The Way You Train Shapes Your Muscle Size and Function - Study in Powerlifters, Bodybuilders & Controls Suggests Effects Go Beyond Hypertrophy & MHC Fiber Composition

Don't worry, this exercise is not going to reverse all the effects of your training. Still, in view of the intriguing results of the study at hand, it would be interesting if the fiber-type unspecific effects in powerlifters are reversed when you stop powerlifting / exercise altogether and/or start lifting with higher volumes and lower intensities (bodybuilding style volume training).

There are visible and invisible differences between bodybuilders, powerlifters and normal men. The former ones are so obvious that it wouldn't be very interesting to address them in a study. The latter, on the other hand, are, other than you'd expect, hardly researched, but - as the results of a recent study from the Manchester Metropolitan University, and a bunch of other European Universities and research centers shows - more pronounced and significantly more fundamental than some of you may have thought.

As Meijer et al. point out in the introduction to their soon-to-be-published paper in the peer-reviewed scientific journal Experimental Physiology, the performance of a power athlete is largely determined by two traits: the maximal force and power generating capacity of the recruited muscles, and the ability to maintain force and power for a prolonged period of high intensity efforts.

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Needless to say that the peak muscle power and force will to some extent dependent on muscle volume and physiological cross-sectional area of the muscle, respectively. In accordance with the above definition of what one's power will depend on, though, the mitochondrial density in the recruited muscle fibres does yet figure as well. I mean, you don't want to run out of steam on your 3rd rep of squats, do you? That's what I thought. Thus, Meijer et al. are right to point out that "[i]deally, an  athlete seeks to maximize both muscle power and endurance" (Meijer. 2015).

Myostatin Limits Muscle Hypertrophy in Everyone! Even Normal Gymrats May Benefit from Blockers, if any of them Actually Worked  Learn more!

The problem with this maxim, however, is that you cannot maximize both, the fibre cross-sectional area (FCSA) and its mitochondrial density. In fact, studies suggest that the FCSA at a given mitochondrial density is limited by the maximal extracellular oxygen tension (Van der Laarse et al., 1997; Wessel et al., 2010) or the myonuclear domain sizes (learn more).

It is thus only logical that studies on myostatin negative animals show that limit the amount of hypertrophy beyond which it becomes disadvantageous for sustainable power (learn more). Weak big, vs. small(er), yet strong muscles. That sounds like powerlifting vs. bodybuilding, right?

Although the fiber composition of bodybuilders, gymrats, endurance rowers and sedentary control differs, it is not - according to the results of the study at hand - the only and maybe not even an important determinant of maximal power (data based on Jürimäe. 1997)

Hold on, why's that even newsworthy? As the authors themselves highlight, their study is the first to show that "long-term resistance exercise, represented here by power athletes and body builders, increases the force generating capacity of muscle fibres" (Meijer. 2015). Now, this alone is not really exciting, what is intriguing, though, is that "this increase in force was only in power athletes associated with a significant increase in the power generating capacity of single muscle fibres" (ibid.) - and thus largely independent of the fiber type composition of the muscles (learn more).

Accordingly, on single fiber basis, the power generating capacity of a body builder (BB) is not only lower than that of a powerlifter, it's actually not even higher than that of an untrained individual (C) - and that despite the fact that the individual muscle fibers are significantly larger. As the authors further explain, "[t]his unexpected observation was explicable by a lower fiber specific tension in BB compared to C fibres". In this context it is important to point out that the C and PA group in the study at hand performed a comparable, albeit relatively low amount of aerobic exercise, it is thus "likely that the effects shown in PA can be attributed to the high-intensity low-volume resistance training," (ibid.), alone.

Well, that's obviously what Meijer et al. thought, as well, when they phrased the following hypotheses about the way the muscle fiber specific tension (F0) of 12 male bodybuilders (BB | BB: 29.8 ± 4.8y; 177.8 ± 4.1 cm; 91.7 ± 13.4 kg), 6 male powerlifters / power athlete (PA | 23.4 ± 3.9 y; 185.0 ± 4.3 cm; 103.0 ± 7.3 kg) and 14 non-competitive / weight lifting controls (C | 24.0 ± 3.5 y; 180.9 ± 5.3 cm; 77.9 ± 6.3 kg) differ in the introduction to their latest paper:

"PAs is characterized by high-intensity low-volume resistance training with supplemental aerobic exercise. Since BBs train for bulk and PAs for function we hypothesize that fibres from PAs will have a higher specific power and F0 than those from BBs. We expect an increase in specific power and F0 in PAs and BBs (for BBs especially in type II fibres) compared to C." (Meijer. 2015). 

To test whether this hypothesis is correct, the researchers compared muscle fibre contractile properties of biopsies taken from m. vastus lateralis of 12 bodybuilders (BB; low- to moderate-intensity high-volume resistance training), 6 power athletes (PA; high-intensity low-volume combined with aerobic training) and 14 controls (C). To do that you have to take samples from the muscle and test the maximal isotonic contractions on a single muscle fibre in vitro.

Figure 1: Typical examples of three IIA muscle fibres. Circles represent the measured force-velocity data. The continuous line shows the fitted force-velocity curve and the dashed line shows force-power curve (top). Specific tension of skinned m. vastus lateralis fibres is inversely related to muscle fibre cross-sectional area (bottom) - For both rows of data: Non-resistance trained controls (left), bodybuilders (middle), power athletes (right | Meijer. 2015).

