Let the Chips Fall Where You Want
These questions ultimately point to nutrient partitioning, an issue that understandably slips through the cracks. And that's okay because we can generally count on the laws of thermodynamics to strip our physique goals down to the bare-bones basics of eating more or less to bulk up or get shredded, respectively (with heavy training in either context, of course).
However, we do have some pull in getting nutrients to go where we want them to, albeit marginally. Optimization of our food intake, within reason, is the name of the game. Now, it's time to sift through the sand and uncover the gems in partitioning.
Glucose Disposal Agents
Also known as insulin sensitizers or insulin mimetics (mimickers), these include alpha lipoic acid (ALA), chromium, vanadium, cinnamon, and vinegar.
So, the good news is that whole-body insulin sensitivity is improved by the use of any one of the above, and that includes muscle cells. This helps muscle glycogen resynthesis following exercise. The problem: that includes fat cells as well. A contemporary (and bright) theorist once pointed out that the problem with Ceylon cinnamon is that it indiscriminately dumps glucose to whatever cells are willing to take it, but the same can be said for glucose disposal agents in general. In the end, it's a crapshoot, and they don't provide the control over nutrient diversion that we're after.
So, when a study comes out that finds improved post-exercise glycogenesis using vinegar or, say, caffeine, we must ask if adipocytes are also enjoying the same benefit. By the way, fat cells have the same GLUT4 (glucose transporter type 4) receptor found on muscle cells that has been implicated as one of the mechanisms in improved insulin sensitivity. Use of these agents would be advantageous to Type 2 diabetics, who have abnormally high blood sugar and could benefit from improved glucose clearance regardless of the route.
I mentioned caffeine just a while ago, and I'm sure you're wondering why I lumped it in with the insulin mimetics. And you'd be justified; under normal conditions, caffeine actually induces acute resistance to insulin. Not necessarily a bad thing for healthy people; high blood levels of free fatty acids (also called "non-esterified fatty acids", or NEFAs) lower the rate of amino acid oxidation (caffeine creates a protein-sparing environment).
To be thorough, researchers back in 2008 found that post-workout co-ingestion of caffeine with CHO amplified glycogen resynthesis. However, a closer look at the study reveals that the dosing that the protocol called for (around 574 grams of caffeine) was grossly unrealistic. Not safe for application.
Still, caffeine has other merits, and this is a good segue into the topic of lipolysis, respiratory quotient (RQ), and beta-oxidation.
If we can't reliably partition nutrients into the desired tissue compartment, can we at least reliably influence what comes out? The answer to that question is yes.
I once discussed the dual use of yohimbine and caffeine in an older post that has grown quite popular to viewers.
To summarize some of what I said in that post, Y and C make fat release, transport, and burning possible in that small segment of the population dealing with stubborn fat. Y, in particular, is profoundly anti-lipolytic and has implications in fat burning at rest.
That's because resting lipolysis is under the control of the alpha-adrenoceptors, and Y conveniently blocks one of them (the one most intimately linked to fat release).
In fact, a study referenced in the clinical pharmacology section of the Proceedings of the British Pharmacological Society showed Y to enhance not only exercising, but also resting, lipolysis. In other words, it may even be useful to dose yohimbine at rest.
That's great news for couch potatoes watching their ESPN or surfing the Internet all day. And due to Y's mechanism of action, I'd expect any additional fat oxidation to be meaningful because the fat is actually reaching the mitochondria unimpeded (this has to do with a phenomenon known as fatty acid cycling, which I'll save for another post).
With that said, depletion training or restricting carbs (or both) would further improve fat oxidation by lowering one's RQ, which is influenced by muscle glycogen levels. That would conceivably magnify Y's effects.
Fish Oil
While the acute benefits that fish oil supplementation was purported to have never panned out, a mere 3 weeks of supplementation did reduce cortisol levels, which might minimally improve partitioning.
However, it could be argued that fish oil supplementation would also blunt the perks that come with YC ingestion: heightened catecholamine levels and blood FFAs. Yohimbine also significantly increases cortisol secretion, but its anti-lipolytic effects outweigh any negative impact it has on partitioning. Clearly, both sides must be weighed and a poison picked if one is to facilitate his or her physique goal.
And by the same token, the myriad of health benefits conferred by fish oil, in addition to its newfound effects on increased protein synthesis and sensitivity to amino acids (Martin Berkhan recently expounded on these in exhausting detail), makes it a legitimate tool in altering body composition.
So, when a study comes out that finds improved post-exercise glycogenesis using vinegar or, say, caffeine, we must ask if adipocytes are also enjoying the same benefit. By the way, fat cells have the same GLUT4 (glucose transporter type 4) receptor found on muscle cells that has been implicated as one of the mechanisms in improved insulin sensitivity. Use of these agents would be advantageous to Type 2 diabetics, who have abnormally high blood sugar and could benefit from improved glucose clearance regardless of the route.
Psychotropics and Nootropics
To be thorough, researchers back in 2008 found that post-workout co-ingestion of caffeine with CHO amplified glycogen resynthesis. However, a closer look at the study reveals that the dosing that the protocol called for (around 574 grams of caffeine) was grossly unrealistic. Not safe for application.
Still, caffeine has other merits, and this is a good segue into the topic of lipolysis, respiratory quotient (RQ), and beta-oxidation.
