Serum & Intramuscular Testosterone, DHT and Androgen Receptor Response to High vs. Low Volume Training

Another set for another ng of testosterone? Does it work that way and is it worth it - not just on paper, but in terms of real gains?

I know that we don't know! And among the many things we don't know the influence of the post-workout elevation in the long-thought "anabolic" hormones testosterone, growth hormone, and co. is unquestionably one of my personal favorites. You've read about it, here at the SuppVersity many times and I got to tell you in advance that the absence of convincing evidence for / against its importance will become a problem in the bottom line of today's SuppVersity article dealing with the intriguing results of an experiment that has been conducted by Lukas J. Farbiak as part of his Honors Thesis (Farbiak. 2013).

"Effects of Lower- and Higher-Volume Resistance Exercise on Serum Total and Free Testosterone, Skeletal Muscle Testosterone and Dihydrotestosterone Content, and Skeletal Muscle Androgen Receptor mRNA Expression and Protein Content"

That's quite a title for a thesis right? Well, one thing's for sure: Having the words, "high, "low", "training volume", "resistance exercise", "total and free testosterone", "dihydrotestostereone", etc. all in the headline is certainly an advantage when it comes to findability of a paper - or in this case - a thesis in a database. And in fact, it was really the title of the 91 page piece that has caught my eye, a couple of days ago - what peaked my interest, though were the research hypotheses Farbiak, whose thesis was by the way overseen by Darryn Willoughby, formulated:

• H1 : Following the HV [high volume] exercise bout involving both upper- and lower-body resistance exercise, a significant increase in serum testosterone will occur compared to the LV [low volume] exercise bout only involving lower-body resistance exercise. 
• H2 : Following the HV exercise bout involving both upper- and lower-body resistance exercise, a significant increase in muscle testosterone and DHT content will occur compared to the LV exercise bout only involving lower-body resistance exercise. 
• H3 : Following the HV exercise bout involving both upper- and lower-body resistance exercise, a significant increase in AR mRNA expression and protein content will occur compared to the LV exercise bout only involving lower-body resistance exercise.

I took the liberty of highlighting three things in Farbiak's hypotheses, which tell you why you want to know the outcome of the study, even if the current "state of the research" questions the significance of exercise-induced elevations of androgens in terms of their ability to elicit muscle growth.

What's special, here, is that we are not measuring serum levels exclusively, but get a much more detailed picture of the endocrine response to high vs. medium volume training.

Why would the internal androgen levels differ from those outside of the cell? The notion that this could and in fact is the case did not arise before Hammes et al. discovered that contrary to the previously heralded position that says that only free testosterone levels would matter and that the latter would be able to enter the cells via passive diffusion, the entrance of testosterone into the cell is actually governed by (attention please) megalin, a low density lipoprotein receptor (LDR) related  protein. According to Hammes, SHBG can bind to megalin can internalize the SHBG + androgen pair into the cytoplasm, where the binding globulin is degraded and the steroid will be released to the cellular environment.It goes without saying that this changes the interpretation of previous data and provides a whole new perspective on the androgen - muscle interaction with the formerly "passive" bound testosterone suddenly having the ability to promote hypertrophy.

In this context the relation of free androgens, androgen receptor expression and the presence and concentration of intra-muscular may well provide first insights into why previous studies, which have predominantly relied on the determination of serum levels without even checking,

• whether there were enough receptors to (this is an oversimplification) transduct the anabolic signal of workout induced increases in testosterone to the muscle cells, and
• to which extent the changes in extra-cellular androgen levels correlate with the amount of testosterone and DHT that's actually in the muscle.

Now that I have your full attention let's take a look at what kind of workout program we are dealing with in the study at hand, for which the researchers recruited 10 "apparently healthy resistance trained  [regular,  consistent  resistance  training (i.e. thrice weekly) for  at least 1 year prior to the onset of the study], men between the ages of 18-30" (Farbiak. 2013).

"In a randomized, cross-over design, participants visited the laboratory on 5 separate occasions in the following manner: visit 1 = entry/familiarization session, visit 2 = testing/resistance exercise session 1, visit 3 = 24 hour follow-up for session 1, visit 4 = testing/resistance exercise session 2, visit 5 = 24 hour follow-up for session 2. Relative to the testing sessions (visits 2 & 4), participants performed a resistance exercise session involving the knee extension exercise on two occasions separated by one week. One session constituted the control session and was preceded by rest and the other was preceded by the experimental session and preceded by a bout of high-volume, moderate-intensity upper-body resistance exercise using short rest periods." (Farbiak. 2013).

The dependent variables, i.e. serum free and total testosterone, intra-muscular testosterone, DHT and  AR  receptor mRNA, as well as protein expression were determined on all, but the initial entry/familiarization visit.

The workout itself (remember this is not a chronic resistance training study, as the one by West et al. (2012) which is - at least to my knowledge unique wrt to the real-world relevance of the data; learn more) consisted of

• LV - low volume: 5 sets of 5-RM (90%-95% 1-RM) of the bilateral knee extension exercise with 3 minutes of rest between sets.
• HV - high volume: Upper-body resistance exercise protocol of 4 sets of 10-RM each of the bench press, seated row, and overhead shoulder press exercises immediately prior to the knee extension protocol. 
• the initial load was set at 80% of the 1-RM for each participant. 
• if muscle fatigue/failure occurred during a set, a spotter provided assistance until the participant completed the remaining repetitions and resistance was reduced for subsequent sets

In all cases, 2 minutes of rest separated sets and exercises. All training sessions were conducted in
the Baylor Laboratories for Exercise Science & Technology (BLEST) and supervised by study personnel.

Figure 1: Sum total and free testosterone in response to high and low volume training (Farbiak. 2013)

Now, the data in figure 1 actually mirrors what we already know: The overall serum response to high volume training is more pronounced that that to playing around on a leg extension machine (which happens to be the favorite benchmark for the / I repeat myself / likewise not very useful studies on PWO protein synthesis).

"Several studies have shown that acute resistance exercise bouts elicit a testosterone response (Kraemer. 1990; Kraemer, Gordon et al., 1991; Kraemer, Hakkinen et al., 1999; Spiering, Kraemer. 2008; Roberts. 2009). Such exercise bouts shown to elicit a testosterone response need to consist of a high intensity (load) (85%-95%) of one repetition max and meet a minimum threshold, and moderate to high volume (set x number of reps x intensity). Exercises that utilize large muscle groups (i.e. power clean, squats, and dead lifts) as well as performing exercises involving large muscle groups first, with short rest periods (30-60 sec) have shown to elicit the greatest response (Kraemer, Marchitelli et al., 1990; Spiering, Kraemer et al., 2008; Vingren, Kraemer et al., 2010). [...] It is known that the testosterone response resistance exercise is highly variable (Kraemer, 1988). Thus, it is possible that after multiple years of resistance training, the initial phasic response of the hypothalamus gonadal axis (aka. testosterone axis) response elicited by resistance exercise bout un trained individuals has become blunted from habitual resistance exercise. However, it is necessary that further research be conducted to elucidate why this blunted response occurs." (Farbiak. 2013; my emphasis of the key points)

As far as the differential response of free and total testosterone is concerned the tendency for both to go hand in hand has been observed in previous studies, as well (Durand. 2003; Kraemer. 1990; Kraemer. 1991; Kraemer. 1999; Spiering. 2008; Roberts. 2009). What's "new" or let's say something we have much less reliable data on are the changes that take place within the muscle (see figure 2)

Figure 2: Intra-muscular androgen & -receptor mRNA & protein expression (Farbiak. 2013)

Interestingly, enough those potentially far more relevant changes take place on a very different time-scale. While we do see the touted increases in serum testosterone in the immediate vicinity of the workout, the corresponding intra-muscular levels are actually declining from pre to post (red vs. blue bars). As Farbiak points out, these changes were yet statistically non-significant and to thus correspond to previous results presented by Vingren & Kraemer et  al. in 2008 (Kraemer. 2008). The same goes for the DHT response that did not make it past the p > 0.05 mark of statistical significance (FYI: this means the chance that this is just a statistical artifice is >5% and thus "not significant").