As the data in Figure 1 shows, the scientists' analysis of their subjects' muscle fibers produced unsurprising and surprising results:

• BBS have larger muscle fibers (unsurprising) - The fibre cross-sectional area (FCSA) was 67% and 88% (P<0.01) larger in BB than in PA and C, respectively.
• There's no difference in fiber size between C and PA (surprising?) - Unlike the difference between bodybuilders, power athletes and control, the existing difference in fiber size between PA and C did not reach statistical significance. 
• BB and PA fibres are stronger (unsurprsing) - BB and PA fibers developed a higher maximal isometric tensions (32%, 50%, P < 0.01) than those of C. 
• BB & C fibers are significantly weaker than PA fibers (unsurprising) - The specific tension (F0) of BB fibres was 62% and 41% lower than that of PA and C fibres (P < 0.05), respectively. 
• The increased peak power of PA fibres was not related to fibre type (surprising) - Irrespective of fibre type, peak power (P) of PA fibres was 58% higher than that of BB fibres (P < 0.05), while BB fibres –despite considerable hypertrophy- had similar PP as C fibres. 

With the latter result standing in contrast to the long-held believe that training induced changes in fiber composition like an increase in the proportion of power-specific MHC IIa,b fibers in power athletes and an increase in "enduring" type II fibers (MHC IIx) in bodybuilders were responsible for the strength and power differences, the study at hand provides initial evidence that that the effects of the way you train go way beyond selective type IIa,b vs. type IIx hypertrophy.

Sedentary Individuals, Endurance & Strength Athletes: Their Fitness, Training & Hormones and How They Effect the Ratio of Fast- to Slow-Twitch Fibers | learn more.

Bottom line: The study at hand provides the first reliable evidence that high-intensity low-volume resistance training as it is performed by power lifters triggers significantly different adaptational processes than the low- to moderate-intensity high-volume resistance of bodybuilders - adaptational processes that go beyond the fiber-specific hypertrophy effects that are responsible for the alleged muscle fiber composition changes in trainees.

Since the former is a completely novel result, we can only speculate about the underlying mechanism. Meijer et al. "postulate that the decrease in specific tension is caused by differences in myofibrillar density and/or post-translational modifications of contractile proteins" (Meijer. 2015).

That's obviously a very unspecific hypothesis that warrants further investigation and elaboration in future studies; not just to confirm it, but also to elucidate (a) the time it takes for these changes to take place and (b) whether they are reversible by (1) changing the way you train (2) staying away from the gym, altogether | Comment on Facebook!

References:

• Jürimäe, Jaak, et al. "Differences in muscle contractile characteristics among bodybuilders, endurance trainers and control subjects." European journal of applied physiology and occupational physiology 75.4 (1997): 357-362.
• Meijer et al. "Single muscle fibre contractile properties differ between bodybuilders, power athletes and controls." Experimental Physiology (2015): Accepted article.
• Van Der Laarse, W. J., et al. "Size principle of striated muscle cells." Netherlands journal of zoology 48.3 (1997): 213-223.
• Van Wessel, T., et al. "The muscle fiber type–fiber size paradox: hypertrophy or oxidative metabolism?." European journal of applied physiology 110.4 (2010): 665-694.

Intermittent Fasting Works, But is It Better Than "Regular" Dieting? What Do the Latest Reviews / Meta-Analyses Say?

Don't eat unless this brunette,... ah, I mean her clock tells you to eat. That's intermittent fasting (IF) - well, at least one out of at least three versions of eating by the clock people call "intermittent fasting". Needless to say that this doesn't make it much easier to decide if IF works or not.

It has been some time since I wrote about "Intermittent Fasting" ("lean gains"-style, i.e. eat in a 6h-8h window everyday), "Fasting" (don't eat at all) and "Alternate Day Fasting" (eat very little / usually ~800kcal one day / and normal the next one, repeat). Against that background it is worth devoting a whole SuppVersity Research Update to the latest studies and reviews of IF and ADF.

In the corresponding papers, Tinsley and La Bounty review the "effects of intermittent fasting on body composition and clinical health markers in humans", Varady et al. discuss "the determinants of weight loss success with alternate day fasting" and Seimon et al. address the question whether "intermittent diets provide physiological benefits over continuous diets for weight loss?", as part of a short report in form of a systematic review of clinical trials.

So, where do I start? I guess it would be best to build the article around the most extensive and for many of you probably most interesting analysis by Seimon et al. that's about to be published in one of the next issues of Molecular and Cellular Endocrinology: "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials" (Seimon. 2015)

Do you have to worry about muscle loss and metabolic damage, when you're fasting?

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Usually I don't do this, but in view of the tons of articles I have already written about Intermittent Fasting, I feel like it is possible to start with the conclusion which says that "[i]ntermittent fasting thus represents a valid – albeit apparently not superior – option to continuous energy restriction for weight loss." Accordingly, the question I still owe you an answer to is "WHY?", i.e.: "What makes intermittent fasting 'a valid' weight loss strategy?", and "Why is it 'valid - albeit nor superior'?" Well, the answers to these questions are neither straight forward nor can they be answered objectively. As every review and/or meta-analysis, Seimon's paper ends with the researchers' subjective interpretation of selected, objective data. Data from a total of 40 publications involving humans of any age or body mass index that had undergone a diet involving intermittent energy restriction, 12 with direct comparison to continuous energy restriction. What all of these studies have in common is that they measured one or more of the following variables: Body weight, body mass index, or body composition before and at the end of energy restriction.

Table 1: The Aguin study is one out of many that shows that both intermittent and chronic energy restriction work and produce statistically (see p-values) identical changes in body composition, size and relevant markers of lipid and glucose metabolism (Arguin. 2012)

What they did not share, though, was the type of "Intermittent Fasting". Practically speaking, this means that 31 of the 40 publications "involved ‘intermittent fasting’ of 1-7-day periods of severe energy restriction" - were thus rather "fasting" or "alternate day fasting" than classic "intermittent fasting" studies. More specifically: Seimon et al. also included studies like Arguin et al. (2012) in which the subjects were either dieting for 15 weeks at a moderate energy restriction or for 3 cycles of 5 week at higher energy deficits were interspersed by 3 cycles of 5 weeks on a calorically sufficient diet and the results were compared after each intervention, as well as one year thereafter. These obviously more important parameters are summarized in Table 1, and they don't show any inter-group differences.

