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what's up everyone

toddparker — Sat, 19 May 2012 16:15:34 GMT

Hey guys...new to the site and just wanted to say hey.

Been into fitness and sports for a lot of years, but just recently getting back into lifting and building again. Just looking to get stronger, bigger, tone and lean up...etc. Also...Finding that as I am getting into my 30's it isn't so easy anymore. Been a fun challenge.

Hoping you guys can point me in the right direction of some good workouts routines, etc. I have always kind of trained the same old way, 4 sets of 10, increase weight every couple weeks, etc. Yawn. I know there is a lot of new stuff out there that I am just not familiar with yet. Thanks for the help...great site and looking forward to getting acquainted.

New to the site - hello from TrainerSteve

TrainerSteve — Fri, 18 May 2012 22:54:52 GMT

Hi,

I'm new here so I thought for those who are interested, a quick bio:

I was an IT executive for 27 geekie years. My ADHD took over (lol) and I just could not attend another boring meeting, so I thought, at 43 years old, what I wanted to do when I grew up was to be a personal trainer.

Fast forward through owning my own company, working as a Fitness Director at several, and now working as a personal trainer at 2 locations, and a competitive NPC bodybuilder - I'm quite a happy guy right now. I live with my girlfriend, who also is a competitive NPC Figure athlete and she is going for her pro-card this summer. She and I "show-prep" competitors, and we both work for the NPC as expeditors. Life is bliss...

Always open to learning more and more and more, especially about nutrition. I'm certified in a bunch of things, but the main one is NASM-CPT. Been into fitness since big Arnold was king of the ring, around 36 years of training myself. Finally figured out HOW to train about 5 years ago, and my body has definately changed.

Thats it for now - thanks for reading and I hope I can learn and add some good knowledge from my own years and years of personal experience.

Steve

Important Read regarding Meal Timing and Frequency

The Solution — Wed, 16 May 2012 13:01:25 GMT

Thanks to Alan Aragon!Hierarchy of Importance

When speaking of nutrition for improving body composition or training performance, it's crucial to realize there's an underlying hierarchy of importance. At the top of the hierarchy is total amount of the macronutrients by the end of the day. Distantly below that is the precise timing of those nutrients. With very few exceptions, athletes and active individuals eat multiple times per day. Thus, the majority of their day is spent in the postprandial (fed) rather than a post-absorptive (fasted) state. The vast majority of nutrient timing studies have been done on overnight-fasted subjects put through glycogen depletion protocols, which obviously limits the applicability of the outcomes. Pre-exercise (and/or during-exercise) nutrient intake often has a lingering carry-over effect into the post-exercise period. Throughout the day, there's a constant overlap of meal digestion & nutrient absorption. For this reason, the effectiveness of nutrient timing does not require a high degree of precision.

The Primary Laws of Nutrient Timing
The First Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing.
The Second Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing.
NOTE: Please do not misinterpret the above to mean that timing is irrelevant. On the contrary, it's very relevant. Timing just happens to have MUCH LESS impact on results than hitting your macro totals for the day. This doesn't diminish the fact that people need to individualize their meal timing so that it maximizes their training performance (& does not hinder it). The latter manipulations vary widely, because people have different training protocols, goals, and tolerances. For example, some people experience their best training performance in an immediately fed state, while others do best in a semi-fasted or fasted state. Endurance athletes who neglect carbohydrate timing will not optimize their training capacity. Strength/power athletes with minimal endurance demands have much less of a concern for this. There's no way to 'universalize' a nutrient timing prescription that applies to everyone & all types of athletes. But to reiterate, macro totals for the day overshadow timing in terms of importance, especially for bodybuilding. If macro totals for the day are not hit, the most precisely neurotic timing of meals is all for sh!t.
I also suggest you read:

http://www.ncbi.nlm.nih.gov/pubmed/19943985This study shows there was no difference in weight loss between subjects with high/low meal frequencies.

http://www.ncbi.nlm.nih.gov/pubmed/9155494Evidence supports that meal frequency has nothing to do with energy in the subjects.

http://www.ncbi.nlm.nih.gov/pubmed/11319656Yet again, no difference in energy in the subjects compared to 2 meals/d to 6 meals/d.

