My view of the bodybuilding coaches' beliefs that underpin promoting exogenous insulin in order to aid exercise-induced fat oxidation

[Type-IIx]

This post is to answer a question sent by PM out in the open, as an illustration of the absence of rational drug use among even the most highly respected coaches to serve a given objective.

On the topic of combined DNP & slin: The two simply work at cross-purposes, as quoted. On this, I have in the past stated that:

DNP certainly does block the anabolic effects of exogenous insulin as it sabotages the proton pump and interferes with Pi groups' uptake into the mitochondrial matrix, reducing substrates for ATPase.

Growth requires ATP. The practical purpose of exogenous insulin is growth. DNP works at cross-purposes with this (its purpose is fat loss and it's a very blunt instrument at that).

Insulin promotes skeletal muscle hypertrophy by increased muscle protein synthesis, b) reduced proteolysis, and c) transmembrane transport of AAs (non-BCAAs).

Only one of these (b) is particularly useful in skeletal muscle with the use of DNP for the preservation of muscle and strength. I'd suggest that androgens accomplish anticatabolism in skeletal muscle at low doses better than insulin.

[link]

You might see coaches (incorrectly) making claims that insulin can promote fat loss (they believe that exogenous insulin can support exercise-induced fat oxidation by blunting hyperglycemia). This is false, of course.

There is only a weak association between insulin sensitivity and maximal fat oxidation (in non-insulin users). This relates to the etiology of insulin resistance: normally (without exogenous insulin), as someone tends towards an obese phenotype, they will see systemic insulin resistance.

What one must understand is that the bodybuilding community equates "hyperglycemia" (blood glucose elevation) with "insulin resistance." This is false - because both high systemic (blood, plasma) glucose AND high systemic (blood, plasma) insulin reflect insulin resistance. That is, elevations to either, and especially to both, reflect insulin resistance.

To illustrate this point, HOMA-IR (a quantitative measure of insulin resistance) can be expressed by the formula fasting insulin * fasting glucose / 405 (or fasting serum insulin (μU/ml) * fasting plasma glucose [mmol/liter] / 22.5).

Exogenous supra-physiological insulin promotes insulin resistance (i.e., insulin toxicity) by several mechanisms, one is that with prolonged hyperinsulinemia, there is diminished autophosphorylation of the IR, and subsequent PI3K-AKT signaling is affected, thereby reducing GLUT-4 translocation in skeletal muscle.

Insulin is antilipolytic leading to attenuated fat availability and oxidation during exercise. Even fasting insulin levels (1.4 - 14.0 µIU/mL or 9.7 - 97.2 pmol/L) are sufficient to inactivate hormone sensitive lipase (HSL; the rate limiting step in mobilization of adipocytes) by ~50%.

The effect of insulin on lipid metabolism is as follows: (a) It decreases the rate of lipolysis in adipose tissue and hence lowers the plasma fatty acid level, (b) it stimulates fatty acid and triacylglycerol synthesis in tissues, although only to a minor extent in humans, (c) it increases the rate of very-low-density lipoprotein (VLDL) formation in the liver, (d) it increases the uptake of triglyceride from the blood into adipose tissue and muscle, (e) it decreases the rate of fatty acid oxidation in muscle and liver, (f) it increases the rate of cholesterol synthesis in liver.

 

[M@NU]

what is your take on all those guys running inj. L-Carnitine + around 2iu pre fasted cardio then (the insulin mainly to "shuttle" the L-carnitine)? It has quite the hype on some other boards and some "gurus"
ive always assumed it blunts fat loss since even 2iu exogenous insulin should have an effect on lipolysis. What do you think?

 

[Rido]

what is your take on all those guys running inj. L-Carnitine + around 2iu pre fasted cardio then (the insulin mainly to "shuttle" the L-carnitine)? It has quite the hype on some other boards and some "gurus"
ive always assumed it blunts fat loss since even 2iu exogenous insulin should have an effect on lipolysis. What do you think?

