Science Round-Up Seconds: Optimal Health & Fitness Best Promoted W/ Intense Exercise. News on PUFAs & Thyroid Metabolism. Manganese the Anti-Sugar Glue Mineral!?

There may be a hitherto overlooked "enzymatic connection" between low thyroid function (spec. "low T3 syndrome" or starvation-/overtraining-induced reductions in thyroid levels) and "insufficient" levels of the long-chain varieties of both, omega-3 (EPA, DHA), as well as omega-6 (GLA, ARA) fatty acids.

I must admit that Carl & I did much to my own surprise cover more ground than I thought we would - and that despite his lengthy rant about the FDA ;-) That said, there is still enough for a second serving, aka the "Seconds", featuring news like:

• The optimal exercise for health and fitness is intense - SuppVersity readers & Superhuman Radio listeners knew it all along, the comfort zone won't enforce adaptation
• PUFAs and the thyroid - insufficient conversion of LA and ALA with low T3 levels; probably also relevant everyone who enjoys starvation and overtraining
• Manganese an anti-sugar glue mineral - study shows manganese protects blood vessels in a high glucose environment from the from monocyte adhesion and subsequent endothelial dysfunction

Contrary to previous shows it does not really matter, whether or not you have already or are still going to listen to the show. If you want, or your schedule doesn't allow otherwise, you can very well start with the Seconds, though - and that despite the fact that the author(s) of book of etiquette probably won't appreciate that ;-)

Scientists listen to the SuppVersity science round: Working out glycogen-depleted rules

8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists:- that's the headline of an October 2012 SuppVersity post

(Taanaka. 2013) -- The headline of this paragraph is obviously meant to be funny, but still. It's a funny coincidence that Hiroaki Tanaka, Kazuhiro Morimura and Keisuke Shiose from the f Fukuoka University in Fakuoka, Japan have just published a review on what the title tells us is An optimal exercise protocol for improving endurance performance and health and the protocol they suggest is basically very similar to the one(s) you will have heard about on the Science Round-Ups of December 8 and December 21, in which we broached the same issue of training in a glycogen depleted state, I also addressed in a post from October 2012 (see image on the right).

Obviously the review that has just been published in the The Journal of Sports Medicine and Physical Fitness has been written before my article, but it's still nice to see that the conclusions the Japanese researcher draw are virtual identical to what you read and heard on the SuppVersity and Super Human Radio, before:  

1. Tell me about efficacy: 4-6×30 s supramaximal sprint cycling Wingate tests are as effective as 40-120 min exercise session s at 65% of VO2Peak (Burgomaster. 2008); 7×30 s “all-out” bouts and 3×20 min bouts at approximately 87% of VO2peak could induce a similar increase in PGC-1α (Psilander. 2010); learn more about HIIT
   The optimal exercise protocol to improve health and endurance performance was discussed in re-lation to exercise-induced gene expression of PGC-1α.
2. Training intensity is a critical factor in PGC-1α gene expression and requires trainees to work out at a high(er) intensity broaching the lactate threshold (=no hours of endurance training, but glycolytic exercises such as sprinting or plyometrics)
3. HIIT does  not simply offer a way to meet the criteria in (2), it is also highly time efficient and improves aerobic capacity to a much greater extend than classic steady state cardio training
4. Training a glycogen depleted state renders submaximal continuous exercise a viable alternative to high intensity workouts.

Actually it would be ideal if I wouldn't have to repeat that whenever this issue comes up, but just to make sure: Do never forget that training  glycogen depleted is something like an intensity technique. Just like training past failure on every set, heavy eccentrics or planned phases of deliberate overreaching, it can set you up for overtraining and the Athlete's Triad, when your diet and / or recovery times are off.

PUFAs and the thyroid - insufficient conversion of LA and ALA with low T3 levels

(Swenne. 2013) -- This is not what the Peat-anians (or whatever you may call the friends of Dr. Ray Peat's theories may call), are now thinking about. At least at first sight, it would appear that it's quite the opposite of Peats anti-thyroid theory of polyunsaturated fatty acids (PUFAs).

