25g Whey Protein or 10g of EAAs Maximize Post Workout Protein Synthesis Without Additional Carbs

While this probably won't end the debate on whether post-workout carbohydrate intake is a good or a bad thing, a recent review of the literature presented by Steward M. Phillips at the The Summer Meeting of the Nutrition Society (Phillips. 2010) suggests that the addition of carbs to your post-workout shake is at least unnecessary, as long as you have a sufficient amount of leucine and EAAs in it:

The increment in [muscle protein synthesis] MPS is maximally stimulated at a dose of protein of approximately 25 g or 10 g EAA. This rise is based solely on protein consumption and is not augmented by carbohydrate, at least when protein is adequate.

Also, the type of protein is of utmost importance. Phillips recommends whey protein or (please note that it is not whey and EAAs) a blend of EAAs at dosages of 25g and 10g, respectively.

Figure 1: Whole blood leucine concentration (μM) following resistance exercise from subjects who consumed 500 ml fluid skim (low fat) milk and an isonitrogenous and isoenergetic quantity of a soya drink (drawn with data from Wilkinson et al.).

As can be seen from figure 1, even skimmed milk, which is only partially whey, produces a larger increase in whole blood leucine than soy protein (soy is for girls only, anyway ;-) Consequently, you should prefer dairy proteins or whey concentrates, isolates or hydrosolates as your post workout protein sources.

Skipping Breakfast Makes You Fat, but NOT by Increasing Appetite

You will certainly have heard of the scientifically proven correlation between skipping breakfast and getting obese. At least for children a group led by Tanya VE Kral (Kral. 2010) has now found "Omitting breakfast affected children’s appetite ratings but not their energy intake at subsequent meals." Astonishing as this may sound, the results of their investigation are unequivocal:

There was no significant main effect of breakfast condition on energy intake at lunch (P = 0.36) or throughout the remainder of the day (P = 0.85). There was a significant main effect of breakfast condition (P = 0.04) on total daily energy intake, which indicated that on the day when the subjects did not eat breakfast, they consumed 362 fewer calories over the course of the day than when they did eat breakfast. On the day when no breakfast was served, subjects
indicated that they were significantly hungrier, less full, and could consume more food before lunch than on the day when they did eat breakfast (P , 0.001).

Bottom line, eating less or rather not eating less by not eating at the right time makes children and most probably adults fat. As far as the reasons for this observation are concerned, the researchers speculate that ...

It is possible that children who regularly skip breakfast may show different energy intake patterns throughout the day compared with children who regularly eat breakfast and who may skip breakfast only occasionally. In other words, the long-term effects of skipping breakfast on energy intake may develop over time and may involve learning of new eating patterns.

These eating patterns will of course center around over-eating at night and would thus provide the body with an abundance of energy right when he needs it the least. It stands to reason that this may contribute to obesity, especially in view of the reduction in metabolic rate triggered by skipping breakfast. So, if you are one of those who "simply can't eat something in the morning", a meal replacement shake might be something worth considering.

15-30% Increase in Protein Synthesis if Protein is Ingested After Exercise

What common sense already told us has now been proven again in a scientific study published by the American Society for Nutrition (Pennings. 2010). Protein synthesis is greater if protein is consumed after exercise. And these results hold true for both, young and old.

As a marker of protein synthethis, the scientists investigated the response of exogenous phenylalanine on a 20-g bolus of intrinsically l-[1-¹³C]phenylalanine-labeled protein which was administered either at rest or after exercise:

[...] Muscle protein synthesis rates calculated from the oral tracer were 0.0620 ± 0.0065%/h and 0.0560 ± 0.0039%/h for the rest condition and 0.0719 ± 0.0057%/h and 0.0727 ± 0.0040%/h for the exercise condition in young and elderly men, respectively (age effect: P = 0.62; exercise effect: P < 0.05; interaction of age and exercise: P = 0.52).

