Selenium & Skin Cancer. ALA, Inflammation & Muscular Adaptations. Eccentric Training & Oxidative Muscle Fibers. Tip of the Day: Have Plenty & Regular Sex For Your Brain

Certain "behaviors" during spring break can give your brain a neuro-anabolic break.

13% and 15% that's the number of Canadian University Students who claim to do what it takes to keep their brain volume at least stable over the spring break. 13% of the female and 15% of the male student and female students, respectively, that's also the SuppVersity Figure of the Week and at the same time the relative number of students who openly declared that they were about / had previously engaged in "casual sexual activity" on the upcoming / past spring break trip to Daytona Beach, Florida (Maticka-Tyndale. 1998)

Who said our youth did not know what's good for them?

Since the pertinent study preceded the Glasper study addressed in the current installment of on short notice by 15 years, these results just go to show you that we know instinctively what's necessary to counter the effects of the alcohol over spring-break ;-)

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Selenium and skin cancer (Cassidy. 2013) -- I guess you will remember the debate that arose after the data from the selenium + vitamin E large scale trial hit the mainstream media news. Hell broke lose and people did (unfortunately) not only start questioning the usefulness, but also the safety of all vitamin supplements - and that quite frantically (cf. "Ask Dr. Andro, Are Vitamin Pills Bad for Me?").

The results of a recently published study by scientists from the Huntsmen Cancer Institute (no that's not "Paleo" ;-) in Salt Lake city could shed at least some new insights into the very mixed results we are seeing in the studies on vitamins and/or minerals with anti-oxidant prowess:

"Taking A Multivitamin is a Question of Faith", above all (read more)

"We studied the effects of Se in vitro on UV-induced oxidative stress in melanocytes, and on apoptosis and cell cycle progression in melanoma cells. In vivo, we used the HGF transgenic mouse model of UV-induced melanoma to demonstrate that topical treatment with l-selenomethionine results in a significant delay in the time required for UV-induced melanoma development, but also increases the rate of growth of those tumors once they appear. In a second mouse model, we found that oral administration of high dose methylseleninic acid significantly decreases the size of human melanoma xenografts." (Cassidy. 2013)

In other words, in as much as they are able to postpone / prevent the occurrence of cancer by protecting the healthy cells, their protective effect is not tissue specific and will - once the bad guys have appeared on the scene protect the cancer from your bodies own, as well as the pharmacological inflammatory anti-cancer machinery.

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Alpha lipoic acid does not hamper exercise induced intramuscular ROS production & DNA damage (Fogarty. 2013) -- I know this does not really sound like good news to some of you, but you will be surprised that even the authors of the study at hand feel that it is.

While this is not directly related to the intramitochondrial ROS production, I still reccomend, you read my previous article on the purported "nutrient partitioning effects" of ALA before you go and buy a year's supply. (learn more)

The scientists from the University of Ulster recruited 12 of this in the world of scientific paper "rare specimen" of healthy male study participants (age 28 + 10 years, stature 177 +/-12 cm and body mass 81 +/-15 kg) and had them take either 2x1,000mg of regular alpha lipoic acid twice a day or placebo.

Wouldn't it be better to use R-ALA? I am telling you this now for the 1124th time: There is no reliable evidence for the superiority of R-ALA over regular ALA, the majority of the studies showing benefits of ALA supplementation has been conducted with the 50% r-enantiomer and 50% s-enantiomer version and if you have ever heard of the hormesis hypothesis (=low (eu-)stress induces beneficial adaptation) you would rather ask, "isn't it likely that taking R-ALA would not have yielded the same beneficial effects?"

The caps were to be taken in addition to the regular diet, the young men were following and were supposed to build up a protective anti-oxidant belt against the exercise induced oxidative assault of 100 isolated and continuous maximal knee extensions in the non-dominant leg after 14 days of supplementation.

"[The ALA preload] increase[d] plasma antioxidant status and attenuates lipid peroxidation and DNA damage following maximal, eccentric muscle contractions[, but] had no protective effect on muscle mitochondrial DNA damage."

