Carbs Before Workout Won’t Lock Your Ab Fat in its Stores | Plus: Wired for Laziness, Standing for Your Health and ‘Cardio’ Reversibly Promotes Microbial Diversity in Guts

Spiking insulin w/ high GI carbs before a workout doesn’t blunt the release of fat from the stores covering your abs.

Whenever I hit on journals like the latest issue of Medicine in Sports Science, a publication by the American College of Sports Medicine. I contemplate using them as a resource for an installment of the short news – albeit only if more than one of the studies in said journals are actually worth talking about.

For the November issue of Medicine in Sports Science, this was the case for four studies. First and foremost, probably Baur’s experimental counterevidence to the hypothesis that the carbohydrate-induced surge in insulin would ‘seal’ your subcutaneous body fat stores.

It may not be necessary to attack your ab-fat, but fasting does have a handful of benefits:

Monthly 5-Day Fast Works

“Lean Gains” Fast Works

Habits Determine Effects of Fasting

Protein Modified Fast 4 Health

IF + Resistance Training = WIN

ADF Beats Ca-lorie Restriction
  • Eating carbs before a workout won’t prevent you from shedding ab fat (if you’re in a deficit) – Results independent of the GI of the pre-workout carbs — Insulin is the hormonal boogie man of our time, among other things because it will reduce the oxidation of fatty acids (while increasing that of glucose, by the way). Now, scientists from the Florida State University have been able to show that the overall reduction in fatty acid oxidation is not associated with a reduced subcutaneous central adipose tissue (SCAAT) lipolysis, i.e. the release of stored body fat from the fat cells that are covering your abs – at least not in trained runners.

    For their study Daniel A. Baur, et al. recruited N=10 trained male runners who completed three experimental trials consisting of 30 min at 60% VO2max, 30 min at 75% VO2max, and a 5-km time trial (TT). Thirty min prior to exercise, participants consumed one of three beverages: 1) 75 g low glycemic index modified starch supplement (UCAN), 2) 75 g high glycemic index glucose-based supplement (G), or 3) a flavor-matched non-caloric placebo (PL). SCAAT lipolysis was assessed via microdialysis.

    Figure 1: The scientists measured the release of glycerol from the subcutaneous adipose tissue directly and the lack of difference between placebo, glucose and the slow-digesting UCAN resistant starch refutes the hypothesis that carbs before workouts would lock your body fat in place (Baur 2017).

    While the scientists did confirm the previously established significant reduction in total fat and increase in glucose oxidation w/ high GI (=highly insulinogenic) carbs,  they were unable to determine a difference in SCAAT lipolysis at rest or during running – independent of either exercise intensity or the glycemic index of the carbs the subjects ingested.

    In view of the fact that only small amounts of body fat are actually lost during exercise, the implications of this revelation are yet not 100% clear.

    Since there were no performance differences between high and low GI carbs, Baur et al. are however generally correct, when they posit that their results support “current sport nutrition guidelines suggesting there is little extra value in ingesting low glycemic index carbohydrates prior to exercise when compared to more traditional high glycemic index carbohydrates” (Baur 2017).

    What you must not forget, though, is that liberating fat (i.e. lipolysis) is only the first step of losing body fat. What’s even more important is that you have an adequate energy deficit that will then prevent that the fat is restored to the fat cells it came from.

  • Are some of us genetically “wired” to be lazy and inactive? A recent study by J. Timothy Lightfoot colleagues suggests just that — The Texas A&M University researchers found that “physical activity level, measured in various manners, has a genetic component in both humans and non-human animal models” (Lightfoot 2017). In their consensus paper, the authors present the results of an American College of Sports Medicine-sponsored roundtable and provide a brief review of the theoretical concepts and existing literature that supports a significant role of genetic and other biological factors in the regulation of physical activity.

    As the authors highlight, human behavioral traits are usually determined by both environmental/social and biological factors. Against that background it is, as Lightfoot et al. point out, “alarming that the vast majority of the literature on physical activity has excluded biological factors as potential determinants of physical activity levels in humans” – and that despite the fact that “even a brief and targeted literature review […] shows conclusively that physical activity level is strongly influenced by biological mechanisms” (Lightfood 2017).

    Figure 2: Conceptual holistic model of physical activity (Lightfood 2017).

    To summarize the summary of the research the US researchers present in their paper isn’t just beyond the scope of this installment of the short news but also more or less nonsensical. Accordingly, I would like to highlight only a few key aspects and concepts: If we define “physical activity” as any locomotion or movement that is the result of skeletal muscle contraction, the volume of physical activity (including everything from fidgeting to running a marathon),

    • is controlled by the central reward center of the brain (primarily structures in the striatum),
    • correlates with peripheral cardiovascular and musculoskeletal capabilities associated with high and low-activity profiles,
    • is subject to significant influence from genomic and other biological factors, such as sex and other hormones, and illness and disease, which may cause changes in inflammatory signals and metabolite levels that participate in the regulation of daily physical activity level,
    • will be affected by environmental factors such as diet and the presence of environmental toxicants that may augment/inhibit physical activity level regulatory mechanisms, and
    • is heavily influenced by social-environmental factors that may influence activity.

    The question is thus not “Is it in your genes, your character your environment or your upbringing, it’s rather “How do all three of them interact to determine your activity levels?”

  • Stand up for health – Multi-component workplace intervention that promotes standing and or walking during office times triggers significant health improvement — In fact, not one, but several cardio-metabolic health risk biomarkers were progressively reduced in the 136 desk-based workers /65% women, mean±SD age=44.6 ±9.1 years) from seven worksites who participated in Elisabeth AH Winkler’s latest study.
    Figure 3: The increase in walking time was mediocre aat best, but the increase in time the subjects spent standing was significant – 1h per 16hr, with health-relevant consequences in form of reduced blood pressure, trigs, an improved total/HDL ratio, reduced body weight and fat mass, as well as waist reductions and improvements in insulin when considering both, standing and walking instead of sitting.

    “The Stand Up Victoria intervention consisted of organizational support (senior management support, a team champion who sent emails containing the intervention messages); environmental modification (sit-stand workstations); and, individual health coaching (including goal setting and tracking). 

    The intervention was tapered over 12 months with intensive components (e.g., health coaching and team champion emails) ceasing after 3 months. It primarily targeted reductions in workplace sitting time, especially sitting accrued for ≥30 minutes at a time continuously. 

    The main message was to ―Stand Up, Sit Less, Move More” (Winkler 2017).

    While the individual response to the intervention was found to be highly variable, the composition was statistically significant (with the 95% confidence region excluding no change) and was very close to the point indicating a drop in mean baseline sitting of 1 hour/16 hours awake, when only the subjects standing time is considered.

    That’s not impressive, but it was still associated with highly significant health benefits: The scientists found that the greatest degree and/or widest range of cardio-metabolic benefits appeared to occur with long-term changes, and when increasing ambulatory activities, with reductions in systolic blood pressure occuring as early as after three months and significant improvements in cardiometabolic risk scores, weight, body fat, waist circumference, diastolic blood pressure, and fasting triglycerides, total/HDL cholesterol and insulin after 12 months.
    In contrast to what another recent study seemed to suggest standing alone seems to suffice to trigger many of the beneficial effects. Significant differences between standing and stepping were, after all, “only observed for systolic blood pressure and insulin; both favored stepping” (Winkler 2017). That doesn’t change the fact, though, that stepping would trigger overall greater improvements than standing.

  • First study to conclusively demonstrate that exercise changes your microbiome — Scientists from the University of Illinois confirm that exercise training induces compositional and functional changes in the human gut microbiota.