So overall, this is a non-negligible increase in the calculated protein synthesis rate by 15% and 28% in the young and old subjects, respectively. It does however not answer the question, whether administration of the same 20g of marked protein right before exercise would not have increased protein synthesis to an even greater extent. Personally, I feel that for people on an everyday exercise regimen keeping protein intake high 24/7 will certainly be the best solution, even if it is just via an occasional protein shake at work (and thus probably "before workout).

L-Citrulline Against Arterial Stiffness

You probably know it from the ingredient list of your pre-workout or amino acid product, l-citrulline. Being a possible precursor of l-arginine it is included in those formulas to increase nitric oxide levels and deliver those "skin bursting pumps" the advertisements brag about.

In a recent study, scientists from Japan (Ochiai. 2010) found that 1 week of l-citrulline supplementation at 5.6g/day effectively reduced arterial stiffness in 15 healthy males:

Compared with the placebo group, baPWV [index of arterial stiffness] was significantly reduced in the l-citrulline group (p<0.01). No significant differences in blood pressure (BP) were found between the two groups, and no correlation was observed between BP and baPWV. The serum nitrogen oxide (NOx, the sum of nitrite plus nitrate) and NO metabolic products were significantly increased only in the l-citrulline group (p<0.05). Plasma citrulline, arginine and the ratio of arginine/asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase (arginine/ADMA ratio) were significantly increased in the l-citrulline group compared with the placebo group (p<0.05, p<0.01, p<0.05, respectively). Moreover, there was a correlation between the increase of plasma arginine and the reduction of baPWV (r=-0.553, p<0.05).

Beyond the reduction in arterial stiffness, these results confirm the hypothesis that l-citrulline effectively increases NO metabolism (probably even more than l-arginine) AND, what's even more important, reduces an endogenous inhibitor of NO synthase, so that more nitric oxide may be produced.

Further Evidence Against Anti-Oxidant Supplementation: Vitamin E + Alpha Lipoic Acid Reduce Skeletal Muscle Mitochondrial Biogenesis

Mass media and supplement companies will make you believe: "It is all about anti-oxidants" - Well, making money these days may in fact be all about anti-oxidants, but at least for athletes supplementing exogenous anti-oxidants may not be so wise as their producers would have us believe.

Yet another recent study on the "beneficial" effects of anti-oxidants on reactive oxygen specimen (ROS) found that, at least for athletes blocking natural increases in ROS may also inhibit the intended adaptive responses:

Consistent with augmentation of skeletal muscle mitochondrial biogenesis and antioxidant defenses, following training there were significant increases in PGC-1α mRNA and protein, COX IV and cytochrome C protein abundance, citrate synthase activity, Nfe2l2 and SOD2 protein (P<0.05). Antioxidant supplementation reduced PGC-1α mRNA, PGC-1α and COX IV protein, and citrate synthase enzyme activity (P<0.05) in both sedentary and exercise-trained rats.

In view of the fact that there are virtually no studies that confirm a beneficial or ergogenic effect of anti-oxidants, specifically vitamin E in athletes or trained human beings, you may be better off keeping your supplemental vitamin E intake within reasonable limits (i.e. ~12mg = 100%RDA).

Want to Lose Fat? Don't Reward Yourself with Food!

At my gym, I see it over and over again: people staring at the calorie counter of the stairmaster, dreaming of the pot of icecream which is already waiting for them in the fridge. Don't be so stupid or you will end up like the "non-responders" in a recent study on exercise-induced weight-loss done by scientists from the University of Leeds (Finlayson. 2010).

The scientists observed 34 sedentary obese males and females who participated in a 12-week supervised exercise intervention prescribed to expend 500 kcal/day, 5 d/week and classified them into responders (losing weight) and non-responders (maintaining or even increasing weight). By this means the scientists identified a certain pattern of increased appetite in high-fat sweet foods in the non-responders:

 Food reward (ratings of liking and wanting, and relative preference by forced choice pairs) for an array of food images was assessed before and after an acute exercise bout. Results. 20 responders and 14 non-responders were identified. R lost 5.2 kg ± 2.4 of total fat mass and NR lost 1.7 kg ± 1.4. After acute exercise, liking for all foods increased in NR compared to no change in R. Furthermore, NR showed an increase in wanting and relative preference for high-fat sweet foods.