Now this is actually awesome news, because it shows that ALA blunts the systemic oxidative damage only, while leaving the local intra-muscular oxidative damage of which the researchers rightly point out that "a substantial body of literature documents" the beneficial effects of ROS on "cell adaptation associated with exercise training" (Fogarty. 2013). In other words: It's unlikely ALA will hamper your gains.

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Eccentric training for bigger stronger muscles? (Hody. 2013) -- At first sight the conclusion of a soon-to-be-published study from the University of Liège in Belgium, which says:

"Our data suggest that the eccentrically biased contractions in mice induced specific adaptations in protein expression and muscle fiber composition which may reflect a more oxidative muscle phenotype." (Hody. 2013)

appears to suggest that the longstanding wisdom that eccentric reps are (given you get adequate rest) profoundly anabolic was inaccurate. If you use your knowledge about the enormous degree of type I fiber hypertrophy in bodybuilders (cf. fig.1 here), however, the information that eccentric training causes a shift in the muscular phenotype towards a predominantly oxidative slow-twitch fiber make-up, would at least the part about the muscles becoming "bigger" will remain intact.

Figure 1: Effect of five training sessions of variable duration (75-135 min / increasing from session to session) with 48h breaks between sessions on the muscle fiber make-up of mice (Hody. 2013)

Now, don't be afraid that your eccentric biceps curls could eventually make you weak. There are some "on the other hands" attached to the study results. The first and most important one of these is the mere fact that the largest increase occurred in type IIa fibers which are also often referred to as "oxidative" muscle fibers, but are actually more of an "jack-of-all-traits" fiber type, which happen to do most of the work in the BB-relevant 6-15 rep range. Secondly, the training downhill-running protocol the adult C57BL6 mice were exposed to. Downhill-running, may be eccentric, but it is also an endurance and no strength training regimen, and will thus have a tendency to promote the

No pain inflammatory signaling, no gain? In the long(er) run this could in fact be true (learn more). And what would be more fitting to induce the former if not eccentric training?

That being said, it is only logical that whatever growth / genera adaptation mechanism a given exercise regimen may be triggering, the trained muscle group and in this case also the trained fiber-type will benefit the most. Moreover, scientists and laymen tend have a very different understanding of a "shift in fiber type composition" by which the former don't imply loss of any fibers, while the latter misunderstand the ratios for absolute values and fool themselves to believe that results like the ones of the study at hand were about "losing precious type II" (=fast twitch, glycolytic, "lift heavy, but short") muscle fibers. What they are really about, is yet the accentuated ability of the highly stressing eccentric reps to induce more than just a "balooning up" of the muscles and induce profound structural adaptations, the importance of which I have highlighted only a couple of days ago in the context of my post on satellite cells (read up on that one).

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Only regular sexual intercourse keeps your brain healthy and in shape (Glasper. 2013) -- No, I am not going to start this comment with a reference to certain old men who met a couple of days ago in Rome. I will rather stick to the relevant facts and inform you that you better make sure you get laid this weekend. Why? Easy, a recent study by scientists from the University of Maryland and Princton University shows quite impressively that our body notices that we are useless once we give up reproducing. So useless, in fact, that he even does not bother to repair our brains any longer:

In a past installment of On Short Notice you have already learned what the female orgasm could be for, remember? Which brings up the question will the women benefit, as well? Likely.

"Sexual experience enhanced the number of newly generated neurons in the dentate gyrus with both single and repeated exposures in middle-aged rats. Following continuous long-term exposure to sexual experience, cognitive function was improved. How-ever, when a prolonged withdrawal period was introduced between the final mating experience and behavioral testing, the improvements in cognitive function were lost despite the presence of more new neurons." (Glasper. 2013)

You want a bottom line? Well, let's make it fast, I feel I got to do something for my brain, now! Have sex, have it regular and have plenty of it (the rodents did it at least once a day) and when the new pope calls, tell him it's just for your brain health ;-)

Note: Although I deliberately wrote this part of On Short Notice, I hope that you are all old enough to know that getting drunk and having unprotected sexual intercourse with the next best person you can find "spring break style" is an absolute no-go. Not just for Catholics, but for any sane human being who has not already drowned his last neuron in alcohol.