    What is particularly interesting is that these changes are (a) dependent on obesity status, but (b) independent of diet … what is not surprising, though, is that the changes were also “contingent on the sustainment of exercise” (Allen 2017).

    Figure 4: The changes in the bacterial diversity were associated with significant changes in body composition (A lean mass, B body fat %), bone mineral density (C) and physical fitness (D VO2max) over the course of 6 exercise weeks (E6). Just the microbiome, which returned to baseline after the intervention, these benefits were largely lost during the subsequent 6 weeks washout (W6 | Allen 2017)

    In the study at hand, the amount of exercise that had to be sustained was an endurance-based exercise training that was done on 3 days/wk and at progressing durations and intensities (from 30 to 60 minutes/day and from moderate (60% of heart rate reserve [HRR]) to vigorous intensity (75% HRR)) – once the subjects stopped training, their bacterial diversity bounced back to baseline diversity levels, of which the existing evidence suggests that they are too low to support optimal health (Lloyd-Price 2016).

    Ah, and by the way: In contrast to what you may expect, it were not the obese subjects who benefitted most: At least when it comes to the exercise-induced increase in fecal concentrations of short-chain fatty acids (SCFAs), the effects were in fact “lean only”, i.e. they were not observed in obese, participants. 

The results of the Baur study are in line w/ Schoenfelds “Cardio on Emtpy” study from 2014 | more.

Bottom line: Even though I have pointed out previously that a lack of ill effects on lipolysis does not necessarily mean that you will effectively lose as much subcutaneous body fat regardless of whether you ingest or abstain from carbs before a workout, the results of Baur’s experiment can partly explain why doing your cardio fasted is not going to help you shed more body fat or lose that fat faster… “you don’t?” No, you don’t. If you still believe that (re-)view my article about Schoenfeld’s seminal paper on “Fasted Cardio” from 2014, which didn’t find any benefit of doing fasted cardio in a 4-week study with a controlled moderate energy deficit | Comment on Facebook!

  • Allen, Jacob M., et al. “Exercise Alters Gut Microbiota Composition and Function in Lean and Obese Humans. Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017.
  • Baur, Daniel A., et al. “Adipose Lipolysis Unchanged by Preexercise Carbohydrate regardless of Glycemic Index.” Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017
  • Lightfoot, J. Timothy, et al. “Biological/Genetic Regulation of Physical Activity Level: Consensus from GenBioPAC.” Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017
  • Lloyd-Price, Jason, Galeb Abu-Ali, and Curtis Huttenhower. “The healthy human microbiome.” Genome medicine 8.1 (2016): 51.
  • Winkler, Elizabeth AH. “Cardiometabolic Impact of Changing Sitting, Standing, and Stepping in the Workplace.” Medicine & Science in Sports & Exercise: Post Acceptance: November 21, 2017.

Carbs Before Workout Won’t Lock Your Ab Fat in its Stores | Plus: Wired for Laziness, Standing for Your Health and ‘Cardio’ Reversibly Promotes Microbial Diversity in Guts syndicated from


No Native Advantage: RCT Compares High-Leucine “Native” Whey to Regular Concentrate – Finds NO Difference in MPS

Is the literally “raw” raw material that’s used to manufacture “native whey” worth the extra bucks the final products cost? Native whey fails the real world test.

In February this year, I already predicted that the “benefits” of “native whey” will probably turn out to be practically irrelevant. In the corresponding article “Native Whey, a Superior Muscle Builder? Recently Observed Impressive Absorption Rates Tell You Nothing About ‘Gains'” (re-read it).

Back in the day, I made a point that the improved amino acid kinetics, i.e. the more rapid appearance of amino acids Hamarsland et al. observed in their first study this year (Hamarsland 2017) for native compared to ‘regular’ whey protein was unlikely to trigger significant differences in actual protein synthesis – let alone long-term gains.

Now, a recent study by Hamarsland et al. (2017b) confirms just that – as early as in the title, by the way: “Native whey protein with high levels of leucine results in similar post-exercise muscular anabolic responses as regular whey protein: a randomized controlled trial” (Hamarsland 2017b).

Read about exercise-related studies at the SuppVersity

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Study Indicates Cut the Volume Make the Gains!

As the researchers point out in the introduction to their paper, protein is not just needed as a substrate for protein synthesis and thus the accrual of lean muscle mass, it can also stimulate protein synthesis. In this context, leucine has been found to be one of, if not the main agent to drive the increase in mTOR, a protein that controls the process of protein synthesis.

Native whey has more leucine than regular whey, so it should be more anabolic, no?

The authors’ hypothesis in the study at hand was that “native whey[, which is produced by the filtration of unprocessed raw milk and has been found to induce greater leucine blood concentrations than WPC-80 (Hamarsland 2017a), would be [a more potent stimulator of MPS than WPC-80] (Hamarsland 2017b).

Accordingly, the authors compared the time-dependent changes in mTORC1 substrate signal in response to either native whey protein or a regular whey protein concentrate (WPC80) when both were ingested at a dosage of 2 × 20 g after a resistance exercise session and controlled to the effects of milk providing 20g of protein at even lower relative amounts of leucine than WPC80.

Figure 1: Authors’ illustration of the experimental design (Hamarsland 2017b)

The study was a double-blinded, partial crossover, randomized control trial. Each participant was assigned to one of two groups. The randomization was stratified based on lean body mass. The milk group did the protocol once, whereas the whey group was exposed to the protocol two times, once consuming WPC-80 and once consuming native whey, in a randomized order, approximately two weeks apart.

Exercise protocol: leg training, only

3 h after a standardized breakfast participants performed an intense bout of high-load leg-resistance exercise. 20 g of protein from milk, WPC-80 or native whey, were ingested both immediately after, and again 2 h after exercise. Blood samples were collected from an antecubital vein to measure changes in blood concentrations of amino acids, glucose, insulin, urea and creatine kinase (CK). MPS and related intracellular signaling were measured during a 5-h recovery period combining biopsies and tracer infusion of [2H5]phenylalanine. In addition, we measured recovery of muscle force-generating capacity by maximal isometric voluntary contractions (MVC) for 24 h after exercise.

The results were quite unequivocal: real benefits of “nativity” couldn’t be observed

In line with the results of the previously discussed study, native whey increases the blood leucine concentrations to a greater extent than WPC-80 and milk (P < 0.05). What it did not do, however, was to trigger a significant increase of the phosphorylation of p70S6K, an mTOR target protein that controls the actual rate of protein synthesis – for p70S6K, an advantage was only observed over milk and that only 180 min after exercise (P = 0.03).

Figure 2: The increased phosphorylation of p70S6k did not translate to sign. increased rates of protein synthesis; * different from resting values. # different from milk at the corresponding time point, p < 0.05 (Hamarsland 2017b).

What is even more important, though, is that the actually measured muscle protein synthesis rates did not differ between the whey groups. For both whey proteins, the protein synthesis increased significantly 1–3 h hours after the exercise – with WPC-80 (0.119%), and 1–5 h after exercise with native whey (0.112%).

The only thing that is noteworthy, here, is that this increase in protein synthesis appears to be non-significantly more sustained in the native vs. concentrate group. That’s probably also why only the native whey group saw a statistically significant increase over milk during the whole 1–5 h period after the workouts (0.112% vs. 0.064, P = 0.023), while the overall increase in FSR in the concentrate group didn’t reach statistical significance (the difference we see here is yet practically irrelevant, for the practitioner one won’t have an advantage over the other… after all, there’s almost no and certainly no statistically relevant difference between native and whey concentrate).