How much weight / fat loss and health improvements can you expect? While the Seimon study is excellent for detail, Tinsley's and La Bounty's short review features the more concise overview of the figures - albeit with the same general message, i.e. "intermittent fasting (in the broadest sense) works, but whether it's more effective than continuous energy reductions must be determined on an individual level". This does not negate that (a) alternate-day fasting trials of 3 to 12 weeks in duration appear to be effective at reducing body weight ( 3%–7%), body fat ( 3–5.5 kg), total cholesterol ( 10%–21%), and triglycerides ( 14%–42%) in normal-weight, overweight, and obese humans, and (b) that whole-day fasting trials lasting 12 to 24 weeks also reduce body weight ( 3%–9%) and body fat, and favorably improve blood lipids ( 5%–20% reduction in total cholesterol and 17%–50% reduction in triglycerides). Research on time-restricted feeding aka "lean gains"-style intermittent fasting, on the other hand, is still "too limited" (ibid.) to draw clear conclusions.

Now, while the Arguin study is not correctly summarized in the tabular overview of all studies they reviewed, the most important information, i.e. the fact that the cyclic diet does not provide any significant advantages or disadvatages over continuous dieting is true. Based on the meta-analysis by Seimon et al., the following take-home messages can be stated:

• The drop out rates were comparable for interventions involving intermittent energy restrictions (IER) and continuous energy restrictions (CER).
• Significant reductions in body weight, size (waist, hip, etc.) and adiposity can be achieved with both intermittent energy restrictions (IER) and continuous energy restrictions (CER).
• If we go by weight loss which happens to be the most frequently measured study outcome in Seimon's selection of studies, the results are comparable for IER and CER.

• 

  Study suggests: Your goals may determine whether a low or high fat diet is the better basis for your alternate day fasting fat loss diet | more

  A reduced drive to eat, on the other hand, appears to be a unique advantage of intermittent energy restrictions, where eating very little for a fixed time period appeared to be easier to handle for the subjects then the grazing that's part of many CER interventions.
  
  This is an important results, after all, one of the mainstream arguments against intermittent or alternate day fasting is that they will trigger an overcompensation on the (re-)feeding day - a phenomenon that was not observed.
  
  On the contrary, "participants only consuming an average of 95% of their calculated energy needs on feed days" (Seimon. 2015). This is particularly noteworthy because "this apparent suppression of the drive to eat occurred despite decreased circulating levels of the appetite-reducing hormone, leptin, following IER" (Seimon. 2015). Whether this is related to an increase in ketone bodies in the IER studies that was non-existent or less pronounced in the CER trials will still have to be elucidated, though.
• A trend towards mood disturbance, tension, anger and confusion was observed in only one study. A study by Hussin et al. (2013) that was done in aging normal-weight men and the results of which stand in contrast to what Johnson et al. found in overweight subjects in 2007.
  

  

  Figure 1: Intermittent energy restrictions (IER) appear to be better suited for the obese, whose mood improves during th fast, while the mood of lean subjects decreases sign. (Hussin, 2013 & Johnson. 2007).

  In conjunction with the increased drop-out rates in Hussin's study, we may argue that a lack of triglyceride and FFA releasing adipose tissue may make IER interventions harder to adhere to - probably, because of a simple lack of available energy during the fast.

• 

  So, "Intermittent Fasting Does Now Make You Fat"? Do the Facebook Posts Lie? Not Necessarily, but Many People Forget that IF Works Only if it Reduces Your Energy Intake | more

  In view of the sign. reductions in leptin in IER interventions it is hardly surprising that Seimon et al. didn't find convincing evidence that IER would ameliorate the reduction in resting metabolic rate that's an inevitable (temporary) side effect of any dieting regimen.
  
  One (de Groot. 1989) out of three studies that made a direct comparison between the two even found a further reduction in resting metabolic rate (RER) in the IER group, the others found no difference (Hill. 1989; Harvie. 2011; Arguin. 2012). Overall, it would yet appear as if any potentially existing difference was negligible.
  
  Other metabolic adaptations such as a reduced IGF1 production were observed only in trials where the subjects fasted with liquid meals (Kroeger. 2012).
• No difference and on average comparable improvements in glucose homeostasis were observed in the 20 studies that tested respective parameters in detail. While there are individual studies that suggest advantages for one or another method, the overall picture that emerges is that there are no systematic differences - a conclusion that would also explain the - in parts - contradictory results from pertinent studies.
• Lastly, it must not go unmentioned that the addition of exercise to IER will make it - just as it is the case for CER, by the way - more effective and will thus shed more fat (and maintain more lean mass) than IER alone.
  

  

  Figure 2: The combination of alternate day fasting and exercise reduces uncontrolled and emotional eating in 64 obese subjects over the course of a 12-week study (Bhutani. 2013).

  Somewhat surprising, but in view of the overall anti-appetite effect of fasting not impossible is that the combination of exercise with IER also reduced the subjects' craving for uncontrolled and emotional overeating (Bhutani. 2013).

In view of the fact that only 12 of the 40 publications included in Seimon's review directly compared IER with CER, it is yet important to remember that we are far from being able to tell who will benefit most and who least from "intermittent fasting" (in the broadest sense). If you review the above summary of the results, you will yet have to agree that it would appear as if men and women who still have a ton of weight to lose could fare better with intermittent or alternate day fasting, while lean individuals may, but don't necessarily have to struggle with the lack of readily available energy during the fast.

Figure 3: While race matters and Caucasians appear to do much better on alternate day fasting regimen, the baseline body weight (and BMI | not shown) doesn't make a difference in the 4 ADF trials Varady et al. reviewed (2015).

At least in the 8-week ADF studies Varady et al. reviewed in their previously mentioned short report in Obesity Research and Clinical Practice, however, the initial body weight was not a good predictor of weight loss success. Rather than that, "[s]ubjects aged 50—59 y achieved greater (P = 0.01) weight loss than other age groups" and "Caucasian subjects achieved greater (P = 0.03) weight loss than other races" (Varady. 2015) with the alternate day (ADF) version of "intermittent fasting".