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That's it for today, and I guess with the Glasper study in the back of your head, I don't have to tell you that there are other things than hanging out in front of the computer, TV or even the gym that can be done on the weekend, right? Enjoy!


References:

• Cassidy PB, Fain HD, Cassidy JP, Tran SM, Moos PJ, Boucher KM, Gerads R, Florell SR, Grossman D, Leachman SA. Selenium for the prevention of cutaneous melanoma. Nutrients. 2013 Mar 7;5(3):725-49.
• Fogarty MC, Devito G, Hughes CM, Burke G, Brown JC, McEneny J, Brown D, McClean C, Davison GW. Effects of α-Lipoic Acid on mtDNA Damage following Isolated Muscle Contractions. Med Sci Sports Exerc. 2013 Mar 6.
• Gasper ER, Gould E. Sexual Experience Restores Age-Related Decline in Adult Neurogenesis
  and Hippocampal Function. Hippocampus. 2013 [Epub ahead of print]
• Hody S, Lacrosse Z, Leprince P, Collodoro M, Croisier JL, Rogister B. Effects of Eccentrically and Concentrically Biased Training on Mouse Muscle Phenotype. Med Sci Sports Exerc. 2013 Feb 22. 
• Maticka-Tyndale E, Herold ES, Mewhinney D. Casual sex on spring break: Intentions and behaviors of canadian students. Journal of Sex Research. 1998; 35:3.

No Pain no Gain? What Can We Learn From the Time Course of Muscle Damage After Eccentric Workouts. Plus: What's that Got to Do With Your Doctor Sending You to the ER

Concentration curls are among those exercises, where eccentrics can easily be incorporate. Plus. As the EMG Series shows, this increases the biceps activity by almost 50% compared to the regular barbell curl (learn more). But will it also make you grow faster?

Just let me get this straight right away: I am well aware that it is still debated if and if so to which extend skeletal muscle damage affects or even determines the training induced gains in strength and/or lean body mass and it is not my intention to rekindle this never-ending debate. At least in my humble opinion, it does yet appear that a certain degree of "damage" is necessary for "optimal" gains. Anything that passes this threshold is however, as Schoenfeld points out in what I believe is the most recent review of the literature, not going to "further augment muscle remodeling and may in fact interfere with the process" (Schoenfeld. 2013).

The potential of negative interference is obviously particularly pronounced, when the the potentially muscle damaging physical activity is performed during the recovery phase. But how long it going to take until the repair and restructuring processes are completed?

In other words: How long would be optimal rest interval for someone who trains really intense with a focus on eccentric overload? 
 
At first sight it seems as if the results of a recent study from the State University of Campinas should help us to bring light into the darkness, but as we are soon going to see, things are (once again) more complicated than common sense would tell us.

The main intension of the researchers was to (I quote) "observe the time course of muscle damage and inflammatory responses to resistance-training with EO [eccentric overload]" (Neme Ide. 2013). To this ends, they recruited 3 women and 5 men in their early twenties who had at least one year of previous strength training experience and had them perform a standardized workout program with the following parameters:

No idea how to schedule your workouts? Learn how to do that and much or in the Step By Step Guide to Your Own Workout Routine!

• total duration: 13 sessions (total) distributed evenly across 7 weeks; 2x full body workouts trained every Tuesday & Thursday

• set & rep scheme: 4 sets of 8 reps at 80% of the 1-RM max for eccentrics; since that's more than you can "lift", i.e. move concentrically, the researchers who supervised the sessions had to help the participants on the eccentric part of the movement

• exercises: classic full body workout consisting of bench presses, 45-degree leg presses and bent-over rows

The blood samples were taken 96h after training session 2, 7, 9, 11 and 13, respectively and the creatine kinase, CRP and various hematological parameters were measured to evaluate the impact the eccentric workouts had on ...