Whey is more than a potent muscle builder. Learn more in my 2014 article “Whey Beyond Brawn: 10+ Things You Probably Didn’t Know Whey & Peptides That Form During its Digestion Can Do: From A as in Vitamin A Uptake to Z as in CanZer Protection” | read it.

Bottom line: In view of the lack of practically relevant beneficial effects on post-workout protein synthesis (at a moderate dose, by the way), spending the extra money for “native” whey protein, i.e. whey protein made from unprocessed milk (vs. the remnants of the cheese-making industry) cannot be recommended.

Since this allegedly superior form of whey didn’t show a sign. different glucose/insulin response, produced the same increase in CK, a marker of exercise-induced muscle damage, and failed to reduce the loss in muscle contractility and/or facilitate a faster recovery, of isometric knee extensor force-generating capacity, either, there’s also no other reason to spend the extra-bucks — at least if athletic performance and skeletal muscle hypertrophy are your primary goals.

I would not exclude that it may have additional or more pronounced effects on your glutathione status, but the latter has – as far as I know – not been studied and appears, IMHO, not extremely likely (also because “native” is not unprocessed, it’s just sourcing a different raw ingredient that will then undergo the same treatment processes as regular whey for safety reasons) | Comment!


  • Hamarsland, Håvard, et al. “Native whey induces higher and faster leucinemia than other whey protein supplements and milk: a randomized controlled trial.” BMC Nutrition 3.1 (2017a): 10.
  • Hamarsland, H. et al. “Native whey protein with high levels of leucine results in similar post-exercise muscular anabolic responses as regular whey protein: a randomized controlled trial.” Journal of the International Society of Sports Nutrition (2017b) 14:43.

No Native Advantage: RCT Compares High-Leucine “Native” Whey to Regular Concentrate – Finds NO Difference in MPS syndicated from

Leucine, Whey Concentrate, Hydro Whey or Soy – How do They Affect Beginner’s Early Muscle & Strength Gains?

12 weeks of serious resistance training will transform the body of beginners, but it’ll do that regardless of whether you supplement with protein or not, doctoral thesis shows.

The headline of today’s SuppVersity article summarizes the research question of a recently published doctoral thesis by Christopher Brooks Mobley (Mobley 2017). In that, Mobley started with the hypothesis that “[w]hey protein in combination with resistance training will provide the greatest
anabolic and ergogenic response” – Was he right? Well, without giving away too much, the most appropriate one-word-answer to this question is “No!”

How’s that? Well, let’s take a look at diet, training, and supplementation and you may be realizing why the only “magic” whey did was to increase the skeletal muscle satellite cell pool (learn more about Whey’s effect on satellite cells).

High-protein diets are much safer than some ‘experts’ say, but there are things to consider…

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Protein Timing DOES Matter!

High Protein not a Health Threat

For his doctoral thesis, Mobley recruited seventy-five untrained, college-aged males (mean±SE; age=21±1 yr, body mass=79.2±0.3 kg; exlusion criteria were: engaging in any regular exercise program for at least 6 months prior to study initiation, already consuming a high-protein diet (>2.0 g/kg/d), using anabolic enhancing agents (e.g., anabolic steroids, supplemental protein, creatine monohydrate, or prohormones), or having any medical or orthopedic condition(s) that would hinder them from participating in the study).

Figure 1: Graphical overview of the study design; IMTP, isometric mid-thigh pull (Mobley 2017).

The subjects were randomly assigned to an isocaloric (~200kcal), lipid- (2-4.5g), and organoleptically-matched (=appearance, taste, texture, and packaging were indistinguishable) maltodextrin placebo (PLA, n=15) twice a day [post-workout (training day) or with any meal (non-training day) and pre-bed], or they received the active treatment containing…

  • leucine (LEU, n=14), 
  • whey protein concentrate, 80% protein (WPC, n=17),
  • whey protein hydrolysate,  67% of peptides as <5 kDa in 80% protein (WPH, n=14), or 
  • soy protein concentrate, 80% protein (SPC, n=15) group.

At a dosage of that would provide a standardized amount of 2x3g of leucine per serving. And, yes, that means the participants in the leucine group received only 2x3g leucine per day… nothing else.

Participants performed whole-body resistance training three days per week for 12 weeks while consuming supplements twice daily. 

The training protocol followed a daily undulating periodization (DUP) model, with individual workouts being based on free-weighted barbell squats, bench press, deadlifts, and bent-over rows for …

  • 4 sets of 10 repetitions (Monday or Tuesday), 
  • 6 sets of 4 repetitions (Wednesday or Thursday), and 
  • 5 sets of 6 repetitions (Friday or Sunday). 

All participants were supervised by laboratory personnel for each training session to ensure that proper lifting technique is executed, and training volumes for each session will be recorded. Participants that missed more than 4 of the 36 planned session were not included in the analysis due to lack of training compliance.

Table 1: Overview of the periodization scheme, with intensities, expressed relative to estimated one repetition maximum (calculated per the NSCA’s recommended guidelines, i.e. 3-RM/0.93 | Mobley 2017).

Eventually, Mobley lost 13 participants due to lack of compliance with supplementation or resistance training. Furthermore, one subject in the WPC group had to withdraw from the study due to a musculoskeletal injury sustained during training.

With data from DXA (incl. hydration test), ultrasound assessment and muscle (and fat) biopsies the study provides very comprehensive and reliable data

A brief glimpse at the results of the 4-day food logs, the scientists evaluated to analyze their subjects’ diets revealed …

  • no differences in caloric and macronutrient intakes (i.e., total and relative calories, protein, carbohydrates, and fats) did not differ between groups at the beginning of the study. T1 (all ANOVA p-values >0.50),
  • increased caloric intakes in all groups specifically in the time after the deload, when the intensity was increased (training sessions T20 to T39) without an effect o supplementation,
  • significantly increased daily protein intakes in all groups, with an expectable group x time effect favoring WPC/WPH/SPC in terms of both, total and relative protein intake.

In contrast to the diets, the training sessions did not show significant group effects, with neither, training volume, nor intensity and/or strength gains during the intervention showing inter-group differences (ANOVA, p=0.286 | see Figure 2).

Figure 2: Total volume lifted during the 12-week training intervention (panel a) as well as pre- and post-intervention 3-repetition maximum (RM) squat values (panel b), 3-RM bench press values (panel c), and isometric mid-thigh pull (IMTP) peak force values (panel d); * within-group increase from pre- to post training (p < 0.05 | Mobley 2017).

Against that background, it becomes less surprising that there were no changes in body mass, muscle mass, fat mass, and vastus lateralis muscle thickness between groups.

Figure 3: Changes in body composition variables and vastus lateralis muscle thickness between groups (Mobley 2017).

In fact, Figure 2, which illustrates the strength gains, and Figure 3, which illustrates the size gains, look surprisingly alike. They confirm the efficacy of the workout, but fail to confirm the expected anabolic benefits of (whey) protein… with one exception:

Satellite cells thrive on whey but don’t seem to be needed

As already hinted at, the effects of whey protein on satellite cell proliferation is not a “new” result. In fact, SuppVersity readers have known about the pro-myogenic activity of whey ever since July 2014, when I wrote an article titled “Accelerated Satellite (= Muscle Precursor) Cell Proliferation is Yet Another Way for Whey to Promote Muscle Gains” (read it).

Figure 4: Satellite cell and myonuclei number in type II muscle fibers (Mobley 2017).

In view of the lack of downstream effects on the myonuclei number in type II fibers (note: satellite cells are precursors of myonuclei, they provide a pool for both, the formation of new myonuclei and the replacement of damaged ones | learn more and even more), it is yet only mildly surprising that the increased satellite cell activity didn’t translate to size or strength gains.