I thought carnitine with insulin was advised in the "loading phase"

Or eat some fast carbs to increase insulin secretion

 

[Type-IIx]

what is your take on all those guys running inj. L-Carnitine + around 2iu pre fasted cardio then (the insulin mainly to "shuttle" the L-carnitine)? It has quite the hype on some other boards and some "gurus"
ive always assumed it blunts fat loss since even 2iu exogenous insulin should have an effect on lipolysis. What do you think?

This use does relate to using slin (+ L-carnitine) to increase FA utilization, by the fact that slin promotes the uptake of L-carnitine into skeletal muscle, modestly increasing skeletal muscle carnitine stores.

I think that the combined use of slin & L-carnitine does achieve the objective of promoting exercise-induced fat oxidation. You've raised an interesting factor: the addition of L-carnitine + exogenous slin does accomplish this.

There's evidence that hyperinsulinemia + hypercarnitinemia can increase muscle carnitine stores, thereby enhancing glycogen sparing (via ↑FA utilization), increasing total work (modestly). The evidence suggests that there is a low practical limit to the amount of FAs that can be shuttled above base-line (due, e.g., to malonyl CoA) - limiting the extent of L-Carnitine's performance enhancement. With respect to resistance training, L-carnitine can decrease pain perception & muscle damage, perhaps by enhanced blood flow via increased vasodilation, decreasing some metabolic stress markers, enhancing recovery. However, I would note that the evidence that L-carnitine can up-regulate AR (but increase IGFBPs, which may either decrease or increase IGF-I bioavailability) is equivocal - I wouldn't rely on this to support a view that L-carnitine is potently synergistic with AAS or GH/IGF-I.

My view is that this is conceptually interesting, but that L-carnitine is not potently ergogenic for bodybuilding (but may be for an endurance athlete). Still, I like to think about these things, and CPT1 & the carnitine system are interesting pathways that are important to understand. But as for efficacy - I wouldn't say that L-carnitine is particular outstanding.

Basically, I would say that the multipotent effects of slin on metabolism are conducive to growth (muscle anabolism & glycogen supercompensation) but still, even with the interesting addition of L-carnitine, not so conducive to fat loss.

 

[hudson98]

This use does relate to using slin (+ L-carnitine) to increase FA utilization, by the fact that slin promotes the uptake of L-carnitine into skeletal muscle, modestly increasing skeletal muscle carnitine stores.

I think that the combined use of slin & L-carnitine does achieve the objective of promoting exercise-induced fat oxidation. You've raised an interesting factor: the addition of L-carnitine + exogenous slin does accomplish this.

There's evidence that hyperinsulinemia + hypercarnitinemia can increase muscle carnitine stores, thereby enhancing glycogen sparing (via ↑FA utilization), increasing total work (modestly). The evidence suggests that there is a low practical limit to the amount of FAs that can be shuttled above base-line (due, e.g., to malonyl CoA) - limiting the extent of L-Carnitine's performance enhancement. With respect to resistance training, L-carnitine can decrease pain perception & muscle damage, perhaps by enhanced blood flow via increased vasodilation, decreasing some metabolic stress markers, enhancing recovery. However, I would note that the evidence that L-carnitine can up-regulate AR (but increase IGFBPs, which may either decrease or increase IGF-I bioavailability) is equivocal - I wouldn't rely on this to support a view that L-carnitine is potently synergistic with AAS or GH/IGF-I.

My view is that this is conceptually interesting, but that L-carnitine is not potently ergogenic for bodybuilding (but may be for an endurance athlete). Still, I like to think about these things, and CPT1 & the carnitine system are interesting pathways that are important to understand. But as for efficacy - I wouldn't say that L-carnitine is particular outstanding.

Basically, I would say that the multipotent effects of slin on metabolism are conducive to growth (muscle anabolism & glycogen supercompensation) but still, even with the interesting addition of L-carnitine, not so conducive to fat loss.

