2-aminoisoheptane aka DMHA or Octadrine, a Legit DMAA Successor? Structure, Effects & Sides Suggest: "Maybe"

2-aminoisoheptane aka DMHA or Octadrine, a Legit DMAA Successor? Structure, Effects & Sides Suggest: "Maybe"

cognitive performance DMAA DMHA fat burner health lose fat performance preworkout PWO stimulant stimulants

DMHA is rather a stim than a fat burner. But I guess it will be marketed as both.

If you are following the supplement market closely, you will have seen the first products with a new stimulant on the shelves. 2-aminoisoheptane or DMHA - a supposedly worthy successor to DMAA aka "geranamine" (the stuff in the old Jacked3D) with unquestionable structural similarities to the original banned stimulant and a questionable efficacy and safety profile. With two other non-OTC agents that have been (ab)used to lose body fat for decades, namely ephedrine and clenbuterol, DMHA, which is also called octadrine and correctly labeled "2-amino-6-methylheptane" shares a history as an asthma agent (Monroe. 1947).

DMHA will be banned, when this article is a SV Classic and caffeine again the stim of choice

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Aside from the previously cited study by Monroe et al., a study that showed weak, but existing cytoxic effects in cancer cells by Craciunesco et al. from the early 1980s and an old safety study in rodents and guinea pigs by Fellows (1947), which allows us to estimate the "safety range" of the agent at a human equivalent roughly < 400mg (in rodents, the equivalent dose will already trigger tremors and sign. increases in activity), there's unfortunately no scientific evidence to prove that the agent is (a) safe for human consumption and/or (b) even works as it is supposed to.

Whether the active substance in Eskay Oralator inhalants from the 1940s is a legitimate successor to DMAA can thus only be answered based on speculation and information from the first users, as well as the fact that the agent ended up on Rasmussen et al's recently published list of "novel stimulants in supplements" that are supposed ot "substitute for recently successful products based on ephedrine and amphetamine" (Rasmussen. 2015 | see Table 1 #8).

Table 1: Trivial and chemical names of the compounds supplement companies have dug up in articles from the 1940-50s to replace banned substances in their products (Rasmussen. 2015).

So let's look at what we have: The obviously unreliable user feedback is positive and in line with the implications of the fact that DMHA shares the same structural characteristics which allowed DMAA to interact with the trace amine associated receptor 1 and modulate dopamine and norepinephrine by increasing their production and reducing their reuptake.

Figure 1: It is not difficult to see the structural ressamblance of "geranium" or "geranamine" aka "DMAA" (found for ex. in the old "Jack3D") and "octadrine" aka "DMHA" (as it is found in supps like "InfraRed") when you compare the two.

The structural resemblance to DMAA (see Figure 1) is yet not the only thing the two agents with similar acronyms have in common. Another one is the lack of compelling scientific evidence of their efficacy and safety: Just like DMHA now, DMAA had no no real scientific backup when it first appeared on the radar of the average supplement junkie and it still blew many away - in the positive sense of being happy w/ the results,... at least until the stimulant effects wore off and the crash turned the positive into similarly negative feelings.

Remember the craze about tainted charges of DS Craze with more than just dendobrium | read more

Speaking of supplement junkies... in view of the facts that corresponding products are already on the market, we are certainly going to learn relatively soon about the efficacy and safety of this compound from hundreds if not thousand of human guinea pigs on "the boards" (fitness forums).

Don't be one of those guinea pigs that use an untested product of which I am sure it's going to be banned soon based on hearsay only - regardless of what you hear about purported α-2 receptor activity (like yohimbine) or the fact that it supposedly has similar effects as high dose caffeine or DMAA, but without the crash, by the way | Comment!

References:

• Craciunescu, D. G., et al. "Structure-antitumour activity relationships for new platinum complexes." Chemico-biological interactions 42.2 (1982): 153-164.
• Fellows, Edwin J. "The pharmacology of 2-amino-6-methylheptane." Journal of Pharmacology and Experimental Therapeutics 90.4 (1947): 351-358.
• Monroe, Russell R., and Hyman J. Drell. "Oral use of stimulants obtained from inhalers." Journal of the American Medical Association 135.14 (1947): 909-915.
• Rasmussen, Nicolas, and Peter HJ Keizers. "History full circle:‘Novel’sympathomimetics in supplements." Drug Testing and Analysis (2015).
• Thompson, W.F. - Memo, ‘Low CNS Inhaler’, 22 December 1941; R.S. Fox memo, ‘Disposal of Certain Patent Cases’, 22 March 1942; M.T. Rabbitt to Thompson re ‘Chronologic Report on the Study of Normal-Amylmethyl Carbinamine Sulfate’, 7 June 1945. All in the archives of the California Institute of Technology, Gordon Alles papers, box 15, unlabelled folder.