While, obviously, many of you may suffer from those "symptoms" the way to get and stay lean is not to give in to those lustrous desires, but to make healthy food choices 24/7 no matter how many calories you think you have left in the gym hours before.

Creatine Prevents Statin Induced Myopathy

In the Observations section of the November issue of Annals of Internal Medicine Shewman & Craig (Shewman. 2010) report beneficial effects of creatine supplementation in patients on statin drugs:

Myopathy scores were significantly higher after the statin-only treatment phase than at baseline but did not differ from baseline after the other treatment phases. Creatine loading plus maintenance creatine therapy prevented myopathy symptoms in 8 of 10 patients receiving statins. After these 8 patients stopped maintenance creatine therapy and developed myopathy symptoms while receiving statins alone, reloading creatine decreased symptoms to baseline levels. Also, increasing the creatine dosage from maintenance to loading diminished myopathy symptoms to baseline levels in 1 patient who developed symptoms 6 days after a statin was added to maintenance creatine therapy. No significant differences in vital signs or laboratory test results were observed.

So, in case you really think you need to continue taking statins, it may be worth investing a few cents into some plain creatine monohydrate to keep side effects at bay.

L-Arginine @5g/Day Reduces Lactate Levels in Male Athletes

While the NO-hype of the last years unquestionably is/was a scam, l-arginine, the amino acid that does not build muscle via increased NO-production, transpires to be ergogenic via very different mechanisms.

Scientists from Iran (Mozezzaneh. 2010) have now found that 5g of supplemental l-arginine significantly decreased the blood lactate levels of athletes (N=30) in the course of a 3 week supplementation period, but failed to induce consecutive or concurrent increases in VO2 max (a direct marker of exercise capacity):

Blood lactate level was significantly decreased in the L-arginine group compared to the placebo one. There was no significant difference between the two groups in VO2max at anaerobic threshold. Only in the L-arginine group, VO2 max at anaerobic threshold was significantly increased. In addition, there was no significant difference in VO2 max at anaerobic threshold for the placebo group.

If you remember the previous news on arginine, you may understand that I will repeat my advice not to flush your good old pre-workout down the toilet. Even if it was just for the cosmetic pump and the decrease in lactic acid, this is probably more than some newer and probably fancier products will provide.

DHT Safer Than Previously Thought: High Blood DHT does not Induce Prostate Cancer

Regular visitors of the SuppVersity will know that the stigmatization of DHT goes without reasonable and conclusive scientific research. In their editorial to the Annals of Internal Medicine Swerloff & Wang (Swerloff. 2010) conclude from the results of more recent studies into the various effects of DHT on different tissues:

In normal men, serum DHT levels are approximately 10% of the serum testosterone levels, whereas intraprostatic DHT levels are much higher than serum levels, with the intraprostatic DHT–testosterone ratio being 7 to 8 (12). Although the authors did not measure DHT levels in
the prostate after DHT administration, Page and coworkers (13) recently reported that prostatic DHT levels did not increase when pharmacologic doses of DHT were administered (Page S. Personal communication.). These findings are consistent with those of Marks and colleagues (12), which demonstrated that administration of testosterone to mildly testosterone-deficient men increased serum testosterone levels but did not increase either prostatic DHT or testosterone concentrations. Thus, it seems that the amplifying 5alpha-reductase system is so efficient in regulating intraprostatic DHT levels that substrate (for example, testosterone) concentrations are limiting only at very low levels. Furthermore, the ability of the 5alpha-reductase system to produce high tissue levels of DHT in organs, such as the prostate, indicates that even high levels of DHT in the blood remain much lower than the levels reached in the prostate and thus have little influence on prostate growth. In contrast, high levels of DHT in the blood will act as a hormone and thus produce real effects in tissues with less dominant testosterone to DHT-amplifying systems, such as muscle, fat, and bone marrow. Although the present study was not adequately powered to definitively answer the question of long-term safety of testosterone use, these data do show that a 10-fold increase in serum DHT levels had no significant effects on prostate size, serum DHT, and International Prostate Symptom Score, suggesting that the modest increases of serum DHT seen after testosterone treatment may not have a clinically significant effect on prostate health.