No, the reason is not too much protein in the diet: I guess you have already been speculating about potential reasons why the intervention “failed”. Well, my personal first guess that a high baseline dietary protein intake would explain the lack of effect. After all, the dietary protein intake was low and the whey concentrate, hydrolysate and soy protein groups did consume significantly more total protein than the placebo or leucine group (2g/kg vs. 1.3g/kg).

Gains are not the only reason to supplement with whey protein. Only recently scientists have found that increasing your protein intake, specifically at breakfast, and getting that extra protein from whey facilitates weight loss, waist reductions and significant improvements in glucose management | more.

So, if it’s not what I would like to call a ‘saturation effect’, what else could explain the null findings in the study at hand? Here’s what Mobley suggests: (1) young, male newbies are already gaining size and strength rapidly – in combination with the advanced (and potent) workout regimen in the study at hand, the gains may have been so rapid that it was simply physiologically impossible to augment them even further; (2) the baseline protein intake may not have been high, but it was – at least in the eyes of some researcher – within the threshold that’s necessary to maximize you gains (cf. Hoffman 2007 | the paper suggests that 1.2 g/kg/d of protein is adequate to support muscle anabolism with resistance training); (3) lastly, the training was intense and had a decent volume, but compared to what some more experienced athletes are doing in the gym, it may still not have been prolonged and/or strenous enough to increase the protein requirements and thus see benefits in response to increased protein intakes and/or the anti-inflammatory effects of whey protein.

The last-mentioned hypothesis would also be in line with the increased satellite cell counts Mobley observed in the whey concentrate and hydrolysate groups. An even harder, higher-volume workout would, after all, have triggered greater muscle damage and thus increased the number of satellite cells required to repair the damaged muscle tissue. Accordingly, it would be interesting to repeat the study in already trained individuals following an even more intense resistance training regimen. It is not unlikely that this study would produce the results Mobley expected to observe even in the study at hand, namely that “[w]hey protein in combination with resistance training will provide the greatest anabolic and ergogenic response” (Mobley 2017) | Comment!


  • Hoffman, Jay R., et al. “Effects of protein supplementation on muscular performance and resting hormonal changes in college football players.” Journal of sports science & medicine 6.1 (2007): 85.
  • Mobley, Christopher. “The Effects Of Leucine Or Different Protein Supplements On Muscle Hypertrophy After 12 Weeks Of Resistance Training In Untrained Men.” Dissertation submitted to the Graduate Faculty of Auburn University in partial fulfillment of the Requirements for the Degree of Doctor of Philosophy of Exercise Science (2017).

Leucine, Whey Concentrate, Hydro Whey or Soy – How do They Affect Beginner’s Early Muscle & Strength Gains? syndicated from

Move Qi, relieve pain

relax in hammockRelieving pain can be that simple.

Qi (energy) is the basis of the physical structures of the body. When the Qi is plentiful and flowing, we experience ease of movement. Abundant and flowing Qi manifests as supple and toned muscles and flexible joints.

Qi flows through pathways called meridians.

SherlockBecause Qi is energy, it is challenging to observe.
Similarly, the meridian lines are also energetic, and therefore out what is readily perceptible by our five senses.

We know that blood flows through hundreds of miles of blood vessels in an organized manner: from the heart, out to all areas of the body, and back to the heart. Blood is easy to see, but not so easy to feel moving through our vessels.

Qi also moves within an organized web of meridians.

Just like blood, every cell in our body requires Qi. Qi is hard to see but easier to feel than blood. For instance, in a moment of anger, you can feel a rush of energy (Qi) moving upwards. In contrast, in a moment of sadness, you can feel the pull of Qi downwards. In anger, the Qi is rushing upwards, and our physical body is propelled upright, perhaps even yelling.

The energetic roots of pain

In many cases, physical pain is due to slow or blocked Qi flow.
Qi is slowed down by a blockage in the meridian. This energetic pattern is called “Qi Stagnation.” As the Qi builds up behind the blockage, energetic pressure builds and we may experience pain in the area of the blockage, or anywhere along that particular meridian.

For example, pain between the shoulder blades.
Have a look at the picture below of the Bladder Meridian. Notice how it is located between the shoulder blades and continues down the legs to the feet.

Bladder Meridian

Bladder Meridian pathway shown on the right side of the body. The meridian is also located on the left side.

Relieve back pain with Meridian Massage

Step 1
Gently massage the whole length of the Bladder Meridian, from upper back, down the back of the legs, along the outer foot, and the 5th toe (the Bladder Meridian ends at the nail bed of the 5th toe).
Now we have touched into the whole meridian and hopefully encouraged the Qi to flow a little more.

Step 2
Next, we massage acupoints on the Bladder Meridian (referred to as “Bladder points”) to amplify the flow of Qi and clear blockages from the meridian. The Bladder Meridian has 67 points. We only need to activate a few of these to clear blockages and encourage the flow of Qi. I use a couple of local points (points at the area of pain), and a few distal points (points away from the pain).

In this case, I would gently massage the following Bladder points:

Local points: BL 13, BL 14, BL 15
Distal points: BL 36, BL 57, BL 60

Bladder Points to relieve pain between the shoulder blades

Bladder Points to relieve pain between the shoulder

Meridians and points are on both sides of the body

Although the pain is often on one side, I massage the meridians and points on both sides of the body.
As the energetic blockages let go, and the Qi returns to harmonious flow, the pain dissipates. Qi Stagnation is the root of many conditions of muscle tension and pain. By combining the Meridian Massage Approach with your other hands-on skills, you can relieve stubborn patterns of pain.

The post Move Qi, relieve pain appeared first on Big Tree School of Natural Healing.

Move Qi, relieve pain syndicated from

From Hero to Zero – “HMB Doesn’t Work at All… in Athletes and Trained Individuals”, Latest Meta-Analysis Suggests

If we go by the results of this latest meta-analysis, athletes and experienced gymrats don’t benefit from HMB supplements.

Roughly 4 years ago, HMB, which, once hailed as “as potent as a weak androgenic steroid”, had been forgotten by most fitness enthusiasts, when – all of a sudden – a single study by Wilson et al. put it back into the limelight. In fact, there’s hardly a study that has been so heavily debated in the fitness geek community as Wilson’s infamous HMB paper with the steroid-like gains from March 2014 (Wilson 2014). Since Wilson’s paper has (as of now) not been retracted, it does seem odd that a group of scientists from Chile and Spain write in the conclusion of a new meta-analysis that’s about to be published in the Journal of Science and Medicine in Sport (Sanchez-Martinez 2017) that they found “no effect of HMB supplementation on strength and body composition in trained and competitive athletes” (Sanchez-Marrinez 2017)… unless, obviously, the study was not included. But let’s address one thing after the other.

Learn more about the potential beneficial effects of HMB at the SuppVersity:

HMB For Fat Loss?

Hica & HMB in Yogurt

More on HMB Free Acid

Wilson’s Infa-mous HMB Study

HMB + Whey = Useless?!

HMB Lower Body Fat, Higher T?

The aim of this new meta-analysis was – much in contrast to previous meta-analyses – to “examine the evidence for the effectiveness of beta hydroxy-beta-methylbutyrate supplementation interventions on modification in strength and body composition in trained and competitive athletes” (my emphasis in Sanchez-Martinez 2017). In that, Sanchez-Martinez et al. defined trained and competitive as follows:

  • ‘Trained’ = subjects w/ at least one year of weight training experience
  • ‘Competitive Athlete’ = subjects who compete at college or professional levels

Furthermore, all studies had to be randomized controlled or crossover trials. They had to use standardized or controlled diet, and strength or sports training, to include measurements of body mass, fat-free mass, fat mass, bench or leg press strength, and to include sufficient information for calculating the effect sizes (ES).

