I-Force Dexaprine Ingredient Write-Up.

Figure 1: I-Force Nutrition's
newest fat burner Dexaprine

Just received an email from the marketing guys @I-Force Nutrition informing me that "Dexaprine is finally here...". Well, to be honest, I had not been waiting for it, but the email intrigued me and I would like to give you a brief rundown on the ingredients, which are "guaranteed to give you more energy, increased appetite suppression, and insane mood enhancement than you have ever experienced!" - I don't know about you, but I think I have heard similar claims before ;-)

Ok, here we go: One bottle of Dexaprine, which is 39.99 (pre-order offer @ I-Force webshop) has 60 servings (serving size 1 capsule) of the "thermogenic powerhouse" (I love these advertisment guys) @ 600mg of the following ingredients

• Thermophoric Amine Mood Enhancing Complex,
  which is basically just synephrine (from citrus aurantium) + geranamine (which is also known as 1,3-dimethylamylamine, 4-methyl-2-hexylamine, or as I-Force has it on the label 1,3-dimethylpentylamine)
  
• Extended Release Energy Complex,
  which is a combination of caffeine and theophylline, with the latter having identical beneficial (stimulant, beta receptor agonism, etc.) as well as detrimental (e.g. temporary insulin resistance in muscle tissue, cf. Colnes. 2010, adrenal problems due to long term (over-)use etc.) effects on perceived energy and weight loss, but a longer half-life, which is even prolonged by the concomittant admistration of caffeine (Jonkman. 1991)
  
• Anabolic Protein Synthesis Enhancing Complex,of which I think that it is completely mislabeled, because it is a combination of the two diiodo-L-Thyronines (also known as T2s), 3,3'-T2 and 3,5-T2, of which I have already written in a paper for a German BodyBuilding and fitness magazine (click here for Google-translation) that their impact on metabolic rate (in non-hypothyroid individuals) is probably negligible and would - according to the mice studies that are presently available - require much higher doses than those present in current "thyroid stimulating" products to up-regulate UCP significantly above "normal" levels.

So, overall this does leave us with a probably relatively long lasting stimulant that will enable you to work harder and thus burn more calories and subsequently more fat. Not bad, but nothing new or even revolutionary here.

On a side note: As it is quite often the case in the supplement industry, Dexaprine is deliberately named to sound similar to a potent drug, the synthetic amphetamine Dexedrine (has up to 15 mg dextro-Amphetamin per cap). This practice is about as shabby as calling a product XYZ-"drol". The latter, i.e. the "drols", have incidentally been banned by bodybuilding.com - good idea, guys ;-)

Want to Burn More Fat During Your Cardio Training? Eat Low Carb Before Workout!

Modulation of substrate utilization is the key to effective weight loss. For years we have been told that "training in the zone" (referring to a specific heart rate) would do the trick - recent research does yet suggest otherwise: High Intensity Interval Training (HIIT) has been shown to be at least as effective in burning off unwanted body fat, as the longstanding "gold standard", Low Intensity Steady State (LISS) in the "fat burning zone".

Researchers from the Department of Exercise Science and Sports Studies at Springfield College, Springfield, MA, USA, have now found that apart from the type of exercise you chose to perform, the nutrition, especially in the hours before working out, determines whether you will predominantly burn fat or carbs to sustain the workout.

In their study (Gregory. 2011), Gregory et al. compared the metabolic responses of a group of 8 "active, pre-menopausal" women to a 30 minute exercise regimen performed after either a low carbohydrate (LC: 392 kcal @ 15% carbohydrate, 68% fat, and 18% protein) or a low fat (LF: 396 kcal @ 78% carbohydrate, 7% fat, and 15% protein) meal. Respiratory gas exchange (RER), blood glucose (G), insulin (IN), triglycerides (TG), and free fatty acids (FFA) were measured. While "no significant differences existed between test meals for fasting blood measurements", the post-exercise results showed significant differences:

Postexercise (PE) FFA (mEq·L-1) levels were significantly greater following LC [1.1 (0.3) vs. 0.5 (0.3)]. PE TG (mg·dL-1) levels were significantly greater following LC [152.0 (53.1) vs. 114.4 (40.9)]. RER was significantly lower at all time points following LC compared to LF.

With the respiratory gas exchange being a measure of the relative contribution of fatty acids to fulfill the exercise-induced energy demand (Chessex. 1995), the researchers rightly conclude "ingestion of a single LC meal resulted in greater lipid oxidation at rest and during exercise as compared to a single LF meal." But, let's be honest - did you expect anything else?