Finally, the 1st Blood-Flow Restriction + Classic Training Periodization Study is There and the Gains are Impressive

Finally, the 1st Blood-Flow Restriction + Classic Training Periodization Study is There and the Gains are Impressive

BFR blood flow-restriction build muscle build strength periodization

No, the study did not use a simple rope or band to restrict blood flow. Instead an automated system was used that kept the pressure at stable 100mmHg.

As a SuppVersity reader you know that blood flow restricted training is - at best - as effective as regular resistance training and can thus only be recommended as an adjunct to your regular training (efficacy unproven) or replacement for injured athletes. With a recent thesis by Daniel Cortobius and Niklas Westblad from the Swedish School of Sports and Science, the former use gets scientific backup.

The aim of the bachelor students' study was to investigate how a periodized combination of classic resistance and blood flow restricted resistance exercise (BFRE) compares to regular training when it comes to increase in quadriceps muscle growth and strength.

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Now as great as this sounds, the study has several important weaknesses (few, though, considering the fact that this is undergrad research) due to which it should be considered a "proof of concept", not a "classic + BFR is better than classic alone" study:

• untrained subjects - 10 males and 10 female (4 dropouts), to be specific, 
• no dietary standardization (only a 21g vegetable protein shake after workouts),
• unilateral (=one leg only) resistance training for the legs, only, and 
• the lack of a non-BFR periodized control group 

Without control group, it should be quite obvious that the magnitude of the results of the strength and ultrasound tests Cortobius & Westblad performed before and after the subjects trained for 10 weeks must be interpreted with utmost caution.

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What did the workouts look like? "After two familiarization sessions subjects performed three sessions per week in leg press and leg extension, except for week 4 and 8 were subjects performed five BFRE training sessions Monday to Friday" (Cortobius. 2016)." During the weeks, the subjects did three sets with 70-75%, 63-67,5% (90% of Monday) and 80-85% of their individual 1RM for 10-12, 10-12 and 5-7 reps on Monday, Wednesday and Friday of weeks 1-3 and 5-7. During the classic training weeks 9-10, they did 2-3 sets of 10-12 reps at 70-75% on Monday, 1 set of 10-12 reps at 63-67,5% (90% of Monday) on Wednesday and 2-3 sets of 5-7 reps at 80-85% on Friday.

During the BFR weeks, subjects exercised every day, but switched back and forth between leg extensions and presses with the former being done on Monday, Wednesday and Friday, and the latter being performed only on Tuesday and Thursday. Both exercises were performed wearing an automated cuff that was set to regulate the pressure at 100mmHg during the workouts. The BFR workouts, itself, consisted of four sets of unilaterally leg press or leg extension the subjects did at a set pace of 60 BPM and 50 BPM for the extensions and press, respectively. As usual, the intensity was reduced for the BFR weeks: 20 % of 1RM in leg extension and 30 % of 1RM in the leg press. With the short rest of thirty seconds after the first set of 30 reps, the 2nd set of 10 reps and the third and fourth set, during which the subjects performed to concentric failure, the BFR workouts were yet still pretty intense. 

This does not refute the authors' conclusion that their findings, namely a significant increase of vastus lateralis muscle thickness by 15,1 % ± 7,6 (p ≤ 0,01 | no difference between genders), as well as leg press 1.RM by 59,1 % ± 27,4 (p ≤ 0,01), and leg extension 1RM by 19,8 % ± 13,1 (p ≤ 0,01), suggest superior effects of periodized BFR + regular training on muscle growth in comparison with most other strength training studies.

Figure 1: Size (left) and strength (right) gains over the 10-week study period / no sign. sex-differences (Cortobius. 2016).