Interesting Post, so overall you do not think injectable L-carnitine is highly effective for gaining muscle, recomposition, or fat loss? Sorry if I misread your post.

I also was wondering your opinion on some related questions.

1. Would you say talking short-acting slin pre-workout would hinder fat loss in a cut (deficit)? Would it help maintain LBM (I assume yes to this).

2. I have read some people say a small amount of fat intake can be beneficial when using slin pre-or post because fat is stored within muscle, and the slin can shuttle the fat into the muscle and create fullness. I always assumed this was bs (we should not eat any fat in our pre-post workout slin meals because it is more likely stored as fat).

Thanks

 

[Type-IIx]

Interesting Post, so overall you do not think injectable L-carnitine is highly effective for gaining muscle, recomposition, or fat loss? Sorry if I misread your post.

I also was wondering your opinion on some related questions.

1. Would you say talking short-acting slin pre-workout would hinder fat loss in a cut (deficit)? Would it help maintain LBM (I assume yes to this).

2. I have read some people say a small amount of fat intake can be beneficial when using slin pre-or post because fat is stored within muscle, and the slin can shuttle the fat into the muscle and create fullness. I always assumed this was bs (we should not eat any fat in our pre-post workout slin meals because it is more likely stored as fat).

Thanks

Another conceptually interesting posting.

Yes - my view is that L-carnitine even in combination with slin is only modestly performance enhancing for bodybuilding. Its ergogenic features relate primarily to glycogen sparing (increasing training volumes, i.e., most beneficial to aerobic endurance sport), but with some improved recovery, decreased metabolic stress, decreased pain & muscle damage, etc. I think L-citrulline actually accomplishes more than L-carnitine for resistance training given their similarities mechanistically (i.e., improved vasodilation, blood flow) and the difficulty in meaningfully increasing muscle carnitine stores along with limitations to CPT1 transport.

Short-acting slin used in a cut would simply not be a compound I would necessarily opt for (unless we are using high dose rhGH - which is a possibility - in which case, we become principally concerned with maximizing bioavailable IGF-I, which slin aids with). Though certainly, it is a superior choice here versus Lantus by contrast. But say we do opt for it for the sake of this hypothetical - then, during a cut, I would be very concerned about hypoglycemia (more often undetected than not) with the pre-workout use of slin. I would suggest that the risk/reward given the hypoglycemic risk would be such that it tends to outweigh the benefit of profound glycogen repletion/supercompensation sans depletion (slin + exercise & GLUT-4 translocation).

Given this, I'd shift the burden of providing a rationale back on you - what is your rationale for pre-workout slin in an energy deficit with the objective of minimizing skeletal muscle loss & maximizing adipose tissue loss? I'll provide you a bit of help in this: glycogen repletion (supercompensation sans depletion) has some benefits (e.g., H₂O influx, improving strength through mechanical properties, increases muscle protein synthesis; cell stretching and anabolic signaling). Some considerations: what are you doing with your training, macronutrient intakes, and weekly protocol? If this remains fixed, consider the consequences. Contrast slin's muscle/protein anabolic mechanisms with that of androgens. Then, take a look at what slin accomplishes (or hinders) systemically: are the effects on the muscle tissue sufficient to outweigh the effects on systemic lipid metabolism?

Finally, on the matter of slin & IMTG stores. IMTG stores account for ~1% of muscle weight, but because fat is less dense than skeletal muscle, the volume of fat in a fully fat-loaded muscle cell may exceed 2% of muscle volume. Does the task of using slin to replete these small stores justify the ends (e.g., are you 90 kg at 15% b.f., or 120 kg at 7%?) This use case to me might be rationally supported for an advanced super heavyweight IFBB pro during peak week (as a one-time bolus), but not for a case of regular slin administration in a highly motivated recreational that is essentially in a continuous off-season.

 

[hudson98]

Thank you for the reply, good information.

I am not very scientific but my rationale (it may be flawed) for using slin would be.