As far as the androgen receptor mRNA expression is concerned a often-cited (also by me, here at the SuppVersity) by Kraemer et al. observed a reduction in response to a single bout of resistance exercise, (Kraemer. 2010). The latter does actually conflict with in-vitro studies that suggested that the presence of higher testosterone levels would lead to an increased expression of androgen receptor mRNA and proteins - an observation of which Farbiak points out that it does not only stand in line with a previous study by Willoughby  and  Taylor (Willoughby. 2004) who observed a

"+35% and +43% increases in AR mRNA expression 48 hours after the first and third resistance exercise bouts, with a peak increase of 68% in AR mRNA expression occurring 48 hours after the second resistance exercise bout within the resistance exercise group" (Farbriak. 2013)

which was ascribed to corresponding increases in serum testosterone levels. In view of the fact that the latter were absent in Farbiak's subjects, it is not surprising that the existing increases in AR receptor mRNA in the study at hand did not reach statistical significance. Similarly, Farbiak was not able to show significant alterations in androgen receptor protein content in response to either LV or HV bouts of resistance exercise, which leaves us with pretty much of a null result and raises the question...

What do we make of this null result?

I guess the first thing would be to take a look at the underlying "mathematical" reason for the non-significance of the results... standard deviations - HUGE standard deviations, indeed. So huge that I initially thought that this must be a mistake, I mean if you have a mean pre-testosterone level of 43.59 ng/dl and a standard devition of 43.03 ng/dl, i.e. 99%, what can you expect? Now this is an extreme example, but in view of the relative small number of participants it should suffice to tell you that - maybe - we should not focus that much on statistical significance, here?

Suggested read: "Advanced Trainees Benefit from Increased Training Volume! Greater & Steadier Strength Gains with 8 Sets of Squats. Plus: Over 6 Weeks, 1 Set and 4 Sets Equally (In-)Effective." If higher volume begets higher T-responses and the latter is blunted in advanced trainees, it would appear logical that they benefit from doing more (learn more)

Schoenfeld mentioned similar effects in a whole host of pertintent studies in his excellent review of the literature on the effects of the exercise induced hormonal changes on muscle hypertrophy (I mentioned this review before, e.g. March 2, 2013; March 4, 2013). So it could simply be inter-individual variability that skewed the results. If that was the case, it is however unlikely to assume a dose-response relationship between any (serum or intramuscular) changes in androgens / androgen receptor expression and skeletal muscle hypertrophy - I mean that would imply much more pronounced differences in muscle growth in response to a workout than the real world results do indicate.

Another factor that may have influenced the results is the high training experience (>8 years) of the participants in the Farbiak study, if the initially cited hypothesis that the androgen response to exercise declines in experienced athletes turns out to be true, the non-significance of the endo- and paracrine hormonal response in the study at hand could well be "normal" and no anomaly. And if that was the case, it would suggest that the changes that were observed in previous studies, many of which were conducted on rookies, do matter - at least to a certain degree.

To use this as the only explanation for the (comparatively) exorbitant gains training noobs experience once they pick up their first dumb- and barbells would yet be shortsighted. To add it as yet one of the many confounding factors, on the other hand, would make perfect sense, as it would stand in line with the (comparably) short-term detrimental effects chronic resistance training without off-times has on the protein synthetic mTOR response to exercise (learn more about exercise induced "mTOR resistance").

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Bottom line: To sum it up, while we do now have another puzzle piece, it looks as if it only made us realize that our 1,000 piece puzzle is in fact a 10,000 piece puzzle and that it will probably require more than just a handful of follow up study to investigate the numerous factors "such as age, time of day [not all trainees trained at the same time, so the circadian rhythm may be an issue, in the study at hand], and training experience" (Farbiak. 2013) of which Farbiak speculates in the discussion of his honors thesis that they may account for the observed discrepancies and inconsistencies in testosterone response to acute resistance exercise... ah, and once we've done that, we would need more studies like the one by West et al. (2012) to see the real world implications. I guess, we better issue a bond to get those finance, right?

References:

• Farbiak, LJ. Effects of Lower- and Higher-Volume Resistance Exercise on Serum Total and Free Testosterone, Skeletal Muscle Testosterone and Dihydrotestosterone Content, and Skeletal Muscle Androgen Receptor mRNA Expression and Protein Content. A Thesis Submitted to the Faculty of Baylor University In Partial Fulfillment of the Requirements for the Honors Program. May 2013.
• Durand RJ, Castracane VD, Hollander DB, Tryniecki JL, Bamman MM, O'Neal S, Hebert EP, Kraemer RR. Hormonal responses from concentric and eccentric muscle contractions. Med Sci Sports Exerc. 2003 Jun;35(6):937-43.
• Hammes A, Andreassen TK, Spoelgen R, Raila J, Hubner N, Schulz H, Metzger J, Schweigert FJ, Luppa PB, Nykjaer A, Willnow TE. Role of endocytosis in cellular uptake of sex steroids. Cell. 2005 Sep 9;122(5):751-62. 
• Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, Fleck SJ. Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol. 1990 Oct;69(4):1442-50.
• Kraemer WJ, Gordon SE, Fleck SJ, Marchitelli LJ, Mello R, Dziados JE, Friedl K, Harman E, Maresh C, Fry AC. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int J Sports Med. 1991 Apr;12(2):228-35.
• Kraemer WJ, Häkkinen K, Newton RU, Nindl BC, Volek JS, McCormick M, Gotshalk LA, Gordon SE, Fleck SJ, Campbell WW, Putukian M, Evans WJ. Effects of heavy-resistance training on hormonal response patterns in younger vs. older men. J Appl Physiol. 1999 Sep;87(3):982-92.
• Kraemer WJ, Ratamess NA. Hormonal responses and adaptations to resistance exercise and training. Sports Med. 2005;35(4):339-61.
• Roberts MD, Dalbo VJ, Hassell SE, Kerksick CM. The expression of androgen-regulated genes before and after a resistance exercise bout in younger and older men. J Strength Cond Res. 2009 Jul;23(4):1060-7. 
• Schoenfeld BJ. Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design. J Strength Cond Res. 2013 Jun;27(6):1720-30.
• Spiering BA, Kraemer WJ, Anderson JM, Armstrong LE, Nindl BC, Volek JS, Maresh CM. Resistance exercise biology: manipulation of resistance exercise programme variables determines the responses of cellular and molecular signalling pathways. Sports Med. 2008;38(7):527-40.
• Spiering BA, Kraemer WJ, Vingren JL, Ratamess NA, Anderson JM, Armstrong LE, Nindl BC, Volek JS, Häkkinen K, Maresh CM. Elevated endogenous testosterone concentrations potentiate muscle androgen receptor responses to resistance exercise. J Steroid Biochem Mol Biol. 2009 Apr;114(3-5):195-9.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012 Jul;112(7):2693-702.
• Willoughby DS, Taylor L. Effects of sequential bouts of resistance exercise on androgen receptor expression. Med Sci Sports Exerc. 2004 Sep;36(9):1499-506.

Ramadan Improves Body Composition of Young & Older Men, Young Women Don't Benefit and Women >37y Become Fat During the Fast - Implications for Intermittent Fasting?

It may not be "paleo conform", there but the traditional Ramadan menu is 100% home-made from fresh foods - that alone will make a huge difference.

"I hear you..." What's that supposed to mean? Well, in a way I am running the SuppVersity for me, because I like the idea that people like you come here and think "Hey, today I've learned something new", "... read something interesting" or at even"... have been enlightened". On the other hand, this entails that I got to tailor the topics to your interests as well and since the short Facebook item on the effects of Ramadan fasting on body composition I posted on Facebook, a couple of days ago, which spiked so much interest, I will take it up and write a whole article about this soon-to-be-published study from the Mashhad University of Medical Science and the University of Nicosia (Norouzy. 2013).

Ramadan is not "intermittent fasting"...