So after all, this means that

1. you do not have to take Finasterid or other side-effect-loaden bullsh* if you are on TRT
2. you may benefit from the positive effects on libido, alpha-male feeling and probably muscle growth of reasonably elevated DHT-levels without having to worry about your prostate
3. you better not believe every "scientific fact" that is covered in mainstream media

Trigonella foenum graecum Slightly Increases Testosterone, but Fails to Illicit Gains in Lean Body Mass

A recently published study by Colin Willborn et al. (Willborn. 2010) found that supplementation with 500mg of the purported aromatase inhibitor Trigonella foenum graecum did increase total testosterone +6.57% and bioavailable testosterone +12.26%  over an eight week period. Yet, the ingredient that is part of several commercially sold "muscle builders" did not increase lean body mass in thirty resistance-trained men.

Figure 1: Body-fat loss from baseline testing (T1) through Week 8 (T3), mean Delta ± SD.

What it did do, however, was to support a reduction in body fat (-2.0%), beyond the one seen in the placebo group (cf. figure 1). This is particularly interesting, because the hormonal data shows that the extract in fact failed to block aromatization effectively; this may be concluded from the fact, that apart from the rise in testosterone, there was a minor increase in estrogen, as well. In view of the lack of strength gains

No significant changes were detected among groups for Wingate peak or mean power, total body weight, dihydrotestosterone, hemodynamic variables, or clinical safety data.

and the overall safety of the extract, this might be something more geared for the dieters out there than for those of you who are looking for a test booster to build some mass.

1046 ng/dL Increase in Testosterone for 1.5kg Lean Body Mass in 16 Weeks

Before you read on: This was a study done on 112 men aged 65–90 years, so the results are only partly significant in view of the effects of testosterone supplementation on younger men.

In a double-masked 2x3 factorial design the scientists administered testosterone gel (5g/day vs. 10g/day via Leydig cell clamp) and rhGH (0 vs. 3 vs. 5 µg/kg/d) to the subjects who had a mean baseline testosterone level of 493ng/dL. They summarize the results for the testosterone and the testosterone + rhGH groups as follows:

Increases in total testosterone of 1046 ng/dL (95% confidence interval = 1040–1051) and 898 ng/dL (95% confidence interval = 892–904) were necessary to achieve median increases in lean body mass of 1.5 kg and appendicular skeletal muscle mass of 0.8 kg, respectively, which were required to significantly enhance one-repetition maximum strength (≥30%). Co-treatment with rhGH lowered the testosterone levels (quantified using liquid chromatography–tandem mass spectrometry) necessary to reach these lean mass thresholds. 

So, in view of supplement producers boasting with "all natural" products boosting natural testosterone levels by up to 80% , the fact that a 112% boost in testosterone delivered a mediocre increase of 1.5kg in lean mass over 16 weeks should remind you that even with the most effective natural test booster, a sound nutritional regimen and an intense workout plan are a must to see those results in muscle tone and size you are probably striving for.

Combination of Selenium & Vitamin C Effectively Raises Testosterone Levels in Rats

Although this is an older study (Lodhi. 2009), I found it particularly interesting that other than individual supplementation with vitamin C (group II) or selenium (group III), the combined administration (group IV) of 500 mg/L vitamin c in drinking water and 1.5 mg/kg selenium in chow significantly raised the testosterone to cortisol ratio of the rodents (cf. fig 1).