Figure 1: Illustration of the role of the blocked (X) desaturase (DS) enzymes Delta-6 and Delta-5 in the formation of long-chain omega-6 (top) and omega-3 (bottom) fatty acids

After all, the results, Swenne and Vessby present in a paper that has been published only a couple of days ago in Acta paediatrica point towards an inhibitory effect of low thyroid function (specifically low triiodothyronine = T3 levels) on PUFA metabolism.

Stupid question of the day: "But Arachidonic Acid (ARA) is bad anyway, so why would I care - I mean, I take my fish oil" I am fully aware that the screwed up worshiping of omega-3 and the overgeneralized demonization of omega-6 fatty acids make questions like this appear logical, if not "smart". In fact, they do yet only reveal the public ignorance towards the complex interactions and the importance of proper ratios of both types of polyunsaturated fatty acids.

In an exercise scenario comprising a 4x/week classic body building strength training regimen, for example, the ingestion of 1g of arachidonic acid on a daily basis has been shown to have anti- not pro-inflammatory effects (-15% IL-6; Roberts. 2007)

Upon closer scrutiny of the actual data, it does yet turn out that the starvation induced alterations of omega-3 essential fatty acid (EFA) metabolism the Swedish scientists observed in 227 adolescents with eating disorders went hand in hand with the down-regulation of T3 levels. This observation alone does therefore not suffice to settle the "chicken or egg question" (i.e. what comes first?). The researchers' analysis of the activity of the desaturase enzymes (see figure 1), which convert the short chain omega-3/6 to long-chain omega-3/6 fatty acids would yet suggest a causative relationship between the reductions in active thyroid hormone and the subsequent deficiency of the long-chain polyunsaturated fatty acids EPA & DHA (omega-3) and GLA and arachidonic acid (omega-6). Now things become really interesting, when we also take into consideration that previous studies have shown that

"[i]nsulin appears to stimulate both desaturases, while hormones that increase blood sugar concentrations such as glucagon, adrenalin and corticosteroids are inhibitory for both enzymes." (Swenne. 2013)

This in turn brings us right back to the Athlete's Triad (read more about the Athlete's Triad in the respective SuppVersity Special) where the continuous lack of readily available energy results in low insulin levels and chronically elevated glucogon, adrenalin and corticosteroid levels, so that long-chain PUFA supplementation (and this includes the omega-6 fatty acids GLA and ARA) would appear to be indicated for (chronically) overtrained athletes, as well.

Manganese protects endothelial cells of diabetic rodents

(Burlet. 2013) -- In the latest issue of the Journal of Biological Chemistry, Elodie Burlet and Sushil K. Jain from the Louisiana State University Health Sciences Center report that administration of a whopping dose of 16 mg/kg body weight of manganese chloride (this equals ~4mg of elemental manganese) to Zucker diabetic fatty rats (standard model of diet-induced diabetes) significantly reduced the binding of immune cells to the endothelium and will thus have an ameliorative effect on the development of cardiovascular diseases.

As the data in figure 2 goes to show you the human equivalent of ~50mg/day elemental manganese did also induce statistically highly significant reductions in cholesterol and - what's probably of greater real-world relevance in view of the CVD-risk - a 60% reduction (!) in triglycerides in the diabetic rodents.

Figure 2: Relative expression of markers of binding of immune cells to the endothelium and cholesterol and triglyceride levels in diabetic rodents with or without additional 4mg/kg elemental manganese in their drinking water (Burlet. 2013)

Among the plethora of (trace-)minerals manganese certainly is one of the least known and that despite the fact that it plays an absolutely crucial role in blood glucose management. In view of the fact that it is known to raise not decrease blood glucose, it is however understandable that detailed information about this trace mineral the levels of which are tightly regulated by our bodies is scarce - I mean, the number of people suffering from hypoglycemic episodes is several magnitudes smaller than the number of (pre-)diabetics. Moreover, the beneficial effects on blood lipids have also been confirmed in different scenarios such as a rodent model of menopause (Bae. 2011)

