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marylin monroe
Showing posts with label lose fat. Show all posts
Showing posts with label lose fat. Show all posts

Intelligent Weight Loss Workouts: 45 Min of HIT'14 = "High Intensity Thinking" Help Resolve HIS New Year's Resolution

High intensity thinking - intelligent weight loss workouts
It's almost 2014! Actually it is already 2014; at least for my friends in the "Far East" (HAPPY NEW YEAR!) and thus almost too late for the annual "I want to lose weight" new year's resolution. Ok, you as a SuppVersity reader should actually know better, but just in case you are still planning to make the weight loss happen solely by increasing your workout volume, I would suggest that you replace some classic HIT training with the revolutionary HIT 2.0 - high intensity thinking regimen (warning: doing this too often may actually build more brain than muscle mass ;-). 

Well,... now that I take a closer look at the results of this recent study from the University of Quebec here,  I have to realize that this will only work if you are a man. But don't worry, I am pretty sure there is something to be learned for the ladies in the last SuppVersity article of 2014, as well ;-)

All jokes aside, your brain is a sucker for energy!

I guess you will be familiar with the over-cited fact that "the human brain is only 2% of the weight of the body, but it consumes about 20% of the total energy we need every day"... I know that's boring, but actually that's quite an important point, because it tells you that your brain is not just a sucker for energy, but also a sucker for new information, which will in turn increase the energy requirements of the insatiable heap of neurons in your skull. Why? Well, our brains need energy to process each and every of these information chunks - max. 30W per opeartion, if the currently heralded estimations are correct. I know that sounds tremendously much, but if we performed only one of these operations per minute, you would hardly burn the energy equivalent of 1/25 of a 70-85% chocolate bar during your high intensity thinking sessions.

Against that background it's all the more impressive that Emilie Pérusse-Lachance and her Canadian colleagues were able to measure a significant increase in energy expenditure, when they had their 35 subjects (22 men and 13 women; aged 24 ± 3 years) read a 10-page text and write a summary of approximately 350 words using a computer in the "mental work condition" of their study.
Figure 1: Energy expenditure in kcal/45min in the control and the mental work condition, left; energy intake during the buffet ca. 15min after the control and mental work condition, right (Pérusse-Lachance. 2013)
If you take a look at the data in Figure 1, you will also notice that the scientists original hypothesis, which was that they would observe a similar hyperphagic (=hunger ➲ increased energy intake) response to in the "mental work" condition as Chaput et al. who conducted two very similar studies in 2007 and 2008.  The actual study outcome does yet tell a different story: While the female study participant did in fact supercompensate for the extra-energy they had to spent, when they were not watching TV and lolling around like in the control condition, the men were probably so immersed in their thoughts that they simply forgot to eat... ok, I guess you already realized that this was an ad-hoc hypothesis to make sure you don't realize that neither I nor the scientists have any clue what the underlying reasons of this sex-difference were.

I would even guess that the women did not even notice that they were overcompensating. If you take a look at the subjective hunger scores that have been assessed by seven visual analogue scale questionnaires the participants had to fill...
  1. at the beginning (T-60/60 minutes before the buffet), 
  2. after the experimental session (T-15/15 minutes before the buffet), and 
  3. after the buffet-type meal (T0, T60, T120, T180, and T240).
...those will tell you that the ladies either claimed to, or actually weren't more hungry than in the control condition. In view of the irrefutable evidence that they still ate more (see Figure 1) this may look awkward. When it's all said and done, these contradictory result does yet only confirm that you cannot trust people, when they tell you "I am never hungry and actually don't eat that much.... I have really NO clue where that belly comes from". This may even be their own perception, but that does not change that it is usually not in line what happens at the buffets, dinner tables and - most importantly - during the snack breaks people take during not after their high intensity thinking regimen all over the world.
Figure 2: Change in energy balance (kcal) in the "exercise" condition in the course of which the subjects walked on a treadmill for 45 min, waited for 15 minutes and were then allowed to avail themselves of as much food as they wanted at the buffet - further evidence that the "exercise just makes you hungry" hypothesis is bunk.
Bottom line: By now you should have realized that this article must not be taken too seriously. Though,... if this type of heavy brain lifting would have women eat 15.3% (=121kcal/day) more and men 16.1% (=267kcal/day) less every day it would probably have a non-negligible impact on your chances of living up to your new year's weight loss resolution in 2014.

But don't worry, ladies. Life is not so unfair as it may seem. All you have to do to achieve an almost level playing field is to convince him that a 45 min walk in the park with you is much more fun than 45 min of high intensity thinking. And if that's  not convincing enough, show him the data in Figure 3 and tell him that real exercise (in the study 45min of paced walking) will help both of you improve your energy balance - his by -31% (-516kcal) and yours by -23% (-184kcal).
References:
  • Chaput, J. P., & Tremblay, A. (2007). Acute effects of knowledge-based work on feeding behavior and energy intake. Physiology & behavior, 90(1), 66-72.
  • Chaput, J. P., Drapeau, V., Poirier, P., Teasdale, N., & Tremblay, A. (2008). Glycemic instability and spontaneous energy intake: association with knowledge-based work. Psychosomatic medicine, 70(7), 797-804.
  • Pérusse-Lachance, E., Brassard, P., Chaput, J. P., Drapeau, V., Teasdale, N., Sénécal, C., & Tremblay, A. (2013). Sex Differences in the Effects of Mental Work and Moderate-Intensity Physical Activity on Energy Intake in Young Adults. ISRN Nutrition, 2013.

Modifying Set Numbers: 1, 3, or 5 Sets - How Many Shall We do per Exercise in 2015? First Study to Investigate Potential Benefits of 5 Sets in the Long (6 Months) Run

I have to admit. I am surprised that the total lean mass didn't but the sleeve size of the subjects did benefit from increasing the number of sets from 1 to 3 and from 3 to 5 sets. For legs this would have been something I would have expected. For arms, which are trained with almost every other exercise? No, not really.
With their latest study, scientists from the University of Rio Grande do Sul, the University of Wisconsin-Eau Claire and the Federal Universities of Rio de Janeiro and Maranhão tried to fill the gap that exists with respect to studies comparing the effects of multiple sets, greater than 3-sets, on strength and muscle hypertrophy over long training periods. Accordingly, the aim of the study was to compare the effects of 1, 3 and 5-sets on the changes in the muscle strength and endurance, muscle hypertrophy, vertical jump performance and body composition over the course of a six months standardized training regimen.

The hypotheses of the study was that multiple sets would result in greater changes in training outcomes than single sets and that there would be a dose response for training outcomes.
Are you looking for other muscle builders than volume increases?

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Pre-Exhaustion Exhausts Your Growth Potential

Full ROM ➯ Full Gains - Form Counts!

