Timed Ingestion of 3x21g of Whey Protein + Exercise Sheds 14% Abdominal Fat in Overweight Subjects Within 4 Months

Minimal effort, minimal results - While you can lose weight by just adding whey protein to your diet, your success will more than double, when you're willing to work (out) for it four times a week!

It's not a secret that things that diet and exercise are the keys to weight control and health in the 21st century. If you skip only one of the two you can hardly expect optimal results. In that, it is often said that weight, or rather fat loss requires a significant reduction of one's total energy intake; and for athletes and already lean individuals, this may in fact be the case. For the average "free-living overweight or obese" individual, however, the dietary changes that are required can be as simple as adding three servings of 21g of whey protein to their regimen on a daily basis (the scientists found no overall increase in energy intake, this means the 252 extra kcal/day from whey were effectively compensated for by the overweight subjects of the study at hand.

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Before you go ahead and buy a bag of whey from the next best Internet supplement vendor, though, I have to tell you that why alone may have some beneficial effects. Without regular exercise, however, you are not going to shed those ~10% abdominal fat, the subjects in the PRISE, i.e. protein, resistance exercise, interval sprint exercise, stretching/yoga/ Pilates, and endurance exercise, group saw over the course of the 16-week study period.

Table 1: Overview of the exercise program in the PRT and the PRISE group (Arciero. 2014)

ASs you can see in Table 1, the subjects trained four times a week. They did so at different rates of perceived effort (RPE) and they performed

• upper-body resistance exercise (UB) for the chest, shoulders, biceps, triceps, and back,
• lower-body resistance exercise (LB) for the quadriceps, hamstrings, calves, and abdomen, 
• sprint interval training, and endurance training (type C) like walking, jogging, running, cycling, swimming, elliptical, rowing, rollerblading, cross-country skiing, etc. and
• supervised stretching, yoga and pilates workouts (in the PRISE group, only, where
  the four types of exercise were cycled on a weekly basis, such that participants performed each of the four exercises, 1 day/wk for a total of four exercise sessions/wk)

and one session (X), where they were free to chose whatever they wanted to do (i.e. resistance training, conditioning exercises, etc.).

All that without dietary intervention!? It sounds hard to believe that simply adding whey protein to the diet of 79 overweight / obese subjects would have such a profound impact on their body composition, but the scientists did in fact prescribe nothing else than the timed ingestion of 23g of whey protein (1) within 1 h of waking in the morning, (2) mid-afternoon or within 30 min following an exercise session and (3) withing 2 h of going to bed at night (total protein intake ended up at ~1.3-1.5g per kg body weight). Otherwise, all participants were instructed to consume their habitual diet ad libitum throughout the 16-wk intervention.

Only the increase in protein was stat. sign. across all groups (Arciero. 2014)

In the introduction I did yet already hint at the fact that the addition of 252kcal/day from the whey protein did not increase the subjects overall dietary intake (~2,000kcal/day). Against that background it's obvious that the provision of extra whey protein induced voluntary changes in the macronutrient composition of the diet that reached statistical significance for protein (+6%, +9% and +6% in the protein, protein + resistance training and PRISE group, respectively). For fat and carbohydrates the dietary changes were too different from subject to subject (meaning some reduced fat, others carbs) to reach statistical significance - which obviously does not mean that they were not reduced!

During all sessions, the subjects use medicine balls, physioballs, rubber tubes, and bands, which were incorporated into a dynamic warm-up, footwork and agility drills, resistance and power movements, and core and body weight exercises (e.g., lunges, squats, and jumping rope).

Figure 1: Relative changes in body mass, fat mass (subcutanous, visceral and in the abdominal region) and waist circumference over the course of the 4 months study (Arciero. 2014).

If you think that's more than you can handle, you better take another look at the results in Figure 1. Are you really sure you don't have the guts (don't tell me you don't have the time, if you have time to watch TV and lie around lazily on your sofa) to work out on Monday, Tuesday, Thursday and Friday?

I must say that the changes in lean mass are disappointing. Maybe a focus on higher intensity resistance training would have helped build the usually relatively muscled (from carrying an obese body) legs of the overweight / obese participants.