Primary outcome = strength, secondary outcome = body composition changes

Effect size (ES) was calculated through Cohen’s d (difference between two means divided by a
pooled standard deviation for two independent samples) and 95% CIs were calculated for each study by means of t-scores, number of participants, and SD (When the SD was unavailable, it was calculated from the square root of the sample size multiplied by the standard error of the mean). ES was interpreted as follows: <0.2, trivial; 0.2–0.6, small; 0.6–1.2, moderate; >1.2, large.

Figure 1 (left): PRISMA 2008 (see Liberati 2009) flow diagram of the process of study selection| Table 1 (right): Main characteristics of selected studies based on PICOS recommendations (Martinez-Sanchez 2017).

Next to the primary and secondary outcomes (strength and body composition changes), the authors also conducted a stratified exploratory analysis comparing (i) HMB doses (3g/d, 3g/d time-release and 6g/d); (ii) duration of intervention (<4week or ≥4week); (iii) training level (trained or competitive athletes); and (iv) diet co-intervention (with or without extra supplementation) as distinguishing characteristics.

The Wilson study/-ies are not part of the meta-analysis

If you scrutinize the overview in Table 1 you will recognize that neither the initially cited study by Wilson et al. nor its follow-ups made the cut. I have to admit that I am not sure why this is the case. Maybe it’s as simple as the lack of information about the subjects’ training experience in years. Since they are described as “resistance trained” and had an average squat, bench press, and deadlift of 1.7 ± 0.04, 1.3 ± 0.04, and 2.0 ± 0.05 times their body weight, respectively, it is yet almost impossible that they didn’t train for at least one year. Maybe I have overlooked an important exclusion criterion, but of those listed in the flow diagram in Figure 1, none seem to apply to Wilson 2014. It may thus have been the ongoing criticism and scrutiny from the scientific community (Phillips 2017) that turned the balance against the inclusion of Wilson’s HMB research.

What do previous meta-analyses say? As the authors point out, to-date, three meta-analyses have been carried out in different populations. The first one, by Nissen and Sharp (2002), concludes that HMB is an effective supplement for gaining fat-free mass and strength when taken in conjunction with resistance training in both trained and untrained healthy adults. The second one by Rowlands and Thomson (2009) reports only trivial gains in trained men and a small effect in untrained men. And, in the third one, Wu et al. (2015) conclude that HMB supplementation, when added to a resistance-training program, prevented fat-free mass losses in older adults.

Be that as it may, for the remaining 6 studies in the meta-analysis, the results (see Figure 2) clearly support the initially quoted conclusion that there’s no physiologically relevant “effect of HMB supplementation on strength and body composition in trained and competitive athletes” (Sanchez-Martinez 2017).

Figure 2: Effects meta-analysis of HMB on strength (left) and body composition (right). Abbreviation: ES = effect size; n = number of subjects. p-value <0.05 was used for significant findings (Sanchez-Martinez 2017).

More specifically, the studies which were mostly (one exception) performed in men (19.5 ± 1.43 and 25.5 ± 4.3 years | N = 8-32 participants) and dosed HMB at 3 g per day, usually administered in form of 3 separate doses (mostly as HMB-calcium, no free acid, two studies used time-released HMB), show:

  • HMB did not generate any appreciable effect on bench press strength (ES = 0.00; 95% CI −0.32 to 0.32; p= 0.99), or leg press strength (ES = −0.09; 95% CI −0.46 to 0.28; p= 0.65). 
  • there were no statistically significant effects of HMB supplementation on body composition, i.e. body mass (no effect), fat-free mass (trivial positive; ES = 0.16) or fat mass (small negative; ES = -0.2 effect = small fat loss).

Neither the changes in body composition nor the previously mentioned NULL-effect on bench press and leg press strength had a statistically relevant heterogeneity. The scientists still conducted a subgroup analysis which did – and that’s not really surprising, then – “not present any significant effect when carried out for the subgroups (HMB doses, duration of intervention, training level, and diet co-intervention) and exclusion sensitivity analysis (p>0.05)” (Sanchez-Martinez 2017).

“HMB ‘Likely’ Protects ‘Muscle Quality’ & ‘Possibly’ to ‘Likely’ Cuts Inflammation During 23-Day Intense Military Training” – You may remember from the last HMB article on the SuppVersity that independent studies rather describe the benefits of HMB supplementation as “hypothetical” than as “convincing” | read more

Bottom line: When only studies in previously trained individuals and competitive athletes, i.e. those with the greatest interest in spending money on HMB-supplements are tested and the contested HMB research by Wilson et al. is excluded, “HMB supplementation [does] not generate any significant effect on strength (bench and leg press) nor body composition (body mass, fat-free mass, and fat mass)” (Sanchez-Martinez 2017).

In their discussion of the differential effects on body fat, the authors do yet rightly point out that the discrepancies, e.g. one study in judo athletes showing sign. reductions in body fat mass while no change was observed in a sample of collegiate football players, could be a result of the “interaction between supplementation and sport specific training (i.e., volume, intensity, duration, sports discipline etc.) – this, in turn, gets us back to the Wilson-study/-ies, in which both, training volume and intensity were significantly higher than in most previous HMB studies.

Speaking of “HMB studies”, even if it may not answer the question if HMB is useful for athletes ‘once and for all’ (no study or meta-analysis will do this, btw), the fact that Sanchez-Martinez et al. found only 6 studies that qualified for their meta-analysis clearly indicate that more research is necessary – also to answer the often-heard question whether the free acid form of HMB is in fact superior to it’s slower-digesting calcium-equivalent (note: in this meta-analysis the studies using slow-release HMB showed better results than those with the fast(er) digesting regular Ca-HMB; since it’s absorption speed is supposedly the reason for the superior effects of HMB, it is unlikely that the null effect that was detected in the meta-analysis at hand was a result of the studies’ use of the allegedly inferior Ca-HMB).

In that, Sanchez-Martinez et al. speculate that the reason why trained individuals appear to benefit even less than untrained or elderly subjects is that “athletes generally follow a regular optimized training (balance between training load and recovery), allowing them to significantly reduce muscle protein breakdown” – which is, as you as a SuppVersity reader know, where HMB appears to excel (learn more) … be that as it may: Overall, the contemporary evidence (minus the ‘Wilson-paper‘) suggests that there may be “possible benefits of HMB in untrained, but not in trained and competitive athletes” (Sanchez-Martines 2017) | Comment!


  • Liberati, Alessandro, et al. “The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration.” PLoS medicine 6.7 (2009): e1000100.
  • Nissen, Steven L., and Rick L. Sharp. “Effect of dietary supplements on lean mass and strength gains with resistance exercise: a meta-analysis.” Journal of Applied Physiology 94.2 (2003): 651-659.
  • Phillips, Stuart M., et al. “Changes in Body Composition and Performance With Supplemental HMB‐FA+ ATP.” The Journal of Strength & Conditioning Research 31.5 (2017): e71-e72.
  • Rowlands, David S., and Jasmine S. Thomson. “Effects of β-hydroxy-β-methylbutyrate supplementation during resistance training on strength, body composition, and muscle damage in trained and untrained young men: A meta-analysis.” The Journal of Strength & Conditioning Research 23.3 (2009): 836-846.
  • Sanchez-Martinez J., et al. “Effects of beta-hydroxybeta-methylbutyrate supplementation on strength and body composition in trained and competitive athletes: A meta-analysis of randomized controlled trials.” Journal of Science and Medicine in Sport (2017): accepted manuscript. doi: 10.1016/j.jsams.2017.11.003.
  • Wilson, Gabriel J., et al. “The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study.” European Journal of Applied Physiology (2014).
  • Wu, H., Xia, Y., Jiang, J., Du, H., Guo, X., Liu, X., … & Niu, K. (2015). Effect of beta-hydroxy-beta-methylbutyrate supplementation on muscle loss in older adults: a systematic review and meta-analysis. Archives of gerontology and geriatrics, 61(2), 168-175.

