.

.
marylin monroe
Showing posts with label regeneration. Show all posts
Showing posts with label regeneration. Show all posts

On Short Notice: Retinoic Acid vs. Lung Cancer / Metabolic Effect of Fats in Cerebral Fluid / Nucleotid Supplements Instead of Icepacks // Ibuprofen & Leaky Gut / Fish Oil Enema & Colitis / Fructose, Glut-5 & Obesity + More!

Image 1 (Coloribus): Unquestionably a great add, but the (Ex-)Marlboro man would be better off with a piece of liver than a carrot ;-)
Just as I promised I am pumping out another set of "short notice" items. To make sure not to be confused with what I have once heard someone call a "pubmed warrior", I did however spike today's episode with three longer items and saved a couple of mini-items for the next week. I hope you enjoy the ride and don't forget to copy "Fatfree" who asked for more in-depth info on TUDCA after reading last Saturday's installment of this series (see "Testosterone - 12% Drop With 75g Glucose? Low T3 Syndrome - Can TUDCA Help?"). If there is more information that would make a longer post worthwhile and I find the topic interesting enough to spent the time on doing the research, I am always willing to comply with wishes like this :-)

Retinoic acid (not beta carotene!) can protect smokers from lung cancer

In a paper that has just been published in the Journal of Food Sciences, Xue et al. report that the epigenetic switches retinoic acid (active, real vitamin A) triggers in cancer cells of lung cells in cigarette-smoke exposed rodents does effectively counter the upregulation of the 120 mostly cell-differentiation and proliferation related genes scientists believe to be a causative factor in the etiology of lung cancer. This is particularly interesting, because supplementation with larger amounts of the vitamin A precursor beta-carotene has been found to pose a serious health risk for smokers. With a passive smoke exposure equivalent to 80 nonfiltered commercial cigarettes the per day it is almost marvelous how effective the 10mg/kg bodyweight of all-trans retinoic acid were.
Figure 1: While all-trans-retinoic acid (left, bottom) appears to have potent anti-lung-cancer effects the β1-apocarotenoids our bodies produce from beta carotene could potentially negate these beneficial effects (see "Anti-Vitamin A Effects of Beta Carotene"); this would also explain why previous research has shown that beta-carotene supplements are potentially hazardous for for smokers (cf. Druesne-Pecollo. 2010)
I guess, the most studious among you will probably already know how the differing effects of vitamin A (real ATRA) and beta carotene come about, right? In my recent blogpost on the "Anti-Vitamin A Effects of Beta Carotene", I did actually provide a mechanistic explanation as the metabolic byproduct that arises from high dose beta carotene supplementation will block the retinoic acid receptor (similar to the way a SERM blocks the estrogen receptor) and thus inhibit the inhibitory effects of real vitamin A on the occurrence and progression of cancerous growth.

Image 2: Helicobacter pylori, ain't the reason you get lung cancer, but smoking will help him to prepare the breeding ground for gastric cancer.
Apropos lung cancer, a study by Koshiol et al. has recently refuted the claim that Helicobacter pylori (H. pylori) infections would increase the risk of lung cancer (Koshiol. 2012). Previous research from the German Center for Research of Ageing, on the other hand, found conclusive evidence that the combination of h. plyori and smoke increases the risk of gastric cancer by more than 600% (Brenner. 2002)! But don't worry, all-trans-retinoic acid can take care of that, as well. At least in the Petri dish, incubation of human gastric cancer cells with ATRA lead to immediate growth arrest (Zhang. 2005)... and did I mention it does the very same thing to pancreatic cancer, breast cancer and leukemia cells?
Implications: Regardless of whether you live with a chainsmoker, work in a bar or are stranded on a lonely island, where your campfire is the only source of smoke in your life, try to get your real vitamin A (=retinol) from fatty animal products and forget about beta carotene supplements (even if you brought some to your lonely island ;-). With fatty fish, a piece of liver every now and then, butter, eggs, etc. and large amounts of green leafy vegetables and a reasonable amount of whole fruits (no juices!) you are guaranteed not to fall short of any of these "vitamins A" (retinol and beta carotene) and the multitude of other potent carotenes that would be missing from your supplements anyway.