Figure 1: Effect of vitamin C and/or selenium supplementation on testosterone to cortisol ratio

Although it is uncertain if human beings will react similarly, both selenium and vitamin c are major players in the human antioxidant system, which has profound influence on stressors (cortisol) and endocrine function. And a higher testosterone to cortisol ratio (anabolic status) certainly won't hurt your efforts to get fitter, bigger, stronger or healthier - whatever your goals are ;-)

Sebacic Acid, an Ingredient of Castor Oil, Helps with Diabetes

In a recent study, European scientists (Membrez. 2010) found that sebacic acid, a natural ingredient of castor oil improves blood sugar control in a mouse model of diabetes.

The scientists fed their mice a diet containing 1.5% or 15% of sebatic acid (SA) over a period of 6 weeks and found:

After 42 days of supplementation, fasting glycaemia and HbA1c were ∼70 and 25% lower in the SA_15% group compared with the other groups showing a beneficial effect of SA on hyperglycaemia. During OGTT, plasma glucose area under the curve was reduced after SA_15% compared with the other groups. This effect was associated with a tendency for an improved insulin response. In the liver, Pck1 and FBP mRNA were statistically decreased in the SA_15% compared with Ctrl suggesting a reduced hepatic glucose output induced by SA.

While these are certainly encouraging results, it remains questionable whether or not it would be feasible for humans to achieve sufficiently high sebatic acid intake to reap the benefits of this previously ignored constituent of castor oil.

Taurine Effective Against High Fructose Induced Symptoms of the Metabolic Syndrome

Regular visitors of the SuppVersity know about the diverse positive effects of dietary taurine on health, body composition and exercise performance. Now, a recent study by Mesallamy et al. (Mesallamy. 2010) found another good reason for the non fish-eaters among you (fish is particularly high in taurine) some supplemental taurine in your diet / supplement regimens.

Figure 1: Effect of HFD and taurine supplementation on weight gain at days 0 and 35 of feeding.
Each value is expressed in grams. (Mesallamy. 2010. Fig. 1)

The scientists put rats on either a control diet or high fructose diet (HFD), with both groups receiving additional 300 mg/kg/day taurine via intra-peritoneal (i.p.) route for 35 days. While the decrease in body weight gain illustrated in figure 1 is relatively low, the overall effect of taurine on makers of the metabolic syndrome was significant:

Fructose-fed rats showed significantly impaired glucose tolerance, impaired insulin sensitivity,
hypertriglyceridemia, hypercholesterolemia, hyperhomocysteinemia (HHcy), lower total antioxidant capacity (TAC), lower paraoxonase (PON) activity, and higher nitric oxide metabolites (NOx) concentration, when compared to rats fed on control diet. Supplementing the fructose-fed rats with taurine has ameliorated the rise in HOMA by 56%, triglycerides (TGs) by 22.5%, total cholesterol (T-Chol) by 11%, and low density lipoprotein cholesterol (LDL-C) by 21.4%. Taurine also abolished any significant difference of TAC, PON activity and NOx concentration among treated and control groups. TAC positively correlated with PON in both rats fed on the HFD and those received taurine in addition to the HFD.

While the human equivalent dose of the 300mg/kg taurine used in the study is about 100mg for a person weighing 70kg, previous studies on the positive health effects of taurine have used 1.5-3.0g of taurine - and this would also be my suggestion for those of you who have now become interested in the health benefits of this sulfur-amino acid.

Olive Leave Extract Equally Effective at Lowering Blood Pressure as ACE Inhibitor Captopril

For those who read yesterday's news on the negative effect of caffeine on exercise induced blood pressure response, it might be of interest that no more than 500mg of Olive (Olea europaea) leaf extract may well counteract the negative effect of caffeine intake and help with triglyceride levels, as well.