I once discussed the dual use of yohimbine and caffeine in an older post that has grown quite popular to viewers.
To summarize some of what I said in that post, Y and C make fat release, transport, and burning possible in that small segment of the population dealing with stubborn fat. Y, in particular, is profoundly anti-lipolytic and has implications in fat burning at rest.
That's because resting lipolysis is under the control of the alpha-adrenoceptors, and Y conveniently blocks one of them (the one most intimately linked to fat release).
That's great news for couch potatoes watching their ESPN or surfing the Internet all day. And due to Y's mechanism of action, I'd expect any additional fat oxidation to be meaningful because the fat is actually reaching the mitochondria unimpeded (this has to do with a phenomenon known as fatty acid cycling, which I'll save for another post).
With that said, depletion training or restricting carbs (or both) would further improve fat oxidation by lowering one's RQ, which is influenced by muscle glycogen levels. That would conceivably magnify Y's effects.
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| Find a brand with a good amount of EPA and DHA. |
While the acute benefits that fish oil supplementation was purported to have never panned out, a mere 3 weeks of supplementation did reduce cortisol levels, which might minimally improve partitioning.
However, it could be argued that fish oil supplementation would also blunt the perks that come with YC ingestion: heightened catecholamine levels and blood FFAs. Yohimbine also significantly increases cortisol secretion, but its anti-lipolytic effects outweigh any negative impact it has on partitioning. Clearly, both sides must be weighed and a poison picked if one is to facilitate his or her physique goal.
And by the same token, the myriad of health benefits conferred by fish oil, in addition to its newfound effects on increased protein synthesis and sensitivity to amino acids (Martin Berkhan recently expounded on these in exhausting detail), makes it a legitimate tool in altering body composition.
GLUT4 and the Controversy of Carb Cutoffs
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| How the last meal before a carb cutoff might look. |
The idea of cutting out carbs from one's meals before it got too late in the evening gained quite some notoriety several years ago. I first heard about the practice from advocates of Doggcrapp, or DC, Training. Because thermodynamics trump the "carb cutoff" rule, it just wasn't necessary to resort to macronutrient separation.
However, if we are nitpicking, GLUT4 sensitivity is higher during the first half of the day than it is the latter half. Short-term fasting (assuming no stimulant use) increases this effect. Considering this, the body is technically less receptive to the downstream effects of insulin on GLUT4 translocation and subsequent glucose uptake as the day wears on.
But then we return to the crapshoot model of generalized insulin sensitivity, where fat cells are more likely to soak up the glucose as well. So, more likely than not, the timing and composition of meals (excluding a low carb diet's effect on lowered RQ) is a moot point.
Refeeds
The dietary practice with probably the most diverse range of partitioning effects is the carb-centric refeed, which is leveraged extensively in Lyle's Ultimate Diet 2. But it needs to be coupled with the right kind of training, which happens to be the key factor in getting the right kind of partitioning to happen, and without which the carb load would be fruitless.
In The Ketogenic Diet, Lyle used research to give a rough guideline of fat intake concurrent with the carb-up that likely wouldn't go toward storage, assuming full glycogen depletion. I will issue a similar recommendation: don't restrict, but don't go to excess. By the way, the nature of the fat being consumed affects the insulin response to a meal (unsaturated fats attenuate the response, but saturated fats amplify it).
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| A food hedonist's carb-centric haven. |
The dietary practice with probably the most diverse range of partitioning effects is the carb-centric refeed, which is leveraged extensively in Lyle's Ultimate Diet 2. But it needs to be coupled with the right kind of training, which happens to be the key factor in getting the right kind of partitioning to happen, and without which the carb load would be fruitless.
In The Ketogenic Diet, Lyle used research to give a rough guideline of fat intake concurrent with the carb-up that likely wouldn't go toward storage, assuming full glycogen depletion. I will issue a similar recommendation: don't restrict, but don't go to excess. By the way, the nature of the fat being consumed affects the insulin response to a meal (unsaturated fats attenuate the response, but saturated fats amplify it).
A Concentric-centric Mindset
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| My childhood buddy Ryan at 16. |
A string of studies in the 90s revealed the detrimental impact of eccentric exercise on glycogen resynthesis.
On the other hand, it is the concentric portion of contraction that generates improved partitioning (the "metabolic stress" model of training). This is the reason that Bryan Haycock advocates "pulsing" in his novel HST (Hypertrophy-Specific Training) protocol. Training is one of the few things that can preferentially improve GLUT4 translocation on muscle cells. That and the inhibitory effect of exercise on fat lipoprotein lipase (LPL) and acylation-stimulating protein (ASP) within the fat cell make for a hard case for improved nutrient uptake into the fat cell.
Conclusions
In the end, only some of the above mentioned techniques aimed at improving nutrient partitioning are actually worth investing time, energy, and money in.
Training and refeeds are the winning ticket to diverting incoming calories away from adipocytes and shuttling them toward muscle cells instead. Their prudent application can be more readily appreciated for those bulking up.
But fish oil and YC also carry great utility in the contexts of health and fat loss, respectively (also, fish oil, as Martin mentioned, has implications for sarcopenia in the elderly). They may not directly influence partitioning per se, but they are worthwhile toys that may be taken out of the box when the time calls for it.
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