Type of fatty acids in cerebral fluid determine metabolic rate

Image 3: Assuming that the fatty acids you eat also float around in your brain peanut oil (1-2.5% C:24) is the worst edible oil for anyone who is concerned about his overnight energy expenditure.
A study that has just been published on PLos ONE provides astonishing insights into how long chain fatty acids (saturated fats) in your cerebral fluid could (we are dealing with observational human data from a metabolic ward study, here) slow down your fat loss or even make you gain weight by decreasing overnight energy expenditure. With correlations in the range of -0.6, lignoceric acid (C24:0, as in peanut oil) and Cerotic acid (C26:0; as in beeswax) are by far the worst offenders, as far as overnight energy expenditure are concerned; and though the design of the study did not allow for any conclusions on the underlying mechanisms, the fatty acid induced suppression of the nocturnal surge in growth hormone could be one potential and at least in my humble opinion not very far-fetched cause for this effect. Interestingly, things look completely different for the plasma levels of these fatty acids, which showed the exact opposite +0.6 correlation with 24h energy expenditure. Other noteworthy results were
  • significant correlations of the mono-unsaturated fatty acids palmitoleic and oleic acid in the cerebrospinal fluid with higher rates of fatty acid oxidation (relative to carbs, not total) and 
  • significant correlations of the omega-6 fatty acids linoleic (18:2n6), dihomo-g-linolenic acid (20:3n6) and arachidonic acid (20:4n6), the omega-3 fatty acids linolic acid and docosapentaenoic acid (DPA, C22:5n3) and the omega-9 fatty acid mead acid (C20:3n9) with better glucose clearance.
And no, the much-lauded fish-oil, i.e. the EPA and/or DHA content of the cerebrospinal fluid, had no significant effect on glucose tolerance. A result, by the way, which reminds me of another study I came across recently:  In their four day supplementation trial Miller et al. observed vast differences between the incorporation of EPA and DPA (docosapentaenoic acid, the one that did correlate - weaker than the omega-6s, though - with improved glucose tolerance) into plasma and red blood cell lipids subsequent to the oral provision of 8g/day of each to ten healthy women. Their observations and the respective alterations in EPA and DHA in the DPA supplementation group Miller and his colleagues concluded that DPA could serve as a reservoir of the major long-chain n-3 fatty acids (LC n-3 PUFA) in humans - exciting stuff and probably something you will read more about, here at the SuppVersity in the future.
Image 4: The data would support the use of MUFA and omega-6 laden olive and high MUFA macadamia oils, if we know how their consumption effects the fatty acid flux in our brains.
Implications: Due to our lack of knowledge about the ultimate determinants of cerebrospinal fluid fatty acid composition it is hard to say if these results do imply that you better focus on MUFAs in view of their beneficial effect on both glucose clearance and respiratory quotient - and still the usefulness of MUFA and omega-6 laden olive oils, which have time and again been shown to produce all sorts of favorable changes in glucose, fat and overall energy metabolism would support the notion that there is a direct or indirect downstream effect of higher intakes of the respective fats, their occurrence in our cerebrospinal fluid and their downstream metabolic effects.