• muscle damage - indicated by the amount of creatine kinase (CK) that leaked from the musculature into the blood,

• overall inflammation - indicated by the change in C-reactive protein (CRP) levels, 

• hemtaological paramaters - including red blood cell count (RBC), hemoglobin concentration (Hb), hematocrit (Ht), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), erythrocyte distribution width (RDW), white blood cell (WBC) count, lymphocyte (LYNF) count, neutrophil (NEUTR) count, and platelet count (PLT).

The reasoning behind the constant monitoring of CK, CRP and blood parameters was that the scientists expected that there would be an attenuation of the damaging effects of the workouts as the participants bodies got accustomed to the bi-weekly torture.

Don't let your Dr send you to the ER without letting him know that you trained the day before you got your latest bloodwork done.

If you take a look at the creatine kinase (CK) data I plotted in figure 1 (left) there are two things you should take a mental note of. Firstly, the increase in creatine kinase is "exorbitant" and could - assuming your doctor either doesn't know you are strength training or has no clue about the effects a heavy workout can have on the amount of the enzyme that "recycles" creatine into pohosphocreatine (PCr) that's floating around in your blood stream - be enough to have your physician send you to the ER - misdiagnosis: rhabdomyolysis (please bear in mind that Kraemer et al. (2004) suggest a reference interval for physically active subject of 1,309U/L; that's almost 4x more than the regular lab range that usually says everything past 400U/L would be pathological)

Figure 1: Creatine kinase (CK) levels (left) and C-reactive protein (CRP) levels (right) at different timepoints of the 7-week exercise intervention (Neme Ide. 2013)

And secondly, this increase in creatine kinase is hard to predict and varies from subject to subject (the numbers in the upper line of the label of the horizontal axis are the subject numbers):

"CK and CRP presented significant changes at specific time points, but not for all subjects. Four subjects presented significant changes in CK activity at P2 (+1719%, +1250%, +1281%, and +312% resp.), and other two at P13 (+391% and +139%, resp.). For CRP six subjects presented significant changes at P2 (+1100%, +243%, +3800%, +2500%, +1400%, and +2400%, resp.), one at P4 (+567%), other at P9 (+3200%), three at P11 (+300%, +3400%, and +3900%, resp.), and other at P13 (+1500)." (Neme Ide. 2013)

Interestingly, there was no significant correlation between the changes in creatine kinase (CK) and C-reactive protein (CRP) as you would expect if muscle damage and systemic inflammation went hand in hand.

Accommodation? yes! Unequivocal results? No.

Despite the fact that the expected pronounced initial CK response was present only in four out of the eight individuals, the scientists are confirmed that the data they gathered does support their initial hypothesis that there would be an attenuation of muscle damage in the course of the 7-week study period and ascribe the latter to the repeated bout effect a term, scientists use to refer to the protective effects a single bout of eccentric exercise has on the muscle damage during subsequent bouts (Mc Hugh. 2003).

"The potential adaptations that explain the phenomena have been categorized as neural, mechanical, and cellular. Regarding the cellular adaptations there is evidence of longitudinal addition of sarcomeres and adaptations in the inflammatory response following an initial bout of eccentric exercise, limiting also the proliferation of damage." (Neme Ide. 2013)

While a similar trend was observed for the CRP levels, the initial increase of the latter was by far less pronounced than for the CK values, so that the levels remained within the physiological norm for active people (the average CK values, on the other hand, were 2x elevated over the already high reference interval for physically active individuals).

Changes in hematological parameters were the exception

In case your workout program looks anywhere like Adelfo's Overkill Program from April 2013, you better make sure to come up with a new one after no more than max. 3-4 weeks!

If we acknowledge the reasoning Plaisance and Grandjean present in their 2006 review of the literature and take the comparatively low exercise related increases in C-reactive protein levels (CRP) as an indicator of damage in non-skeletal muscle tissue, it is also not surprising that this unquestionably intense and obviously muscle damaging exercise regimen did not have more pronounced effects on the blood panel of the study participants.