In a double-blind, randomized, parallel and active-controlled clinical study (Susalit. 2010) an international team of scientists found that after a run-in period of 4 weeks continued subsequently by an 8-week treatment period supplementation with Olive (Olea europaea L.) leaf extract (EFLA®943) at 500 mg twice daily was equally effective in reducing blood pressure as the ACE inhibitor Captopril, which was given at the dosage regimen of 12.5 mg twice daily for the first two weeks and (if necessary) at 25 mg twice daily for the rest of the treatment period:

After 8 weeks of treatment, both groups experienced a significant reduction of systolic blood pressure (SBP) as well as diastolic blood pressure (DBP) from baseline; while such reductions were not significantly different between groups. Means of SBP reduction from baseline to the end of study were −11.5 ± 8.5 and −13.7 ± 7.6 mm Hg in Olive and Captopril groups, respectively; and those of DBP were −4.8 ± 5.5 and −6.4 ± 5.2 mm Hg, respectively.

What is even more intriguing is the concomitant reduction in triglyceride level, which was observed exclusively in the Olive, but not in Captopril group.

Figure1: Plasma Triglyceride levels throughout the study in the subgroup with baseline triglyceride level of > 200 mg/dl (Susalit. 2010).

So, if you are on blood pressure medication, you may well consider talking to your doctor if you could test-drive some Olive leaf extract to get off those nasty ACE inhibitors. But beware, I strongly advise against dropping the ACE "cold turkey"! It would rather be wise to reduce the dosage and to simultaneously begin supplementing Olive leaf extract to see how your body reacts.

Caffeine Blunts Exercise Induced Hypotensive Response and Increases Post Exercise Blood Pressure

I told you about the positive effect of caffeine supplementation on the post high intensity interval training fatty acid oxidation, only yesterday. Today, I have to tell you that all that could be a bad idea, if you are prone to hypertension, because, as scientists from Brazil found (Cazé. 2010), the same caffeine that may make you shed some additional grams of fat, will block the hypothensive, i.e. blood pressure lowering effect of exercise and may drive an already high blood pressure into the danger zone:

Seven hypertensive subjects (52.3 +/-3.3 years), being 5 women, accomplished two walk sessions with 40 minutes of duration, in two days of training, having previously ingested CA (4 mg/kg of body weight) or placebo (PL). BP and heart rate were verified previously to the ingestion, after 15, 30, 45, 60 minutes of the ingestion, at rest and with 10, 20 and 30 minutes after exercise. [...] BP mean increased from 124.9/80.9 mmHg before ingestion to 129.4/84.3 mmHg 60 minutes later (p< 0.05). In the recovery period, after 30 minutes of exercise, hypotensive answer was observed in the PL procedure (decrease of 122.6/79.4 mmHg to 115.7/78.6 mmHg), while in the procedure with CA, BP was significantly higher than at rest (increase of 124.9/80.9 mmHg to 136.9/90.9 mmHg, p<0.05).

If you already have blood pressure issues and are exercising in order to get rid of these, it would thus be wise to refrain from caffeine consumption before or in the course of your exercise sessions.

HIIT + Caffeine = Increase in Post Exercise Fat Metabolisation

HIIT and Caffeine have both been highly advocated for fat loss by professionals and personal trainers all over the world. Now, a recent study (Gerber. 2010) by provides clinical evidence for the effectiveness of the combination of both.

Gerber et al. had six participants complete two exercise trials consisting of 30 min of HIIT (20s cycling at 150% VO2max with 40s rest), followed by a time to exhaustion (TTE) test at 150% VO2max with prior ingestion of 5 mg/kg of either caffeine or placebo (Caltrate) in randomised order and found:

During recovery from TTE, plasma glycerol was significantly increased with caffeine (p<0.05), with a similar trend for plasma FFA (p=0.1). VO2 was significantly elevated in the caffeine trial compared to placebo after both HIIT and TTE exercise bouts (p<0.05), and plasma uric acid was significantly higher after caffeine following TTE (p<0.05).

So, after all, "bro-science" sometimes is not far away from "pro-science" and some advice you frequently hear in the gym is actually worth following.