Say on a cut I eat 2,000 calories. I intermittent fast until around 4pm. So my body is burning fat during that period. Then at 4pm I take my pre-workout meal say 50 protein, 50 carbs, and 5 iu of slin.

We know slin inhibits fat loss, but I am eating the majority of my daily calories pre-and post workout (during the window slin is active) so I would not be burning fat during this time anyway, so there is not really anything to inhibit.

Or if we take it to the extreme say someone does alternate day fasting and eats 0 calories day 1, and 4000 calories day 2 (for an average of 2000 per day which will cause weight loss over the week).

The slin is used on the 4,000 calorie days pre and post, so it isn't active on their fasting days where the actual fat loss is occurring. So they would get the benefits but I would assume it wouldn't impair fat loss.

Assume this person us using HGH as well.

 

[Type-IIx]

Thank you for the reply, good information.

I am not very scientific but my rationale (it may be flawed) for using slin would be.

Say on a cut I eat 2,000 calories. I intermittent fast until around 4pm. So my body is burning fat during that period. Then at 4pm I take my pre-workout meal say 50 protein, 50 carbs, and 5 iu of slin.

We know slin inhibits fat loss, but I am eating the majority of my daily calories pre-and post workout (during the window slin is active) so I would not be burning fat during this time anyway, so there is not really anything to inhibit.

Or if we take it to the extreme say someone does alternate day fasting and eats 0 calories day 1, and 4000 calories day 2 (for an average of 2000 per day which will cause weight loss over the week).

The slin is used on the 4,000 calorie days pre and post, so it isn't active on their fasting days where the actual fat loss is occurring. So they would get the benefits but I would assume it wouldn't impair fat loss.

Assume this person us using HGH as well.

OK, so I understand that dietary practices like these attach with a sense of identity & purpose in people. Please don't view this as any sort of an assault on yourself.

The combined use of slin & intermittent fasting (IF)/time-restricted eating (TRE) is highly irrational - it may be the most irrational application of slin use I've considered (it never occurred to me that they'd be combined until now).

To start, IF and time-restricted eating are inapposite bodybuilding practices because of significant protein catabolism/muscle loss during periods of starvation.

The metabolic benefits ascribed to intermittent fasting & time-restricted eating related to reduced IGF-I & insulin (and benefits, therefore, to longevity, reduced cancer risks, diabetes, etc.) Thus, the use of slin contravenes these objectives of the diet..

IF/TRE are a convenient way for those on a typical work schedule to restrict calories. Yet rather sub-optimal for bodybuilding objectives.

Insulin use is optimized in a caloric surplus for the purpose of growth. It profoundly increases serum insulin (of course) & IGF-I.

This proposed protocol might reduce systemic blood glucose - but without any apparent aim. I understand there's a hyperfocus on lowering blood glucose even in healthy persons - a current trend - but as this thread's title post indicates, insulin resistance & hyperglycemia are separate concepts, and ideally one has healthy blood glucose levels, rather than the lowest levels attainable.

Combined IF/TRE & slin would seem to eviscerate both the purpose of slin and of IF/TRE. Given a weekly energy deficit, growth - the primary purpose of exogenous insulin - is impaired by IF/TRE. By using exogenous slin, blood insulin & IGF-I levels are profoundly elevated - impairing the metabolic benefits of IF/TRE.

 

[hudson98]

Thank you for the reply, not offended in the least. I understand why Slin and IF now makes no sense.

I was a bit surprised that you feel that IF would be more catabolic when dieting, or are you talking just in extreme cases like 24 hour fasts?

Say for example

A person has a maintenance of 3k calories, and is dieting on 2k calories. Their feeding window is 3pm until 10pm, with training around 5pm.

Assume they are using a small amount of AAS 200mg Tren/300mg test, 4iu HGH.

I assume your stance is they would lose more muscle than then if they ate 6 meals at regular intervals? I'm not arguing against (you know more than me) just wanted to clarify.