Battle the Rope to Get Ripped & Strong

Study Indicates Cut the Volume Make the Gains!
In view of the fact that the subjects were 48 men from the Brazilian Navy School of Lieutenants (mean ± SD age = 24.4 ± 0.9 yrs; body mass = 79.3 ± 9.1 kg; height = 174.5 ± 5.5 cm) who were familiar with all sorts of body weight "strength training" drills, but had not trained on any of the Life Fitness machines that were used in the study, it's not unlikely, though, that even one set of bench presses, leg presses, lat pulldowns, leg extensions, leg curls, biceps curls, ab crunches and triceps extensions, which were performed thrice a week, would suffice to produce significant results (also compared to the regular military training the men in the control group performed).
Figure 1: Overview of the 6-week resistance training protocol used in the study at hand.
All exercises were performed with a weight of 8-12RM (meaning the subjects failed after 8-12 reps) and a rest interval of 90 to 120 seconds between sets and exercises. The training resistance was increased by 5-10% for the next session when subjects were able to perform more than 12 repetitions in all sets of an exercise.
Remember? A 2012 study by Robins et al. suggested that experienced strength trainees need 8, not 4 or 1 set for legs | more
What's different to previous studies? As previously mentioned this is the first study to compare three set-ranges (1, 3, 5 sets) over a long study period. Accordingly, it's not necessarily surprising that the results of the study at hand stand in conflict to studies by Bottaro et al. (2011) ot Hanssen et al. (2013),  which found no significant difference between one and three-set training protocols. On the other hand, the results are partly in line with those of a 2007 study by Rønnestad, et al. who found benefits of three sets, albeit only for the legs. Overall, the total training volume (number of exercise) and study length of the previous studies was yet lower than that of the study at hand. This suggests that it may be the 2x higher volume difference between 4x1 vs 4x3 as in Ronnestad et al. (2007) and 8x1 vs. 8x3 vs. 8x5 in the study at hand that may have made all the difference.
The scientists made sure that all subjects participated in at least 95% of the training sessions (missed no more than four sessions). All training sessions were monitored by an experienced investigator and the subjects were not allowed to perform aerobic or flexibility exercises during the six month training period. What the scientists found was:
  • Figure 2: Changes in body composition (top) and bench press & lat pulldown 5RM (Radelli. 2014).
    All training groups recorded significant strength gains for bench press (BP), front lat pull down (LPD), shoulder press (SP) and leg press (LP) (p≤0.05) exercises, but the 5RM (maximal weight the subjects could lift 5 times) increased significantly more for both bench presses and lat pulldowns in the 5- SETS compared to the other training groups (p ≤ 0.05). 
  • In the 20RM (maximal weight with 20 reps) bench press tests both the 3- and 5-SETS groups saw significantly greater strength increases than the 1- SET group, with the 5-SETS protocol also producing significantly greater increases in strength, than the 3-SETS group (p≤0.05). 
  • In the 20RM leg press tests only the 5-SETS protocol yielded significantly greater strength gains than the 1-SET protocol. 
  • For the 3- and 5-SETS groups the scientists also observed significant increases in elbow flexor muscle (biceps) thickness (MT) with the 5-SETS increase being significantly greater than the other two training groups (p≤0.05). 
In spite of these differences, all training groups decreased percent body fat, increased fat free mass and vertical jump ability (p≤0.05), with no differences between groups. In spite of that, "the results demonstrate a dose response for the number of sets per exercise and a superiority of multiple sets compared to a single set per exercise for strength gains, muscle endurance and upper arm muscle hypertrophy" (Radelli. 2014).
Example Split-Routine for 2015: If you still need inspi- ration here is an example of how you could train using the 5 sets per exercise principle in a 2-day + cardio split in 2015:
(Mo) Push day: Squat, bench press, military press, nose breaker, calf raises
(We) HIIT day 10x45sec sprinting or cycling at maximal velocity, 2 min walking / slow cycling
(Fr) Pull day: Pull up, DB row, biceps curl, stiff legged deadlift, abs.
Same procedure as in the study at hand, 90-120s rests between sets, 8-12RM (to failure).
Bottom line: If we go solely by the results of the study at hand, it would appear prudent to add a set or two to your training regimen. In view of the fact that most of you will probably be training according to a body-part split, I doubt that you will be doing significantly less than 5 sets for any of your muscle groups, anyway. In view of the absence of beneficial effects on the body composition and considering the fact that the arms, of all muscle groups, were the only ones that grew significantly, it's still questionable how beneficial a volume increase in 2015 would be.

As a SuppVersity reader you will also be aware that previous studies showed that a higher volume training is beneficial for the legs ("8 sets of squats outperform 1 and 4 sets" | read more). This result was yet observed in highly trained individuals and stands in contrast to the recent revelation that you can "Cut the Volume, Still Make the Gains!" (read more). I would thus suggest you keep that in mind, when you plan your 2015 workout routine. 5 sets per body part!? Fine! 10 sets for legs? Fine! But four exercises à 5 reps for chest? Madness! Comment on Facebook!
References:
  • Bottaro, M., et al. "Resistance training for strength and muscle thickness: effect of number of sets and muscle group trained." Science & Sports 26.5 (2011): 259-264.
  • Hanssen, K. E., et al. "The effect of strength training volume on satellite cells, myogenic regulatory factors, and growth factors." Scandinavian journal of medicine & science in sports 23.6 (2013): 728-739.
  • Radaelli, Regis; Fleck, Steven J.; Leite, Thalita; Leite, Richard Diego; Pinto, Ronei S.; Fernandes, Liliam; Simão, Roberto. "Dose Response of 1, 3 and 5 Sets of Resistance Exercise on Strength, Local Muscular Endurance and Hypertrophy." Journal of Strength & Conditioning Research: Post Acceptance: December 24, 2014. doi: 10.1519/JSC.0000000000000758
  • Rønnestad, Bent R., et al. "Dissimilar effects of one-and three-set strength training on strength and muscle mass gains in upper and lower body in untrained subjects." The Journal of Strength & Conditioning Research 21.1 (2007): 157-163.

Forskolin: Friend or Foe? Stories and Studies About Fat Loss, Lean Gains, Topical Cellulite Treatment, Testosterone, Cancer, Hepatotoxicity, Drug Interactions & More

There is a single human study that would suggest that forskolin would make you get closer to this classic physique w/out tons of salad (who said that's necessary anyway?).
Since Maxim asked in one of his more recent comments about the usefulness and/or downsides of forskolin, I dediced to dedicate this Sunday (finally again?) to answering a user question and am going to briefly sum up some older and the few novel findings on forskolin I am aware of.

For those of you who find that boring: Don't blame Maxim alone, another reason for this decision was that I have seen discussions on forskolin resurface elsewhere on the Internet. By the way, I write re-surfaced, because forskolin has once been hailed as a testbooster and fat loss adjuvant, but as the prices increased and people came out with faked or low-quality products that did not yield results, the market collapsed.

What is forskolin and where does it originate from?

As usually there is more than a single answer to this question. The most straight forward general ones are probably (a) it is a white to white with yellow cast powder, or (b) a labdane diterpenoid with antihypertensive, positive inotropic, platelet aggregation inhibitory and adenylate cyclase activating properties. Moreover, forskolin is able to activate the adenylate cyclase and thus increase the intracellular cyclic AMP levels in most tissues and cells. And hat  it's called forskolin, because it is derived from the Indiant plan Coleus forskohlii is probably something 99% of you knew already.

The reason I suppose that Maxim got interested in it, is that it is commonly used in cell studies to raise the levels of cyclic AMP (cAMP; cf. Alasbahi. 2012) and did a pretty impressive job in the recently discussed PGC-1a study. On the other hand, it did also increase the expression of the aromatase enzyme in the Yang study mentioned in the "Natural Sildenafil & Testosterone Alternative" post on which Maxim replied with the initially mentioned comment.

"Wait, wasn't it supposed to be a testbooster and now it also inhibits myostatin and increases estrogen? What does this stuff not do?" - Well, forskolin is, above all, a cAMP modulator

Forskolins chemical structure. Sometimes it's also referred to as Colforsin; 7-beta-acetoxy-8, 13-epoxy-1-alpha, 6-beta, 9-alpha-trihydroxylabd-14-en-11-one; or Coleonol (img. from Sigma-Aldrich's product database)
I know that sounds confusing, but in essence forskolin does nothing but increasing cAMP levels in almost all types of cells. cAMP a breakdown product of ATP (=> cAMP => AMP) in turn is one of those molecules which exert most their effects as intracellular signal transducer. In that, it is involved in the activation of protein kinases and regulates the effects of adrenaline and glucagon. It also modulates the calcium channels and contributes to growth hormone release; unfortunately, cAMP has also been implicated in the proliferation of not very beneficial cell growth aka cancer. The same ion-flux mediation has recently been implicated in the etiology of ADHD, as well (Arnsten. 2012).