Table 1: Average manganese content of selected foods (download full list from the USDA, here)

Since manganese also figures in  the enzymatic cascades which underly protein metabolism, bone formation, the synthesis of the neurotransmitter GABA and is an essential constituent of the eponymous manganese superoxide dismutase, one of the most important enzymes in the endogenous anti-oxidant system of the mitochondria, it is actually no wonder that manganese is officially considered one of the "essential trace minerals". With an adequate intake of 2.3mg for men and 1.8 mg for women (according to the Linus Pauling Institute) and it's abundance in Western type diets (>10mg/day), full-blown deficiencies are yet rare.

A 1987 study by Friedman et al. did yet show that a diet that contains insufficient amounts of manganese will result in skin rashes and pathologically low cholesterol levels. Since high levels of manganese are also implicated in the development of Parkinson's or rather a "Parkinson like disease" that's induced by manganese accumulation, but does not involve degeneration of midbrain dopamine neurons, supplementation with larger amounts of manganese without knowing one's dietary intake (better even tissue and serum levels), supplementation high(er)-dose supplementation is thus counter-indicated. Whether human type II diabetics can benefit from supplementation and which dosages are save and effective will still have to be elucidated.

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That's it already: In case you want more short news, even before the official installment of "On Short Notice" is posted tomorrow (don't as me what's going to be in there, I have no clue as of yet ;-), I suggest you visit the SuppVersity Facebook Page and check out these

• NON-ergogenic gadget of the week - Holographic wrist band meant to increase performance turns out to worsen performance compared to performance worse than "placebo"  (read more)
• The anti CVD taurine <> cholesterol connection - High serum taurine levels protect people with abnormally high cholesterol from cardiovascular disease (read more)
• Tennis elbow? Ultrasound and laser therapy show promise in treatment of medial and lateral epicondylitis, review says. (read more)
• Milk - What's good for the young ones can't be bad for the elderly, right? Right! Japanese 70+-agers' BMI and HDL levels benefit from milk consumption (read more)

as well as the other news I  have already posted + those that are going to appear within the next 24h and before the short news are even written (let alone published ;-).

References: 

• Bae YJ, Choi MK, Kim MH. Manganese supplementation reduces the blood cholesterol levels in Ca-deficient ovariectomized rats. Biol Trace Elem Res. 2011 Jun;141(1-3):224-31.
• Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M, Macdonald MJ, McGee SL, Gibala MJ. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. J Physiol. 2008; 586: 151-160.
• Burlet E, Jain SK. Manganese supplementation reduces high glucose-induced monocyte adhesion to endothelial cells and endothelial dysfunction in zucker diabetic fatty rats. J Biol Chem. 2013 Jan 17.
• Friedman BJ, Freeland-Graves JH, Bales CW, et al. Manganese balance and clinical observations in young men fed a manganese-deficient diet. J Nutr. 1987;117(1):133-143.
• Psilander N, Niklas P, Wang L, Li W, Westergren J, Jens W, Tonkonogi M, Michail T, Sahlin K, Kent S. Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise. Eur J Appl Physiol. 2010; 110: 597-606.
• Roberts MD, Iosia M, Kerksick CM, Taylor LW, Campbell B, Wilborn CD, Harvey T, Cooke M, Rasmussen C, Greenwood M, Wilson R, Jitomir J, Willoughby D, Kreider RB. Effects of arachidonic acid supplementation on training adaptations in resistance-trained males. J Int Soc Sports Nutr. 2007 Nov 28;4:21.
• Swenne I, Vessby B. Relationship of Δ(6) -desaturase and Δ(5) -desaturase activities with thyroid hormone status in adolescents with eating disorders and weight loss. Acta Paediatr. 2013 Jan 19.
• Tanaka, H, Morimura K, Shiose H. An optimal exercise protocol for improving endurance performance and health. J Phys Fitness Sports Med. 2013; 1(4): 595-604.