Only two subjects presented significant changes in neutrophils with an unpredictable up and down for subject 7 and a significant 60% increase after the final session in subject 6. In view of the fact that subject 7 was also the only one with detoriations in almost all other blood parameters, it's yet pretty unlikely that this was a result of the workout protocol and not the result of some sort of infection or whatever.

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Ok, so what exactly have we learned now? This is actually a pretty good question. I guess one thing we have learned is that physically active individuals can actually shock their doctors with "exorbitantly" high (yet still normal) creatine kinase levels. This does not mean that you can simply ignore constantly elevated / abnormal CK values, but it's important to realize that the 400U/L range your lab report lists is probably not sufficient for your personal CK values if you get blood drawn in the vicinity of a hard workout (on a related note: especially when you are low-carbing and eating high amounts of protein the increase in CK usually goes hand in hand with increases in the "turn protein to energy" enzymes AST and ALT, which are in this case not necessarily indicative of "liver damage").

There is evidence that the expression of the local factions of IGF-1, MGF & Co., depends on the exercise induced wear and tear  (learn more), it would be stupid to assume that there was no turning point at which the beneficial damage turns against you.

What we unfortunately didn't learn (and I feel that the scientists really missed out on this opportunity) is what the underlying reasons of the differential CK response to the workout may have been. Would it really have been too difficult to ask the "non-responders" what kind of exercise protocol (including set + rep schemes, frequency, weights and exercises) they had been following before they enrolled in the study? I don't think so. In fact, I would rather argue that it would have been obligatory. For me, for example, the eccentrics would have been the only novel stimulus in this workout. I have however been training with a female friend of mine a couple of days ago who would certainly qualify as having been training for at least a year and following a training program consisting of 3–5 sets of 6–12 repetitions with 1-2-minute rest interval between sets, performed 4-5 times per week (these were the inclusion criteria for the study at hand), for whom all of the exercises would have constituted a whole new stimulus in and out of itself (she usually works out on those fancy machines).

Now this may be a pity, but int the end, the differential CK response could have been totally irrelevant anyway. The pertinent evidence from human studies may be more than scarce, but if we go by the few studies we have, it appears that even a 5x higher CK response to eccentric exercises as it was observed in the non-preconditioned group in a 2011 human study by Flann et al. does not result in significantly different increases in either muscle size, or strength (cf. figure 2).

Figure 2: Strength and hypertrophy (left) and creatine kinase (CK, right) response in pre-trained and naive individuals in the course of an 8-week eccentric training protocol (Flann. 2011)

The fact that Neme Ide et al. did not measure the strength and/or hypertrophy response, still baffles me. I do however believe that (most) scientists are not just clever, but also very rational beings and therefore I would suspect that there is soon going to be a follow-up paper with the respective data. Why's that? Well, in a scientific community, where the number of publications is unfortunately more important than their quality, tricks like these may eventually give you the edge over the competition on your next job application ;-/

References:

• Flann KL, LaStayo PC, McClain DA, Hazel M, Lindstedt SL. Muscle damage and muscle remodeling: no pain, no gain? J Exp Biol. 2011 Feb 15;214(Pt 4):674-9.
• Kraemer WJ, French DN, Paxton NJ, Häkkinen K, Volek JS, Sebastianelli WJ, Putukian M, Newton RU, Rubin MR, Gómez AL, Vescovi JD, Ratamess NA, Fleck SJ, Lynch JM, Knuttgen HG. Changes in exercise performance and hormonal concentrations over a big ten soccer season in starters and nonstarters. J Strength Cond Res. 2004 Feb;18(1):121-8.
• McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports. 2003 Apr;13(2):88-97. R
• Neme Ide B, Alessandro Soares Nunes L, Brenzikofer R, Macedo DV. Time course of muscle damage and inflammatory responses to resistance training with eccentric overload in trained individuals. Mediators Inflamm. 2013;2013:204942.
• Schoenfeld BJ. Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy? J Strength Cond Res. 2013 May;26(5):1441-53.