Still, it's not all about c-AMP. Probably cAMP unrelated downsides of coleus forkohlii are for example:
  • forskolin induces hepatic CYP2C enzymes and coleus forskohlii extract and thus attenuates the anticoagulant action of warfarin. (Yokotan. 2012) 
  • even more than isolated forskolin, coleus forskohlii  messes with the hepatic enzyme cascade (P450) and has even been shown to be hepatoxic in a study published in the July issue of the Journal of Toxicology (Virgona. 2012)
On the other hand there are a handful of benefits, e.g.
  • Figure 1: Effects of 12 weeks on 2x250mg (10%) forskolin on testosterone (free and total) and lean & fat mass (Godard. 2005)
    In a 2005 study (Godard. 2005), which caused quite a stir in the health and fitness community back then, Godard et al. observed profound beneficial effects of testosterone and body composition (cf. figure 1) after the ingestion of 2x250mg of a 10% standardized forskolin (Forslean).

    Now, the unfortunate truth is that the15 subjects (average age, BMI, and body fat percent were 24.4 +/- 5.9 years, 32.5 +/- 4.1 kg/m2 , and 35.2 +/- 8.3%) who had been randomized to the active arm of the study, and the 15 participants in the placebo arm (28.7 +/- 8.6 years, 32.6 +/- 3.8 kg/m2 , and 35.0 +/- 7.3%) were non-active sedentary overweight/obese (BMI 26 kg/m2 or more) individuals. Add the funding by Sabinsa (Forslean producer) to the equation and decide for yourself how relevant you think the results are going to be for you...
  • In several in-vitro studies, forskolin has been used as a positive control to compare the effects of other compounds on the testosterone release in leydig cells. Lin et al. for example used it in 2001 as a comparison for lactate and found a ~3x increase in testosterone release in incubated leydig cells (Lin. 2001). A similar study by Yu et al. showed that the addition of green tea catechins lead to an additional stimulation of forskolin induced testosterone production in cell cultures (Yu. 2010).
  • Figure 2: Results of 12-week intervention w/ forskolin containing topical cream (Roure. 2011)
    As part of a topical cosmetic slimming product combining tetrahydroxypropyl ethylenediamine, caffeine, carnitine, retinol and, obviously, forskolin it has shown some promise as a topical anti-cellulite and toning agent (Roure. 2011). The clinical study was however financed by Johnson & Johnson and I am not sure how much of the effects were actually brought about by forskolin (the placebo was a basic gel with the same texture containing mainly water, gelifying and preservative systems). So take the data in figure 2 with a grain of salt, ladies - I bet 12 weeks on this product are not going to be exactly inexpensive.
    • The administration of forskolin in conjunction with rutin (the glycoside between the flavonol quercetin and the disaccharide rutinose), vitamin B1 & B2 in a 2010 study by Pescosolido et. al. lead to a significant reduction in intra-ocular pressure in 15 glaucoma patients after 40 days (Pescosolido. 2010). Similar results were observed in a 2012 study for forskolin and rutin alone (Vetrugno. 2012)
    • An in-vitro study by Cristobal et al. provides first evidence for the ability of forskolin to restore PPA2 in acute myeloid leukemia. That would make it a potential candidate for the treatment of this type of cancer, but to my knowledge there is as of yet not even a rodent study that would support these in-vitro results. Moreover, previous studies have suggested that Forskolin may even favor the proliferation of other types of leukemia (Kobayashi. 1994)
        Time to weigh the "established" benefits and downsides

        Figure 3: Effect of different doses of forskolin with and w/out epinephrine on FFA release from rat adipocytes - watch out this is from yet another in-vitro study with rodent cells (Litosch. 1982)
         In view of the fact that the aforementioned study by Godard is the only human study is only backed up by in-vitro data from rodent studies (Litosch. 1982, cf. figure 3), the fat loss benefits are as  Jeukendrup et al. point out in their 2011 review of purported fat burners...
        "[...] promising, there is [yet] only one study at the present time and more work is required before forskolin can be recommended as a fat metabolism-enhancing substance." (Jeukendrup. 2011)
        If you add to this the host of wanted and unwanted, known and unknown side effects that occur in response to the coleus foskohlii induced cytochrome P450 modulation (e.g. the mice in the aforementioned study by Virgona lost some visceral fat, but the costs were increased fat deposition in the liver and elevated transaminase levels).

        With the questionable "fat loss" benefits (remember stress is also a powerful lypolitic and the problem is not to get the fat out of the cell, but rather to burn it), and the almost non-existant human data on the purported testosterone boosting effects, this should be reason enough not to buy more than one bottle for a test-run. After which I highly suggest to do some lab work to see if whatever good or bad you believe you are feeling is an actual boost in T (check T-levels) or hepatic side effects (check ALT, AST & ALP).

        Note (update in response to comments): As far as the hepatoxicity is concerned the suggested dosage of 2x 250mg coleus forskholii most supplements come with may be higher than the medium dose in the study by Virgona, but is still probably "liver save" if you double dose on that, you are however landing in the no-man's land (=not tested for) gray zone between the medium dosage and the "danger zone" of  ~49mg/kg per day (human dose equivalent) that was tested in the study. Don't freak out, if you did that in the past, the levels return to normal afterwards and temporarily elevated ALT + AST or ALP levels do not necessarily mean that your liver is whacked forever ;-)

        References:
        • Alasbahi RH, Melzig MF. Forskolin and derivatives as tools for studying the role of cAMP. Pharmazie. 2012 Jan;67(1):5-13.
        • Arnsten AF, Jin LE. Guanfacine for the treatment of cognitive disorders: a century of discoveries at Yale. Yale J Biol Med. 2012 Mar;85(1):45-58. Epub 2012 Mar 29.
        • Godard MP, Johnson BA, Richmond SR. Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men. Obes Res. 2005 Aug;13(8):1335-43. 
        • Jeukendrup AE, Randell R. Fat burners: nutrition supplements that increase fat metabolism. Obes Rev. 2011 Oct;12(10):841-51. 
        • Kobayashi K, Nishikawa M, Omay SB, Toyoda H, Deguchi K, Shirakawa S. Forskolin potentiates G-CSF-induced proliferation of a murine myeloblastic leukemia cell line. Leuk Res. 1994 Feb;18(2):111-7.
        • Lin H, Wang SW, Wang RY, Wang PS. Stimulatory effect of lactate on testosterone production by rat Leydig cells. J Cell Biochem. 2001 Jun 26-Jul 25;83(1):147-54.
        • Pescosolido N, Librando A. Oral administration of an association of forskolin, rutin and vitamins B1 and B2 potentiates the hypotonising effects of pharmacological treatments in POAG patients. Clin Ter. 2010;161(3):e81-5. 
        • Roure R, Oddos T, Rossi A, Vial F, Bertin C. Evaluation of the efficacy of a topical cosmetic slimming product combining tetrahydroxypropyl ethylenediamine, caffeine, carnitine, forskolin and retinol, In vitro, ex vivo and in vivo studies. Int J Cosmet Sci. 2011 Dec;33(6):519-26.
        • Vetrugno M, Uva MG, Russo V, Iester M, Ciancaglini M, Brusini P, Centofanti M, Rossetti LM. Oral administration of forskolin and rutin contributes to intraocular pressure control in primary open angle glaucoma patients under maximum tolerated medical therapy. J Ocul Pharmacol Ther. 2012 Oct;28(5):536-41.
        • Virgona N, Taki Y, Yamada S, Umegaki K. Dietary Coleus forskohlii extract generates dose-related hepatotoxicity in mice. J Appl Toxicol. 2012 Jun 22.
        • Yokotani K, Chiba T, Sato Y, Taki Y, Yamada S, Shinozuka K, Murata M, Umegaki K. Hepatic cytochrome P450 mediates interaction between warfarin and Coleus forskohlii extract in vivo and in vitro. J Pharm Pharmacol. 2012 Dec;64(12):1793-801.
        • Yu PL, Pu HF, Chen SY, Wang SW, Wang PS. Effects of catechin, epicatechin and epigallocatechin gallate on testosterone production in rat leydig cells. J Cell Biochem. 2010 May 15;110(2):333-42.