And if you want to do some more detailed digging, you can read:

http://www.ncbi.nlm.nih.gov/pubmed/1905998Eur J Clin Nutr. 1991 Mar;45(3):161-9.LinksInfluence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism.

http://www.ncbi.nlm.nih.gov/pubmed/11319656Int J Obes Relat Metab Disord. 2001 Apr;25(4):519-28.LinksCompared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter.

http://www.ncbi.nlm.nih.gov/pubmed/18053311Br J Nutr. 2008 Jun;99(6):1316-21. Epub 2007 Dec 6. LinksAcute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency.

http://www.ncbi.nlm.nih.gov/pubmed/1905998Eur J Clin Nutr. 1991 Mar;45(3):161-9.LinksInfluence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism.

http://www.ncbi.nlm.nih.gov/pubmed/11319656Int J Obes Relat Metab Disord. 2001 Apr;25(4):519-28.LinksCompared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeterhttp://www.ncbi.nlm.nih.gov/pubmed/18053311Br J Nutr. 2008 Jun;99(6):1316-21. Epub 2007 Dec 6. LinksAcute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency.

http://www.ncbi.nlm.nih.gov/pubmed/9155494Br J Nutr. 1997 Apr;77 Suppl 1:S57-70. LinksMeal frequency and energy balance.

http://www.ncbi.nlm.nih.gov/pubmed/15806828Forum Nutr. 2003;56:126-8.LinksHighlighting the positive impact of increasing feeding frequency on metabolism and weight management.

http://www.ncbi.nlm.nih.gov/pubmed/9504318Int J Obes Relat Metab Disord. 1998 Feb;22(2):105-12.LinksEvidence that eating frequency is inversely related to body weight status in male, but not female, non-obese adults reporting valid dietary intakes.http://www.ncbi.nlm.nih.gov/pubmed/15085170Int J Obes Relat Metab Disord. 2004 May;28(5):653-60. LinksDecreased thermic effect of food after an irregular compared with a regular meal pattern in healthy lean women.

http://www.ncbi.nlm.nih.gov/pubmed/15220950Eur J Clin Nutr. 2004 Jul;58(7):1071-7. LinksRegular meal frequency creates more appropriate insulin sensitivity and lipid profiles compared with irregular meal frequency in healthy lean women.

http://www.ncbi.nlm.nih.gov/pubmed/17228037Obesity (Silver Spring). 2007 Jan;15(1):100-6. LinksAssociation of eating frequency with body fatness in pre- and postmenopausal women.

http://www.ncbi.nlm.nih.gov/pubmed/15640455Am J Clin Nutr. 2005 Jan;81(1):16-24. LinksComment in:Am J Clin Nutr. 2005 Jan;81(1):3-4.Beneficial metabolic effects of regular meal frequency on dietary thermogenesis, insulin sensitivity, and fasting lipid profiles in healthy obese women

http://www.ncbi.nlm.nih.gov/pubmed/10578205Int J Obes Relat Metab Disord. 1999 Nov;23(11):1151-9.LinksAcute appetite reduction associated with an increased frequency of eating in obese males.

he postexercise "anabolic window" is a highly misused & abused concept. Preworkout nutrition all but cancels the urgency, unless you're an endurance athlete with multiple glycogen-depleting events in a single day. Getting down to brass tacks, a relatively recent study (Power et al. 2009) showed that a 45g dose of whey protein isolate takes appx 50 minutes to cause blood AA levels to peak. Resulting insulin levels, which peaked at 40 minutes after ingestion, remained at elevations known to max out the inhibition of muscle protein breakdown (15-30 mU/L) for 120 minutes after ingestion. This dose takes 3 hours for insulin & AA levels to return to baseline from the point of ingestion. The inclusion of carbs to this dose would cause AA & insulin levels to peak higher & stay elevated above baseline even longer.

So much for the anabolic peephole & the urgency to down AAs during your weight training workout; they are already seeping into circulation (& will continue to do so after your training bout is done). Even in the event that a preworkout meal is skipped, the anabolic effect of the postworkout meal is increased as a supercompensatory response (Deldicque et al, 2010). Moving on, another recent study (Staples et al, 2010) found that a substantial dose of carbohydrate (50g maltodextrin) added to 25g whey protein was unable to further increase postexercise net muscle protein balance compared to the protein dose without carbs. Again, this is not to say that adding carbs at this point is counterproductive, but it certainly doesn't support the idea that you must get your lightning-fast postexercise carb orgy for optimal results.