From Hero to Zero – “HMB Doesn’t Work at All… in Athletes and Trained Individuals”, Latest Meta-Analysis Suggests syndicated from

Cold Water Immersion Blunts PWO Cell Swelling | 12mg Capsaicin Boost 1.5k TT Running Performance, Reduce RPE | BIA Underestimates Athlete’s Body Fat-% by up to 10%

If you want to show off your “guns” cold water immersion (CWI) may be counterproductive in the short- and long-run. In the hours and days after the workout, you’ll miss the swelling, over weeks you’ll blunt ‘ur gainz.

No, today’s article is not about the effects of cold water on a man’s “most personal parts”. Rather than that, it’s – at least in parts – about the latest study from the University of Trás-os-Montes & Alto Douro in Portugal which shows that the immediate post-workout application of cold water immersion will significantly reduce the swelling of your biceps you’d normally see last for days after a workout.

This paper, alongside the latest research on the ergogenic effects of capsaicin supplements on short-medium distance running and the surprisingly position-depending inaccuracy of multi-frequency bioimpedance measurements of the body composition of collegiate football players, are the studies discussed in today’s installment of “On Short Notice“.

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  • Cold water immersion (CWI) shuts off PWO inflammation in biceps muscle (Matos 2017) — A recent study by Matos et al. 2017 highlights once more the potency of cold water immersion (CWI) as a useful acute treatment to prevent post-workout inflammation. A good thing if you have to compete again in the next 24h, but – as previous research showed – a double-edged sword when it comes to the adaptational processes to exercise, i.e. the “training effect”, which is blunted when the regular inflammatory process is disturbed or inhibited.

    In the corresponding experiment, the Portuguese scientists tried to verify the effects of CWI on muscle swelling by measuring the muscle thickness (MT) of their subjects’ elbow flexors after a standardized resistance training protocol (RT).

    Figure 1: Graphical illustration of the study design (Matos 2017).

    Eleven males were submitted to an RT (see Figure 1), performed in two different weeks. In one of the weeks, subjects experienced a passive recovery. In the other, subjects were submitted to a CWI (20 min at 5-10°C). Ultrasound (US) images were taken pre-, post-, as well as 24h, 48h and 72h post-exercise, to evaluate the MT.

    The results were simple: CWI works and it does so pretty well. The muscle thickness of both exercise (RT) and control (CA) arm was significantly higher 48h and 72h post-exercise when subjects were submitted to a passive recovery compared with the CWI (p=0.029, p=0.028 and p=0.009, p=0.001, 48h, 72h, EA and CA, respectively). The swelling was not, however, blocked completely (the trained arm was still thicker than the untrained one).

    Figure 2: Muscle swelling of the biceps before and after the test-workouts w/ CWI or passive recovery; percentages across the bars indicate the relative difference between CWI and no CWI trial (Matos 2017).

    Accordingly, the study at hand confirms the usefulness of CWI as a means to reduce muscle swelling and the associated potential performance impairments. It does yet also reinforce the idea that CWI may blunt the normal inflammatory response to resistance training which would, in turn, explain why previous studies observe a significant negative effect of repeated use of CWI on strength and size gains in response to a standardized resistance training regimen.

  • More evidence in favor of the performance-enhancing effects of capsaicin (de Freitas 2017) — As a SuppVersity reader, you will know that capsaicin, which has long been marketed solely as a thermogenic fat burner, has recently been found to have ergogenic effects, as well. In a new study, de Freitas, Cholewa, Gobbo, de Oliveira, João, Lira, and Rossito investigated the acute effect of capsaicin supplementation on the performance, rate of perceived exertion and blood lactate concentrations during short duration running in physically active adults.

    Ten physically active men (age= 23.5+/-1.9 yrs, weight= 78.3+/-12.4 kg, height= 177.9+/-5.9 cm) completed two randomized, double-blind trials: Capsaicin condition (12 mg) or a placebo condition. Forty-five minutes after supplement consumption, the participants performed a 1500 meter running time trial. Time (in seconds) was recorded. Blood lactate concentration was analyzed at rest, immediately post-exercise, post-5, 10 and 30 minutes during recovery and the rate of perceived exertion (RPE) was collected after exercise.

    Figure 3: 1.5k Time trial performance and rate of perceived exertion in placebo vs capsaicin trial (de Freiatas 2017).

    As you can see in Figure 3, “[t]he time was significantly (t= 3.316, p= 0.009) lower in the capsaicin (371.6 + 40.8 sec) compared to placebo (376.7 + 39 sec). RPE was significantly (t= 2.753, p= 0.022) less in the capsaicin (18.0 + 1.9) compared to the placebo (18.8 + 1.3).

    In view of the lack of effect on lactate levels, which increased over time for both conditions without significant differences between (p>0.05) and considering the short timeframe of the exercise intervention it is unlikely that this performance increase is a result of an increase in fat oxidation as it has been observed in mouse and man (Inoue 2007) in response to the ingestion of capsaicin before. 

  • Multi-frequency bioelectrical impedance analysis (MfBIA) is not an accurate measure of body composition in collegiate football players (Raymond 2017) — If you own a body fat scale, you will be aware that the absolute body fat values these devices calculate based on the resistance your body offers to the current that’s running from your left to your right food or vice-versa are not exactly reliable (I wish I was at the 5% body fat my scale tells me I had left ;-).

    Accordingly, the conclusion that “MfBIA does not appear accurate in examining between-player body composition in college football players” (Raymond 2017) probably won’t surprise you. The reason you may find Christiana Raymond’s latest study still interesting is not that it shows the inefficacy of BIA measurements, anyway. Rather than that it allows us to draw some conclusions about whose values are going to be particularly messed up, because her study is the first to also examine the influence of player position (and thus built) on the agreement between multi-frequency bioelectrical impedance analysis (MfBIA) and dual X-ray absorptiometry (DXA) when assessing total and segmental percent body fat (BF%), fat mass (FM), and fat-free mass (FFM) in NCAA Division I collegiate football athletes.

    Figure 4: It’s not just the body fat percentage that differs according to a player’s position. The average length of an NFL carreer also differs by position w/ wide receivers having the shortest and offensive lineman the longest careers (data from, originally published in “The Wall Street Journal”)

    For the study, forty-four male collegiate athletes (age=19+/-1 yrs; height=1.9+/-1.0 m; weight=106.4+/-18.8 kg) were recruited. Player positions included: offensive linemen (OL; n=7), tight ends (TE; n=4), wide receivers (WR; n=9), defensive linemen (DL; n=6), defensive backs (DB; n=8), linebackers (LB; n=6), and running backs (RB; n=4). Total and segmental body composition measured using MfBIA were compared with values obtained using DXA.

    Figure 5: Difference of DXA – MfBIA-measured body composition by player position (Raymond 2017).