... at least not in the sense it's interpreted by most people.In fact, there are a whole host of differences one could think about, but for our purpose which is the use of intermittent fasting as a way to live healthier and/or improve our physique these are just a couple of examples that come to mind:

• 

  Effect of Ramadan fasting on perceived snack, fluid and food intake in 411 male and 323 female Malaysian Junior Level Muslim athletes (data calculated based on Singh. 2011; originally posted as part of the Intermittent Thoughts on Intermittent Fasting on Sept. 06, 2011)

  The fasting window can actually be pretty small - While all Muslims will eat the lions-share of their energy intake in the evening many rise early (esp. when Ramadan falls into the winter months) and ingest a medium sized breakfast to "make it through the day".
• Food quality (from a health perspective) is not always ideal - While researchers have observed that there seems to be an unconcious increase in protein intake (+6.6% protein; less carbs and fats; Trabelsi. 2011), this is yet not a characteristic feature of the protocol, but rather a result of dining with the family, not snacking and putting an emphasis on whole self-prepared (and more expensive) food.
  
• During the fast Muslims don't drink - This is obviously something anybody following a "lean gains" like intermittent fast or an "alternative day fasting" protocol, where people eat only 500kcal or so two or three times a week and just follow their habitual diet on the other days would not remotely consider. However, in a paper published in the European Journal of Clinical Nutrition in 2003, Leiper, Molla and Molla report that despite the fact that "[d]uring the daylight hours of Ramadan fasting, practising Muslims are undoubtedly dehydrating", it is neither "clear whether they are chronically hypohydrated" nor have there been any "detrimental effects on health [...] directly attribut[able] to negative water balance at the levels that may be produced during Ramadan" observed in any scientifically relevant studies (Leiper. 2003). It is thus relatively safe for us to assume that we can neglect he influence of potential dehydration in our initial analysis of respective studies.
• Other differences  - I guess, I better spend time discussing the latest study and refer you to the Intermittent Thoughts Series, where I discussed the existing differences and implication at length. You can browse the articles here. Start with the first post "Myth #1: A Higher Meal Frequency Equals a Higher Metabolic Rate" from September 4th, 2011 and click yourself through the  rest of the series. You won't regret reading it, I promise ;-)

A one-to-one translation of the results from the study at hand to your efforts of a practical and effective way to lose body fat (this is where it excels - and not in "lean gaining") is thus unwarranted. There may yet still be a couple of things, we can learn from what the observations the Iranian and Greek researchers made in their 240 adult subjects (male: 158) who fasted between sunrise and sunset for at least 20 days.

Figure 1: Body weight and composition before and after Ramadan and percentage changes from baseline according to gender and age; data expressed relative to baseline (Norouzy. 2013)

As the data in figure 1 goes to show you the overall pattern that emerges is positive one. However, the weight the subjects, who were grouped according to age and sex, lost was (as it was to be expected, by the way) not pure fat mass. Still, with the exception of older women all subjects improved their body fat levels.

Is intermittent fasting not for women?

Apropos women, it's not just that the older women (>37y) did actually gain body fat, the already minimal reduction in body fat (%) in the younger women was also non-significant (p = 0.079 vs. p=0.029 in men). Taken together these results appear to suggest that a non-controlled, intermittent fasting regimen that's based solely on the absence of food intake in the course of the day would be beneficial for men only.

Looks good, tastes good, is good - high protein foods! Unfortunately many  women (obyiously not you, right) have still not gotten the message that by simply making sure you have 30g+ of protein in your three-square meals is probably the easiest way to improve both your physique and health. Still, the study at hand provides further evidence that a low protein intake is not all that makes it more difficult for women to lose fat (learn more)

It should be said, though, that these results stand in conflict with previous studies by Husain et al. who report more, not less weight and body fat loss in the 20-45 year-old female subjects of their Ramadan fasting study (Husain. 1987). An observation they pin on the "increase in energy expenditure" that comes with preparing the meal for the whole family... well, you know that I am not afraid of calling *bs* by its name and this explanation certainly is*bs*. It is in fact much more likely that the differences could be explained by a lower overall energy intake just as the increase in body weight Frost & Pirani observed in the young men in another cohort was solely a result of the nightly binges (Frost. 1987). I mean, we all know that women are more likely to be concerned about the detrimental effects of a high food intake in the evening on their body composition, so that it is not unlikely that the 20-45 year old women in the Husain study were deliberately limiting their energy intake, while the men in the study by Frost & Pirani gave in to their ravenous appetite and the delicious meals their wifes, sisters and aunts had prepared (I will leave it up to you if you call the role allocation "traditional" or "chauvinist", btw. ;-)

This is basically also how Norouzy et al. try to explain the inconsistencies that become obvious, when you compare the study at hand to previous results:

"This inconsistency may be a result of the subject characteristics and, in particular, age, sex and physical activity, as well as the number of hours of fasting observed during Ramadan, which varies according to geographical location from 11 to 19 h a day." (Norouzy. 2013)

Furthermore, the majority of previous studies included young subjects aged <35 years; thus, limited information is available on subjects of older ages and according to Norouzy et al. their study was the first to "attempted to compare changes in body weight and composition in different ages and sex" (Norouzy. 2013). In view of the existing differences in resting energy expenditure and physical activity this could well explain part of the differences between the studies and the high amounts of "null results" (=no change at all) other scientists reported (Ati.1995; Finch. 1998; Ramadan. 2002; Yucel.2004).

Figure 2: Dietary energy, macronutrient and fibre intakes before and during Ramadan and percentage changes from baseline according to gender; I must warn you though, according to the scientists dietary records were not available from all participants (Norouzy. 2013)

Going back to the study at hand, the data in figure 2 indicates that neither the general trends, nor the age and sex-specific differences can be fully explained by changes in total energy (due to high variability borderline significant only in men, totally insignificant in women) or macronutrient ratios (insignificant in both); an observation the Iranian researchers try to explain by differences in nutrient oxidation and changes in energy expenditure during the fasting period and add:

Overtraining and undereating will have your thyroid hormones plummet within no more than four days (learn more) - would Intermittent Fasting make that worse, or could it - as I suggest in the bottom line - maybe even postpone the onset of plummeting T3 and increasing rT3 levels by allowing you to eat to satiety once a day? Respective studies are missing, but it does not sound totally implausible!?

"A previous study investigating the effect of Ramadan on the abdominal fat distribution by computed tomography found reductions only in the visceral fat tissue area, and only in subjects in their twenties and in women, and attributed this to fat redistribution because no changes in weight were observed (Yucel et al., 2004). Thus, although this remains to be investigated, differences between sexes and ages may be a result of differences in nutrient oxidation and changes in energy expenditure during the fasting period. For example, as shown in healthy women aged 25–39 years, Ramadan fasting induced a significant decline in carbohydrate oxidation and a significant increase of fat oxidation, as well as a decline in diurnal energy expenditure, which may be attributed to the absence of post-prandial thermogenesis during fasting (Ati al., 1995). A reduction of energy expenditure during Ramadan was also reported in another study (Sweileh et al., 1992)." (Norouzy. 2013)

Now, these changes in (1) fatty acid oxidation (Ati. 1995), (2) improvements in visceral fat (questionable whether those occurred in the study at hand that did not observe sign. reductions in waist circumference in any group) and (3) overall energy expenditure would unquestionably be of interested for the average physical culturist, as well and (1) could in fact be one of the reasons that numerous people report great fat loss following respective regimen. After all, one of the major obstacles of translating fatty acid oxidation to fat loss is that the latter must occur in the presence of an energy deficit or the body fat that's getting oxidized on time-point T1 is going to be replenished from the fats, carbs and protein on time-point T2.

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Exercise prevents, not amplifies, fasting induced protein degradation. In a 2006 paper, Kasperek et al. report that

"Exercise did prevent the increase in the rate of total protein degradation caused by food restriction, which may have important implications in weight reduction diets." (Kasperek. 2006)

And indeed, any type of fast (even an intermittent one) that is intended to improve body composition would be missing out big time without the exercise component - just keep it to a sane level and focus on muscle preserving strength training.

Energy intake counts: If you remember the recent SuppVersity post on the detrimental effects a caloric deficit can have on the thyroid function in the presence of a high volume training regimen after four days only, it may sound hilarious that the bottom line starts with the words "energy intake counts". However, faced with the fact that a very large energy deficit will stall weight loss, people tend to forget that not being in a minimal energy deficit won't allow you to lose weight either (the whole alternate day fasting regimen is based on the simple fact that 90% of the people won't fully compensate for the caloric deficit on the low calorie = fasting days).