If so, do you also believe they will lose less fat than if they ate 6 meals at regular intervals?

I may have to change my practices. Like you said though ,it is very convenient to diet this way but I wasn't aware it was sub optimal (or to a large degree).

 

[Type-IIx]

Thank you for the reply, not offended in the least. I understand why Slin and IF now makes no sense.

I was a bit surprised that you feel that IF would be more catabolic when dieting, or are you talking just in extreme cases like 24 hour fasts?

Say for example

A person has a maintenance of 3k calories, and is dieting on 2k calories. Their feeding window is 3pm until 10pm, with training around 5pm.

Assume they are using a small amount of AAS 200mg Tren/300mg test, 4iu HGH.

I assume your stance is they would lose more muscle than then if they ate 6 meals at regular intervals? I'm not arguing against (you know more than me) just wanted to clarify.

If so, do you also believe they will lose less fat than if they ate 6 meals at regular intervals?

I may have to change my practices. Like you said though ,it is very convenient to diet this way but I wasn't aware it was sub optimal (or to a large degree).

Certainly, in the extreme case of 24-hr fasts, you're risking significant muscle loss. I believe that the time-restricted eating design versus a CKD-style diet (not with an objective to enter ketosis, but rather a cyclical design to promote insulin sensitivity on non-training days with higher monounsaturated fat & non-processed carbohydrate sources) and a high meal frequency (e.g., 6 meals daily, including shakes and high-protein snacks) gets us closer to optimal. Tren, Test & rhGH certainly stave off muscle catabolism, and there's no way to quantify whether you'd be looking at significant muscle loss; but the CKD-style diet is theoretically optimal versus the TRE/IF diet.

At the end of the day, if the only diet design that gets you in a caloric deficit is TRE/IF, then you'll have to use that. Practically, what you can adhere to long-term is what will work best.

 

[Klimmzugernie]

Another conceptually interesting posting.

Yes - my view is that L-carnitine even in combination with slin is only modestly performance enhancing for bodybuilding. Its ergogenic features relate primarily to glycogen sparing (increasing training volumes, i.e., most beneficial to aerobic endurance sport), but with some improved recovery, decreased metabolic stress, decreased pain & muscle damage, etc. I think L-citrulline actually accomplishes more than L-carnitine for resistance training given their similarities mechanistically (i.e., improved vasodilation, blood flow) and the difficulty in meaningfully increasing muscle carnitine stores along with limitations to CPT1 transport.

Short-acting slin used in a cut would simply not be a compound I would necessarily opt for (unless we are using high dose rhGH - which is a possibility - in which case, we become principally concerned with maximizing bioavailable IGF-I, which slin aids with). Though certainly, it is a superior choice here versus Lantus by contrast. But say we do opt for it for the sake of this hypothetical - then, during a cut, I would be very concerned about hypoglycemia (more often undetected than not) with the pre-workout use of slin. I would suggest that the risk/reward given the hypoglycemic risk would be such that it tends to outweigh the benefit of profound glycogen repletion/supercompensation sans depletion (slin + exercise & GLUT-4 translocation).

Given this, I'd shift the burden of providing a rationale back on you - what is your rationale for pre-workout slin in an energy deficit with the objective of minimizing skeletal muscle loss & maximizing adipose tissue loss? I'll provide you a bit of help in this: glycogen repletion (supercompensation sans depletion) has some benefits (e.g., H₂O influx, improving strength through mechanical properties, increases muscle protein synthesis; cell stretching and anabolic signaling). Some considerations: what are you doing with your training, macronutrient intakes, and weekly protocol? If this remains fixed, consider the consequences. Contrast slin's muscle/protein anabolic mechanisms with that of androgens. Then, take a look at what slin accomplishes (or hinders) systemically: are the effects on the muscle tissue sufficient to outweigh the effects on systemic lipid metabolism?