Without a group that trained without cuffs in weeks 4 and 8, too, however, the attribute "superior" is yet practically meaningless. Different subjects, probably different nutrition, different exercises, ... a direct comparison between one study and another is never really valid, even if Cortobius and Westblad are right to point out that that the effects they observed in their study are "much greater than the mean increase of 0.11 % per day reported in a large meta-analysis (Wernbom, Augustsson & Thomeé 2007)" (Cortobius. 2016) - without a control group that trained regularly or simply with slightly higher intensity, but similarly high reps to failure daily during weeks 4 and 8, we have no valid benchmark for the results of the study at hand (so let's hope there's a follow up before the authors' master thesis ;-).

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Bottom line: As happy as I am that this study has finally been conducted (you may remember from previous SuppVersity articles on blood flow restriction that I've argued in favor of periodization to use BFR more effectively), there's no way to tell whether BFR + classic training produces greater gains than classic training alone based on the study at hand.

Therefore, we can only hope that a follow-up study with a 1:1 comparison of periodized BFR and unperiodized regular resistance training will be done to finally answer the question, whether the two weeks of training with cuffs actually promoted additional size and/or strength gains (in my dreams, that study would be done with a full body or at least a complete leg workout in trained individuals, obviously ;-) | Comment!

References:

• Cortobius, Daniel, and Niklas Westblad. "Optimizing strength training for hypertrophy: A periodization of classic resistance training and blood-flow restriction training." (2016).
• Wernbom, Mathias, Jesper Augustsson, and Roland Thomeé. "The influence of frequency, intensity, volume and mode of strength training on whole muscle cross-sectional area in humans." Sports medicine 37.3 (2007): 225-264.

Caffeine Keeps You Going When You'd Usually Rack the Weight - Does That Cause an Increase in Muscle Damage?

Caffeine Keeps You Going When You'd Usually Rack the Weight - Does That Cause an Increase in Muscle Damage?

caffeine CK coffee lactate performance rhabdomyolysis training

With only 65mg of caffeine, an espresso provides only ~12.5% of the amount of caffeine used in the study at hand.

If you've kept an eye on the latest caffeine research you may have noticed that there's an increasing number of studies that fails to find significant performance enhancing effects of caffeine during resistance training sessions (Trevino. 2015). Does this mean that caffeine, a substance that is by the way on the World Anti-Doping Agency's list of prohibited substances useless for gymrats? Certainly not.

One thing most of these studies have in common is that they tested the subjects' strength or power production during short workouts. Studies that investigate the effects of caffeine in higher volume contexts, on the other hand (e.g. Lang. 2015; Thomas. 2015), confirm that caffeine is rightly the most (ab-)used ergogenic among fitness enthusiasts.

You can learn more about coffee and caffeine at the SuppVersity

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Caffeine Resis- tance - Does It Even Exist?

One thing that has recently caught my attention on Facebook is the claim that the performance enhancing effects of caffeine put you at risk of rhabdomiolysis, i.e. the potentially dangerous breakdown of muscle tissue. In theory, it'd appear logical to assume that an agent that has repeatedly been proven to significantly lower the perceived exertion/fatigue as well as muscle pain during exercise could lead to a greater degree of muscle damage during exercise.

Figure 1: Graphical overview of the experimental design of Ribiero's study (Ribiero. 2016).

To test the hypothesis that acute caffeine ingestion could attenuate leg power, and increase blood lactate at the expense of increased muscle damage, researchers from the Federal University of Rio de Janeiro recruited six male pro handball athletes who layed in the first division of the Brazilian National League of Handball (HBNL).

"All of them had at least 5 years of experience in the sport and trained for about 4 hours a day, 4-5 days a week. No athlete had a previous medical history of cardiopulmonary disease or used any medication during the study. The athletes reported intake of ~ 60 mg of caffeine per day (~ 1 cup of coffee)" (Ribiero. 2016).

In a randomized, placebo-controlled, double-blind crossover study, the subjects reported to the laboratory at two occasions after an 8-h fast and at least 24h of caffeine abstinence. 60 minutes after having a standardized breakfast, which consisted of bread, white cheese, and orange juice (CHO: 87 g, 348 kcal; PTN: 13.5 g, 54 kcal; LIP: 7 g, 63 kcal; Total: 465 kcal), they consumed either placebo (PLA), or caffeine (CAF; 6mg/kg body weight) and remained seated for another 60 minutes.