Exercise Research Quickie: HIIT vs. Steady State, More on the Hormonal Response. Light Training, High TUTs & Peak Contractions - Not Just for The Elderly. Train Your Left, Grow Your Right Leg - Contralateral Training Effects

The role of the innervations between our muscles as well as to our brain is often overlooked, when we are talking about size gains. The image shows stained nerve fascicles from the Song study, which brings this wiring back onto the radar.

I know that we have had the short news on Saturday only and that there are of course tons of short news on Facebook everyday, but the studies I am going to present you in this exercise research quickie were so in-between (meaning not really worth a full post, but still way too good to be wasted on facebook) that I decided to devote a post of its own to the research on the hormonal effects of interval vs. steady state training by Hackney et al. (Hackney. 2013b), the impressive and certainly not totally irrelevant effects of slow movement, low-intensity resistance training in the elderly Watanabe et al. describe in their latest paper and the surprising muscle building (Watanabe. 2013) and growth priming carry over effects Song et al. observed in response to unilateral electrical muscle stimulation (Song. 2013).

Although, the latter post is pretty theoretical I hope that all of you will find something that enlightens, amuses or entertains them in this "threesome" ;-)

More T, more DHT, more cortisol - that's the HIIT vs. LISS formula

(Hackney. 2013b) -- In fact the results of two subsequently published papers by Hackney et al. would suggest that it's about as easy. Work out hard and fast and see greater increases in testosterone levels, but also testosterone turnover (into DHT via 5-alpha reductase), but don't forget that aside from these (questionable) anabolic benefits, your thyroid hormone levels are going to take a dive (as reported previously), as well.

Figure 1: Comparison of the hormonal responses measured in the plyometrics (left) and the HIIT vs. LISS (right) study (based on Ozen. 2013 and Hackney. 2013)

The figure above is actually from a post where I discussed this before, so if you cannot remember all the details, briefly go back before you take a look at the summary of results of the more recent study by Hackney.

"Dihydrotestosterone (DHT) - Bigger, Stronger, Faster or just Balder, Fatter and Unhealthier?" That's the question I asked in one of the installments of the Intermittent thoughts on building muscle. A post I would highly suggest you read, by the way ;-)

In this 2nd paper that was published right before Christmas in the Journal of Endocrinological Investigations the researchers were able to show that repeated periods of 90-sec treadmill running at 100-110% maximal oxygen uptake (VO2max) and 90-sec active recovery at 40% VO2max for 42-47 min (which is obviously pretty long!) caused  just a significantly more pronounced increase not just in free testosterone, but also in its conversion to testosterone's big brother DHT (as indicated by statistically higher levels of the 5α-reductase marker 3-α Diol G at 12POST HIIT vs. LISS). This is interesting, as dihydrotestosterone (DHT) which is often falsely associated only with hair loss, prostate cancer and even obesity, does also play an important role in strength development (click here to learn more) and appears to do it's magic via the MAPK receptor. Now, MAPK in turn can activate PGC-alpha and that the latter is way more than just the endurance / mitochondria builder it was long thought to be is something you should still remember from the post on the"The IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects of PGC-1 α-4" (read more).

Bottom line: It is becoming more and more clear that HIIT is in fact somewhat of a chimera that shares beneficial and detrimental effects of both classic cardio and classic strength training with mammoth sessions like the one performed in the studies at hand triggering similar hormonal cascades that will - despite probably causing beneficial adaptations - simply require longer rest times than a classic LISS regimen.