Finally, on the matter of slin & IMTG stores. IMTG stores account for ~1% of muscle weight, but because fat is less dense than skeletal muscle, the volume of fat in a fully fat-loaded muscle cell may exceed 2% of muscle volume. Does the task of using slin to replete these small stores justify the ends (e.g., are you 90 kg at 15% b.f., or 120 kg at 7%?) This use case to me might be rationally supported for an advanced super heavyweight IFBB pro during peak week (as a one-time bolus), but not for a case of regular slin administration in a highly motivated recreational that is essentially in a continuous off-season.

That means if an athlete focus on fat oxidation AND gaining muscle at the same time it would might be clever to do fasted cardio with HGH (1h pre i.m. injection) and later the day the work out routine with HGH and no intra work out carbs (also no eaa due to Leucin) and pin insulin with the post workout meal?

Beneficial or non sense and I shall go back and do my homework?

 

[Type-IIx]

That means if an athlete focus on fat oxidation AND gaining muscle at the same time it would might be clever to do fasted cardio with HGH (1h pre i.m. injection) and later the day the work out routine with HGH and no intra work out carbs (also no eaa due to Leucin) and pin insulin with the post workout meal?

Beneficial or non sense and I shall go back and do my homework?

I don't see morning fasting as optimal due to the issues raised above with respect to TRE/IF (muscle catabolism). I also do not see a rationale for split dosing, as peak GH is most consistently associated with lipolysis. Yes brother, I do not see this protocol as rational (see no rationale to using pure Leucine as it is disgusting and already maximally stimulates MPS in combination with the BCAAs from whey/casein/whole food sources).

 

[Para_33]

This use does relate to using slin (+ L-carnitine) to increase FA utilization, by the fact that slin promotes the uptake of L-carnitine into skeletal muscle, modestly increasing skeletal muscle carnitine stores.

I think that the combined use of slin & L-carnitine does achieve the objective of promoting exercise-induced fat oxidation. You've raised an interesting factor: the addition of L-carnitine + exogenous slin does accomplish this.

There's evidence that hyperinsulinemia + hypercarnitinemia can increase muscle carnitine stores, thereby enhancing glycogen sparing (via ↑FA utilization), increasing total work (modestly). The evidence suggests that there is a low practical limit to the amount of FAs that can be shuttled above base-line (due, e.g., to malonyl CoA) - limiting the extent of L-Carnitine's performance enhancement. With respect to resistance training, L-carnitine can decrease pain perception & muscle damage, perhaps by enhanced blood flow via increased vasodilation, decreasing some metabolic stress markers, enhancing recovery. However, I would note that the evidence that L-carnitine can up-regulate AR (but increase IGFBPs, which may either decrease or increase IGF-I bioavailability) is equivocal - I wouldn't rely on this to support a view that L-carnitine is potently synergistic with AAS or GH/IGF-I.

My view is that this is conceptually interesting, but that L-carnitine is not potently ergogenic for bodybuilding (but may be for an endurance athlete). Still, I like to think about these things, and CPT1 & the carnitine system are interesting pathways that are important to understand. But as for efficacy - I wouldn't say that L-carnitine is particular outstanding.

Basically, I would say that the multipotent effects of slin on metabolism are conducive to growth (muscle anabolism & glycogen supercompensation) but still, even with the interesting addition of L-carnitine, not so conducive to fat loss.

What about using it to drop blood sugar, releasing glucagon, releasing liver glycogen, and the low blood sugar being a stimulus for gluconeogenesis, which would then increase the rate of fat loss as well. With the insulin then being present to shutting the circulating nutrients/sugar into the muscles being worked for cardio preventing atrophy and catabolic effects of cardio ?

I thought this was the thought process behind it.

The Carnitine then being in place to assist with uptake of the ffa being released by cortisol

 

[Type-IIx]

What about using it to drop blood sugar, releasing glucagon, releasing liver glycogen, and the low blood sugar being a stimulus for gluconeogenesis, which would then increase the rate of fat loss as well. With the insulin then being present to shutting the circulating nutrients/sugar into the muscles being worked for cardio preventing atrophy and catabolic effects of cardio ?