In that intermittent fasting or rather the ingestion of one or two large meals instead of many mini-meals may provide an edge over "classic" dieting as it allows for a daily "feast" that could trick your body to believe that the starvation it experienced earlier in the day was already over. This in turn could delay the metabolic slowdown and rock bottom T3 levels Loucks et al. observed in the female participants of their exercise + dieting trial within no more than 4 days (go back and learn all the details about the Loucks study). If that's the case, we would not have an absolute increase in energy expenditure (see pt. 3, above), but at least a relative one - compared to eating 6 mini square meals.

References:

• el Ati J, Beji C, Danguir J. Increased fat oxidation during Ramadan fasting in healthy women: an adaptative mechanism for body-weight maintenance. Am J Clin Nutr. 1995 Aug;62(2):302-7.  
• Frost G, Pirani S. Meal frequency and nutritional intake during Ramadan: a pilot study. Hum Nutr Appl Nutr. 1987 Feb;41(1):47-50.
• Husain R, Duncan MT, Cheah SH, Ch'ng SL. Effects of fasting in Ramadan on tropical Asiatic Moslems. Br J Nutr. 1987 Jul;58(1):41-8.
• Kasperek GJ, Conway GR, Krayeski DS, Lohne JJ. A reexamination of the effect of exercise on rate of muscle protein degradation. Am J Physiol. 1992 Dec;263(6 Pt 1):E1144-50. 
• Leiper JB, Molla AM, Molla AM. Effects on health of fluid restriction during fasting in Ramadan. Eur J Clin Nutr. 2003 Dec;57 Suppl 2:S30-8.
• Ramadan J. Does fasting during Ramadan alter body composition, blood constituents and physical performance? Med Princ Pract. 2002;11 Suppl 2:41-6. 
• Singh R, Hwa OC, Roy J, Jin CW, Ismail SM, Lan MF, Hiong LL, Aziz AR. Subjective Perception of Sports Performance, Training, Sleep and Dietary Patterns of Malaysian Junior Muslim Athletes during Ramadan Intermittent Fasting. Asian J Sports Med. 2011 Sep;2(3):167-76.
• Sweileh N, Schnitzler A, Hunter GR, Davis B. Body composition and energy metabolism in resting and exercising muslims during Ramadan fast. J Sports Med Phys Fitness. 1992 Jun;32(2):156-63. 
• Trabelsi K, El Abed K, Trepanowski JF, Stannard SR, Ghlissi Z, Ghozzi H, Masmoudi L, Jammoussi K, Hakim A. Effects of ramadan fasting on biochemical and anthropometric parameters in physically active men. Asian J Sports Med. 2011 Sep;2(3):134-44.
• Yucel A, Degirmenci B, Acar M, Albayrak R, Haktanir A. The effect of fasting month of Ramadan on the abdominal fat distribution: assessment by computed tomography. Tohoku J Exp Med. 2004 Nov;204(3):179-87.

Triple Your Energy Expenditure During Shuttle Runs + Learn Why Intensity and not Just Weight x Distance Counts

The shorter the distances between the cones on a shuttle run the greater the energy expenditure per meter you are sprinting - in fact the amount of energy you will burn on a 10m run is 3.5x higher than that your body will expend on the corresponding 10m of a 20m sprint - and you bet that this is not a "shuttle run"-specific effect.

I have already hinted at the unfortunate circumstance that trainees and even scientists still adhere to the (obviously) lousy hypothesis that it were possible to calculate the energy expenditure of their participants by simply multiplying the force they apply to move a given object (or themselves) from point A to point B.

It is true that the result, W (as in W-orlkload) = F (as in F-orce) x d (as in d-istance) will "look" like it should tell you the amount of Energy that's been necessary to move the object from A to B, but that would require that (a) all the bio-chemical energy your body produces would be converted to mechanical energy and none would be lost and (b) the acceleration and thus force (F = mass x acceleration) would be constant - both pretty irrational assumption even for a non-physicist, I should say.

Against that background it should not surprise you that a recent study from the School of Sports and Exercise Sciences at the University of Rome does now report:

3.5x higher energy expenditure / m on short (10m) vs. long (20m) shuttle runs

Kinetic measurement / estimation of the energy expenditure - how did that work? (1) The velocity profile during the shuttle runs was determined by means of a high-frequency camera. (2) The video was then analyzed using free software Kinovea-0.8.7 to obtain the actual distance covered by the center of mass of the subject over each nominal 2-m stretch as well as the corresponding time. (3) This allowed for the calculation of the time course of the speed [note to this ends they did not use the time-integral over M x v²/2, which would be how it's done, but simply the peak v-elocity], and, hence, of the corresponding acceleration, as well as the peak speed, which where then used to "estimate" (Buglione. 2013) the energy cost of shuttle running by multiplying it with a variable ny (~0.25; cf. Prampero. 2005) describing the efficiency of mechanical work and adding the result to energy cost of constant speed running.

To measure this difference, Buglione and di Prampero conducted two experiments. For experiment one, they invited

• 29 physically active subjects practicing in various amateur sporting activities, 
• 28 professional soccer players and 
• 8 high-level runners 

for whom the energy costs during the shuttle runs were measured directly by from gas exchange
measurements over 155 trials and

• 10 subjects of 25.4±3.9 age (years), 70.3±2.6 body mass (kg), 1.75±0.05 stature (m) belonging to the Italian national field hockey team

for whom the energy costs were calculated (the math approach) based on a kinetic approach (if you are a physics geek see the box on the right-hand side for more details).

Figure 1: Energy expenditure in J/(kg*m) plotted against running speed in m/s (left) and energy cost of shuttle running, as obtained from the kinetic (CSh-Kin) or energetic approaches (CSh-En) are plotted as a function of average speed over 20 m (open triangles, CSh-Kin; close triangles) and 10 m (open circles, CSh-Kin; dots; Buglione. 2013)

As the data in figure 1 goes to show you the energetic costs for a given sprint (~ interval) distance on the shuttle run increases linearly with the velocity v. The incline, of the graph, on the other hand, is determined by the distance with the a much steeper incline on the short (10m) vs. long (20m) shuttle runs.

Kinetics + math = cheap but not always accurate

Remember the last study involving a shuttle run? It dealt with the ergogenic effects of glycerol (read more).

Interestingly, the results from the direct measurement are in good accordance with those calculated based on the scientists kinetic approach (see figure 1, left; where the energy cost of shuttle running [J/(kg m)] obtained from the kinetic approach (CSh-Kin) is plotted as a function of the corresponding value obtained from the energetic approach (CSh-En)), for the longer distances.

This observation confirms Antonio Buglione and Pietro Enrico di Prampero hypothesis that their "kinetic approach" would qualify to as a assess the energy expenditure during high intensity (intermittent) exercises like the shuttle run over long(er) distances without having to resort to expensive experimental equipment.

Remember: All it takes is a cheap Casio Exilim EX-FH25 to record the runs at a high-frequency of 210 Hz and the video software.

What's the physiological underpinning of the short vs. long difference?

Now, analyzing the underlying physiological mechanisms that yield the directly measured 3.5x increase in energy expenditure during the short 20m shuttle runs was not part of the Italians' study. Therefore we will have to invoke the results of another recently published study by Jared R. Fletcher et al. from the Human Performance Laboratory at the Faculty of Kinesiology of the University of Calgary (Fletcher. 2013), who set out to answer the question: "Can muscle shortening alone, explain the energy cost of muscle contraction in vivo?"

Their results, part of which you can see in figure 2 clearly indicate that the actual energy energy that's necessary to maintain a given torque (which is what you would usually calculate based on the weight and the lever, e.g. the poundage on the bar and the length of your forearm for a simplistic model of a biceps curl), increases almost linearly with the shortening velocity.

Figure 2: The relationship between the rate of energy use to maintain a given torque and magnitude of muscle fascicle shortening (cm).