Bottom line: You can argue simply having that extra whey is also going to help you lose body fat, but compared to the "PRISE"-less combination of protein and resistance exercise, intervals, stretching/yoga/ Pilates, endurance exercise the fat loss from whey alone is not exactly impressive. Ok, it's impressive that simply adding three servings of whey do trigger reductions in body fat, but adding 4 workouts of which only the sprint interval workouts reach a maximal intensity of 10 on the RPE scale for only 30s (!) is what makes the difference between statistically significance, and mirror and "man, you've slimmed down"-comment significance ;-)

Needless to say, though, that completely turning your diet upside down and making exercise an integral part of your everyday life are more promising strategies to lose weight and stave it off than any of the interventions in the study at hand | Comment on Facebook!

References:

• Arciero, Paul J., et al. "Timed-daily Ingestion of Whey Protein and Exercise Training Reduces Visceral Adipose Tissue Mass and Improves Insulin Resistance: The PRISE Study." Journal of applied physiology (Bethesda, Md.: 1985) (2014).

When Timing Matters - Alpha Lipoic Acid: Works Best, When it's Taken 30min Before a High Carb Meal. Can Easily Make You Hypo, if You Forget the Carbs or Have it on Empty

A salad like the one the beautiful young lady is about to eat is not the kind of meal that would require pre-meal lipoic acid supplementation.

Although I am not convinced that alpha lipoic acid (lipoic acid aka ALA) will actually partition glucose preferentially to muscle, because studies indicate that it will increase glucose uptake in fat cells, as well (and that at 10x higher glucose transporter expressions in fat vs. muscle cells; Estrada. 1996; Konrad. 2001), there is still good evidence that it can help people with (full-blown) insulin resistance stash away the glucose they consume, more effectively. To do so, it would appear logical that alpha lipoic acid has to be consumed in the vicinity of a meal.

The question I am trying to answer today is thus: When do you have to take your alpha lipoic acid to ensure optimal glucose "repartitioning"?

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The answer to this question - and I should not have to tell you that - will obviously depend on the pharmacokinetics of alpha lipoic acid. Pharmacokinetics, as they were observed in healthy, not in sick people.

Pharmacokinetics as they were described by Jens Teichert, Robert Hermann, Peter Ruus, and Rainer Preiss in a 2003 article in the Journal of Clinical Pharmacology (Teichert. 2003). In the corresponding experimental trial the plasma concentration-time courses, urinary excreted amounts, and pharmacokinetic parameters of alpha-lipoic acid metabolites were evaluated in 9 healthy volunteers after multiple once-daily oral administration of 600 mg racemic (=regular) alpha-lipoic acid.

"The primary metabolic pathways of alphalipoic acid in man, S-methylation and β-oxidation, were quantitatively confirmed by an HPLC-electrochemical assay newly established prior to the beginning of this study. Major circulating metabolites were the S-methylatedβ-oxidation products 4,6-bismethylthio-hexanoic acid and 2,4-bismethylthiobutanoic acid, whereas its conjugated forms accounted for the major portion excreted in urine." (Teichert. 2003)

The first important finding is that here was no statistically significant difference in the pharmacokinetic parameters Cmax, AUC, and t_max between day 1 and day 4. That's relevant because it means that any prescription we develop based on the results will remain valid for one week, one month and probably the rest of your life.

No, there is no evidence that R-ALA is better than regular ALA: While there is one study showing that a high dose of S-ALA, the second of two isomeres you will find in regular ALA supplements will not increase the glucose uptake into insulin resistant muscle cells in the petri dish (Streeper. 1997), there is no study as of yet that would prove the superiority of R-ALA over racemic mixtures of both R-ALA and S-ALA in human beings. And effects such as those described by Streeper et al. for R-ALA have also been observed for regular ALA dozens of times (Jacob. 1996; Khamaisi. 1997; Weinstein. 2001).

Moreover, despite the prolonged half-lives of the major metabolites compared to the parent drug, no evidence of accumulation was found. Unlike creatine, for example, alpha lipoic acid can thus not be cycled. It has to be taken continuously.

Illustration 1: At least after only four days on ALA its pharmacology in healthy human subjects doesn't change significantly - taking it 30 min before a meal thus appears to be a valid strategy even for chronic use (Teichert. 2003)

The data the scientists collected also indicate that the major pathway through which ALA is elminates is not, as you may expect urinary excretion. In the study at hand, only 12.4% of the administered dose were recovered in the urine after 24 hours as the sum of alpha-lipoic acid and its metabolites. As Teichert et al. point out,...