To add to this... Why has the majority of longer-term research failed to show any meaningful differences in nutrient timing relative to the resistance training bout? It's likely because the body is smarter than we give it credit for. Most people don't know that as a result of a single training bout, the receptivity of muscle to protein dosing can persist for at least 24 hours: Enhanced amino acid sensitivity of myofibrillar prote... [J Nutr. 2011] - PubMed - NCBI

More from earlier in the thread:

Here's what you're not seeming to grasp: the "windows" for taking advantage of nutrient timing are not little peepholes. They're more like bay windows of a mansion. You're ignoring just how long the anabolic effects are of a typical mixed meal. Depending on the size of a meal, it takes a good 1-2 hours for circulating substrate levels to peak, and it takes a good 3-6 hours (or more) for everythng to drop back down to baseline.

You're also ignoring the fact that the anabolic effects of a meal are maxed out at much lower levels than typical meals drive insulin & amino acids up to. Furthermore, you're also ignoring the body's ability of anabolic (& fat-oxidative) supercompensation when forced to work in the absence of fuels. So, metaphorically speaking, our physiology basically has the universe mapped out and you're thinking it needs to be taught addition & subtraction.

Madness at SNO!!!!!

Lnh — Wed, 16 May 2012 03:50:37 GMT

Hey everybody! Just wanted to let you guys know that Sports Nutrition Online has become a retailer for BioPulse Nutrition products.

They have started out with Madness, and plan to carry our future products as they become available.

The products should hit their store at Sports Nutrition Online by the end of the week!!!!

Make sure to check out their site and take a look around.

BMR Calculator / Caloric Intake

IcedCoffee — Sun, 13 May 2012 18:41:00 GMT

Quick question:
I'm interested in how people's caloric intake matches up with their supposed BMRs based on some of the formulas out there. I cant help but feel like my caloric intake has to be WAY under my theorized BMR to lose any bf%. I'd be interested to see how others LBM stacks up with their caloric intake.

Test Factor Advanced redefines test boosting, 3 in 1 anabolic, potent GDA and SERM

SwolenONE — Mon, 07 May 2012 19:33:45 GMT

Shawn Wells and William Llewellyn had their hands full with these innovations that help Test Factor Advanced span multiple product categories and outperform your current test boosters with their well rounded capabilities to impact anabolism from different angles.

Berberine, Corosolic acid and other proven glucose dispersal agents have met their new peer: RC Pensis

http://jrnlappliedresearch.com/artic...4/alsagar1.pdf

Stimulatory Effect of the Aqueous Extract of Ruta chalepensis on the Sex Organs and Hormones of Male Rats. Aly Abdullah Al Qarawi, PhD . Journal of Applied Research. Vol.5,No.1,2005.

The role of NO and cGMP in antispasmodic activity of ruta chalepensis leaf extract on rat ileum. A.A. Moazedi, N. Dabir et al. Pak. J. Bio. Sci. 13(2): 83-87, 2010

Persistent Hyperinsulinemia as a Result of Infusion with Ruta Chalepensis. Othman Al-Sagair,PhD. Journal of Applied Research. Vol.4,No.4,2004

Rehmannia inhibits adipocyte differentiation and adipogenesis. Jiang L, Zhang NX, Mo W, Wan R, Ma CG, Li X, Gu YL, Yang XY, Tang QQ, Song HY. Biophys Res Commun. 2008 Jun 27;371(2):185-90. Epub 2008 Apr 3.

Effects of Rehmannia glutinosa oligosaccharides on proliferation of 3T3-L1 adipocytes and insulin resistance. Guo XN, Zhang RX, Jia ZP, Li MX, Wang J. Zhongguo Zhong Yao Za Zhi. 2006 Mar;31(5):403-7.

ActeoFit represents the first natural SERM:

Acteoside and martynoside exhibit... [J Steroid Biochem Mol Biol. 2006] - PubMed - NCBI

Acteoside and martynoside exhibit estrogenic/antiestrogenic properties. Papoutsi Z, Kassi E, Mitakou S, Aligiannis N, Tsiapara A, Chrousos GP, Moutsatsou P. Journal of steroid biochemistry and molecular biology. 2006, vol. 98, pp. 63-71.

Naturally occurring phenylethanoid glycosides: potential leads for new therapeutics. Fu G, Pang H, Wong YH. Curr. Med Chem. 2008;15(25):2592-613.