But this is not resistance training! While you're absolutely right, jumping is at least as notorious for producing muscle damage as regular resistance training. It is thus unlikely that leg presses or squats would have produced a greater degree of muscle damage than this intense VJ protocol.

After the 60-minute delay during which the serum caffeine levels rose to peak values (see previous SuppVersity article), they performed a short warm-up and a standardized vertical jump test the scientists describe as follows:

Figure 2: Mean leg power during VJ (Ribiero. 2016).

"The VJ performance was evaluated by the jump platform System Optical (Cefise®, São Paulo, Brazil). This equipment consists of a laptop with the software "Jump System" (version 1.0, São Paulo, Brazil), connected by a cable to a resistive (or capacitive) platform (equipped with infrared optical sensors). The timer software is triggered by the feet of the subject at the moment of release from the platform, and will be stopped at the moment of touchdown. This equipment has the same principle of “Ergojump” to inform the flight time (ms) and contact (ms). 

The error of measurement, when compared with film analysis has been reported to be in the order of ± 2% (18). The athlete was positioned, barefoot, in the interior of the platform and the jumps were performed starting from a standing position until approximately at an angle of 90° knee, using help from upper limbs at the time of the VJ execution" (Ribiero. 2016).

The VJ data were analyzed by average leg power (Watts/Kg) generated by the athletes. In that, the scientists separated the total number of vertical jumps into tertiles, so that they could have an understanding of the behavior of the jumps in the 1st tertile (i.e., theoretically better performance), in the 2nd tertile (i.e., theoretically an average performance), and 3rd tertile (i.e., theoretically a drop in performance).

Your muscle is not the only thing that could be overtaxed - Even though the ability to perform more sets / work out more intensely / longer may not have affected the primary marker of muscle damage in the study at hand, the chronic consumption of high doses of caffeine may still pose a risk to your central nervous system and contribute to sympathetic overtraining. Therefore I'd still recommend you stick of max. 400-600 mg caffeine per day and, instead of increasing the dosage, when it stops working, take a "caffeine break" whenever you stop noticing the "caffeine spike".

This allowed Ribiero et al. to make comparisons between groups and to assess the effects of supplementation. Effects of which the data in Figure 3 tells you that they became evident only in the latter tertile of jumps:

Figure 3: Nonlinear regression analyses (polynomial regression 3rd order). Leg of the power generated in each sets of athletes with tertiles in placebo (PLA) and caffeine (CAF) trials (Ribiero. 2016).

As you can see in Figure 2, the subjects hit the wall in said third tertile in the placebo trial. In the supplement trial, on the other hand, the performance decline was significantly ameliorated - not only, but especially during the first and second set (black squares and white circles). This effect becomes even more obvious when you take a look at the leg power the subjects exerted on the jump platform during the jumps in the 1st, 2nd and 3rd tertile (plotted in Figure 2): compared to the use of placebo caffein improved the leg power the of athletes in the 3rd tertile (p <0.05) by 5.23%.

At the same time, however, it lead to a highly significant increase in blood lactate levels (+42.59%) after the execution of vertical jump test (p <0.05). In contrast to what the initially discussed hypothesis would suggest, though, this increase in lactate was not accompanied by significant increases in serum CK levels of the athletes (see Figure 4).

Figure 4: On average, the increase in CK was even lower in the caffeine trial - albeit not significantly (Ribiero. 2015).

So what does that mean? Well, the most obvious answer certainly is that using caffeine to boost your performance beyond "natural limits" is not going to increase your risk of rhabdomiolysis. On the other hand, the study doesn't say anything about the effects on the central nervous system and whether your CNS, not your muscle, could be overtaxed by "going beyond failure" with caffeine.

The potential negative effects of chronic caffeine consumption on the central nervous is a problem I've mentioned in the red box and discussed in previous articles about caffeine.

Unfortunately, this problem has not been sufficiently studied, yet. So, if you're looking for a supplement related topic for your master thesis, boys and girls, the effects of chronic pre-workout caffeine consumption at different dosages on the central nervous system could be just the topic you've been looking for ;-) | Comment on Facebook!