    Compared to DXA, MfBIA underestimated BF% (3.0+/-3.8%), total FM (2.5+/-4.3 kg), arm FM (0.4+/-0.8 kg), arm FFM (1.4+/-0.9 kg), leg FM (2.8+/-2.0 kg), and leg FFM (5.4+/-2.4 kg) (all p<0.001; arm FM p=0.002) and overestimated total FFM (-2.4+/-4.5 kg) (p<0.001). Limits of agreement (LOAs) were: +/-7.39% (BF%), +/-8.50 kg (total FM), +/-1.50 kg (arm FM), +/-1.83 kg (arm FFM), +/-3.83 kg (leg FM), +/-4.62 kg (leg FFM), and +/-8.83 kg (total FFM).

    Beware: BIA systematically underestimates body fat and overestimates lean mass

    In that there’s yet also good news: There was no significant difference between devices for the health-relevant trunk FM (-0.3+/-3.0 kg; p = 0.565) and trunk FFM (0.4+/-2.4 kg; p=0.278), with LOAs of +/-5.92 kg and +/-4.69 kg, respectively.

    Most importantly, however, the researchers found that the “player position significantly affected all between-device mean body composition measurement differences (adjusted p<0.05), with OL demonstrating the greatest effect on each variable” (Raymond 2017) – an observation the scientists from the University of Minnesota interpret in the previously cited way: “MfBIA does not appear accurate in examining between-player body composition in college football players” (Raymond 2017).

Choline Supplementation Accelerates Fat Loss During Crash Diet in Female Athletes: 2g Choline Double the Rate of Fat Loss in the Last Week Before the Competition | more

Bottom line: If you’ve been shaking your head about that lean, but nor ripped guy claiming he went from 10% to 5% body fat when he was using capsaicin “just to improve his performance”, you may be relieved to hear that he may rather have made it from 20% to 15% (which is much easier, by the way than getting into the single-digit range). For a football player from the offensive line, the MfBIA values for body fat are, after all, up to 9.6% lower than those that were measured with the more accurate DXA method.

As I’ve pointed out in relation to previous studies on the accuracy of body impedance analyses, this does not necessarily mean that you have to trash your body fat scale – you will still be able to track your progress, just ignore the absolute value and make sure you always measure well-hydrated and at the same time of the day | Comment!


  • de Freitas, et al. “Acute Capsaicin Supplementation Improves 1500 M Running Time-Trial Performance And Rate Of Perceived Exertion In Physically Active Adults.” Journal of Strength & Conditioning Research: Post Acceptance: November 06, 2017. doi: 10.1519/JSC.0000000000002329
  • Inoue N, Matsunaga Y, Satoh H, Takahashi M. Enhanced energy expenditure and fat oxidation in humans with high BMI scores by the ingestion of novel and non-pungent capsaicin analogues (capsinoids). Bioscience, biotechnology, and biochemistry. 2007 Feb 23;71(2):380-9.
  • Matos, Filipe; et al. “Effect Of Cold Water Immersion On Elbow Flexors Muscle Thickness After Resistance Training.” Journal of Strength & Conditioning Research: Post Acceptance: November 06, 2017. doi: 10.1519/JSC.0000000000002322
  • Raymond, Christiana J. M.S.; et al. “Total And Segmental Body Composition Examination In Collegiate Football Players Using Multifrequency Bia And Dxa.” Journal of Strength & Conditioning Research: Post Acceptance: November 06, 2017. doi: 10.1519/JSC.0000000000002320

Cold Water Immersion Blunts PWO Cell Swelling | 12mg Capsaicin Boost 1.5k TT Running Performance, Reduce RPE | BIA Underestimates Athlete’s Body Fat-% by up to 10% syndicated from

16 Little Known Plants + Phytocompounds to Control(!) Your Cortisol Levels | Plus: A Dozen Better-Known Alternatives

Don’t forget: Cortisol is no stressor, it’s released to help us cope w/ stress.

While I have repeatedly emphasized that the notion of cortisol as the “muscle-catabolic stress hormone” you have to “keep as low as possible” is fundamentally flawed, there are reasons why you may want to control your cortisol levels within what would be considered the circadian normal zone, i.e. high(er) levels of cortisol that get you going upon waking, lower levels of cortisol in the PM and at night to facilitate optimal glucose control, avoid HPTA suppression (=keep normal thyroid, GH, and testosterone/estrogen levels), allow for healthy and recuperative sleep and so on and so forth.

If you are physically healthy and not overweight/obese, you are probably able to achieve this goal if you have the following (health) habits: (1) getting enough sleep (6-8h), (2) adhering to fundamental rules of sleep hygiene (same time, same routine, no blue light exposure before and during the sleep phase, etc.), (3) not starving yourself/depriving yourself of carbs while trying to get away w/ most energy from protein, not fat, (4) controlling your workout volume and using periodization strategies to benefit from temporary overreaching while avoiding chronic overtraining, (5) meditation and other techniques to reduce and/or cope with stress (learn more in “Take control of your cortisol levels“).

Chronically elevated glucocorticoids can occur in the early phase of overtraining:

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Unfortunately, it is not always possible to control/reduce your stress exposure solely by behavioral means. In those situations, medicinal plants that can modulate your hormonal response to stress can come handy. A group of less-known medicinal plants and herbal products has recently been reviewed by scientists from the Shahrekord University of Medical Sciences in Iran (Solati 2017).

For their recently published review, Solati, Heidar-Soureshjani, and Pocock considered all papers describing herbal/medicinal plant treatments that will ameliorate or normalize the production of corticotropinreleasing hormone (CRH), adrenocorticotropic hormone (ADH), or cortisol (CORT), directly.
Of the initial 884 studies that turned out in response to the scientists’ keyword search, the authors excluded 738 because they were, upon closer scrutiny, out of date, had an insufficient scope or were duplicates. Of the remaining 146 studies 30 were excluded, because there was no English-language full text. Another 94 did not measure any of the three target hormones and were likewise eliminated. Eventually, the authors were thus left with only 19 studies they grouped into studies investigating the effects of medicinal plants (meaning you would have to ingest a decoction, brew a tea (water extraction) or simply eat parts of the plant) and phytocompounds (meaning you would have to buy a supplement or extract certain substances from a plant yourself).

Table 1 & 2: Plants (left) and phytocompounds w/ stress modulating effects

Complex blends (proprietary or not) such as Si Ni Tang, a Chinese herbal combination consisting of Glycyrrhiza uralensis, Zingiber officinale, and Aconitum carmichaeli, a traditional mix of Magnolia ofifcinalis and Phellodendron amurense, or Zhi-Zi-Hou-Po, which consists of Gardenia jasminoides Ellis fruit, Citrus aurantium L. fruit and Magnolia offcinalis Rehd. et Wils. bark were not included in the tabular overviews, but still showed promising effects in experimental investigations:

  • Figure 1: Effects of Andrographis paniculata extract (AP), andrographolide (Andro), and Withania somnifera extract (WS) on plasma corticosterone level of chronically stressed rats. Values are Mean ± SEM (n = 6), *p < 0.05 versus normal control; ¥p < 0.05 versus stressed control (Thakur 2014). Note: The classic adaptogen WS performs best.

    Si Ni Tang (Glycyrhhiza uralensis, Zigiber officinale, and Aconitum carmichaeli) modulated increase in corticosterone and therefore helped relieve stress in a rodent model of unpredictable (≠everyday) stressors (41) and modulated both corticosterone and ACTH while increasing the mRNA expression of hippocampal glucocorticoid receptors in another study (Wei 2016).

  • Magnolia officinalis and Phellodendron amurense in stressed human beings yielded a significant decrease in oral cortisol levels over 4 weeks of continuous treatment (Talbott 2013).
  • Zhi-Zi-Hou-Po, consisting of Gardenia jasminoides Ellis fruit, Citrus aurantium L. fruit and Magnolia officinalis Rehd. et Wils. bark, caused normalization of ACTH and CORT levels in a rat model of unpredictable chronic mild stress (Xing 2015).