        22g High EAA (6g) Protein + 36g CHO Pre- / Intra-Workout Boost Fat Oxidation & PWO Resting(!) Energy Expenditure

        I don't doubt that you can do that, too!
        It does sound awkward: If you mix Twinlab: Amino Fuel (22 g protein - 6 g essential amino acids | L-phenylalanine: 633 mg; Lvaline: 781 mg; L-tryptophan: 133 mg; L-threonine: 679 mg; L-isoleucine: 565 mg; L-methionine: 292 mg, L-histidine: 282 mg; L-leucine: 1350 mg; L-lysine: 1449 mg) with a regular  sports recovery drink that contains 36g of simple sugar, down half of the resulting 800ml serving of whatever you want to call this mix immediately before your workout and consume the rest during the rest periods between sets, this will have measurable effects on your resting energy expenditure and fat oxidation.

        From long-term to short time effects

        At first, it does questionably sound counter-intuitive that the ingestion of an EAA + carbohydrate mixture before / during would increase the resting energy expenditure and rate of fatty acid oxidation after your workout. On the other hand, if you think about the long-term effects of corresponding supplement regimen, you don't have to look far, to find evidence that they can promote both, muscle gain and fat loss (Bird. 2006).
        You can learn more about protein intake at the SuppVersity

        Are You Protein Wheysting?

        Cod protein for recovery

        Protein requ. of athletes

        High EAA protein for fat loss

        Fast vs. slow protein

        Too much ado about protein?
        Kyle J. Hackney, Andrew R. Kelleher, and Lori L. Ploutz-Snyder from the Syracuse University speculated that the highly beneficial changes in body composition Bird et al. observed in their study participants over the course of a 12-week strength training + EAA & CHO supplementation that after "[t]hese adaptations may be related to the acute energy expenditure and substrate utilization responses in the postexercise period." (Hackney. 2013)
        Figure 1: The changes in body composition (in kg) in response to 12 weeks of resistance training + placebo, CHO, EAA or CHO + EAA supplementation in 2006 study by Bird et al. "inspired" Hackney et al.
        Against that background, it was only logical to conduct a study to examine how multiple bouts of resistance exercise with and without the strategically timed intake of amino acids affect the resting energy expenditure (REE) and respiratory exchange ratio (RER). The results could after all explain if the long/er) term effects on body composition that have been observed in previous studies using chronic training and supplementation regimen are maybe nothing but necessary consequences of repeated acute increases in REE or decreases in RER (you hopefully remember that a decrease in the respiratory exchange ratio signifies an increase in fatty acid oxidation).

        Experimental design and results

        To this ends, the researchers recruited 10 young (mean age: 23.4y) recreationally trained male participants. All of them had been participating in general resistance training exercise for a minimum of 3 days per week for at least 6 months.
        Figure 2: Changes in resting energy expenditure (kcal/day) and comparison of training volume in 58g CHO (black bars) and EAA + CHO (white bars) trials (Hackney. 2013).
        As you can see in Figure 2, Hackney et al.'s original hypothesis that "intake of amino acids with each resistance exercise session would lead to greater perturbations of REE and RER" (Hackney. 2013) does unquestionably hold for this population of average (rookie) gymrats.

        Whether the scientists "main finding" (Hackney. 2013), i.e. the 3.61% increase in resting energy expenditure (REE) will be similarly pronounced in advanced trainees is yet as questionable as the real-world effects of this artificial value. Despite the fact that Hackney et al. are right, when they say that our resting energy expenditure "represents the largest component of [our] total daily energy expenditure (60–85%) and has been implicated as a major contributor to overall body mass management " (Hackney. 2013), I am not sure how "major" an increase of only 66kcal per day actually is... I mean,  if this pathetic increase in resting energy expenditure was the actual driving force we would need almost 100 days to shed a hilarious pound of body fat (note: the reason I use the flawed 3,500kcal = 1lbs of fat rule of thumb here is that the whole REE calculations would be pointless if you didn't put at least some faith into the "energy in vs. energy out" hypothesis of weight loss - right?)
        SuppVersity Suggested Read: "Fat Loss Principles That Work: 10g+ of EAAs W/ Every Meal. Do Energetic Costs of Protein Synthesis Trigger This Effect?" |  read more
        Bottom line: It stands out of question that your training success can benefit from a high EAA protein source and some carbs you consume before and during the exercise session. Whether the fat loss benefits are actually brought about by the marginally increased resting energy expenditure (REE) is yet something I doubt - it certainly helps fat loss, but clearly isn't its main motor.

        Don't get me wrong, this does not imply that you will benefit from this type of "peri-workout" supplementation. And let's be honest, the end most of you probably don't care about the exact underlying mechanisms, as long as your body composition keeps improving, right?
        References:
        • Bird, S. P., Tarpenning, K. M., & Marino, F. E. (2006). Independent and combined effects of liquid carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations following resistance training in untrained men. European journal of applied physiology, 97(2), 225-238.
        • Hackney, K. J., Kelleher, A. R., & Ploutz-Snyder, L. L. (2013). Amino Acid-Carbohydrate Intake Combined with Multiple Bouts of Resistance Exercise Increases Resting Energy Expenditure. ISRN Nutrition, 2013.

        3g Taurine Improve Post-Workout Glycogen Resynthesis, Protect the Testes of Doping Sinners & Battles Alzheimer's

        Taurine - A useful supplement for chemical, natural athletes and even sedentary slobs who are afraid of diabetes.
        Taurine, or 2-aminoethanesulfonic acid, as Wikipedia says, is an organic acid widely distributed in animal tissues. It is a major constituent of bile and can be found in the large intestine, and accounts for up to 0.1% of total human body weight. That does not sound like much, but taurine has many fundamental biological roles, such as conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling. It is essential for cardiovascular function, and development and function of skeletal muscle, the retina, and the central nervous system and you were thus probably not too surprised, when you've recently read on the SuppVersity Facebook Page that taurine may help with Alzheimer's disease.
        You can learn more about taurine & other amino acids at the SuppVersity

        Taurine Pumps Up Strength & Recovery?