"[t]he results of the present study revealed that urinary excretion of alpha-lipoic acid and five of its main metabolites does not play a significant role in the elimination of alpha-lipoic acid."

This does also imply that biliary excretion, further electrochemically inactive degradation products, and complete utilization of alpha-lipoic acid as a primary substrate in the endogenous metabolism are more likely candidates for the primary pathways of excretion.

Do you remember? ALA has only recently been shown to normalize the high fat diet induced synchronization issues of the internal clocks in rodents (learn more). Interestingly, this was achieved without having to time the ingestion of ALA by simply adding 0.2% lipoic acid to their diets. Against that background it is unlikely that "untimely" supplementation will, as it was the case for meltonin (learn more) - mess with the circadian rhythm. The issue of potential hypoglycemic episodes, on the other hand, is very real and should not be taken lightly - specifically by those of you who don't belong to the ever-increasing (still) minority of insulin-resistant (pre-)diabetics.

What's really relevant is yet not how alpha lipoic acid leaves your body, but rather the time it takes for the serum levels to peak. A time-span, Teichert et al. quantify as ~30 minutes. A value that is in line with the timing a group of German scientists used in the first (and AFAIK only) human study that produced results that would warrant the hype surrounding the use of alpha lipoic acid as insulin sensitizers (Jacob. 1999).

Figure 1: Increase in insulin-stimulated glucose disposal according to treatment (Jacob. 1999)

In said study seventy-four patients with type-2 diabetes were randomized to either placebo (n = 19); or active treatment in various doses of 600 mg once daily (n = 19), twice daily (1200 mg; n = 18), or thrice daily (1800 mg; n = 18) α-lipoic acid.

By the means of an isoglycemic glucose-clamp the authors of the study were able to confirm the results of a previous observations of an increase of insulin sensitivity in type-2 diabetes after acute and chronic intravenous administration of ALA.

The data in Figure 1 (bottom) does yet also tell you that the alpha lipoic treatment did not work for all of the seventy four-patients; and interestingly, the efficacy didn't depend on the amount of the of ALA that was used - more is thus, once again, not necessarily better.

The same timing was used in a 2011 study by Koh et al. who conducted a randomized, double-blind, placebo-controlled, 20-week trial, 360 obese individuals with 1200 or 1800 mg/d of alpha-lipoic acid or placebo.

Figure 2: Changes in Body weight over the course of the 20-week study (Koh. 2011)

Due to the longer duration of the study the scientists were also able to determine the one thing everyone is interested it: weight loss! As you can see in Figure 2, the subjects in the high dose alpha lipoic acid group lost a significant amount of weight, regardless of the fact that they were not even dieting. Needless to say that you cannot expect similar results if you are not obese and diabetic, but if you are significantly overweight or (pre-)diabetic, the Koh study provides a strong incentive to go and buy a bottle of 600mg ALA tablets.

Figure 3: ALA can trigger hypoglycemic episodes, because it blunts gluconeogenesis in the liver (Khamaisi. 1999)

Timing matter for non-diabetics, as well: And even if you are neither one, nor the other, timing matters. Taking alpha lipoic acid before a workout to increase AMPK and hope for increases in fatty acid oxidation is only going to increase your risk of going hypoglycemic (with all its recently discussed potentially obesogenic negative side effects). Similar effects can be expected if you've been fasting, then pop a couple of ALA pills and wait another 1-2h before you're finally giving your body what it will be craving for: sugar.

You think that's just biased bullshit? Well, take a parting look at the data in figure 3. Do you really want to be that normoglycemic guy who ends up in acute hypoglycemia because ALA increased his cellular glucose uptake and inhibited gluconeogenesis, i.e. the production of glucose from fat and/or amino acids in the liver, to an extend that left him hypo?

I don't think so. And I am pretty sure, the ravenous cravings and low energy levels you may be experiencing during and after these episodes are not going to help you achieve the perfect physique you may be thriving for | Comment on Facebook!

