. Screen-Based Entertainment Time, All-Cause Mortality, and Cardiovascular Events. Journal Americal College of Cardiology. 2011; 57(3):292-299
9. Hidde P. van der Ploeg, PhD; Tien Chey, MAppStats; Rosemary J. Korda, PhD; Emily Banks, MBBS, PhD; Adrian Bauman, MBBS, PhD. Sitting Time and All-Cause Mortality Risk in 222 497 Australian Adults. Arch Intern Med. 2012;172(6):494-500
10. Tatiana Y. Warren, Vaughn Barry, Steven P. Hooker, Xuemei Sui, Timothy S. Church, and Steven N. Blair. Sedentary Behaviors Increase Risk of Cardiovascular Disease Mortality in Men. Med Sci Sports Exerc. 2010 May ; 42(5): 879–885
11. Steven K. Galson. Prevention of deep vein thrombosis and pulmonary embolism. Public Health Rep. 2008 Jul-Aug; 123(4): 420–421
12. Katzmarzyk PT, Church, TS, Craig, CL, Bouchard C. Sitting time and mortality from all causes, cardiovascular disease, and cancer. Med Sci Sports Exerc. 2009; 41(5):998-1005.
13. Hamilton MT, Hamilton DG, Zderic TW. The role of low energy expenditure and sitting on obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. Diabetes. 2007; 56:2655–2667. 
14. Hamilton, Marc T., Healy, Genevieve N., Dunstan, David W., Zderic, Theodore W.  Owen, Neville. Too little exercise and too much sitting: inactivity physiology and the need for new recommendations on sedentary behavior. Current Cardiovascular Risk Reports. 2008, 2 4: 292-298.
15. Genevieve N, Dunstan, David W, Jo Salmon, Jonathan E Shaw, Paul Z, Owen, Neville. Television Time and Continuous Metabolic Risk in Physically Active Adults. Med Sci Sports Exerc. 2008 Apr;40(4):639-45.
16. Brooke R. Stephens, Kirsten Granados, Theodore W. Zderic, Marc T. Hamilton, Barry Braun. Effects of 1 day of inactivity on insulin action in healthy men and women: interaction with energy intake. Metabolism. 2011 Jul;60(7):941-9
17. Levine JA. Nonexercise activity thermogenesis (NEAT): environment and biology. Am J Physiol Endocrinol Metab. 2004 May; 286(5):E675-85
18. Levine JA, Lanningham-Foster LM, McCrady SK, Krizan AC, Olson LR, Kane PH, Jensen MD, Clark MM. Interindividual variation in posture allocation: possible role in human obesity. Science. 2005 Jan 28;307(5709):584-6.

Physiology of Dehydration and Overhydration

When the body is in a state of dehydration, many substrates and neurotransmitters are influenced by circulating vasopressin (antidiuretic hormone) and angiotensin II (1,2).

Dehydration can increase levels of cortisol (3). Interestingly, even a decrease in cell volume caused by hypohydration promotes insulin resistance (4,5,6).
Conditions dehydrating insulin target tissues such as hyperosmolarity or amino acid deprivation are associated with insulin resistance; blockage of the cell volume response to insulin may be the common denominator in dehydration-induced insulin resistance (4).

As a consequence of dehydration, the blood–brain barrier permeability is altered by serotonergic and dopaminergic systems, potentially causing central nervous system dysfunction if dehydration is prolonged (7).  

Understanding Scientific Research [2]: Experimental vs. Observational Studies

Not all scientific studies are created equal. There are several types of studies, and  the first distinction is between experimental and observational evidence.

Previously I posted about how to read a study and how a study is structured with different sections. Certain features in each section should be present and be clear. For example, in the discussion section results should be put into context of the overall or similar literature and weighed against it. 

Scientific evidence should be used to figure out what is more likely to be true, and not misused to defend what we want to be true, for whatever reason.

In this day and age, scientific beliefs and (provisional) conclusions must be based on solid evidence. But what constitutes solid evidence? This can be a tricky question because we have several kinds of evidence with different strengths and weaknesses. This alone makes it all more difficult to interpret.

We must be able to recognize what we are looking at and how to distinguish between different types of scientific evidence. Some studies have more weight than others.

Successful Dieting [5/5]: What Is The Best Weight Loss Rate?

The composition of weight loss is important. While greater deficits yield faster weight loss, this strategy makes you lose more lean body mass than slower weight loss programs due to the size of the caloric deficit, and dietary factors. For example, resistance exercise or high protein diets may modify the proportion of weight loss resulting from body fat versus lean tissue (1,2,3).

Lean body mass is lost in concert with body fat during weight loss (4,5). As the size of the caloric deficit increases weight loss coming from lean body mass also tends to increase (6,7,8). 

As I have argued before, not all diets can be considered successful, the importance of keeping lean body mass loses to a minimum during a diet is paramount. That is, the ratio of body fat to lean mass should be high, for example 80% of fat mass to 20% of lean mass.

Gluten Digestion and the Microbiome: Gluten-Eating Bacteria

It is often assumed, and sometimes defended fanatically by certain “groups”, that humans cannot digest gluten, and therefore no single human (with or without CD) should be eating gluten-containing foods, such as wheat. For them the story ends here. But there is a lot more to it.


There is a large variety of bacteria capable of digesting gluten with gluten-degrading proteases naturally present in the upper human gastro-intestinal tract. The oral cavity is colonised with microorganisms that produce proteases capable of hydrolysing peptides rich in proline and glutamine residues. Intestinal dysbiosis is present in celiac disease patients, characterized by increased Gram-negative bacteria, other potentially pro-inflammatory bacteria and reduced bifidobacteria.

Small-intestinal bacterial overgrowth (SIBO) and infections have been suggested to contribute to CD pathogenesis with persistence of gastrointestinal symptoms after gluten withdrawal. Pathogenic enterobacteria could play a role in the switch from tolerance to an inflammatory immune response to gluten, by altering the permeability of the intestinal mucosa.

A lack of maturation of the gut microbiota is observed within the first 2 years of life in infants at risk of CD. The early introduction of gluten and the lack of maturity in the GI microbiota could trigger or accelerate the development of autoimmunity. Bacterial groups related to gluten metabolism are altered in patients with CD.

Either Bifidobacterium could protect against CD, or inherent features of the CD intestine influence Bifidobacterium colonization. Reduced IgA-coated bacteria is associated with intestinal dysbiosis suggesting the existence of a barrier defect, which fails to stabilize the gut microbiota and prevent the host from the invasion of harmful antigens and pathogens.

The induction of gliadin proteolysis in the human gut might not be the solution but the origin of CD, since gliadinases are CD specific. Gliadinases might have a bacterial origin within the duodenum of patients with CD. Gliadin-metabolising bacteria could be absent, or present to a much lower degree, in the duodenum of all non-predisposed individuals.

In CD the mucosal tolerance to the gut microbiota is deregulated. Reductions in beneficial Gram-positive bacteria could favor the residence and interactions of harmful Gram-negative bacteria within the mucosal surface thereby contributing to loss of gluten tolerance.

Either a particular glycosylation pattern in predisposed individuals favors harmful bacterial adhesion, which contributes to CD pathogenesis or modifications in the composition of the intestinal microbiota lead to alterations in the glycosylation pattern and its defensive role of the mucus layer against infections and CD.

Read the Free Full Article @ and learn a ton about gluten with myself and Brad Dieter, PhD 

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