The main finding in this study was that when greater MG fascicle shortening was imposed, the rate of muscle oxygen uptake increased.

We assume this measured oxygen uptake is proportional to the total EC [energy consumption] of the muscle contractions; that is, any anaerobic energy utilization would increase in proportion with the increases in oxygen uptake. (Fletcher. 2013; my emphasis)

Moroever, kinetic (=moving the weight) vs. isokinetic (=static) exercises resulted in significantly greater muscle shortening and greater shortening velocity. I is therefore not surprising that the isokinetic plantarflexion contraction the 19 triathletes who were in the pre-competition phase of their training performed during the testing session (30 reps at 1/s) resulted in a +19% greater energy expenditure than their isometric counterpart.

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Bottom line: Overall, the two studies have a general, and two very practical take home messages. The general one is that you cannot calculate the amount of energy your body will consume during a certain exercise / movement paper based on simplistic equations that have been developed to be applied to standardized weights on straight levers that are moved with constant velocity along strictly linear or circular paths and against constant, at best linearly in-/decreasing resistances.

The practical take home messages, on the other hand, are that you (a) want to maximize muscular activity and that you (b) achieve that with short, intense, fast, yet not ballistic (no cheating the weight over 95% of the distance) kinetic movements. If you doubt the validity of this approach in terms of it's ability to help you shed body fat, you just have to take another look at one of the following posts:

• 

  Another suggested read: "Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!" A perfect example of the fallacy of simplistic energy expenditure calculations (read more)

  From 16% to 8% Body Fat in 10 Weeks: Crossfit Workout Gets The Leanest Shredded - But Only the Fittest Survive (read more)
• Eight HIIT Sessions on the Rowing Ergometer Cut Body Fat, Increase Adiponectin, VO2Max & Performance in National Level Rowers - Workmatched Classic "Cardio" Does Nothing (read more)
• Reduced Exertion High Intensity Training - A Minimalist 2x20s HIIT Protocol For The Male Convenience Generation (read more)
• The Iranian HIIT Solution: Three 200m Sprint Sessions per Week Double Insulin Sensitivity & Normalize Leptin Levels (read more)

Convinced? Well, that's what I'd expect... although, actually I would have hoped that you'd been convinced of the validity of the intensity vs. duration approach to fat loss before. You were? Ok, then today's SuppVersity post will just have reinforced what you already knew ;-)

References:

• Buglione, A. di Prampero, PE. The energy cost of shuttle running. Eur J Appl Physiol. 2013 [epub ahead of print]
• di Prampero PE, Fusi S, Sepulcri L, Morin JB, Belli A, Antonutto G. Sprint running: a new energetic approach. J Exp Biol. 2005 Jul;208(Pt 14):2809-16.
• Fletcher JR, Groves EM, Pfister TR, MacIntosh, BR. Can muscle shortening alone, explain the energy cost of muscle contraction in vivo? Eur J Appl Physiol. 2013 [epub ahead of print]

Beyond Testosterone: 200mg/day of Tongkat Ali (Eurycoma Longifolia) for Stress Management & Improved Mood!?

It does not always take a pill to effectively manage your stress levels. Don't forget to take your well-deserved timeouts - from work and workouts and use a hot bath to "pre-regenerate" (learn more)

While "long jack" as it is also called is probably best known for its testosterone boosting effects  (learn more about Tongkat Ali aka "Ali's Stick") and one of the staple ingredient in the standard OTC-testosterone boosters (previous news), its traditional use as a longevity agent does already hint at the fact that its ability to boost testosterone levels and fertility may actually be mere side effects of a more general effect, of which a recent study from SupplementWatch would suggest that it is the ability of the this herbal medicinal plant that grows in South East Asia (Malaysia, Vietnam, Java, Sumatra,Thailand) to normalize the reaction to all sorts of exogenous stressors (including exercise and everyday stress).

"Our employers produce supplements that work!"

In their recently conducted study, Shawn M Talbott, Julie A Talbott, Annie George and Mike Pugh, of who have all ties (either as employers or sponsors) with the supplement business, found that the administration of 200mg/day of a standardized hot water extract from Eurycoma Longifolia to 63 subjects (32 men and 31 women) had statistically significant beneficial effects on the subjects' psychological

• 

  20x higher doses of TA produced impressive changes in body composition in rodents (read more)

  tension (−11%), 

• anger (−12%), and 

• confusion (−15%)

and physiological

• reduced cortisol exposure (−16%) and 

• increased testosterone status (+37%).

response to moderate everyday stress. The supplement was generally well-tolerated (2 subjects in the
TA group and 1 subject in the placebo group reported feeling unusually fatigued during the first two weeks) and did not produce any changes in the usual markers of hepatic toxicity (ALT; AST).

Putting the results into an unsponsored perspective

The time-course of serum T-levels in users of real gear vs. those who use natty test boosters will have significant effects on the net gains (learn more)

Contrary to previous studies, the researchers did not observe and effects on either body weight, body fat percentage, lean muscle tissue and whatever else you are actually looking for (or are you trying to score higher numbers on a lab report?).

Actually, this is a result which should not surprise you, if you read my various comments on the usefulness / real world effect of moderate changes in the cortisol / testosterone profile on body composition and/or athletic performance (e.g. "Quantifying 'The Big T' - Do increases of testosterone, which are well within the physiological range matter?"; read more).

Moreover, a closer look at all psychological / mood parameters that were accessed, reveals that that the "[m]ood state parameters showed mixed results" with "no effect" being observed "between supplementation groups for indices of Depression, Vigor, or Fatigue [sic!]" (Talbott. 2013). 

Figure 1: Salivary cortisol levels before and after the interention (left; Talbott. 2013) and the questionable reliablility of salivary testosterone measurements due to their susceptibility to simple things like using chewing gums (‘O’ = Orbit, ‘E’ = Extra, ‘D’ = Dentyne; ‘S’ = Spearmint, ‘P’ = Peppermint; cf. van Anders. 2010)

Similarly, the statistically significant reduction in cortisol (compared to the placebo group) is a classic hoax and mere result of significantly elevated cortisol levels in the treatment group before the intervention (see figure 1), which leaves us with a net increase in salivary testosterone that can be brought about by simply chewing a Dentyne Spearmint gum (+150% salivary testosterone in men; +75% testosterone salivary testosterone in women; cf. van Anders. 2010) and puts another question mark behind the physiological relevance of the observations (note: the results could be skewed in both groups, also previous studies have already established the beneficial effects on testosterone levels, so this is more of an "aside" than a valid argument).

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If you follow the "Three Simple Rules of Sensible Supplementation" this will not just save you tons of money, it will also avoid that your breakfast is ever going to look like this. This is not the breakfast of a champion, it's the breakfast of a complete moron who disregards the first, and probably all other rules of "sensible supplementation" (img consumersearch)

Bottom line: While there are probably benefits to Tongkat Ali supplementation. However, studies like the one at hand make them appear to be "larger than life" and will raise expectations the corresponding supplements are not going to satisfy - this is particularly true, when you combine them with the prevalent but unwarranted marketing claims of "steroid like muscle gains" that come with most of the corresponding products.

For people with low-normal testosterone levels, it may still make sense to do a test-run although previous studies would suggest that more than the 200mg/day used in the study at hand will be necessary to elicit noticeable physiological effects, the low dosage could well have psychological benefits. Just don't buy a whole batch and follow the "Three Simple Rules of Sensible Supplementation" (specifically those listed under principle #3) when you insist on giving long jack a try.

References:

• Talbott SM, Talbott JA, George A, Pugh M. Effect of Tongkat Ali on stress hormones and psychological mood state in moderately stressed subjects. J Int Soc Sports Nutr. 2013 May 26;10(1):28.
• van Anders SM. Chewing gum has large effects on salivary testosterone, estradiol, and secretory immunoglobulin A assays in women and men. Psychoneuroendocrinology. 2010 Feb;35(2):305-9.

Overtraining, Undereating & Self-Inflicted Hypothyrodism: Thresholds for Low T3 and High Reverse T3 Levels at 8% & 15% Reduced Energy Intake + Exercise After Only 4 Days!