        Taurine Improves Insulin + Glucose Metabolism

        Taurine ➲ 180% Testosterone Increase

        Taurine + BCAA Work Hand in Hand

        43% Reduced Performance W/ BCAAs

        BCAA Neurotransmitter Depletion
        In the corresponding paper that was published only recently in the ScientificReports on Nature.com Kim et al. report that orally administered taurine via drinking water rescued the cognitive deficits in a standard rodent model of Alzheimer's (APP/PS1 mice) and brought them back up to age-matching wild-type mice.
        Figure 1: Improvement in spatial and hippocampal learning behaviours in taurine-treated transgenic mice. 7-month old wild-type (Wt) and agematched APP/PS1 transgenic (Tg) male mice were orally administered water or taurine (1,000 mg/kg/day) for 6 weeks (n 5 8–10 per group). After 6 weeks, behavioural tests were administered to the 8.5-month old mice. (Left) Y-maze. Average alternation (%) of each group of mice was calculated. (Right) Passive avoidance. Average latency time in seconds for each group of mice was measured (Kim. 2014).
        That's unquestionably impressive, but what's more impressive is that this is by far not the first study to report that taurine exhibits a plethora of physiological functions in the central nervous system.
        But taurine gives me diarrhea! If it does try taking it with a meal that will greatly reduce the risk of having to rush to the toilette and should not reduce the physiological benefits significantly. At least for the muscular effects its unlikely that it will matter at all. For the beneficial effects on the brain, it may be necessary to achieve higher serum peak levels. In view of the fact that the rodents in the aforementioned study by Menzie et al. received the taurine in the drinking water, even this is yet unlikely. If the taurine "goes right through", though, it's certainly not going to help you ;-)
        In a recent review in the scientific journal Amino Acids review, Janet Menzie et al. describe the mode of action of taurine and its clinical application in the neurological diseases: Alzheimer’s disease, Parkinson’s disease and Huntington’s disease and conclude that taurine...
        "[...] functions through multiple neuroprotective mechanisms: regulation of cellular osmolarity , anti-oxidant, neuromodulator of GABAergic transmission, maintenance of calcium homeostasis, inhibition of glutamate excitotoxicity, attenuation of endoplasmic reticulum stress, modulation of mitochondrial pore permeability, downregulation of a range of proapoptotic proteins while upregulating anti-apoptotic proteins and downregulation of inflammatory mediators." (Menzie. 2014)
        Moroever, Menzie et al. believe that there is "strong evidence" of the existence of a specific taurine receptor, which is activated exclusively by taurine, but not by structurally similar amino acids such as glutamate, GABA and glycine and could be responsible for many of the beneficial effects taurine exerts in the context of central nervous system disorders. More specifically existing evidence clearly suggests protective effects in Alzheimer’s, Parkinson and Huntington diseases. Three pathologies that share a number of broad mechanisms: Oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium imbalance, inflammatory changes apoptosis - and *tadaa* a reduced level of (Arai. 1985; Alom. 1991; Molina. 1997).

        Enough of the health stuff, what about the post-workout goodness?

        I know, as long as we are healthy we don't really care about debilitating central nervous system disorders... well, ok. I will spare you my moral pointing finger and get straight to the similarly unsurprising results of a recent study from the University of Tokyo. A study which clearly indicates that the provision of taurine after workouts can lead to a significant enhancement of the already elevated glycogen synthesis after your workouts.
        Figure 2: Muscle and liver glycogen and serum free fatty acids (FFA) before and after the workout (Takahashi. 2014).
        In two rodent studies, the Japanese researchers tested whether the oral administered of taurine  at a dosage of 0.5 g/kg body weight (for human beings that's 0.04g/kg or approximately 3g total | the SuppVersity suggested dose from previous articles, by the way) immediately after treadmill running at 25 m/ min for 90 min would alter the metabolic response and glycogen synthesis after workouts when it was (A) administered alone or (B) as part of a glucose solution containing taurine and glucose at a ratio of 1:2 - in this case 0.5g/kg taurine and 1.0g/kg glucose.
        Figure 3: AUC for glucose after for 60min and 120min after the ingestion of the taurine + glucose solution. As the data indicates taurine helped to "clear" the sugar from the blood stream (Takahashi. 2014).
        As the scientists point out, their "results show that post-exercise taurine administration enhances glycogen repletion in skeletal muscle" (Takahashi. 2014). The underling cause, however, is still speculative. Takahashi et al. believe that it is triggered by
        1. Figure 4: Changes in general oxidative damage (TBARs), protein damage and exercise performance in response to taurine vs. placebo vs. bet alanine supplementation; expressed relative to untrained control (Dawson. 2002).
          an acceleration of glucose uptake, and
        2. an increase in fat oxidation
        of which the latter will have a carbohydrate sparing effect and will thus leave a higher amount of carbs for glycogen repletion. In conjunction with previously established benefits of taurine, such as
        • the attenuation of exercise-induced DNA damage during workouts (young men | Zhang. 2004),
        • the amelioration of cytotoxic (cell damaging) effects of exercise (rodents | Dawson. 2002),
        • an increase in exercise performance (specifically endurance ex. | Dawson. 2002; Miyazaki. 2004),
        • additional effects on the benefits of BCAA intake for the delayed-onset muscle soreness and muscle damage induced by high-intensity eccentric exercise (Ra. 2013),
        • an improvement in osmoregulation (water balance) of the muscle (Cuisinier. 2002), and
        • decreases in oxidative stress during eccentric exercises (Silva. 2011)
        The optimal dosing for performance increments, by the way, is between 1.2-6.0g for 2 weeks (other timing has not been tested, so it's possible that one week will suffice, too). That's at least what the only hitherto published study that investigated the effects of different doses of taurine as a means to improve the endurance performance (Miyazaki. 2004). If you want the nutrient partitioning effects, though, you would have to consume CHO + taurine after the workout - 3g of taurine should suffice. Judged by the hitherto published studies this should automatically help you to increase your workout performance after 2 weeks (the beneficial effects will, just as it is the case for creatine, accumulate until the levels are saturated).

        And there are more benefits - health benefits, for juicers and non-juicers

        The former, i.e. the juicers will probably be happy to hear that taurine does not just have liver protective effects (Miyazaki. 2005), but will also reverse the nandrolone decanoate induced perturbations in sperm characteristics, normalize the serum testosterone level, and restore the activities of the key steroidogenic enzymes in rodents that are treated with nandrolone and taurine (at a dosage equivalent to only 1.3g/day | Ahmed. 2014).

        In spite of the fact that the administration of taurine did also prevent the nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects, I would like to point out that this article is not intended as an incentive for nandrolone doping.
        While taurine is not made from the sperm of Belgian Blues it may still boost your testosterone levels - whether that's going to be by 140% as in this study is questionable, though.
        From performance to health doping: If you are not into "natural performance enhances" and don't care about the direct performance increases, reduced oxidative damage and increases in glycogen repletion during workouts. I would recommend you reread the previous SuppVersity article about the testosterone boosting effects of taurine, it's ability to improve your strength and recovery during and after resistance training sessions, as well as it's ability to improve your glucose metabolism (Franconi. 2006; Carneiro. 2009), to increase your glucose sensitivity (Han. 2004; Nakaya. 2000), to prevent insulin resistance in hyperglycemic states (Haber. 2003), to prevent the development of hypertension as a result of fructose overfeeding (Rahman. 2011), to prevent the cardiac damage due to iron overload (Oudit. 2004), to protect you from the kidney damaging assault of chemotherapy (Saad. 2010), and god knows which benefits I have simply forgotten in the aforementioned list | Comment of Facebook!
        References:
        • Ahmed, Maha AE. "Amelioration of Nandrolone Decanoate-Induced Testicular and Sperm Toxicity in Rats by Taurine: Effects on Steroidogenesis, Redox and Inflammatory Cascades, and Intrinsic Apoptotic Pathway." Toxicology and Applied Pharmacology (2014).
        • Alom, J., et al. "Cerebrospinal fluid taurine in Alzheimer's disease." Annals of neurology 30.5 (1991): 735-735.
        • Arai, Heii, et al. "A preliminary study of free amino acids in the postmorten temporal cortex from Alzheimer-type dementia patients." Neurobiology of aging 5.4 (1985): 319-321. 
        • Carneiro, Everardo M., et al. "Taurine supplementation modulates glucose homeostasis and islet function." The Journal of nutritional biochemistry 20.7 (2009): 503-511.
        • Cuisinier, Claire, et al. "Role of taurine in osmoregulation during endurance exercise." European journal of applied physiology 87.6 (2002): 489-495.
        • Dawson Jr, R., et al. "The cytoprotective role of taurine in exercise-induced muscle injury." Amino acids 22.4 (2002): 309-324. 
        • Franconi, Flavia, et al. "Taurine supplementation and diabetes mellitus." Current Opinion in Clinical Nutrition & Metabolic Care 9.1 (2006): 32-36.
        • Haber, C. Andrew, et al. "N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress." American Journal of Physiology-Endocrinology and Metabolism 285.4 (2003): E744-E753.
        • Han, Jin, et al. "Taurine increases glucose sensitivity of UCP2-overexpressing β-cells by ameliorating mitochondrial metabolism." American Journal of Physiology-Endocrinology and Metabolism 287.5 (2004): E1008-E1018. 
        • Kim, Hye Yun, et al. "Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease." Scientific Reports 4 (2014).
        • Menzie, Janet, et al. "Taurine and central nervous system disorders." Amino acids 46.1 (2014): 31-46.
        • Miyazaki, T., et al. "Optimal and effective oral dose of taurine to prolong exercise performance in rat." Amino Acids 27.3-4 (2004): 291-298.
        • Miyazaki, Teruo, et al. "Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis." Journal of hepatology 43.1 (2005): 117-125.
        • Molina, José A., et al. "Decreased cerebrospinal fluid levels of neutral and basic amino acids in patients with Parkinson's disease." Journal of the neurological sciences 150.2 (1997): 123-127.
        • Nakaya, Yutaka, et al. "Taurine improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous type 2 diabetes." The American journal of clinical nutrition 71.1 (2000): 54-58.
        • Oudit, Gavin Y., et al. "Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model." Circulation 109.15 (2004): 1877-1885.
        • Rahman, Mizanur M., et al. "Taurine prevents hypertension and increases exercise capacity in rats with fructose-induced hypertension." American journal of hypertension 24.5 (2011): 574-581.
        • Saad, Sherif Y., and Ammar C. Al-Rikabi. "Protection effects of taurine supplementation against cisplatin-induced nephrotoxicity in rats." Chemotherapy 48.1 (2010): 42-48.
        • Silva, Luciano A., et al. "Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise." Cell biochemistry and function 29.1 (2011): 43-49. 
        • Takahashi, Yumiko, et al. "Post-exercise taurine administration enhances glycogen repletion in tibialis anterior muscle." The Journal of Physical Fitness and Sports Medicine 3.5 (2014): 531-537.
        • Zhang, M., et al. "Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men." Amino acids 26.2 (2004): 203-207.