Acteoside of Callicarpa dichotoma attenuates scopolamine-induced memory impairments. Lee KY, Jeong EJ, Lee HS, Kim YC. Steroid Biochem Mol Biol. 2006 Jan;98(1):63-71. Epub 2005 Sep 28

Interview With IFPA Pro Tyler Mayer

peruvianiron — Mon, 07 May 2012 13:03:00 GMT

Don't pay attention to Jimmy Maklon's picture LOL

Part 1:

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Part 2:

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Tyler seems like a genuine,nice,humble person.Thanks for taking time to do this interview.Respect. Would have loved to stay more than 5 minutes and ask you something other than if you would sit on my face but teh gf came in lewls. Please stay safe~

The LONG Anticipated MN Test Factor Advanced Write-Up

SwolenONE — Fri, 04 May 2012 15:25:06 GMT

TEST FACTOR ADVANCED�
Extreme Testosterone Support

Combining the clinically proven dosage of D-Aspartic Acid (DAA) with MN�s groundbreaking innovations ActeoFit� and RC Pensis�, Test Factor Advanced� represents the pinnacle of natural testosterone enhancement. Proven to raise testosterone 42% in only 12 days, DAA acts as the backbone of this testosterone-boosting formula. Add to this the SERM-like estrogen management capabilities of ActeoFit�, and the enhanced glycogen utilization and nitric oxide production effects of RC Pensis�, Test Factor Advanced is the best choice to help optimize the lean, dense look of your physique, while at the same time supporting enhanced libido, stamina and energy.

Test Factor Advanced is a multifaceted formula that addresses hormone optimization and muscle growth through several different pathways. While other companies forego putting SERM-like estrogen control ingredients into their testosterone boosters, or are unable to find ingredients that truly work, MN has perfected the technology. The majority of testosterone boosters also do nothing to enhance the utilization of nutrients. Protein synthesis is often limited by the availability of nutrients to the muscles. Thankfully, three years of research from the MN Research and Development team has addressed all of these issues.

Test Factor Advanced� was specifically formulated to support high testosterone levels, low estrogen, enhanced pumps, greater glycogen storage, and more complete nutrient delivery. Help skyrocket your testosterone levels without the use of exogenous hormones or illegal anabolics!

More about the Ingredients:

D-Aspartic Acid: Better known as DAA, this is a rare natural isomer of the more commonly occurring amino acid L-Aspartic Acid. Over the past few years, no single testosterone-elevating ingredient has gained the notoriety, produced the positive results, and been validated by so much blood work, as DAA. This is no surprise; clinical trials performed on human test subjects found 3 g/day of DAA to elicit a 42% average increase in testosterone after just 12 days. It has been long known that such a drastic shift in testosterone production can help bodybuilders and fitness enthusiasts acquire new muscle mass, lose fat, and notice profound strength gains!

ActeoFit�: This high-affinity SERM (Selective Estrogen Receptor Modulator) helps block estrogen receptors, and minimize estrogen related side effects that could otherwise be caused by spikes in testosterone. There are also dozens of studies supporting the use of Acteofit� source herbs in various areas of performance. One study with mice demonstrated a dramatic increase in endurance during exercise, along with reduced muscle breakdown, and improved glycogen stores. This could transfer into better performance, preserved muscle mass, and enhanced energy. Further still, hyperplasia and hypertrophy of muscle cell mitochondria were observed without damage to the myofibril. This may support muscle fiber growth, along with a significant anti-catabolic (protein sparing) effect.

RC Pensis�: Ruta Chalepensis extract, better known as RC Pensis, has shown significant testosterone raising properties, alongside the ability to increase liver and muscle glycogen stores, and promote nitric oxide production. Studies administering this extract orally to male mice have demonstrated a 365-476% increase in serum testosterone levels. Sperm density and testicular weight also increased. Additional, peer-reviewed studies suggest it may improve the anabolic/anti-catabolic action of insulin, increase liver and muscle glycogen stores, and increase nitric oxide (NO) production for stronger erections and an enhanced �pump� effect during exercise.

Diet plan to take control on consumed calories...

micalhassi — Wed, 02 May 2012 08:08:07 GMT

I already work out on a regular basis for 30 mints but I really want to change how I eat and not to eat?. Does this sound diet plan is like a good diet plan to lose weight or need to little change?
Breakfast: Eggs with 2 slice of bread, orange juice.
Lunch: Power-bar
Dinner: Salad and Chicken.
8 to 10 glasses of water throughout the day.