With only 5 out of the 40 studies in Seimon's review having a follow-up and no follow-up in any of the ADF studies in the previously cited short report by Varady et al. (2015), the long-term benefits or detriments must be considered largely under-researched, at the moment, too.

Evidence From the Metabolic Ward: 1.6-2.4g/kg Protein Turn Short Term Weight Loss Intervention into a Fat Loss Diet. 1.6g/kg not 2.4g/kg Offers Optimal Muscle Protection | learn more!

So what's the verdict then? Well, firstly: Intermittent fasting works. It's not exactly well-researched, though. Accordingly, it is difficult to say (a) who would benefit most  / least, (b) which form of intermittent fasting ("lean gains" 6-8h window everyday vs. alternate day vs. total fasting) works best and (c) how (a) and (b) interact with with each other: It is for example well possible that the discrepancy between the effect on appetite in lean vs. obese individuals I highlighted in the main body body of this article occurs only with simple (as in Hussin. 2013), yet not with more complex methods of fasting as ADF or the 6-8h fasting window at a freely chosen point in time.

Overall, the best advise I can give you is thus to try if and which type of intermittent fasting works for you. What I cannot recommend is any form of extended fasting, where you are consuming very low amounts of energy (like 400-600kcal) for more than just one day. In addition, you want to make sure to lift weight and consume enough (~1.5g/kg) protein even on fasting days to conserve lean muscle mass | Comment on Facebook!

References:

• Arguin, Hélene, et al. "Short-and long-term effects of continuous versus intermittent restrictive diet approaches on body composition and the metabolic profile in overweight and obese postmenopausal women: a pilot study." Menopause 19.8 (2012): 870-876.
• Bhutani, Surabhi, et al. "Effect of exercising while fasting on eating behaviors and food intake." J Int Soc Sports Nutr 10.1 (2013): 50.
• de Groot, Lisette CPGM, et al. "Adaptation of energy metabolism of overweight women to alternating and continuous low energy intake." The American journal of clinical nutrition 50.6 (1989): 1314-1323.
• Harvie, Michelle N., et al. "The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women." International journal of obesity 35.5 (2011): 714-727.
• Hill, James O., et al. "Evaluation of an alternating-calorie diet with and without exercise in the treatment of obesity." The American journal of clinical nutrition 50.2 (1989): 248-254.
• Hussin, N. M., et al. "Efficacy of fasting and calorie restriction (FCR) on mood and depression among ageing men." The journal of nutrition, health & aging 17.8 (2013): 674-680.
• Johnson, James B., et al. "Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma." Free Radical Biology and Medicine 42.5 (2007): 665-674.
• Seimon, Radhika V., et al. "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials." Molecular and Cellular Endocrinology (2015).
• Varady, Krista A., et al. "Determinants of weight loss success with alternate day fasting." Obesity Research & Clinical Practice (2015).

Massage Therapy Speeds Recovery in Bodybuilders After Eccentric Workouts - DOMS + CK ↓ / Performance ↑

While many athletes use it and trainers all around the world are convinced that it works, the evidence on what exactly massage therapy does or doesn't do to an exhausted athlete's muscle and lymphatic system is scarce. Even the assumption that it helps reduce DOMS may be based on a placebo effect. After all, it's impossible to conduct a truly double-blinded massage study.

If they can afford it, athletes often employ their own massage therapist. It is commonly believed that sport massage after intensive exercise might improve power and perceptual recovery in sportsmen and -women. As Mehdi Kargarfard et al. (2015) point out in their latest paper, "few studies have been done in this area" to confirm what everyone appears to believe to be a scientific fact" (Kargarfard. 2015).

Accordingly, the researchers' latest study aimed to examine the effect of massage on the performance of bodybuilders - a group of athletes of which only few will be able to afford their own massage therapist, although they may in fact be among those athletes who could benefit most from massage therapy of which scientists believe that it reduces DOMS and speeds up recovery by removing accumulated extracellular fluid from the muscles, thus reducing swelling and pain via increased blood and lymph circulation - and at least the net outcome, i.e. a subjective reduction in DOMS (learn more) has been confirmed consistently (Bąkowski. 2008; Ali. 2012; Andersen. 2013; Visconti. 2014; Urakawa. 2015).

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If we assume that the mechanism has been correctly identified, massage therapy appears to work very differently from ice-baths of which a recent study has shown that it may actually impair the training-induced adaptation process by soothing the fire that's fueling the corresponding processes (learn more in "Using Ice / Cold Water Immersion After Workouts Will Impair Muscle and Strength Gains, as well as Vascular Adaptations").

Table 1: Descriptive statistics of the participants (Kargafard. 2015).

What makes the study particularly interesting is that the N=30 subjects were all healthy young men (28.77 ± 3.54 years) who were free of any supplement and steroid use, but had at least 2 years experience in bodybuilding (Table 1). The participants were randomly assigned using the permuted block randomisation method to either a massage (n = 15) or a control (n = 15) group. Participants were excluded if they had any relative or absolute contraindications to exercise or exercise testing.

• Tests were performed 1 week prior to the commencement of the treatment protocols and conducted during an 8-week preseason training period to limit the training effect. 
• Both groups performed five repetition sets at 75–77% of 1RM of knee extensor and flexor muscle groups. The massage group then received a 30-min massage after the exercise protocol while the control group maintained their normal passive recovery. More specifically, ...

  "... the participants were asked to perform squats to 90º knee flexion for five sets at 75% 1RM until exhaustion (but not less than 10 repetitions); then they had to perform leg press to 90º knee flexion for five sets at 75–77% 1RM until exhaustion (but not less than 10 repetitions). One-minute rest intervals were given between sets. If a participant could not complete 10 repetitions without assistance from the spotters, the initial intensity was reduced until at least 10 repetitions could be achieved. This was followed by a 5-min rest and an isometric protocol to induce DOMS in the right quadriceps muscle" (Kargarfard. 2015).