A  note of caution: Both these studies point to the highly questionable "value" of taking a bunch of people letting them do whatever type of training once, measure some stuff of which you do only have a very rough idea of what it's actually doing and then have a bunch of morons like myself try to come up with "practical implications"

So if you do HIIT, stick to the principles "short and hard" (I would never suggest doing the >40min interval sessions for anyone whose primary goal is to be healthy and look good naked, by the way; add a walk on the treadmill if you want to train longer like on a combined HIIT + LISS cardio only day. But most importantly don't forget to enjoy your well-deserved, highly productive off-time and remember that it's during those hours, when all the hard work is paying off... ah I almost forgot, this is a tried and proven way that happens to be confirmed by studies like Hackney's and not vice versa.

 Light training, high TUTs and peak contractions - not just for the elderly?!

You cannot only implement"light" training into your established routine (see last paragraph), but should also think of the often forgotten benefits of periodization, detraining & co (learn more), as well as times, when you may be injured or otherwise disabled and cannot lift heavy.

(Watanabe. 2013) -- It may sound like a study for the elderly, but just as the best-agers among the SuppVersity readers can learn something from studies done in the the younger fellows, the younger weightlifters may well get some intriguing insights from studies with older participants - studies like the one by Watanabe et al., for example.

When the researchers from the Department of Life Sciences at the University of Tokyo compared the hypertrophy and strength gains of two exercise regimen using a low resistance of 50% of the personal 1-RM max of their 59-76yr old subjects, the scientists found that slow movements with tonic force generation were superior to the regular 1s concentric vs. 1s eccentric reps I guess most of you will be employing in their training routines.

The subjects who had been randomized to the LST group and performed their reps with a 3s concentric, a 3s eccentric and phase and most importantly a peak contraction in-between did gain a similar amounts of strength as those subjects who performed the standard protocol for 10 weeks (the 12-week study had a 2-week familiarization phase), but contrary to they did also record statistically significant increases in muscle size.

Alternative exercises on which peak contractions work well, are the fly (preferably on a machine or using cables), the lat pulldown, cable crunches, all sorts of triceps extensions, the scott curl (where you would do them midrange), every form of calf raises. Always remember, though: A peak contraction is never done in the full stretch position, but always either midrange or as the name implies at the peak of the contraction, before the eccentric phase begins.

So what does that mean? Certainly not that all of you should stop lifting heavy weights, because 50% 1-RM was enough if not superior to the regular 70-90% that are recommended in most serious training regimen. Rather, these results should remind young and old trainees alike of keeping an eye on your form and making sure that you stimulate the muscle and don't just move whatever weight from place A to place B.

That said, try to incorporate peak contractions with every rep on the auxilliary movements of your next workout. Start your leg workout with regular squats, for example, 5x5 TUT 101 (meaning 1s eccentric, 0s rest at the bottom, 1s concentric), but instead of the 4x10 leg extensions you would usually do for your quads, you lower the weight somewhat and do them with a slower rep-speed (somewhere in between 1-3s) and a peak contraction (meaning you really squeeze the muscle in a position, where your knees are almost locked out). Done right, this is going to give the word DOMS (=deep onset muscle soreness) a whole new meaning + you will have to reduce your weights, anyways.

Train your left leg and your right one will grow as well

(Song. 2013) -- Do our bodies know something about aesthetics? Well, if that were the case, the legs of some of the gymbros who "don't train legs, because [they] play soccer" shouldn't look the way they do... but I am digressing here. According to the study by Yafeng Song et al. have just published in the open access journal Plos ONE, there appears to be a certain carry-over effect - at least if the growth stimulus is chronic and profound.

To achieve the latter, i.e. a chronic and profound training stimulus, the researchers from the Umea University in Sweden exposed the soleus and gatrocnemius muscles of rabbits to a 6-week electrical muscle stimulation + exercise protocol and measured muscle changes and inflammation on weeks 1, 3 and 6 of the study. Now, the clue of the study was that the unilateral "exercise" was actually mechanically and electrically enforced, so to say:

"The movements are produced by a pneumatic piston, in which the range of motion can be controlled. The range of movement was set to 9.5 cm, given a range of motion in the ankle of 55–65u of which 20–25u was dorsiflexion and 35–40u was plantarflexion. The right leg was attached to the piston and the pelvis/hip region was strapped down to restrict the motion in the left non-exercised leg. The left leg was unattached. During the plantar flexion of the right leg, an active contraction was induced by electrical muscle stimulation via surface electrodes placed 2 cm apart over the right triceps surae muscle. The stimulation was synchronized with the plantar flexion movement of the piston by a microswitch, which trigged the stimulator unit".