Do you have any suggestions?

2011 IFBB Pro Wheelchair Championships

TheBeastWCBB — Thu, 26 Apr 2012 02:17:30 GMT

2011 IFBB Pro Wheelchair Championships
October 15th, 2011 - Houston, TX
Promoter: Lee Thompson - Thompson Muscle Contest

Results
1st - Harold Kelley
2nd - Jason Greer
3rd - Dan Smith
4th - Ludovic Marchand
5th - Antoni Khadraoui
6th - Reggie Bennett
7th - Nick Scott
8th - Mariusz Kupczak

For More Information:
IFBB Pro Wheelchair Bodybuilding: IFBBWCBB.com - Home
Wheelchair Bodybuilding: Wheelchair Bodybuilding - Home

Official Night Routine Videos:

Harold Kelley - Wheelchair Bodybuilding - Harold Kelley

+ YouTube Video

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Jason Greer - Wheelchair Bodybuilding - Jason Greer

+ YouTube Video

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Dan Smith - Wheelchair Bodybuilding - Dan Smith

+ YouTube Video

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Ludovic Marchand - Wheelchair Bodybuilding - Ludovic Marchand

+ YouTube Video

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Antoni Khadraoui - Wheelchair Bodybuilding - Antoni Khadraoui

+ YouTube Video

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Reggie Bennett - Wheelchair Bodybuilding - Reggie Bennett

+ YouTube Video

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Nick Scott - Wheelchair Bodybuilding - Nick Scott

+ YouTube Video

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Mariusz Kupczak - Wheelchair Bodybuilding - Mariusz Kupczak

+ YouTube Video

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Bonus Video:
Ludovic Marchand (Video in FRENCH) - Wheelchair Bodybuilding - Ludovic Marchand

+ YouTube Video

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Please post on your Facebook, Twitter, BodySpace and other Social Media to help bring awareness to the sport of Wheelchair Bodybuilding.

Thank you,

Nick Scott
CEO/President - Wheelchair Bodybuilding, Inc.

+ YouTube Video
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+ YouTube Video
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+ YouTube Video
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The Kreb's Cycle: Learn it Here.

Andy — Sat, 21 Apr 2012 18:30:41 GMT

Grant Me Your ATPs

Over the past few years it seems to have been a growing trend for companies to throw the mineral acid forms of “Krebs cycle intermediates” into their products; the (sometimes) claimed implications in cell metabolism, however, I digress. It doesn't really make any sense when you look at fundamental biochemistry, which you're about to learn (if you can stay awake). Now, again, the point of this reference piece isn’t to diffuse outrageous claims, but rather to give you a foundational understanding of ATP generation without detracting from its complexity.

Keep in mind that there is a boatload of comprehension involved in truly grasping this stuff, so if you are diving right in without college-level biology and/or general chemistry, kudos.

Two things to note: I will refer to the Kreb’s cycle as the tricarboxylic acid (TCA) cycle throughout the article.

And for sensibility’s sake, I’m going to avoid using biochemical jargon at significant cost of accuracy, but significant worth of clarity. Enjoy!

Holy shit, wtf am I looking at?

I think the real problem with scientific outreach in the States begins with images like this. Even as an aspiring scientist, this depiction of the TCA cycle makes me want to cease giving my last fuck and transfer to the business school. Let’s avert disaster and ignore everything south of pyruvate for now.

The Real First Steps in ATP Synthesis: Glycolysis, Amino Acid Degredation, and Beta-Oxidation

In the TCA cycle, every story (read: well, almost- we’ll get to that in a bit)* begins with pyruvate, and if you’re clever, you’ll notice from the title of this section that there are three routes of ATP formation in metabolism, which abstract it from glucose, amino acids, and fatty acids respectively.

From glycolysis, pyruvate tangles itself up with the pyruvate dehydrogenase complex (PDC) which strips off a carbon, forming Acetyl-CoA. Acetyl-CoA then enters the TCA cycle. This is the most important process to focus on here because it is the most connected to the mechanistic properties of the TCA cycle, which we’ll get into later.