        Adelfo Cerame - Road to Wheelchair Nationals '12: From Man Boobs to Striated Pecs - Looking Back at 2011

        Image 1: Looks like Santa's sweet treats
        just ricocheted off Adelfo ;-)
        Although we are amidst the "holiday season" (you know the time of the year where the term off-season gets a whole new meaning ;-), there is one fellow who must obviously have read my blogpost about the not so amiable gifts Santa has in stock for some of us (cf. "Santa is Coming to Town")... judged by the pictures Adelfo has attached to the latest installment of his amazing "Road to Wheelchair Nationals 2012" series, Santa's sweet treats must have had a fat-burning, muscle-building effect on him. Well, at least this is what you could think, if you did not know how much hard work and dedication it cost him to get to where he is now. But, I guess I will let him tell you the whole story...

        Without the "small" things the bigger one's "lose" all their meaning

        It has been 12 months, now, hwen I got my medical release from the doctor... 12 months from the day I was finally able to leave the bed and go back to work... and eventually (!) go back to the gym and train! For almost all of 2010, I was confined to being bed-ridde. With the deep MRSA infected ulcer on my behind, I even had to lie on my belly - unable to sit, unable to move for almost a year.
        Image 1-2: Looking back at December 2010 - All the abdominal fat and the man boobs that I accumulated after 12 months of being bed-ridden… I just hope that I will never have to go through that again.
        That these memories are coming back now, is probably because New Years Eve is approaching. The last days of a year, where I have made a habit of reflecting on the little things that we usually take for granted. Looking back, none of this things, like being able to go to the grocery store, running errands or doing what I love the most, which obviously is going to the gym, was completely out of reach, back in 2010. Isn't it amazing how we always have to lose something until we appreciate its value?
        Think about it, wouldn't  "Live life… cherish every moment of it… and be thankful for even the simplest things that this life has to offer!" be a much better new years resolution than the usual "I want to lose 5 pounds of fat!" or "I want to quit smoking"?
        For me this (fortunately) temporary loss of mobility and, ultimately, freedom, marked another turning point in my live. I have ever since been trying my best to live life to the fullest, improve and better myself spiritually, mentally and physically. I have begun to cherish the simple things in life, constantly reminding myself that they could be taken away from me (and you!) at any moment. And for me, training, of all these little things, is the one I cherish the most: waking up in the morning, getting into the wheelchair and off the the gym to do the one thing I love the most is something I never want to lose again.

        December 2010 to December 2011 = from man boobs to a striated chest

        I don't know if you can empathize with the way I feel, when I look at the pictures from 2010, now. I mean, you know that about 8-6 weeks ago, I decided that I wanted to look "as stage ready as can be" at my 12-week mark (which actually is today) and today, after 12 weeks of intermittent fasting, eating whole "real foods", and training heavy and intense (plus minimal cardio and abdominal exercises) the result are eventually paying off:


        Stats/Measurements
        • Weight: 141 lb.
        • Waist: 29 in
        • Arms (flexed): 17 ¼” in
        • Chest: 41 in
        • BF%: around 8% [at least that’s what my digital calipers read ;-)]
        As you can see from the images from last year… I don’t have the best genetics in the world (I’m more on the endomorphic side of the body types), and I obviously let myself go (not of my choosing, but due to illness), but my point is: No matter what genetic barriers you think or feel you may have, or how far off you’ve let your body and health go, it’s not impossible to achieve the physique of your dreams, with just a little bit of hard work, consistency and balance.

        I guess, I can say I’m pretty satisfied with what I have achieved so far and I’m definitely looking far better than I was at the my last show in April @ the INBF Natural Buckeye. Fortunately for me, I have 13 more weeks to improve on my physique and push myself even harder with my training and dieting.

        3 things I want to try and improve on within the next 13 weeks…
          You think you could use some advice on your  training, diet and supplementation regimen from someone who knows what it takes to build muscle and lose fat? Reach out to Adelfo via Facebook.
        1. Vascularity… I want people to (figuratively ;-) throw up because they’re so disgusted with how many veins are popping out through my skin. Genetics aside, pushing my body-fat level to the lower limit will be the major factor in achieving that.
           
        2. Maintaining muscle mass and maybe even possibly gaining a little bit more… When you are dieting it is already difficult not to lose at least some of the fullness you have in the off-season. Putting on extra mass, on the other hand, is near impossible. Yet, although I have been dieting hard (and with visible results), I have been getting stronger throughout my prep and those strength gains are still coming... and though we all know that there is no 1:1 (or other quantifiable) relation between strength- and size-gains, I would expect to see at least increases in what people call "muscle density" or "maturity", if I can keep upping the weight on all my major lifts.
           