This is not a "woman thing" only and your T3 levels are not the only thing that's going to "fall flat" if you starve yourself through your workouts! Yep, low libido => low total testosterone => low free testosterone => hypogonadism, that's what we are talking about, guys.

While I did promise to summarize some of the things, I said about creatine kinase, ALT, AST & Co on the last installment of the SuppVersity Science Round-Up on the Super Human Radio Network (I will do that in a future blogpost), today's SuppVersity article will focus on a single and in my experience often misinterpreted and / or overlooked symptom of overtraining that I personally have encountered numerous times in both male and female trainees: Self-induced hypothyrodism, low T3- or the euthyroid sick syndrome are just a couple of names that have been used in the science and laypress to describe this peculiar result of the way trainees deliberately ruin their metabolism by training for hours day in and day out, while following a diet that would hardly nourish a sedentary person, let alone the athlete or fitness model whose physique they are aspiring to achieve.

Pertinent studies are scarce, but they exist

I don't know if the shortage of scientific evidence is a result of the general ignorance of professional athletes, trainers and above all the "average gymrat" that he or she has an organically  healthy thyroid that's just shut off by your body in order not to waste precious muscle and organ weight in a state of constant catabolism.

Despite the scarcity of research, there are two pertinent studies from the Department  of  Biological  Sciences at the College  of  Osteopathic  Medicine of the Ohio  University. Both studies were published in the early 1990s and deal - as you would expect it with female subjects (with no recent history of dieting or weight loss were recruited from the university and surrounding community) who were randomly assigned to a 3x2 experimental design of aerobic exercise and energy availability treatments. The subjects had kept detailed food logs (including weighing and measuring all their foods) before the intervention to have a baseline reading for their energy intake and their heart rates and VO2 max were established during testing seasons before the first workout day.

• 

  Table 1: Detailed information about the participants in the 1993 (Study A) and 1994 (Study B) studies by Loucks et al. (Loucks. 1993 & 1994)

  participants in study A (Loucks. 1993): 51 volunteers 18-29 years of age
• participants in study B (Loucks. 1994): 28 volunteers 18-29 years of age 
• none of the participant was using medication including oral contraceptives, no history of heart, liver, or renal disease, diabetes, menstrual or thyroid disorders, or a history of severe dieting; all had  at least 3 mo of documented menstrual cycles 26-32 days in length and had exercised for only ~60 min per week in the previous 3 months 

Since the basic design of the studies did vary, we are now going to look at the studies separately and in the order in which they've been conducted. This does obviously mean that we'll start with study A the subjects were randomized to groups

• exercising not at all (Z; zero exercise group), 
• expending 1,300kcal/day on low (40% VO2max) intensity exercise (LO)
• expending 1,300kcal/day on high (70% VO2max) intensity exercise (HI)

The exercise was performed under continuous supervision on treadmill and cycle ergometers in 30min and 60min bouts for the high and low intensity groups, respectively.

"So what did happen? Did they drop dead?" Not exactly, no...

Figure 1: Experimental design: dietary energy intake (I), energy expenditure during exercise (E), and net energy availability (A) in the 3 x 2 (exercise X energy availability) experimental design; note: B indicates adequate energy intake, D indicated reduced energy intake (Loucks, 1993)

On the 4 subsequent treatment days the women consumed a liquid clinical dietary product (Ensure, Ross Laboratories, Columbus, OH) was consumed by all subjects as their only food source. The latter contained either

• 30kcal/kg body weight per day (~1,750kcal/day of available energy) in the normal energy group (B) and
• 8kcal/kg body weight per day (~500kcal/day of available energy) in the low energy group (D)

According to the protocol of study A, no effort was made to compensate for the daily energy expenditure and other than the liquid meal replacement Ensure (250 kcal/can, 15% protein, 30% fat, and 55% carbohydrate) the subjects were allowed to consume only plain water.

The blood was sampled for 8 days beginning on the day before the intervention began, in order to track (a) the time course of the development and (b) the persistence of the hormonal changes in the subjects.

Figure 2: Thyroid hormones at the end of the 4-day intervention expressed relative to baseline (Loucks. 1993)

Now, while there were no differences in baseline thyroid status for the participants a brief glance at the data in figure 2 will suffice to see that those were present during and after the intervention. And while the scientists state that ...

"[w]hen dietary energy intake was increased in exact compensation for the energy cost of exercise (LB, HB) [...] even the large volume of exercise performed in this study (similar to running a half marathon each day) had no effect on T3 levels." (Loucks. 1993)

I have my doubts whether "training in the zone" for hours everyday will not shut down the thyroid after 3 weeks and thus 5x the duration of the study. I mean -10% T3 & 5%+ increase in reverse T3 are certainly boding ill (see my comment in figure 2). The data from the two-way ANOVA plotted in figure 3, on the other hand, confirm that the scarcity of energy and thus your bodies' desire to conserve energy is the main factor, here. 

"You're thyroid function is fine - rather high than low!", says the Dr. to the patient

The experiment Loucks et al. conducted does also shows why most patients don't receive adequate counseling (there is no need for treatment) by their doctors and statements like the one above are rather the rule than the exception.

Figure 3: Treatment effects on the changes of total T3 (in nmol/l) in the study particpants of study A (Loucks. 1993)

With normal or low TSH levels (not measured in the study at hand; generally indicating normal or even high thyroid function) and normal or increased T4 levels (this is an exclusive feature of the earlier stages of the overtraining + undereating syndrome) usually being the only additional value you may be able to convince your medical practitioners to measure this appears like an adequate diagnosis. The lowered T3 and even more so the increasing rT3 levels, on the other hand, will go unnoticed by the majority of GPs whose text-book tells them that even a mere TSH test should suffice to determine your thyroid health (in fact that's true, because your thyroid is perfectly healthy).

In a way this is yet better than a Dr. prescribing T4 in these situations. The latter will only be converted to rT3 and can aggrevate the sluggishness and apathy that comes with the low metabolic function due to "low T3 syndrome".

We need more data: Study B (Loucks. 1994)

"How did I let this happen again?", asks Oprah in her own magazine  - the answer is simple, Oprah! Your "diet" programmed the YoYo effect! It happened not after, but right while you were starving... ah, pardon "dieting"! Learn more about the benefits of dieting down slowly.

It goes without saying that the results of study A (Loucks. 1993) of which the scientists themselves point out that it had a "limited purpose" which was to determine (Study B; Loucks. 1994)

1. whether exercise training is capable of altering thyroid metabolism in women, and, if so, 
2. whether this alteration can be wholly explained by the impact of exercise on energy availability, with all other physiological processes occurring during exercise training (i.e., “exercise stress”) having no influence on thyroid metabolism. 

are of low practical relevance, as I would hope that even the most notorious masochists out there won't try to cut on a "8kcal/kg per day" diet... well, I got to qualify this statement, I suppose. In the obese "diets" like that are actually common practice - the "biggest loser" diets often contain 800kcal per day, as does the HCG diet and if you take into account that almost all obese men and a significant amount of obese women weigh more than 100kg, the protocol does no longer seem to be that unrealistic.

Still, I and I would guess, you, as well, will appreciate that Loucks & Heath conducted a follow up study, in the course of which they wanted to elucidate how important the dietary compensation of the exercise induced energy expenditure is, if you want to keep your thyroid hormone metabolism intact. To this ends the subjects were randomly allocated to four groups (ordered from lowest to highest energy intake):

• 10.8kcal/kg LBM available energy -- this is what's left from a baseline intake of 39.5kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric deficit of ~23% below the participants' habitual intake
• 19.0kcal/kg LBM available energy -- this is what's left from a baseline intake of 48.6kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric deficit of ~6% below the participants' habitual intake
• 25.0kcal/kg LBM available energy -- this is what's left from a baseline intake of 53.4kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet that had an identical energy content as the participant's habitual diets
• 40.4kcal/kg LBM available energy -- this is what's left from a baseline intake of 68.4kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric content that was ~32% above the participants' habitual diets (typo in kcal values corrected)
  

All subjects performed the high intensity protocol of the previous study (70% VO2max) and expended 30 kcal kg LBM of energy in daily exercise for four consecutive days beginning on day 2, 3,4, or 5 of the menstrual cycle (this is important, because the energy expenditure during the workouts was obviously not compensated for in the habitual diet). Just as in the previous study the exercise sessions were performed on treadmill or cycle ergomenter, and in 30 min bouts with 10min breaks in between (obviously until the target calorie expenditure was met).