References:

• Lang, K., and E. B. LaFountaine. "Effects of caffeine as an ergogenic aid on weight lifting regimes in male collegiate athletes." International journal of exercise science: Conference proceedings. vol. 12. no. 1. 2015.
• Thomas, Gabrielle. Is coffee an effective pre-workout drink?–The effects of ingesting naturalistic doses of caffeine on one-repetition maximum muscular strength and muscular endurance in females. Diss. Cardiff Metropolitan University, 2015.
• Ribiero, et al. "Caffeine attenuates decreases in leg power without increased muscle damage." Journal of Strength and Conditioning Research (2016): Publish Ahead of Print | DOI: 10.1519/JSC.0000000000001332
• Trevino, Michael A., et al. "Acute Effects of Caffeine on Strength and Muscle Activation of the Elbow Flexors." The Journal of Strength & Conditioning Research 29.2 (2015): 513-520.

Fit and Lean in 4 Min / Week: 1kg Fat Loss, +9% VO2Max, +13% Fat Oxidation - Men Lose Trunk, Women Leg Fat

Fit and Lean in 4 Min / Week: 1kg Fat Loss, +9% VO2Max, +13% Fat Oxidation - Men Lose Trunk, Women Leg Fat

fitness health HIIT lose fat sprints vo2max workouts

No excuse: You don't need an ex-pensive spinning bike for the workout.

This is not an article for the hardcore trainees among you... unless, obviously you are a trainer or have friends and family who fall into the same "I just wannabe fit and healthy" category as the subjects of a recent study by scientists from the Manchester Metropolitan University and the Cambridge University School of Clinical Medicine (Bagley. 2016),  24 men and 17 women with a mean age of 39 (±2) years, a normal weight (BMI 24.6 +/- 0.6) and average fitness levels.

In this group of "normal people", Bagley et al. aimed to examine the hypothesis that very short duration, very high-intensity sprinting exercise (on cycle ergometers) could not just improve their subjects fitness (as measured by VO2max), but also their ability to burn fat and to actually lose it.

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After baseline measurements on the DEXA scan (body fat and lean mass) and cycle ergometers (VO2max), the participants were told to do only one thing: A sprint-interval training (SIT) program on a standard cycle ergometer.

"The training consisted of a 2 min warm-up at a self-selected moderate intensity. This was followed by four bouts of 20 s ‘maximal effort’ sprints at a workload that was set at 175% of the workload attained in the VO2max test. Each of these intervals was separated by 2 min of very low intensity cycling (a workload of approximately 20% of that attained at VO2max). Thus, each training session lasted less than 10 min and only 80 s was completed at an inten sity that would be expected to improve physical fitness" (Bagley. 2016). 

The first training session for each participant, who were told to maintain their their usual dietary and exercise habits throughout the intervention, was fully supervised in the research laboratory. To ensure that the subjects would indeed do their three weekly workouts 80s-workouts, the participants were then provided with clear instructions on the use of the cycle ergometers and the training regimen.

But you said "fit in 4 minutes", now the subjects train for almost 10 minutes? Yes and no. They train for 20 minutes, but the actual "exercise", which is something I define as being significantly exerted is 80s per workout. With three workouts per week, that's 3x80s = 240s = 4 minutes! So, I don't want to hear complaints ;-)

The training work load was increased by 5% every 2 weeks. Gym staff were fully informed of the research and training protocols, they logged the training session and were available to offer advice to research participants if needed during training sessions. Participants maintained a training-log to record workloads during training sessions.

Figure 1: Maximal oxygen uptake and rates of fat oxidation measured during exercise in men and women before and after 12 weeks of SIT; all changes were stat. sign. p < 0.05 (Bagley. 2016).

As you can see in Figure 1, the effects these short, highly time-efficient, and absolutely manageable (everyone can workout at max intensity for 4x20s) had on the subjects' fitness were not just statistically significant, they were also practically relevant and, at least for VO2max, differed significantly for men and women.

But how did they lose weight without dieting? The secret is the proven lack of compensation for SIT sessions, which have been show to be as low as <50kcal/week - compared with endurance exercise where compensation is 10x higher, i.e. 500 kcal/week (Burgomaster. 2008). Still, the direct energy expenditure during the short SIT sessions cannot fully explain the fat loss. Therefore, Bageley et al. speculate that "[o]ther contributing factors might include an increase in post exercise energy expenditure [that's unlikely, learn why] or overall shift towards greater fatty acid oxidation during habitual activities throughout the day" (Bagley. 2016).