        3. Strength… I just don’t want to look the part, but I also want to be strong also. As I already mentioned, this is the first prep I’ve had, where I have not noticed any decline in strength. I partly ascribe this to the combination of intermittent fasting, raw and whole foods eating, and some of the training methods I have used from Rob Regish’s Blueprint, which have really taken the variety of my workout routines to the next level. And I hope that the latest addition of Anadraulic State, Creapure (creatine monohydrate), D-Pol (d-Aspartic acid) and Recycle (a herbal natural test booster) to my supplement regimen will help me with lifting (increasingly) heavy(-ier) lifts throughout the rest of my contest-prep.
        For the time being, I am on my pre-planned last week of the year famine/detox. Those of you who have followed the whole series will remember that I have been quite skeptical about whether the theoretically sensible (cf. Famine/Detox Episode), yet for any bodybuilder totally counter-intuitive idea from Robb Regish's blueprint would work, but the results I had back in October were so convincing that I decided to make it a staple within every macro-cycle of my training. And now, after 12 weeks of intense training and dieting, the time seems to be right.
        Image 4: Example of a "detox meal"
        Recipe of the week: Spartan Detox Food (example meal) - Eat this (or a similar meal) 3x a day to benefit from a simulated "famine".
        • cucumbers, 
        • a handful of fruits, and 
        • a cup of vegetable juice from Trader Joe’s…
        During my last detox, going extremely low on both calories as well as protein and fat worked quite well for me, but in general Rob's protocol allows for a  maximum of 1,200kcal (for you bigger guys out there) and <50g of protein, fill up the rest with veggies, fruit and a lot of water and you are good to go ;-)
        During the 12 weeks, my body has eventually adapted to my diet and training, and is pretty much in an exhausted state, where gains in size and strength usually stall. In order for me to get my body back into a growth state, I have to shock the whole system by putting my body through a mild state of tissue breakdown with added stress (think of it as triggering the alarm). The mild tissue breakdown and added stress through training during the famine phase will accelerate the entire protein turnover cycle. So basically I want to get my body back into a phase where it feels like I just started lifting weights and training for the very first time in order to be in that growth state again, so that, even at an average calorie intake of roughly 1,400 calories per day, I can still maintain (or hopefully build on) the muscle

        Final thoughts... at least for this year ;-)

        Image 4:  No clue what "intermittent fasting is all about"? I suggest you start with reading the first installments of the Intermittent Thoughts, then (click here for Part 1, Part 2, Part 3 and more)
        If there is one thing that I have really come to appreciate during the past weeks, it is yet neither the famine, nor the detox or the different training techniques I have learned. The one thing, I believe has made the biggest difference was intermittent fasting - all I can say is… I love it! The protocol is simple and easy to follow and I was able to tweak it to my liking by applying other methods that have worked for me in the course of the last 4 years of competing. And the results are mind-boggling. I mean, this has by far been the easiest prep I have ever had! Without being distracted with having to prepare meals, I got to focus more on training, school, and fun stuff like social events. Add to that the amazing results I have (and still am) seeing in the mirror and you know why I believe that “IF” is definitely something I can, and will do long-term.

        I will leave it to that for today, and even the year 2011 and wish all of you a happy and safe New Year! And just in case you happen to be one of those people who like to make "New Year's Resolutions"… Good Luck! Let me know how that works out for ya in a week or two? Hahaha! Just kiddin'! But seriously… You shouldn’t have to wait till New Years to make resolutions and set goals ;-)

        The Overfeeding Overview: High Fat, Carb, Protein, MCTs, Leptin, Testosterone, T3 & Reverse T3 - Get an Overview of the Consequences of Short- & Long-Term Overfeeding

        High fat + high carbohydrate foods like mini doughnuts are exactly what you should not eat on a refeed day, let alone during weeks of bulking.
        Do you want to know what happens during days and weeks of gluttony? How the effects "bulking" will have on your body weight and composition, depending on where those extra calories come from? Have you wondered what the optimal nutrient composition on refeed days may look like. And are you concerned about the potential the health consequences of bulking?

        Yes? In this case, I would suggest you take a closer look at the following overview of the research. An overview that is probably not complete, but it should suffice to provide preliminary answers to the aforementioned questions.
        Learn more about the effects of your diet on your health at the SuppVersity

        Only Whey, Not Soy Works for Wheytloss

        Taste Matters - Role of the Taste Receptors
        Dairy Protein Satiety Shoot-Out: Casein vs. Whey

        How Much Carbs Before Fat is Unhealthy?

        5 Tips to Improve & Maintain Insulin Sensitivity

        Carbohydrate Shortage in Paleo Land
        • The amount of weight you gain depends on your genes: They are not the only determinant. That's for sure. A 1990 study by Bouchard et al. still leaves no doubt that your genes are one of the most important determinants of the quantity of weight you gain.

          In said study the researchers from the Laval University fed 24 sedentary young male twins 1,000kcal extra for six out of seven days of the week. In that the study is not the first to investigate the effects of overfeeding on weight gain in twins. It is yet the first and only one that did this over a period of 100 days and thus with a total energy excess of 84,000 kcal on a diet that contained 50 percent carbohydrate, 35 percent fat, and 15 percent protein.
          Figure 1: Comparison of the weight (left) and visceral fat (right) gains in twin pairs; high correlations were observed for both, but the correlation was significantly more pronounced for the unhealthy visceral fat than it was for the mere body weight (Bouchard. 1990).
          The data in Figure 1 does probably not need any extra explanations. In view of the fact that similar results have also been observed in previous studies like Poehlman et al. (1986), it should be obvious that the difference between the weight (left) and visceral fat (right) two identical twins gained was significantly smaller the difference between one twin from pair A and one twin from pair B. The statistical analysis of body fat and waist circumference data revealed similar correlations which were most significant for the visceral fat mass and the waist hip sizes, i.e. those quantities that predict the ill health effects of weight gain best.

          According to Ukkola, et al. (2001), the genetic differences may partly be mediated by differences in the genetic make-up of ones beta-2 adrenoreceptors with specific variants being associated with greater increases in insulin resistance, body weight and subcutaneous fatness. Other candidates are the cholesterol ester transfer protein (CETP) gene which appears to affect adiposity in response to long-term overfeeding (Terán-García. 2008). Other scientists use similar genetic polymorphisms to explain a general resistance to weight gain during overfeeding via genetically determined variations in nonexercise activity thermogenesis (Vanltallie. 2001).
        • Overfeeding fat, carbohydrate or protein, does it make a difference? Studies that compare isocaloric overfeeding are quasi non-existent. What we do have are studies like the one by Horton et al. (1995) that compared high fat vs. high carbohydrate diets (see Figure 2 for macronutrient composition), where the additional energy came from fat or carbohydrates.

          In the Horton study this was a 50% extra that was added in form of fat or carbohydrates on top of the baseline diets of the normal-weight and obese subjects. A 50% extra that lead to significant weight gain.
          Figure 3: Weight gain (left) and increase in energy expenditure (right) in obese and lean subjects in response to carbohydrate and fat overfeeding (Horton. 1995).
          As you can see in Figure 3, both diets led to a rapid increase in body weight, but the trajectory was different. The main and maybe practically relevant difference, though, was that the rapid increase in water and glycogen in the high carbohydrate group was less resilient weight loss in the post-overfeeding period.
        No! Carbs are not necessarily more fattening in the obese. It's a commonly held prejudice that carbohydrates are more readily coverted to fat and stored in the obese, but a study by Minehira et al. that investigated just this found that there was not just no difference in de novo lipogenesis with carbohydrate overfeeding between lean and obese individuals, there was also no increase in de novo lipogenesis, at all, when the when the obese subjects were overfed with a high carbohydrate diet for one day (Minehira. 2004).
        • Figure 4: Proportion of the energy that was stored as body fat (Horton. 1995).
          If we take a look at the proportion of energy that was stored as body fat in Figure 4, it is obvious why the fat gains lasted longer than the carbohydrate gains. Why? Well, simply because the 14-day overfeeding on fat lead to a significantly higher relative increase in body fat.

          Last but not least, it may also be worth mentioning that the the fat gain in the obese group was 89% and 57% higher in the carbohydrate and fat overfeeding group, respectively. An intriguing result that appears to stand in line with dieting studies, where high fat diets are superior to high carbohydrate diets in the obese, but not in lean individuals.

          What was not different for obese and lean individuals, though, was the the fact that the carbohydrate overfeeding lead to higher gains in lean mass than the fat overfeeding. A result that should remind you of a previously reported study here at the SuppVersity, in which a no fat bulk lead to significantly greater muscle and significantly lower fat gains than a low fat bulk (see "If You Go "High Carb", You Better Go Really High!" | more). Overall, "bulking", i.e. eating more than you need on any mixed diet, has repeatedly been shown to produce significant increases plasma Somatomedin-C/Insulin-like Growth Factor (SM-C/IGF-l) and testosterone concentrations as well as insulin, of which Forbes et al. speculate that they promote the lean mass increases that are particularly pronounced when overfeeding is combined with resistance training.