• Participants’ diets and medications were recorded and remained constant throughout the experimental period, which excludes a distortion of the results.

Criteria under investigation included: plasma creatine kinase (CK) level, agility test, vertical jump test, isometric torque test, and perception of soreness.

So why are you confident that massage therapy is not going to backfire? Well, as I pointed out previously in this article, there is no evidence of direct anti-inflammatory effects as they have been ascribed to ice-baths or vitamin supplements that could blunt the necessary hormetic response to exercise. Rather than that, data from a recently published study by Andrzejewksi et al. suggest that repeated massage may contribute to processes of creation of new and development of already existing vascular networks in the skeletal muscle tissue during increased exercise", which is the exact opposite of the proven detrimental effects of ice-baths (Andrzejewski. 2015). It does thus appear very unlikely that the overall long-term effects of massage therapy are going to be detrimental. A long-term study with bodybuilding specific outcomes, like strength and hypertrophy is still necessary, because a low risk of negative effects does not imply that there are going to be increased gains in strength or size.

All variables were measured over 6 time periods: baseline, immediately after the DOMS inducing protocol, right after the massage, and 24, 48, and 72 h after the massage, the scientists describe as follows:

"30-min standardised supine massage was performed by a licensed massage therapist with 3 years of experience on the exercised/right thigh of participants in the massage group after 2 h following the muscle soreness inducing exercise protocol. To maintain consistency and reproducibility for the entire massage procedure, tape-recorded messages were announced to remind the therapist when to change the massage strokes being performed. Western massage techniques of effleurage, petrissage, and vibration were used.

While there are rumors that massage therapy may also help you shed bod weight, this has been shown only for different techniques: "Electro-Cut" Your Body Fat - Study Shows 5.6 cm and 4.9% Reduction in Waist & Body Fat in Young Women in 6 Weeks

Each massage began with 4 min of effleurage consisting of 2 min of light stroking with the palm around the knee, and 2 min of light stroking over the medial thigh. Effleurage was followed by petrissage, which consisted of 2 min of twohanded palm kneading of the anterior thigh muscles, 2 min of two-handed thumb kneading over the medial thigh, 2 min of circular two-handed lifting of the anterior thigh, 1 min of pressing and spreading the tissues perpendicular to the long axis of the thigh, and 1 min of rolling the fingertips over the anterior thigh muscles. Two minutes of vibration was added between the petrissage techniques of circular lifting of the anterior thigh muscles and pressing and spreading the tissues.

The massage was then concluded with 3 min of effleurage over the anterior and medial thigh. While massages were performed on the experimental group, participants of the control group were asked to remain seated and to maintain their normal passive recovery regime as well as to refrain from performing any additional exercises or stretches"
(Kargarfard. 2015).

What the scientists found when they analyzed their results was (a) the obvious, i.e. significant (P < .001) decreases in jumping, agility performance, and isometric torque, but significant (P < .001) increases in CK and muscle soreness levels in all subjects.

Will foam rolling do the same? Whether it will do the same would require future studies with direct comparisons. What I can tell you, though, is that studies by MacDonald et al (2014) and Pearcey et al. (2015) consistently showed similar results, i.e. decreased DOMS and accelerated recovery / preserved muscle function with foam rolling after intense workouts.

There was yet also (b) a significant difference between the control and the massage group who demonstrated a better recovery rate as evidenced by:

• faster recovery of vertical jump performance and maximal muscle torque (measured when subjects were fixed w/ 90º of hip and knee flexion on an isokinetic dynamometer) from 24-72h in response to the  massage therapy,
• reduced increases in creatine kinase (CK) levels, a relatively unspecific marker of muscle damage, after the massage therapy.

What was not observed was a meaningful difference in the agility test, where the pre-test difference was similar before and after the test and treatment.

Figure 1: Creatine kinase (CK | top, left), jump height / distance (bottom, left), agility test times (top, right) and visual analog scale rating for DOMS (bottom, right) for the two study groups (Kargarfard. 2015).

In view of the fact that the study wasn't blinded (for obvious reasons), it is also not clear how much of the subjective reduction in DOMs may just have happened in the subject's head. In conjunction with the previously mentioned faster recovery of performance markers and CK, though, it appears to be very reasonable to follow Kargarfard's conclusion that "As such, a post-exercise massage session can improve the exercise performance and recovery rate in male bodybuilders after intensive exercise" (Kargarfard. 2015).

Since the purported mechanism is very different, it's unlikely that there will be similarly negative long-term consequences as they've been observed w/ ice baths.

Bottom line: In spite of the lack of being double-blinded, the consistency of objective and subjective performance and DOMS markers can be considered sufficient evidence for the existnece of sign. short-term benefits of massage therapy on athletes' recovery.

If we assume my previously mentioned hypothesis that the accelerated manual removal of "debris" after workouts was much different from the anti-inflammatory effects of ice-baths / and cold water immersion therapy is correct, there is also no reason to believe that massage therapy would have a similarly detrimental long-term effect on the training-induced adaptation to exercise as we've recently seen them in response to ice-baths | Comment on Facebook!

References:

• Ali, Rasooli S., et al. "Influence of massage, active and passive recovery on swimming performance and blood lactate." The Journal of sports medicine and physical fitness 52.2 (2012): 122-127.
• Andersen, Lars L., et al. "Acute effects of massage or active exercise in relieving muscle soreness: Randomized controlled trial." The Journal of Strength & Conditioning Research 27.12 (2013): 3352-3359.
• Andrzejewski, Waldemar, et al. "Increased skeletal muscle expression of VEGF induced by massage and exercise." Folia Histochemica et Cytobiologica 53.2 (2015): 145-151.
• Bąkowski, Paweł, et al. "Effects of massage on delayed-onset muscle soreness." Polish Orthopedics and Traumatology 73.4 (2008): 261-265.
• Kargarfard, M, et al. "Efficacy of massage on muscle soreness, perceived recovery, physiological restoration and physical performance in male bodybuilders." Journal of Sports Sciences (2015): Ahead of print.
• MacDonald, Graham Z., et al. "An acute bout of self-myofascial release increases range of motion without a subsequent decrease in muscle activation or force." The Journal of Strength & Conditioning Research 27.3 (2013): 812-821.
• MacDonald, Graham Z., et al. "Foam rolling as a recovery tool after an intense bout of physical activity." Med Sci Sports Exerc 46.1 (2014): 131-142.
• Pearcey, Gregory EP, et al. "Foam rolling for delayed-onset muscle soreness and recovery of dynamic performance measures." Journal of athletic training 50.1 (2015): 5-13.
• Urakawa, Susumu, et al. "Manual therapy ameliorates delayed‐onset muscle soreness and alters muscle metabolites in rats." Physiological reports 3.2 (2015): e12279.
• Visconti, Lorenzo, et al. "Effect of massage on DOMS in ultramarathon runners: A pilot study." Journal of Bodywork and Movement Therapies (2014).

Trying to Lose Fat & Get "Toned" W/Out Training or Diet? Taking 1-3 mg Melatonin Helps Women Lose 7% Body Fat, Gain 3.5% Lean Mass in Recent 12 Months-Long RCT

Since the natural melatonin production decreases as we age, it is (unfortunately) possible that younger women wouldn't see the same benefits as the >56 year-old subjects of the study at hand.

No, I am not recommending laziness here, and I doubt that you will arrive at a cover model physique with nothing but a handful of melatonin pills, but the results of a recent study from the Aarhus University Hospital in Denmark are too intriguing not to devote a whole SuppVersity article to them.

In said study, Anne Kristine Amstrup and colleagues tested whether there's anything to the rumors that have it that "melatonin [has] a positive effect on body weight and energy metabolism" (Amstrup. 2015). As the researchers rightly point out, previous "evidence for this relies mainly on animal models" (ibid). It was thus about time for someone to "determine the effects of melatonin on body composition, lipid and glucose metabolism in humans" (ibid).

Want to learn more about melatonin? The SuppVersity is the place to be.

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In this case, said human beings were 81 post-menopausal Caucasian women (aged 56-73 years) diagnosed with osteopenia (T-score between -1 and -2.5 in the hip or spine). The Danish scientists randomized the women to receive

• either melatonin, at a dosage of 1 or 3 mg per day, or
• an identically looking placebo nightly (timing matters!)

for a total time-period of 12 months. There were no dietary or exercise interventions, but all study subjects received a daily supplementation of 800mg calcium and 20ug vitamin D3 (which obviously wouldn't affect the results, also because all of the participants had taken Ca + D3 for at least 3 months before the study began). With DXA, ...

"To assess body composition, we used a whole body scan by dual X-ray absorptiometry (DXA, Hologic Inc., Waltham, MA, USA). We performed scans at baseline and after one year of treatment. Assessments included total and subtotal body mass (g), lean mass (g), fat mass (g) and percentages of body fat. We calculated body mass index (BMI) as body weight (kg) divided by height² (in metres)" (Amstrup. 2015).

... and a detailed analysis of the blood of their subjects, the body composition and biochemical analyses were similarly thorough as the randomization protocol which was performed by an external pharmacy (Skanderborg Pharmacy).

Beware! If you take melatonin anytime but 1-2h before bed (fasted), it may backfire! If you don't remember why and how timing matters, I suggest you re-read my 2014 article about how taking melatonin at the wrong time of the day may actually make you fat and insulin resistant.

Each block consisted of eight individuals. In the blocks, the women were randomly allocated to treatment, i.e. four received placebo, while two received 1mg of melatonin and two received 3mg melatonin.

Figure 1: Changes in body composition (left) and adiponectin (right) in response to 1-3mg of melatonin taken at night over a 12-months period without further exercise or diet intervention (Amstrup. 2015).

This is also why I have little doubt that we can rely on the data in Figure 1 which shows an astonishingly pronounced reduction in fat mass and a borderline-significant increase in lean mass in the melatonin groups, when the subjects on the placebo supplements gained total (and %) body fat and lost lean mass in the same 12-months period.

Melatonin As Potent as Letrozole in Inhibiting Aromatization | more

You are an athlete who does not care about losing weight? Data from a Spanish study leaves no doubt that you can still benefit from taking melatonin. In their soon-to-be-published study, researchers from the Universidad de Granada a high dose of melatonin restored the normal circadian rhythm of melatonin production, reduced the nocturnal activity and the activity and position during lunch/nap time - "[t]ogether, these data reflect the beneficial effect of melatonin to modulate the circadian components of the sleep-wake cycle, improving sleep efficiency," the authors say (Leonardo-Mendonça. 2015).

The one thing I would still like to repeat is what I already mentioned in the caption of the thumbnail to this article: Since the natural melatonin production decreases as we age and menopaus (Okatani. 2000), it is (unfortunately) possible that younger women wouldn't see the same benefits as the >56 year-old subjects of the study at hand.

Figure 2: Rodent studies also show that melatonin supplementation prolongs the lifespan of the average mouse (Pierpaoli. 1994) and rat (see data in graph) significantly (Oaknin-Bendahan. 1995).

In a similar vein, it cannot be said with any certainty, whether men will benefit to the same extent as the post-menopausal women in the study at hand. While studies in rodents clearly suggest that melatonin works its weight reducing, life pro-longing (see Figure 2) in both male and female middle-aged rodents (Rasmussen. 1999; Wolden-Hanson. 2000), as well as rats who are fed an obesogenic diet like the standard American diet (Prunet-Marcassus. 2003), men are no little mice... but I guess you know that ;-)

So what? Well, melatonin is a hormone, not one with that builds muscle, but as the study at hand proves one with non-debatable "beneficial effects on body composition in terms of reduced fat mass and borderline significantly increased lean mass in post-menopausal women".  What's particularly interesting is that this effect can be achieved with relatively small doses of melatonin (1 and 3mg/d) and without any of the unwanted effects on blood lipids, glucose metabolism or markers of kidney and liver health you would see with other hormonal substances with proven body-recompositioning effects.