*The one exception is protein, for which different amino acids can enter the TCA cycle through different entry points. A class of enzymes called aminotransferases, which exchange an amino acid’s nitrogen for a double-bonded oxygen, catalyzes the reaction that allows certain amino acids to enter the cycle. This image is a hell of a lot less complicated than the one at the top of the page, and it should be quite easy to interpret; if it’s not, ask away.

Beta-oxidation converts fatty acids into 14ATP for every cycle, the number of which depends on the properties of the fatty acid. That might make itself into another detailed article, but that’s all for now.

So, to keep tabs on our progress, we have just covered the mechanisms by which all three macronutrients can become energy in the form of ATP.

So, the TCA Cycle Makes me all my ATPs, Amirite?

Nope. The TCA cycle actually only produces one high-energy phosphate bond per acetyl-CoA metabolized in a process known in biochemistry as substrate-level phosphorylation. It occurs in step-5, forming GTP from GDP. So, if we only get one high-energy phosphate out of all this oxidation, what’s the point?

The Electron Transport Chain and Proton Motive Force

If you recall from secondary school biology, the mitochondria are the cell’s “powerhouse”, generating ATP subsequent to TCA cycle product formation. It’s the reduced (meaning accepted electrons) cofactors formed in the cycle and in glycolysis that are responsible for ATP production, amounting to 10NADH, 2FADH2, and a bunch of protons.

The glycolytic reduced cofactors, which, to clarify, are glorified electron carriers, are transported into the mitochondrion by a cute little piece of biochemical trickery in which electrons are transferred to malate from oxaloacetate in the cytosol. Once it’s in the mitochondrion, the malate is oxidized back to oxaloacetate and viola, you’re left with NADH carrying the pair of electrons.

For housekeeping, note that at this point our reduced cofactors are in what’s called the “mitochondrial matrix”. It is important to understand the structure of a mitochondrion to stay with me through this next part, so stare at this for a while:

What needs to happen next involves a series of transport proteins that act in sequence as the electron transport chain. It really should be called the proton transport chain so people can understand it more easily, because its purpose is to get protons out of the matrix and into the inter-membrane space.

Brief side-note for people who study this stuff:

Moving protons across a membrane isn’t as simple as moving larger ions e.g. Na+ and K+. The reason the electron transport chain is still relatively clandestine is because, if you’re familiar with the concept of proton exchange, hydrogen ions can move along a line of hydrogen-bonding groups within a protein channel. This apparatus is known as the proton wire and it operates mechanistically similar to proton exchange in any other environment; that is, the proton entering the wire may not be the same one that leaves and enters the inter-membrane space. It likely involves a series of conformational changes and acid-base exchanges between adjacent residues.

These proteins, in short, oxidize NADH and FADH2, moving protons into the inter-membrane space. It is a highly exergonic (meaning energy-releasing) process because of a concept called electrochemical potential. The electrons would rather be on the transport proteins’ prosthetic attachments than on the NADH and FADH2, so that’s where they go.

Once the protons are out of the matrix, they create a positive charge in the inter-membrane space, generating a proton motive force. These protons want to get back into the matrix to get away from each other, and we finally arrive at where the ATP is produced en masse, oxidative phosphorylation.

Fucking Finally

ATP synthase is the final enzyme we’ll encounter here, and it’s obvious what it does with all these protons, but it’s mechanism is absurdly complex. For the scope of this reference, know that proton transport is coupled to ATP synthesis because the enzyme is cyclic in nature. Protons basically rotate the enzyme and allow ADP and phosphate to bind to it; the enzyme then attaches the two and forms ATP. Voet et al., the authors of the only necessary reference for this piece, refer to it as a “rotary engine”. It’s not too difficult to conceptualize and visualize by this analogy, so let’s leave it there.

Because proton movement and ATP synthesis are so tightly coupled, scientists can measure exactly how much ATP is formed from each substrate. Turns out that we get 3ATP for every NADH oxidized and 2ATP for every FADH2 oxidized. Notbad.jpg. We end up with about 36 moles of ATP in total for every mole of glucose metabolized.

So there ya have it. I think this reference provides a solid jumping-off point for an in-depth look at fat loss and how we can manipulate it nutritionally and pharmacologically, but until then I hope it helps enough without the supporting cast.

References:
Donald Voet, Judith G. Voet, and Charlotte W. Pratt. Biochemistry: Life at the Molecular Level. 2nd ed. Hoboken, NJ: John Wiley & Sons, 2006.

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