Figure 4: Effects of training at 70% VO2max aiming for a total energy expenditure of 30kcal/kg LBM at different levels of available energy (intake - expenditure in kcal/LBM) on thyroid hormones; values expressed rel. to baseline (Loucks. 1994)

As the literal "blind man" should see, the combination of what most people would not even necessarily call overtraining (after all it's just 4 days and "only" 70% VO2max) reduces the T3 reserves (total T3) to zero and reduce the purportedly active T3 levels by 28% - a reduction that will have a significant impact on how you feel and how your metabolism will function.

Figure 5: The changes in thyroid hormones come "stepwise" with thresholds at 22.5kcal/LBM body weight for FT3 and  ~14kcal/LBM available energy for FT4 and rT3 (Loucks. 1994)

As the text boxes in figure 5 already tell you, we are dealing with a general 2-step mechanism, here, and it it is fully dependent on the extent of the calorie deficit. For a ~8% reduced total energy intake that corresponds to an available energy level of  ~22kcal/LBM, we see "nothing" but a drop in active thyroid hormones FT3, when the energy deficit increases (and I assume when it persists for longer than 4 days), this reduction is no longer enough to minimize the energy expenditure so that your body resorts to what you may term an STRM, a selective thyroid hormone receptor modulator that goes by the telling name reverse T3. Since rT3 is produced from T4 and the other metabolic pathway, the conversion of T4 to T3 is already shutting down, we see an increase in free T4 levels, which will serve as a substrate for the production of rT3 to further slow down the metabolism (in the days/weeks to come TSH will probably go further down so that you will end up with all levels being suppressed and only rT3 high - if anything).

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As you can see, your body is smarter the average starvation dieter thinks he is. So the bottom line is easily formulated: Don't starve yourself if you don't want do feel and look like miserable, hold water, get fat from whatever you eat and end up as a physiological and psychological wrack.

References:

• Loucks AB, Callister R. Induction and prevention of low-T3 syndrome in exercising women. Am J Physiol. 1993 May;264(5 Pt 2):R924-30.
• Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. Am J Physiol. 1994 Mar;266(3 Pt 2):R817-23.

Up Your Coffee Intake & The Temperature of Your Baths to Get in Shape; Up Your Mood W/ Self-Paced Aerobics; Up Your Vitamin D in Time; Up Both Fat & Sugar For Diabesity

Ice cold baths are retarded. A cosy hot tub and a cup of coffee make a way better peak conditioning strategy.

+38% that's the SuppVersity Figure of the Week and it is the fat liberating advantage of the ingestion of 3mg/kg caffeine (in water) before sitting for 30 min in a hot bath (42°C; up to the navel) - yeah, you read me right:  The latest study from the Graduate School at the Department of Health Care of the Soonchunhyang University in the Republic of Korea is about the thermogenic effects of HOT (not cold) baths.

Even in the absence of additional caffeine ingestion the latter increases the amount of circulating free fatty acids by 52% (80% with caffeine) with the ~200-300mg of caffeine before the bath it almost doubles the amount of free fatty acids and increases the circulating leptin levels by 28% (vs. 5.6% w/out caffeine).

Whether the significantly more pronounced reduction in waist circumference (8.9mm vs 6.7mm) Tae-Wook Kim & Jeong-Beom Lee observed in their 9 male subjects (age ~26y; BF% 20%; no habitual caffeine consumers) is yet a result of real fat loss, remains highly questionable. However, even if that's not the case  sitting in a hot tub after having a large cup of coffee would still qualify as a potentially valuable peak-conditioning technique before a contest or photo shoot - or, for the less ambitious, before the high school reunion or the a first date ;-)

Aerobic workouts for a better mood

(Buscombe. 2013) You know these drill instructor classes, where the mostly female participants get their more or less over- and under-sized butts kicked ending up either severely overtrained or chit-chatting with the lady next to them? Yeah, I see - you know exactly what I am talking about ;-)

I guess Richard M. Buscombe and Helen Inskip from the University of London won't like my prelude to their study and there is in fact nothing bad about doing aerobic session like the ones in the Buscombe study, but both, the effects on body composition are about as intensity dependent as the affective changes, Buscome & Inskip measured in their study.

Figure 1: Psychological and physiological effect of 40 min or aerobics at different intensity (Buscombe. 2013)

As you can see in figure 1 the absolute affective change from pre- to post was clearly intensity dependent. Yet despite the fact that the intense workouts had the most significant (beneficial) effect on the feeling scales, the researchers are probably right, when they highlight that

"there was a positive pretest-to-posttest shift in the FS scores, irrespective of the intensity of exercise [and that this] finding supports existing literature advocating the role exercise plays in contributing to positive affective change" (Buscombe. 2013)

Still, in this group of 15 women (medium age 35.08) who think of themselves that they are "fit" or "highly fit", the high intensity (complete routine performed matched to a music with a 140bpm speed) has the greatest reward effect (pre- vs. post).

You have no idea, why I am mentioning the speed of the music here? Read up on the "Accustic Gear" post from 2011 (read more) and the corresponding research overview from April 2013 (learn more) to understand why the rhythm and tempo of the music matters.

In view of the significantly highly rate of perceived exertion and the frustration during the workouts, it does yet stand out of question that the "self-paced" routine, in the course of which

"[t]he participants were instructed that they could add or take away levels from their 'Step' aerobics box, as appropriate [and were allowed] alter the intensity of their session at any stage throughout the course" (Buscombe. 2013)

would be the preferable way to exercise on a regular basis - also, or rather especially because it does not entail the same risk of overtraining as the "push yourself to the limits" high intensity pattern.

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One thing to keep in mind, though, is the fact that not everyone is as willing and able to push him-/herself, when he or she is told that it was not necessary. For less ambitious individuals, the "self-paced" workout may thus well end up mirroring the low intensity routine, in the course of which the participants used only small body movements and minimized any lifting or propulsion actions, performing their workout in sync with a 125 bpm music.

Detrimental effects of vitamin D deficiency on the heart accumulate with time 

(Assalin. 2013) I know that I am already notorious for being the "anti vitamin D guy", but that is about as overgeneralized as the notion that everyone must be taking at least 4k of vitamin D per day. People who have been following the SuppVersity for some time now will be aware that I have always maintained that you go and check your vitamin D levels, supplement, if necessary and re-check after 3-4 months. After all, we all know how detrimental it is to be in a state of full-blown deficiency....

What we did not know - at least up to a couple of days ago, was how "fast" the detrimental effects of vitamin D deficiency can become potentially life-threatening. At least for rodents a recent study from the  São Paulo State University in Botucatu, Brazil, fills this important knowledge gap.

Figure 2: Effects of short (2 months; D2) and long (4 months; D4) on vitamin D deficient diet in the absence UV light on inflammatory markers, anti-oxidant status and heart morphology; data relative to levels after 2 months on the standard diet with 1,000IU vitamin D/kg chow (Assalin. 2013)

The scientists put a group of weanling Wistar rats under non-UV lights on diets containind either 1,000IU VD/kg of chow (C2 and C4) or a vitamin D deficient, but otherwise identical diet for two (D2) and four months (D4), respectively and observed:

• lower beta-hydroxyacyl coenzyme-A dehydrogenase activity and higher lactate dehydrogenase (LDH) activity, as well as 
• increased cytokines release, oxidative stress, apoptosis and fibrosis and 
• left ventricular (LV) hypertrophy and lower fractional shortening and ejection fraction 

in all vitamin D deficient animals. The differences in LDH activity, LV weight, right ventricle weight, and LV mass did yet not achieve statistical significance before the rodents had been kept on the vitamin D deficient diet for four months.