In conjunction with the 14 items from Table 1 + 2 that’s a total of 17 different “herbals” (in the widest sense) you can use as a complement to behavioral modifications to keep your cortisol levels within their normal circadian patters (high in the AM, a steady decline with intermediate increases before/right after meals).

One simply has to repeat, however: goal must not be to annihilate cortisol!

Even if you haven’t read my previous articles about the performance enhancing, inflammation controlling, recovery facilitating and even weight loss and glycemic benefits of normal levels of cortisol, a closer look at the effect summaries in Table 1 + 2 teaches us that…

  • Figure 2: Icariin is better known for its virility effects, but it’s also a potent stress-reducer as a 2010 rodent study (chronic stress vs. control) indicates; sign. reductions in both corticotropin-releasing factor (CRF) and cortisol were observed in response to the HED of 5 and 10 mg/kg Icariin daily (Pan 2010).

    Valeriana jatamansi will also reduce the level of the “happy neurotransmitter” 3-endorphin,

  • Shyusan could reduce the glucocorticoid activity to a degree that will significantly increase your risk of hypoglycemia – especially on low-carb + high protein diets,
  • YZ-50 will impair the natural auto-regulatory mechanisms of the HPA, or
  • Icariin will also reduce the number of serotonin receptors in the hippocampus and frontal cortex and will thus mess w/ your brain chemistry or rather your brains response to a given level of neurotransmitters

Both, the initially mentioned a too drastic reduction of the levels of cortisol and its controlling hormones CRH and ADH, as well as “corollary damage” in form of changes in neurotransmitter levels are something you must at least keep an eye on, when you’re using any of the herbals from Solati et al.’s list to modulate, control, or (if necessary) reduce your cortisol levels.

What other, better-known cortisol controlling agents are there? 

While this review focuses on less well-known compounds. From previous articles or other web sources you will yet know that there is a dozen of better-known alternatives:

Starting with vitamin C that can reduce the cortisol release in response to running an ultramarathon if it’s taken at a high dosage of 1,500mg/d for 7 days before the marathon (do not use chronically or you may impair your gains). An ameliorative effect on the exercise-induced increase in cortisol was also observed in 9 healthy male subjects in response to 15 mmol magnesium-L-aspartate-hydrochloride (that’s 365 mg/d) taken daily for 14 days. What’s odd is that a newer study by Cinar, et al. (2008) in which 10 mg/kg of magnesium sulfate were supplemented, the opposing effects, i.e. an increase in the cortisol response to exhausting exercise was observed. An effect you may remember from another common supplement: caffeine, which will also raise your cortisol levels and your cortisol response to exercise (Lovallo 2006; Slivka 2008).

Amino acid supplements (BCAA 140mg/kg + arginine 100mg/kg + ornithine 80 mg/kg) have also been shown to have complex effects on the cortisol response to exercise, with lower baseline and post-exercise cortisol levels in response to 320mg/kg body weight (vs. placebo) consumed 60 minutes before a standardized workout, but a significantly more pronounced increase of cortisol from pre- to post-exercise (in general, that’s good news: you want a large amplitude in the ups and downs of your cortisol levels) – an effect that was not observed in response to a protein supplement in Fry, et al. 1993 or a protein + carbohydrate mix in Williams et al. (2002).

Figure 2:  Effects of whey (WPI) vs. soy (SPI) PWO supplement on changes in cortisol (nmol·L−1). *Significantly different from PRE value ( p ≤ 0.05), †Significantly ( p ≤ 0.05) different from WPI treatment (Kraemer 2013).

Unlike soy protein, the provision of fast digesting whey protein (which also contains several bioactive peptides) has a small, but measurable effect on the exercise-induced post-workout cortisol spikes (Kraemer 2013).

Another better-known group of cortisol control agents are the so-called adaptogens

Adaptogens are (in herbal medicine) natural substances considered to help the body adapt to stress. Almost all of them will also affect the levels of cortisol, with ginseng, holy basil, ashwaghanda (Withania somnifera, see Figure 1, WS), astragalus, rhodiola rosea and cordyceps having cortisol-reducing, and licorice root and caffeine having cortisol increasing/promoting effects.

Figure 4: Cortisol concentrations in saliva on 4 test days. PC = placebo maintenance followed by 3 × 250-mg caffeine. C300 = 300 mg/d of caffeine at home followed by caffeine challenge on the test day. C600 = 600 mg/d at home followed by caffeine challenge on the test day. PP = placebo at home and placebo on test day. Base 1, Base 2, Base 3 = saliva samples taken immediately before taking a caffeine or pla capsule. PostC = samples taken 1h postdrug. Stress and Recov = samples taken at the end of a 30-min behavioral stress period or after 30 min of recovery (Lovallo 2005).

Especially with respect to caffeine, you should remember, though, that its chronic consumption will significantly reduce its efficacy – if that’s a good or a bad thing, obviously depends on whether your goal is to ameliorate or boost your cortisol levels.

Patented substances and proprietary blends

The DHEA-metabolite 7-keto, but not DHEA itself, can also sign. reduce your cortisol levels by inhibiting the conversion (/activation) of cortisone to cortisol.

Figure 5: 7-Keto inhibits the conversion of inactive cortisone to active cortisol.

The studies showing beneficial downstream effects on metabolism or body composition were however all done in subjects w/ overweight/obesity – there’s yet no doubt that the general effect on cortisol production will occur in lean(er) individuals, as well.

Next to the proprietary DHEA-metabolite, there’s also Cortitrol a proprietary blend of Magnolia (Magnolia officinalis) bark Extract (9.5 mg), Epimedium (Epimedium koreanum, Extract 100 mg which contains Icariin herb ), L-Theanine (TheaPure, 67.5 mg), Plant Sterols (with Beta Sitosterol 55 mg), and Phosphatidylserine (8.3 mg), all of which have some research to back up their effects on cortisol, individually. It is thus not totally surprising that sponsored trials report significant reductions in serum cortisol responses to physical stress (Kraemer 2005).

Take Control of Your Cortisol Levels – Use These 5x Stress-Modulating Diet, Lifestyle & Supplementation Rules Wisely | more

Bottom line: You can find a brief overview of the herbals mentioned in the review at hand in Table 1 + 2. Keep in mind, though, you do not want to annihilate your cortisol levels. Having chronically low levels of cortisol can trigger hypoglycemic episodes (often w/ a racing heart and/or high blood pressure, because an increase in catecholamines needs to compensate the lack of cortisol), general fatigue, exuberant inflammation, joint pain, allergies, sleeping problems, etc.

Ideally, you’d get a 4x/d salivary cortisol baseline reading to know if your fat belly is in fact caused by high cortisol levels, not simply by eating too much, before you embark on any (higher dose) supplement regimen for cortisol control.

Plus: If you stumble across one of the referenced write-ups on commercially available cortisol blockers, make sure to check if the studies that are quoted are even relevant for you. 7-Keto, for example, has decently convincing results in the short run in obese/heavily inflamed individuals. Neither its long-term safety, nor its efficacy in healthy, lean, athletic folks has been studied sufficiently, though | Comment!


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  • Smriga, Miro, et al. “Oral treatment with L-lysine and L-arginine reduces anxiety and basal cortisol levels in healthy humans.” Biomedical Research 28.2 (2007): 85-90.
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16 Little Known Plants + Phytocompounds to Control(!) Your Cortisol Levels | Plus: A Dozen Better-Known Alternatives syndicated from