Will Melatonin Reduce Your Testoste- rone Levels? A Review of the Existing Evidence Experimental Human Data Says: Unlike in rodents, the longterm administrationf melatonin to men appears to rather increase vs. decrease their T levels.

In this context it is also worth mentioning that the authors believe that their "findings may be explained by a melatonin-driven increase in osteogenesis resulting in decreased adipogenesis". Bone instead of fat cells? Well, as SuppVersity reader and follower of the SuppVersity Facebook News-Channel you will have read about the cellular underpinnings of this transformation before. Against that background it is not unreasonable of Amstrup et al. to conclude that "[o]n the basis of [their] study, melatonin maybe an interesting therapeutic agent for future treatment strategies against [...] age-related changes in body composition"  (Amstrup. 2105). Whether it is a must have supplement for younger (more athletic) individuals, though, will have to be determined in future human trials, of which I doubt that they will be publicly funded  | Comment on FB!

References:

• Amstrup, et al. "Reduced fat mass and increased lean mass in response to one year of melatonin treatment in postmenopausal women: A randomized placebo controlled trial." Clinical Endocrinology (2015): Accepted article.
• Leonardo-Mendonça RC,  et al. "The benefits of four weeks of melatonin treatment on circadian patterns in resistance-trained athletes." Chronobiol Int. 11 (2015): 1-10. 
• Oaknin-Bendahan, Sol, et al. "Effects of long-term administration of melatonin and a putative antagonist on the ageing rat." Neuroreport 6.5 (1995): 785-788.
• Okatani, Yuji, Nobuyuki Morioka, and Akihiko Wakatsuki. "Changes in nocturnal melatonin secretion in perimenopausal women: correlation with endogenous estrogen concentrations." Journal of pineal research 28.2 (2000): 111-118.
• Prunet-Marcassus, Benedicte, et al. "Melatonin reduces body weight gain in Sprague Dawley rats with diet-induced obesity." Endocrinology 144.12 (2003): 5347-5352.
• Rasmussen, Dennis D., et al. "Daily melatonin administration at middle age suppresses male rate visceral fat, plasma leptin, and plasma insulin to youthful levels." Endocrinology 140.2 (1999): 1009-1012.
• Wolden-Hanson, T., et al. "Daily Melatonin Administration to Middle-Aged Male Rats Suppresses Body Weight, Intraabdominal Adiposity, and Plasma Leptin and Insulin Independent of Food Intake and Total Body Fat 1." Endocrinology 141.2 (2000): 487-497.

Food Matrices: Protein & Fat Ameliorate Glucose Spikes After Standardized Glucose Load | Plus: Timing Matters if You Want to Turn Regular into Resistant Starch

This is what it's all about. Real food does not come in form of "macros". It comes in form of complex food matrices that determine its effect on one's health - including one's glycemic health.

You will probably remember that I have touched on a specific aspect of the effects of and interactions between different macronutrients in what scientists often refer to as "food matrices" on the glycemic response to standardized glucose loads in previous articles like the famous "True or False?" article that dealt with the question: "Will Adding Fat to A Carby Meal Lower the Insulin Response?" (read it).

You don't remember this or any of the other articles? Well, in that case, I probably have to tell you again that the mere fact that the postprandial glucose are lower does not mean that a certain food or combination of certain macronutrients would increase your insulin sensitivity (adding fat to a high carbohydrate meal certainly doesn't do that, believe me).

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While this is possible for certain supplements like berberine and other AMPK activators, it is mandatory that we differentiate the following three cases:

1. Reduced postprandial blood glucose levels in response to an increase in insulin sensitivity as it is triggered by exercise or AMPK activators,
2. Reduced postprandial blood glucose levels in response to increased insulin levels as they occur with the co-ingestion with whey protein and
3. Reduced postprandial blood glucose levels in response to increased insulin levels and a decreased rate of absorption of glucose as it is the case if you add fat to carbohydrates.

That was too fast? Too complicated? Or both? Never mind. The discussion of two recent articles from the Lund University and the Yong Loo Lin School of Medicine (see blue box) will hopefully help you understand the difference - I promise ;-)

Let's take a look at study design, results and implications

In their study, Wathik Alsalim and his colleagues from the Lund University in Sweden and the Consiglio Nazionale delle Ricerche in Italy investigated the integrative impact of macronutrients on postprandial glycemia, β-cell function, glucagon and incretin hormones in man. The subjects were male and female Caucasian subjects, aged 30-70 years and BMI 20-35 kg/m², without diabetes (normal fasting glucose and normal HbA1c) or with T2D without any pharmacological glucose-lowering therapy and HbA1c <60 mmol/mol (<7.8%).

"Exclusion criteria were liver disease, diabetic nephropathy, proliferative diabetic retinopathy, pregnancy or breast feeding, treatment with oral antidiabetic or insulin, previous myocardial infarction, coronary heart disease or angina pectoris, previous surgery on the gastrointestinal tract, larger surgical intervention the last 12 weeks or treatment with oral steroids or thiazide diuretics" (Alsalim. 2015).

Participants were studied at the Lund University's Clinical Research Center on four occasions in a randomized cross-over design, separated by at least four and maximally eight weeks. After overnight-fast (no food after 10pm), subjects were provided with antecubital vein catheter. After two baseline samples at 5, and 2 mins, they ingested in randomized order either one of the macronutrients alone

• glucose - 330kcal = 83g; Skåne University Hospital Pharmacy, Lund, Sweden,
• protein mixture - 110kcal = 30g; ISO WHEY protein consisting of milk and egg protein
• fat emulsion - 110kcal = 24ml; 50% long-chain triglycerides and 50% water;

The response to the individual macros was then compared to the ingestion of a 550kcal meal containing 330kcal (60%) from glucose, 110kcal (20%) from protein and 110kcal (20%) fat - a proportion of which the scientists say that it "was selected to represent a common meal with 60% carbohydrate, 20% protein and 20% fat" (Alsalim. 2015).