Overall, the increase in VO2max averages out at 9% - the reasons for the sex-differences is not clear. After all, the scientists point out that men have been shown to have higher gains in VO2max following conventional endurance exercise. The mixed results of previous studies into the effects of sprint interval training, however, are mixed and thus not necessarily contrary to the evidence from the study at hand. While Scalzo et al. (2014), for example, found that young women had similar gains in VO2max as young men, the results Allemeier et al. (1994) et al. presented in the Journal of Applied Physiology suggest that men don't see any increase in VO2max. What could be the reason? Well, this is what the scientists say:

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"A higher relative amount of lean mass in men compared to women, coupled with a higher relative body fat mass in women compared to men, may go some way in explaining the differences between men and women in maximal oxygen consumption. However, the supply of oxygen to the working skeletal muscles is thought to be a limiting factor in VO2max, so the higher VO2max response in women might point to higher adaptations of oxygen supply than those in men following SIT, but more focused studies examining cardiac output, blood volume, haematocrit and blood flow distribution are needed to clarify this finding.

Conversely, after regular endurance training, men had higher gains in VO2max compared with women. It is possible that the training volume (higher in endurance) and training intensity (higher in SIT) lead to disparate adaptations between men and women in the oxygen carrying capacity of blood (eg, total blood volume, haemoglobin or cardiac output) or local vasculature, but physiological mechanisms driving such responses are unclear" (Bagley. 2016).

No sex differences were observed for the measured health markers, namely glucose, insulin, HOMA, triglycerides, total cholesterol or LDL - only for HDL there was a significantly more pronounced increase in the female vs. male subjects. Eventually, the improvement of the total cholesterol to HDL ratio was yet similarly pronounced in both sexes (-16% in the men, -11% in the women).

Figure 2: Body composition before and after 12 weeks of SIT; * after the categories denotes p < 0.05 (Bagley. 2016).

The previously discussed changes were accompanied by a significant loss of total, leg and trunk fat, as well as significant increases in lean mass in both groups - with inter-sex-differences in total body mass, body fat %, leg fat, and lean mass. That's quite a result, if you take into account the total and actual exercise time the subjects had to invest.

Want to lose >6kg in 6 weeks with more effort, here's how you do it!

Bottom line: I am not sure how feasible this protocol would be for an obese person, but in the healthy normal-weight subjects in the study at hand, the 12x4 minutes of working out intensely made quite a change. Ok, you have to work out thrice a week, but 10 minutes on an exercise bike? That's something you could easily do every morning before showering or when you come home from work.

Ah, and before I forget to highlight that - even though the fat loss in the female subjects may have been smaller than in the male subjects, the women lost fat where many of them hate it the most: on their legs - not bad!? Comment!

References:

• Allemeier, CRAIG A., et al. "Effects of sprint cycle training on human skeletal muscle." Journal of Applied Physiology 77.5 (1994): 2385-2390.
• Bagley, Liam, et al. "Sex differences in the effects of 12 weeks sprint interval training on body fat mass and the rates of fatty acid oxidation and VO2max during exercise." BMJ Open Sport & Exercise Medicine 2.1 (2016): e000056.
• Burgomaster, Kirsten A., et al. "Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans." The Journal of physiology 586.1 (2008): 151-160.
• Scalzo, Rebecca L., et al. "Greater muscle protein synthesis and mitochondrial biogenesis in males compared with females during sprint interval training." The FASEB Journal 28.6 (2014): 2705-2714.

Raw Milk + Honey Accelerates DOMS Recovery of Trained Athletes Compared to Chocolate Milk, But There's a Catch...

Raw Milk + Honey Accelerates DOMS Recovery of Trained Athletes Compared to Chocolate Milk, But There's a Catch...

chocolate milk dairy DOMS honey milk performance raw milk

While many US officials still believe that raw milk was a threat to public health. The internet is full of (often hilarious) health claims related to raw milk and the ill effects of pasturization. Could the study at hand provide evidence this is not complete bogus?

Maybe you remember that I have been talking with my friend Carl Lanore about raw milk, pasteurization and (even worse) homogenization several times when I still had the time to do the weekly SuppVersity Science Round-Ups on SuperHumanRadio. Until now, the evidence for the often proclaimed benefits of raw milk are skinny. With the publication of a recent study by Andrew Hatchett and colleagues from the Franklin Pierce University this evidence the number of relevant studies has therefore increased significantly.