I thought this was the thought process behind it.

The Carnitine then being in place to assist with uptake of the ffa being released by cortisol

Gluconeogenesis does not increase the rate of fat loss, it is the process of synthesizing glucose from AAs and lipids. Glucagon decreases glycolysis (the use of glucose as the cell's preferred energy substrate to perform cellular metabolism [respiration primarily] and perform work) and increases gluconeogenesis (raising blood glucose levels).

As such, stimulating gluconeogenesis (an anabolic process) does not increase fat loss in itself.

 

[he-man 100]

This post is to answer a question sent by PM out in the open, as an illustration of the absence of rational drug use among even the most highly respected coaches to serve a given objective.

On the topic of combined DNP & slin: The two simply work at cross-purposes, as quoted. On this, I have in the past stated that:


[link]

You might see coaches (incorrectly) making claims that insulin can promote fat loss (they believe that exogenous insulin can support exercise-induced fat oxidation by blunting hyperglycemia). This is false, of course.

There is only a weak association between insulin sensitivity and maximal fat oxidation (in non-insulin users). This relates to the etiology of insulin resistance: normally (without exogenous insulin), as someone tends towards an obese phenotype, they will see systemic insulin resistance.

What one must understand is that the bodybuilding community equates "hyperglycemia" (blood glucose elevation) with "insulin resistance." This is false - because both high systemic (blood, plasma) glucose AND high systemic (blood, plasma) insulin reflect insulin resistance. That is, elevations to either, and especially to both, reflect insulin resistance.

To illustrate this point, HOMA-IR (a quantitative measure of insulin resistance) can be expressed by the formula fasting insulin * fasting glucose / 405 (or fasting serum insulin (μU/ml) * fasting plasma glucose [mmol/liter] / 22.5).

Exogenous supra-physiological insulin promotes insulin resistance (i.e., insulin toxicity) by several mechanisms, one is that with prolonged hyperinsulinemia, there is diminished autophosphorylation of the IR, and subsequent PI3K-AKT signaling is affected, thereby reducing GLUT-4 translocation in skeletal muscle.

Insulin is antilipolytic leading to attenuated fat availability and oxidation during exercise. Even fasting insulin levels (1.4 - 14.0 µIU/mL or 9.7 - 97.2 pmol/L) are sufficient to inactivate hormone sensitive lipase (HSL; the rate limiting step in mobilization of adipocytes) by ~50%.

The effect of insulin on lipid metabolism is as follows: (a) It decreases the rate of lipolysis in adipose tissue and hence lowers the plasma fatty acid level, (b) it stimulates fatty acid and triacylglycerol synthesis in tissues, although only to a minor extent in humans, (c) it increases the rate of very-low-density lipoprotein (VLDL) formation in the liver, (d) it increases the uptake of triglyceride from the blood into adipose tissue and muscle, (e) it decreases the rate of fatty acid oxidation in muscle and liver, (f) it increases the rate of cholesterol synthesis in liver.

@Type-IIx
This is a very interesting topic.
The arguments of the crowd advocating insulin use to increase fat loss are usually that lowering blood glucose with exogenous insulin will cause a release of glucagon ,lipase and catecholamines which will overpower the antilipolytic effect of insulin. And that with no blood glucose available as fuel the energy has to come from somewhere (bodyfat).

 

[Type-IIx]

@Type-IIx
This is a very interesting topic.
The arguments of the crowd advocating insulin use to increase fat loss are usually that lowering blood glucose with exogenous insulin will cause a release of glucagon ,lipase and catecholamines which will overpower the antilipolytic effect of insulin. And that with no blood glucose available as fuel the energy has to come from somewhere (bodyfat).

Insulin suppresses hormone sensitive lipase, glucagon is not lipolytic in humans, and I have no idea from where the claim that insulin releases catecholamines originates. With no blood glucose available the human dies (it's true the brain can use ketones for fuel, a separate argument).