I will spare you the further details... just think of a modern rabbit torture machine that was designed to "work the rabbits right extremities out". As you would expect from any good torture machine this device brought about a significant amount of tissue damage and a corresponding increase in the number of necrotic fibers.

Figure 2: Variability in fiber size, fibers with internal nuclei, inflammation in soleus (left) and gastrocnemius muscle (right) in response to the exercise + electrostimulation program. Mind the similar responses in the exercised (E) and the non-exercised (NE) limb (Song. 2013)

Now what's surprising though is the fact that despite the local damage, the inflammation had a systemic component, which happened to be more pronounced in the untrained soleus vs. gastrocnemius muscle (slow vs. fast twitch, by the way).

Against that background it is still only a little less surprising that the variability in fiber size, the number of fibers with internal nuclei (=sign of restructuring process, cf. "The Skeletal Muscle Hypertrophy 101") and even the fiber splitting were virtually identical. After all, this would mean that systemic parameters do matter. But haven't we just discarded this notion yet another time in the first of the items in today's exercise research quickie? Yes we have, but in that case we were talking about the usual subjects, the "anabolic" and "catabolic" hormones, Song et al. on the other hand speculate that

"[t]he collateral muscle changes and inflammation after unilateral EMS/E observed in this study may be caused by [a] neuronal mechanism. Since there is some evidence for a commissural system in the spinal cord that mediates transmedian signaling with a fairly precise bilateral representation, nerve signals from the trained side may pass over to the contralateral muscles through commisural inter-neurons. If this is the case, unilateral injury caused by EMS/E may cause a cross-transfer up-regulation of neuropeptides that can be involved in the inflammatory response in the contralateral muscles." (Song. 2013)

The researchers indicate that their current, as well as previous results from their laboratory would support this hypothesis and that any systemic or circulatory effects must actually be excluded, because these would not have occurred only focally, but generally within all muscles. They also point towards previous studies in which the signalling between contralateral and ipsilateral limb was blocked and the observed cotralateral responses were abolished.

So what's the point? I will openly admit that the practical relevance of these results (esp. for you as a hopefully healthy trainee) is as of now still very questionable, but the fact alone that it brings the nervous system back on the "scientific" radar was certainly worth including it in this "threesome" - don't you think so? No, well... maybe you like the scientists own rational who argue that the findings are (a) important in the context of a wide range of musculoskeletal and neuromuscular disorders and (b) relevant for each and every unilateral exercise experiment, where the contraleteral limb is used as a control - and you know there are plenty of them!

References:

• Hackney AC, Kallman A, Hosick KP, Rubin DA, Battaglini CL. Thyroid hormonal responses to intensive interval versus steady-state endurance exercise sessions. Hormones (Athens). 2013a Jan-Mar;11(1):54-60.
• Hackney AC, Hosick KP, Myer A, Rubin DA, Battaglini CL. Testosterone responses to intensive interval versus steady-state endurance exercise. J Endocrinol Invest. 2013b Dec;35(11):947-50.
• Ozen, SV. Reproductive hormones and cortisol responses to plyometric training in males. Biol Sport.2013; 29 (3).
• Song Y, Forsgren S, Yu J, Lorentzon R, Stål PS. Effects on contralateral muscles after unilateral electrical muscle stimulation and exercise. PLoS One. 2013;7(12):e52230.
• Watanabe Y, Tanimoto M, Ohgane A, Sanada K, Miyachi M, Ishii N. Increased muscle size and strength from slow-movement, low-intensity resistance exercise and tonic force generation. J Aging Phys Act. 2013 Jan;21(1):71-84.