News on the Taurine vs. Beta Alanine Antagonism

Those of you who have been following the SuppVersity for some time, may remember my blogpost on the antagonism of Taurine and Beta Alanine on a cellular level and the possible detrimental effects of high dose Beta Alanine supplementation on Taurine content of muscle fibers. Now, scientists from Australia and the USA have investigated the effect of Taurine and Beta Alanine on mdx mice, which are a model of Duchenne muscular dystrophy. These mice have naturally low levels of Taurine, which further decrease in the process of muscular degeneration and - as one would expect - did benefit from 4 weeks of  3% Taurine supplementation via drinking water. Supplementation with 3% Beta Alanine, on the other hand did not worsen the symptoms, as one might have expected, but "b-alanine supplementation reduced fatigue (p < 0.05) in both control and mdx mice". Furthermore...

Taurine supplementation had no effect on the recovery of the control group, [while] b-alanine supplementation improved recovery in the control mice up to 10 minutes with no significant difference between supplement groups observed after this time.

In view of the fact, that, hopefully, none of you suffer from Duchenne muscular dystrophy, I will probably have to put my previous warning, not to consume Beta Alanine without concurrently supplementing Taurine, into perspective. I do yet stick to my recommendation not to overdo it on the Beta Alanine, if not detrimental, it would at least be a waste of money, because research has shown that after a few weeks of 3-5g Beta Alanine a day, muscle carnosine levels saturate.

Glycogen-Depletion Has no Effect on Selected Marker of Skeletal Muscle Adaptation

In a recently published study, Camera et al. (Camera. 2010) investigated the effect of isolated glycogen depletion on the rpS6 phosphorylation, a process which is closely related to the insulin/insulin-like growth factor (IGF) signalling pathway that is generally believed to be part of the positive adaptation processes of resistance exercise.

By having their subjects perform a unilateral cycling exercise the evening before the test session, the scientists established a "divergent muscle glycogen content that was  higher in the control leg (Norm) than in the Low leg at rest (383 ± 43 vs. 184 ± 14 mmol/kg dry wt; p < 0.05)". Thus, with the "normal" leg, they had an intra-(not inter-)individual reference for the results of the muscle biopsy after the testing protocol. Other than one might suspect, there was yet no difference between the rpS6 phosphorylation in the glycogen-depleted vs. the normal leg, which lead the scientists to conclude:

These results indicate that low muscle glycogen levels fail to suppress phosphorylation of a key component in skeletal muscle translation initiation following high-intensity resistance exercise when protein/carbohydrate supplementation is provided during recovery.

If we assume that the psS6 phosphorylation is in fact an adequate measure of the anabolic response to exercise training, we may further assume that the practice of "training" does not preclude positive adaptations, if proper amounts of nutrients (in the study these were (20 g whey protein + 40
g maltodextrin) are absorbed in the course of the recovery period.

High Protein Diet vs. Insulin Sensitivity - Effective for Sedentary Women, as Well

I think while I do not have to repeat the importance of a healthy diet, especially the women among you may still think of pasta, rice, grain and vegetables as being the primary or even single ingredient in such a diet, so I consider it my duty, to report the results of a 2010 study (Jung. 2010) published in the October issue of Medicine & Science in Sports & Exercise. The examined the effect of an exercise program and two different dietary regimens (high carbohydrate, HC vs. high protein, HP) on 181 sedentary women (44±12 yrs; 92±17 kg; 44±5 % fat).

Diets consisted of 1,200 kcal/d for 1-wk and 1,600 kcal/d for 9 wks. Diets were 55% CHO, 15% P, and 30% F (HC) or 7-15% CHO, 55-63% P, and 30% F (HP). Exercise groups participated in a supervised fitness program (3-d/wk) that involved 30 min of circuit-style resistance training interspersed with callisthenic exercises.

The results are equivocal, the HOMA, i.e. an index which measures insulin resistance and sensitivity "increased to a greater degree in the HP group (1.48±0.4) while glucose decreased to a greater degree in the HH group (-13.3±5 mg/dL).", meaning that the high protein diet helped to get off / alleviate the carbohydrate addiction, while the high carb diet made things even worse. These results lead the scientists to conclude:

A HP diet during resistance training promotes more favorable changes in HOMA and individuals with higher HOMA values experience a greater reduction in fasting glucose levels.