Figure 1: To allow for maximal control, the "meal" (macro composition on the right) was a shake (Alsalim. 2015).

Water was ingested at the same time of each load to standardize the ingested volume to 400ml; all ingestions were consumed within 5 min. Blood samples were taken throughout a 300min period after each challenge test.

Both vegetable oils and ghee had identical (beneficial) effects on the starch composition, but they have to be added  during boiling or before frying and boiling (Kaur. 2015).

Modifying the glycemic potential and starch content of foods with fats - In the initially cited article, Collier & O'Dea restricted their study to potatoes, only. In a more recent study, Kaur et al. investigated the effects of adding fat to white bread and rice, as well and what's even more important they did so during, not after the cooking process. In other words, instead of "buttering" potatoes, as Collier et al. did it, Karr et al. conducted a study in which they assessed the starch digestibility of white and red rice prepared with 2 oil types: vegetable oil (unsaturated fat) and ghee (clarified butter, saturated fat) added at 3 different time points during the cooking process (“before”: frying raw rice in oil before boiling, “during”: adding oil during boiling, and “after”: stir-frying cooked rice in oil | details).

Unfortunately, the results are less "unique" than the design of the study. (A) Red rice produced a slower digestion rate than white rice. (B) The digestibility of white rice was not affected by oil type, but was affected by addition time of oil, in general. (C) Adding oil “after” (stir-frying) to white or red rice resulted in higher slowly digestible starch. In that, (D) adding the fat before or during cooking and frying respectively had the most significant effect on the subject's postprandial glycemic response and the resistant starch content of the food.

Now, guess what? Yes, yes, and no ... the glucose meal was not the most insulinogenic one. Accordingly, we have to be careful not to mistake the scientists' conclusion that "[a]dding protein and fat macronutrients to glucose in a mixed meal diminishes glucose" (Alsalim. 2015) as evidence that fat and protein will reduce the potential obesogenic effect of carbohydrates. After all, the data in Figure 2 leaves no doubt that we are not talking about effect (a) from our list at the beginning of the article, i.e. a reduction in glucose excursions in response to "an increase in insulin sensitivity as it is triggered by exercise" (see introduction).

Figure 2: Glucose and insulin response as well as corresponding insulinogenic index and insulin clearance of the individual macros and the mixed meal - all data expressed relative to the values of 110kcal of glucose (Alsalim. 2015).

Rather than that, the reduced glucose AUC was a result of (c), i.e. an increase in insulin levels due to increased insulin production, as well as a decreased clearance of insulin and a decreased rate of absorption of glucose (-16%, -52%, -59% and -70% reduced glucose influx through the portal vein at 30, 45, 60 and 90 min after the meal) - and with the increased insulin levels you will also run an increased "risk" of fat storage (whether you gain weight will still depend on your overall energy intake not your insulin levels, though).

Figure 3: Insulin is not always the bad guy. A 2004 study by Hallschmid, et al. shows that it's centrally mediated effects in the brain can actually help men (but not women) lose weight effortlessly, when they administer it cyclically (only chronically elevated insulin levels are truly problematic) intranasally.

At this point, it may be necessary to point out that the increase in insulin in response to the co-ingestion of protein and fat does not imply that guzzling glucose on its own would be healthier than eating a mixed meal. In conjunction with the increases in the important (fat burning) satiety hormone GLP1, which were observed only in the diabetic subjects, though, these changes are yet far more beneficial for the average type II diabetic than they are for the lean athlete, who doesn't need the extra-insulin to maintain normal blood glucose levels and may even consider them an obstacle on his / her way to single-digit body fat levels.

So what? Just as the previously discussed study on butter + potatoes, the study at hand does not confirm that you just have to add fat (and protein) to a meal to stay lean and healthy forever. The GLP-1 increase, which occured only in the diabetics, and the significant increase in insulin production, which occurred in both diabetic and healthy subjects, fully explain the reduced glucose spikes and can be considered "beneficial" only for type II diabetics, who can thus compensate their insulin resistance w/ even more insulin. For lean / healthy individuals who get the questionable benefit of increased GIP and insulin levels, but don't benefit from the increase in GLP-1, the benefits - if there are any - are less obvious.

Are You Afraid that the Fructose Boogieman Clogs Up Your Liver? Citrulline or Alanine, Glycine, Proline, Histidine and Aspartate Mix Will Protect You + Maybe Lean You Out

If there's an advantage of adding protein and fat to carbs in order to reduce the postprandial glucose excursions in lean individuals, that's probably not the often heard of "stay lean" effect, but rather a long(er) term health advantage. Elevated postprandial glucose levels have after all been linked to type II (as a consequence of the ill effects of elevated glucose on your pancreas | Robertson. 2003) and type III diabetes (type III = all sorts of downstream effects of constantly elevated glucose levels like Alzheimer's | Steen. 2005), increased inflammation and cardiovascular disease risk and a lot of other ailments you certainly want to avoid even more urgently than being pot-bellied or "chubby" | Comment on Facebook!

References:

• Alsalim et al. "Mixed meal diminishes glucose excursion compared to glucose by several adaptive mechanisms in man." Diabetes, Obesity and Metabolism (2015): Accepted article.
• Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr. 1983 Jun;37(6):941-4.
• Hallschmid, Manfred, et al. "Intranasal insulin reduces body fat in men but not in women." Diabetes 53.11 (2004): 3024-3029.
• Kaur B, Ranawana V, Teh AL, Henry CJ. "The Glycemic Potential of White and Red Rice Affected by Oil Type and Time of Addition." J Food Sci. (2015).
• Robertson, R. Paul, et al. "Glucose toxicity in β-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection." Diabetes 52.3 (2003): 581-587.
• Steen, Eric, et al. "Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease-is this type 3 diabetes?." Journal of Alzheimer's disease 7.1 (2005): 63-80.