References:

• Estrada, D. Elizabeth, et al. "Stimulation of glucose uptake by the natural coenzyme α-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway." Diabetes 45.12 (1996): 1798-1804. 
• Jacob, Stephan, et al. "The antioxidant α-lipoic acid enhances insulin-stimulated glucose metabolism in insulin-resistant rat skeletal muscle." Diabetes 45.8 (1996): 1024-1029.
• Jacob, S., et al. "Oral administration of rac-α-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial." Free Radical Biology and Medicine 27.3 (1999): 309-314. 
• Khamaisi, Mogher, et al. "Lipoic acid reduces glycemia and increases muscle GLUT4 content in streptozotocin-diabetic rats." Metabolism 46.7 (1997): 763-768.
• Khamaisi, Mogher, et al. "Lipoic acid acutely induces hypoglycemia in fasting nondiabetic and diabetic rats." Metabolism 48.4 (1999): 504-510.
• Koh, Eun Hee, et al. "Effects of alpha-lipoic acid on body weight in obese subjects." The American journal of medicine 124.1 (2011): 85-e1. 
• Konrad, Daniel, et al. "The Antihyperglycemic Drug α-Lipoic Acid Stimulates Glucose Uptake via Both GLUT4 Translocation and GLUT4 Activation Potential Role of p38 Mitogen-Activated Protein Kinase in GLUT4 Activation." Diabetes 50.6 (2001): 1464-1471. 
• Streeper, Ryan S., et al. "Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle." American Journal of Physiology-Endocrinology And Metabolism 273.1 (1997): E185-E191.
• Teichert, Jens, et al. "Plasma kinetics, metabolism, and urinary excretion of alpha‐lipoic acid following oral administration in healthy volunteers." The Journal of Clinical Pharmacology 43.11 (2003): 1257-1267. 
• Weinstein, Randi B., Hans J. Tritschler, and Erik J. Henriksen. "Antioxidant alpha-lipoic acid and protein turnover in insulin-resistant rat muscle." Free Radical Biology and Medicine 30.4 (2001): 383-388.

Unexpected Performance Increments in Elite Wrestlers in Response to Well-Timed Arginine Supplementation: 5.8% Increased Time to Exhaustion, No Recution in O2 Cost!

Science is still wrestling with evidence in favor vs. against l-arginine

Actually the study at hand is not really exciting, the researchers from the Near East University Medical School in Cyprus recruited nine male national and international level wrestlers put them on more or less standardized diets, forbid them to work out and or use caffeine, stimulants or other ergogenic supplements and fed them 1.5g arginine per 10kg body weight (that's 12grams for someone with a body weight of 80kg).

Aside from the dosage, which would be on the higher side compared to the average arginine trial, there were no significant differences to study protocols you know.

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The subjects reported to the laboratory fasted in the AM, they have followed identical diets before both the active and the placebo trial and they had to perform one of those arduous pedal until you drop exercise tests on a cycle ergometer...

There was one difference, however. The subjects were not allowed to start working out immediately after they'd washed down the arginine / placebo supplement. Instead, they had to wait for sixty minutes for the arginine peak in plasma (Gannon. 2002).

Figure 1: Time to exhaustion and lactate levels increased, the VO2 costs of which you could expect that they decreased and would thus allow for the increased time to exhaustion, on the other hand, didn't change (Yavuz. 2014)

And voila! As you can see in Figure 1, Yavuz, Turnagol and Demirel observed a significant performance increase in the arginine trial.

In that, it is quite astonishing that these improvements occurred in the absence of changes in VO2 consumption. A reduction in O2 cost, as it was reported by Bailey et al. (2009) would after all be the most obvious explanation of the ergogenic effects of arginine.

Suggested Read: Arginine a BAT Building WAT Killer & Repartitioning Agent? Plus: The Arginine Enriched Biscuits Diet ;-) | read more

Bottom line: Previous results of studies with arginine supplementation on performance are rather inconsistent and it is difficult to say whether these differences can be explained by the length of the supplementation period, the combination of arginine with different components, different doses of arginine, different exercise protocols, different fitness levels of subjects (endurance trained athletes, physically active healthy men, or combat sports athletes as in the study at hand). Even the hitherto overlooked exact timing of supplementation and workout could make all the difference - so in case you still have a truckload of arginine lying around at home, remember to take it on an empty stomach and 60 minutes before your workouts.

Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Gannon, Mary C., Jennifer A. Nuttall, and Frank Q. Nuttall. "Oral arginine does not stimulate an increase in insulin concentration but delays glucose disposal." The American journal of clinical nutrition 76.5 (2002): 1016-1022.
• Yavuz, H. U., H. Turnagol, and A. H. Demirel. "PRE-EXERCISE ARGININE SUPPLEMENTATION INCREASES TIME TO EXHAUSTION IN ELITE MALE WRESTLERS." Biol. Sport 31 (2014): 187-191.