What makes the study so relevant? Well, it was a randomized human trial in twenty healthy male collegiate sprint football (mean age 20y; height ~175cm, weight ~80kg; 1RM back squat of ~125kg; 80% RM back squat of ~100kg), not any old rodent study.

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There's one thing that reduces the relevance of the data, though. Instead of objective markers of recovery, such as post-recovery strength tests or at least CK and LDH levels, the scientists gave their subjects a questionnaires, prior to completing a lower extremity DOMS protocol, to determine the level of discomfort and functional limitations at baseline.

Upon a second visit to the lab, the subjects were then randomly assigned to consume 240 mL of raw milk (RMS sweetened with honey to make up for the sugar in the chocolate milk) or a chocolate milk "placebo" (CMS) before completing the same set of exercise and filling the same set of questionnaires immediately post, 24-, 48- and 72-h post DOMS protocol. Additionally, the scientists contacted the subjects 10 days after the test to learn if any negative effects were experienced as a result of ingesting either solution.

Figure 1: Changes in reported visual acuity scale (VAS) score regarding lower extremity muscle soreness pre-exercise induced muscle soreness (EIMS) protocol, directly post EIMS, 24 h, 48 h and 72 h post-EIMS for both the Raw Milk Solution (RMS) group and the Chocolate Milk Solution (CMS | Hatchett. 2016).

As you can see in Figure 1, both groups reported an increase in lower extremity discomfort at each data collection interval post-DOMS protocol (post, 24-, 48- and 72-h). In that, the participants who received the raw milk saw an initially higher increase in DOMS which then dropped to a slightly lower levels than in the chocolate milk group after 72h.

Milk and diabetes? Scientists get to the bottom of anti-diabetic effects of milk: It's the mix that makes all the difference: While individual components may not be present in sufficient concentration to produce a physiological effect such an effect may be obtained by several components acting in concert.  PPAR-α, -β and -γ agonists as well milk fat bioactive compounds that induce uncoupling protein-1 expression in brown adipose tissue may explain the suppression of diet-induced obesity and improvement in insulin sensitivity, review concludes (Parodi. 2016).

The scientists' statistical analysis of the difference, revealed that the relevance of the differences at baseline and 24h post is unclear, while the advantage of the raw milk at 48h and 72h was likely relevant. The 10-day follow-up did, as you probably already expected, not reveal any negative side effects. Overall, the results were thus in line with previous studies suggesting that the consumption of a milk-based solution with an elevated carbohydrate level reduces the DOMS (Cockburn. 2012).

As the scientists point out, though, it "has not been reported prior to this study is the difference between a raw milk solution and a commercially available milk solution with elevated carbohydrate levels" (Hatchett. 2016). So, does raw milk actually work the magic that its advocates say is lost due to the pasteurization process which is supposed to denature the macronutrients and many of the micronutrients present in the milk? Maybe...

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Maybe? Yes, maybe! Firstly, the difference between the groups is small and only "likely" relevant. Secondly, the measures are subjective and (at least for a physicist like myself) not really reliable. And thirdly and most importantly, the honey the scientists added to the milk could have made all the difference. After all, honey contains a number of antioxidants from a variety of sources, including polyphenolics; and polyphenols, albeit from other sources, have previously been shown to reduce lipid peroxidation by inhibiting peroxyl radical activation and stabilize cell membranes ... and yes, these are putative mechanisms for reducing DOMS by the means of polyphenol supplements (Radak. 2012) | Comment on Facebook!.

References:

• Cockburn, Emma, et al. "Effect of volume of milk consumed on the attenuation of exercise-induced muscle damage." European journal of applied physiology 112.9 (2012): 3187-3194.
• Hatchett, Andrew, et al. "A Comparison between Chocolate Milk and a Raw Milk Honey Solution’s Influence on Delayed Onset of Muscle Soreness." Sports 4.1 (2016): 18.
• Parodi PW. "Cooperative action of bioactive components in milk fat with PPARs may explain its anti-diabetogenic properties." Med Hypotheses 89 (2016):1-7.
• Radak, Zsolt, et al. "Nitric oxide: Is it the cause of muscle soreness?." Nitric Oxide 26.2 (2012): 89-94.