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Bottom line: Given the fact that the animals in the study did not consume any vitamin D and were - due to being exposed to evanescent (non-UV) light unable to produce even minimal amounts of vitamin D, the study results confirm that you can survive without supplements for a couple of weeks. On the other hand, they underline the importance of getting your vitamin D levels checked regularly. After all, we do as of yet have no idea to predict, where you as an individual are on the 25OHD spectrum ranging from deficient to over the tops - for some it may suffice to get regular sun exposure in the summer, for others 5,000IU of D + sunlight may still not suffice to keep their levels in the normal range: Don't be cheap! Get your levels checked.

What's the best diet to induce metabolic syndrome? The SAD diet!

(Pranpawit. 2013) The research design of the latest study from the Institute of Food, Nutrition and Human Health at the Massey University looks like Araya Pranprawit, Frances M. Wolber, Julian A. Heyes, Abdul L. Molan and Marlena C. Kruger wanted to participate in a competition, where those researchers win whose rodents gain the maximal amount of weight in the minimal amount of time. I mean, if you put the little critter on either

• control: 23% protein, 12% fat, 55% starch, 11% sugar
• high sugar (HS): 22% protein, 18% fat, 60% sugar
• high fat (HF): 16% protein, 60% fat, 20% starch, 4% sugar
• high fat + high sugar (HFHS): 19% pro, 40% fat, 41% sugar

the question that remains is not: "Are the rodents going to develop diabesity"?, but rather "Which group of rodents will die from the consequences of it first?" ... well, guess what, in the end this was more or less what the scientists wanted to find out.

Image  from NYC Dept. of Health & Mental Hygiene: The words on this poster from a 2009 campaign in the NY subway must be taken literally (learn why)!

Since published data with regards to diet‐induced metabolic syndrome in the SD rat model remain inconsistent, it is hypothesized that different types and amounts of diet as well as the period of time the animals are exposed to the experimental diet may significantly affect metabolic parameters in SD rats. Therefore, the objective of the present study was to compare the effects of consuming diets high in saturated fat, high in sucrose, and the combination of high saturated fat plus high sucrose, for a short time (4 weeks) and a long time (8 weeks), on selected markers related to metabolic syndrome in order to identify the optimal diet and experimental period for establishing metabolic disorder in the SD rat model (Pranpawit. 2013)

While the rodents in the HFHS and the HS diets consumed about the same amount of fat, those who had been randomized to the high fat (only; HF) diet obviously did not really enjoy their chow. At least weight-wise these rodents consumed significantly less food than their peers and still gained (due to the high energetic density of the chow) significantly more weight than the rodents in the "pure sugar" (HS) diet (see figure 3).

Figure 3: Weight and fat gain, as well as changes in Homa-IR (insulin resistance) and serum cholesterol; * indicates expressed in reference to control group at 2 weeks (Pranpawit. 2013)

As you can see the actual fat gain was slightly more pronounced in the high fat + high sugar diet (no this does not stand in contrast to yesterday's post on insulin not increasing fat storage, because we are not dealing with insulin sensitive critters here, but with severely obese pre-diabetics with elevated FFA levels, which do not require prior conversion to fat to be stashed away).

SAD, but true: "Human Study Shows: Three Days on "High Fat" Standard American Diet Produce Heart Healthier LDL Particle Profile Than NCEP  Approved Low Fat Diet" (read more).

"In all groups, fasting glucose, insulin concentrations (and insulin resistance (HOMA‐IR index) significantly increased between the 4 week and 8 week time points (p = 0.05; data not shown), indicating that these parameters increase with age regardless of diet. At 4 weeks, test diets had no effect on fasting glucose compared to CONT. HS, HF, and HSHF slightly elevated insulin and HOMA‐IR (Fig. 1). At 8 weeks, glucose was slightly elevated in test groups compared to CONT. HS had no measurable effect on insulin or HOMA‐IR, while HF slightly increased and HFHS strongly increased these parameters, although this did not reach statistical significance." (Pranpawit. 2013)

Somewhat surprisingly, none of the test groups differed from CONT as far as the weights of liver, kidney, pancreas, or caecum (data not shown) are concerned. The only, yet statistically non-significant difference was a "tendency for an increase in pancreas size with body weight" (Pranpawit. 2013). Moreover, rats on fat‐containing diets had markedly heavier abdominal white adipose tissues compared to CONT and this effect was unsurprisingly greater after 8 weeks on the diet compared to 4 weeks.

What's certainly interesting and an observation that flys right in the face of the generally held believe that it was the dietary fat that would precipitate to a messed up cholesterol metabolism is the fact that the rodents in the HS group showed elevated circulating cholesterol levels, as well. The often touted effect of sugar on the elevation of triglycerides, on the other hand, was absent unless the rodents received additional fat in their so that the combination of exogenous and endogenously produced (by fatty acid synthesis) fat reached a level that could not be compensated for by an increase in fat storage and/or oxidation.

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Suggested read: "Standard Am. Diet Has 'Optimal' Fatty Acid Ratio to Induce Diabesity. Plus: Doubling SFA Would Yield More Benefits Than Halving Them" (read more)

Bottom line: While we have to be careful about direct extrapolation of conclusions pertaining to the corresponding effect in human beings, it is still interesting to see that (a) the high sugar diet with literally no fat produces a "skinny, but sick" (remember those rodents were not fat) phenotype that is characterized by a messed up glucose and cholesterol metabolism in the absence of obesity and insulin resistance, that (b) taking fasting or postprandial glucose levels as a means to judge the insulin sensitivity is not generally accurate and overestimated the de facto non-existent insulin resistance in the high sugar group (HS), that (c) it's rather the rise in free fatty acids than the carbs that are responsible for both the developing insulin resistance (in the HF group in the presence of low fasting glucose; cf. (b)) and last, but most intriguingly that "the starch‐based control diet may also gradually cause impaired glucose tolerance" and is thus not exactly healthier for the glucose metabolism of the rodents than the high fat or even the high fat + high sugar diets.

If we had to pick a "winner" to be awarded the grand prize for the most metabolically damaging diet it would thus (without question) be the high fat + high sugar diet, which does - not much to your surprise as I would get - actually show a high resemblance to the SAD diet with a relatively high content of saturated and omega-6 fatty acids (from lard, in the case of the study at hand) and tons of simple sugar. The high fat (only) diet and the high sugar (only) diet, on the other hand lead to obesity and insulin resistance, respectively - both did thus fail to induce the key features of the metabolic syndrome, the presence both.

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That's it for today and aside from the obligatory information that you can find addition real short (and I mean "short" as in few words) short news on www.facebook.com/SuppVersity, e.g.

• 

  Most nuts deliver way less energy than the label or calorie tables tell you - for almonds, for example it's ~35%  less (learn more)

  More direct evidence for the free fatty acid - muscular glucose uptake connection: Reducing the amount of free fatty acids in the blood has immediate effects on the ability of the muscle (esp. of diabetics) to take up glucose (read more)
• The verdict on nuts: Not only are nuts not fattening, a recent meta review suggests that incorporating them into your diet may even yield reductions in BMI and more important waist circumference (read more)
• Stupid fools! "Reduced fat" labels are a signal to overeat... well, sort of at least the average customer is more likely to overeat, when the label tells him/her "this food is not as bad as the real deal" (read more)

there is just one thing left to do for me, which is to wish all of you a great Saturday morning, noon, afternoon and evening (whatever your clock may tell you it is now and will be in a few hours :-)

References:

• Assalin HB, Rafacho BP, Dos Santos PP, Ardisson LP, Roscani MG, Chiuso-Minicucci F, Barbisan LF, Fernandes AA, Azevedo PS, Minicucci MF, Zornoff LA, Rupp de Paiva SA. Impact of the Length of Vitamin D Deficiency on Cardiac Remodeling. Circ Heart Fail. 2013 May 24.
• Buscombe RM, Inskip H. Affective change as a function of exercise intensity in a group aerobics class. Journal of Exercise, Science & Fitness. 2013 [epub ahead of print]
• Pranprawit A, Wolber FM, Heyes JA, Molan AL, Kruger MC. Short-term and long-term effects of excessive consumption of saturated fats and/or sucrose on metabolic variables in Sprague Dawley rats: A pilot study. J Sci Food Agric. 2013 May 24.