          In a more nutrient-type specific study b by Dirlewanger that did not focus on the weight gain or anabolism, but on the leptin response and the increase in resting energy expenditure the subjects experienced a significant increase in leptin (+28%) and resting energy only in the high carbohydrate, yet not in the fat overfeeding arm of their study in young, lean individuals (Dirlewanger. 2000). Other studies, without clear distinction between high carb and high fat overfeeding, indicate that fast food like burgers or fries is an effective short-term leptin stimulator, too - at least if it's consumed in a single binge (Kolaczynski,. 1996).
          Figure 5: Energy partitioning in young men upon overfeeding with ~5,000kcal per day - mostly carbohydrates, i.e. 1% protein, 3% fat, and 86% carbohydrate (Acheson. 1988).
          In the short run, like on refeed days, for example, carbohydrate overfeeding has another advantage over fat overfeeding, because it takes roughly 500g of carbohydrates (that's 2,000kcal) before even a single gram of those carbs is converted to fat and potentially, but not necessarily stored as body fat (Acheson. 1988) - at "only" 400kcal extra from carbs for one day there was no net lipogenesis at all (see Figure 5). This result is corroborated by data from McDevitt et al. (2000) who observed that the fat gain with fat overfeeding starts with day 1, while there is a time gap in the increase in body fat with carbohydrate overfeeding (McDevitt. 2000).
        If you consume sugar on a refeed, should you prefer glucose, sucrose of fructose? In view of the fact that I don't suggest you refeed more than 1-2 days and considering the fact that you want to get the majority of your carbs from starches on a true bulks, it does not really matter. In fact, studies show no difference in de novo lipogenesis in 96h overfeeding studies between pure glucose and sucrose, which is a 1:1 combination of fructose or fructose in two studies in lean and obese women by (McDevitt. 2000 & 2001). In the long run, consuming amounts of fructose you could only get by drinking a couple of bottles of coke everyday, will yet not be favorable for your health - even if taking fish oil can blunt the increase in hepatic de novo lipogenesis, it won't blunt the insulin resistance (Faeh. 2005).
        • Figure 6: Schematic representation of the main lipid metabolic pathways affected in skeletal muscle during 4 weeks of fat overfeeding. Genes indicated in white boxes were down-regulated during the dietary study, whereas genes indicated in gray boxes were up-regulated (Meugnier. 2007).
          Fat overfeeding, on the other hand, has been show to favor fat storage not just because the dietary fat can be stored without being converted to triglycerides, but also because metabolic and genomic investigations show that the lipid oxidation rate tends to decrease, and 55 genes in the skeletal muscle were modified.

          Modifications of which Meugnier et al. show that they stimulate the synthesis of triacylglycerol, inhibit lipolysis and reduce the oxidation of fatty acid oxidation, while promoting the development of adipocytes with an excess of only ~550kcal/day from fat per day (see Figure 6).

          Another potential explanation is the change in thyroid hormones, of which the data in Figure 7 from an overfeeding study by Danforth Jr., et al. (1979) tells you that the high protein overfeeding despite a 29.8% lower total energy intake triggered the most, the carbohydrate diet the 2nd most favorable (=in favor of greater energy expenditure) effects on the thyroid hormone.
          Figure 7: Effects of overfeeding with carbohydrates, fats, and protein on thyroid hormones (Danforth, Jr. 1979).
          Accordingly, high protein diets, of which we know for sure that they are the most satiating hypercaloric diets (followed by high carb and high fat | Johnstone. 1996) and have the highest thermogenic effect (see Figure 8) and can help dieters avoid the yoyo effect after a diet (Lejeune. 2005), should have the least negative impact on your physique.
          Figure 8: Estimates thermic effect of carbohydrates fats, protein, and alcohol in % energy of the energy that's ingested in form of the respective nutrients (Joosen. 2006).
          And in fact, Jose Antonio et al. (2014) have recently been able to show that a diet that contains fivefold more protein than the FDA recommends (4.4g/kg | 307g/day) is not just benign but will, in conjunction with exercise, will have significant beneficial effects on the physique of healthy resistant trained men (learn more). Furthermore studies indicate that a high protein content may also ameliorate negative effects such as an increase in intrahepatocellular lipid deposition in humans (Bortolotti. 2009).
        Beware of bulking the way you did in your twenties! It's almost certainly going to make you fat, because studies indicate that age correlates with a decreased increase in energy expenditure in response to overfeeding (Roberts. 1996). Since the difference is particularly pronounced on day 1 of the respective overfeeding period (see Figure on the left), I would also refrain from excessive "refeed days" if I were 60+ years old, like the subjects in the study by Roberts et al. from which I grabbed the graph that displays the energy expenditure on a diet that contained 956kcal extra per day (phase II in this study).
        • Classic overfeeding studies with protein as a single nutrient are yet unfortunately rare. Even less, namely nothing, is known about the effects of ketogenic diets, which is why it's at the moment impossible to tell whether a hypercaloric high fat diet that is devoid of carbs and low enough in protein to actually induce ketosis will have the same negative effects as a high fat diet that still contains 15-30% carbohydrates and some protein.
          Based on the studies we have, it's yet quite certain that the combination of some carbs and a high amount of fat is the most obesogenic variety of "bulking" you could possibly select. Therefore - with the exception of ketogenic diets, where corresponding data is still missing, the rule of thumb is: The more fat in the diet, the more rapid the body fat, but not necessarily the body weight gain.
        • MCT overfeeding is less obesogenic - The reason that rodents that are overfed with medium-chain triglycerides (Geliebter. 1983) and assumable human beings store less fat than on long-chain triglycerides as you will find them in your bacon, sausages, dairy & co is an increase in thermogenesis that has been observed in both rodent and human studies.
          Figure 10: Metabolic rate in healthy men after the ingestion of isocaloric fat meals containing MCTs or long chain triglycerides (Hill. 1989).
          As you can see in Figure 10, this effect does not diminish over time - at least, when only the effect of the infusion of MCTs versus long-chain fatty acids is concerned. In view of the rodent study by Geliebter et al. (1983) and the results of the study by Hill et al. (1989), it appears to be quite obvious that MCTs constitute a valuable addition to hypercaloric diets. The often-heard claim that they cannot be stored as fat is yet misleading - even if they are oxidized in the liver, the increase in available energy will increase the storage of energy from other nutrients. The dream of eating as much as you want without gaining weight does therefore remain a dream - at least for all of us who don't harbor a gene defect that blunts the storage of fat.

          Still, in theory it would appear as if using MCTs in a dieting context makes sense. In reality, studies have shown that using MCTs as a major source of your dietary fats does not lead to significant long-term improvements in  fat or general weight loss - even if 27% of an 800kcal/day starvation diet were pure MCT oil (Yost. 1989).

        Fivefold More Than the FDA Allows: Extreme High Protein Diet (4.4g/kg | 307g/day) Benign & Non-Obesogenic. Plus: Macronutrient Prescription & Changes in Food Quality | more
        Alright, so what's the bottom line, then? I guess, in view of the fact that we still have few studies on high protein overfeeding and no studies on overfeeding on ketogenic diet, a conclusive bottom line cannot be reached, yet. What appears to be true, though is that a diet containing some carbohydrates and a large amounts of fat is the worst choice you can make, when you are bulking.

        A protein and a high(er) carbohydrate, as well as a correspondingly low(er) fat content on the other hand, appear to be the way to go at least in the short run. In the long(er) run, on the other hand, the differences between higher fat and higher carbohydrate overfeeding appears to disappear - albeit with a small, but potentially practically significant difference in terms of the amount of body fat you will gain (see Figure 4) | Comment on Facebook!
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