Cooling trained muscles appears do decrease regeneration

Soon to be published in the Journal of Strength and Conditioning Research are the results of a randomized cross-over study into the effects 15 minutes of icing applied 0h, 3h, 24h, 48h and 72h after an intense eccentric arm workout with 6 sets of elbow extension performed at 85% maximum of the voluntary maximal load had on the subjective as well as measurable (inflammatory cytokines, creatine kinase (CK-MB), hemoglobin and oxygenation were assessed) regeneration of 11 young male college baseball players (Tseng. 2012).
Figure 2: Inflammatory cytokines, creatine kinase and visual analgue scale data on subjective perception of fatigue at different timepoints before and after the eccentric arm workout (data adaptedm from Treng. 2012)
As you can see from the data in figure 2 the icing did have a somewhat bizarre effect on the inflammatory and subjective indexes of muscular regeneration. While...
[...] significant change in the levels of IL-1β, IL-8, and IL-1 were observed following the muscle-damaging eccentric exercise in either the control or topical cooling conditions and no differences in these cytokines were found between the control and cooling trials throughout the 72 h observation period (data not shown in figure 2, Tseng. 2012).
The levels of the pro-anabolic cytokine IL-12 (Argile. 2001), TNF-α, and IL-6 were significantly lower 24h after the workout (see figure 2, left; p < 0.05). There were yet no significant differences at other time-points ant both the CK-MB, as well as the fatique score (figure 2, right) suggest that the overall regenerative capacity was compromised by the repeated cooling of the strained musculature.
Image 4: If you use a 41°C hot bath 48h before a workout to "pre-generate", you don't even need to ask yourself whether or not the results of the study at hand conclusively imply that icepacks are detrimental and their use after workouts has to be avoided at all costs.
Although I must admit that this is not a settled case for me, until we understand the unexpected dip in IL-12, TNF-α, and IL-6 after 24h and its relation to the obvious increase in muscle damage (CK) and corresponding fatigue levels, it would appear prudent not to make use of an icepack as your regenerative means of choice.

Instead, I would suggest you follow the example of the young lady on the left and take "pregenerative" measures by taking a 41°C hot bath 48h before a strenuous workout. As you will probably remember from my previous article on the Touchberry study (read full story based on Touchberry. 2012) this will not just keep the damage at bay, but may also help you on your quest to a more muscular physique. And if you want to do your immune system a favor, check out the on very short notice item about RNA + DNA precursor supplementation further down...

On Very Short Notice

  • Image 5: Adding ibuprofen on top of exercise will make your gut look like a riddle screen.
    Ibuprofen makes an exercise-induced leaky gut even leakier - The use of NSAIDs such as aspirin and ibuprofen has long been implicated in the etiology of all sorts of gastrointestinal problems ranging from benign gastroinstestinal distress, over gastrointestinal bleading, ulcers etc. to all sorts of cancers. Researchers from the Top Institute Food and Nutrition at the University of Maastricht in the Netherlands have now found that the way by which ibuprofen aggravates the exercise-induced small intestinal injury and induces an even more pronounced gut barrier dysfunction in healthy individuals than exercise alone, may not just contribute to the occurrence of the aforementioned pathologies, but also precipitate to systemic diseases. After all, it opens up the doors to pathogens and toxins, which would otherwise be blocked by an intact intestinal barrier (van Wijck. 2012).
    N-acetyl-L-cystein (NAC) a potent natural anti-inflammatory which has also  been shown to reduce exercise induced inflammation (see "NAC Improves Markers of Oxidative Stress Induced by High Intensity Exercise") and glutamine (in the dos Santos study a HED of "only" 3-5g/day), on the other hand, exert protective effects on the integrity of the intestinal barrier (Sun. 2002; dos Santos. 2010).
  • Fish oil enema ameliorates colitis - When administered intra-rectally at a human equivalent dose of  ~13ml, fish oil effectively ameliorated the mucosal damage in experimentally induced ulcerative colitis in rat; flax oil and the corn oil control, on the other hand, did not prevent the increase in colonic weight / /length ratio and the associated histological changes 24h after Aisha Mohamed Dugani, Ahlam Elhelawi and Aisha Edrah had administered 1ml of 4% acetic acid to induce the colic (Mohamed Dugani. 2012). These results stand in line with general colon-protective effects of fish oil, observed in other studies and it's likely that they are a direct consequence of its non-negligible anti-inflammatory effect - which does not change my assessment that healthy physical culturists should not take more than max. 2g of supplemental fish oil per. The evidence supporting any beneficial effects on non-insulin-resistant, non-obese, non-hypertriglyceremic individuals is simply non-existent.
  • Image 6: No, this certainly does not look as if the conjugated linolic acid would work in horses as it does in mice ;-)
    Species specific effects of CLA: Horse don't lose weight, either - You will probably remember my recent post on the adipose tissue destroying effects of CLA (cf. "CLA Destroys Body Fat") in rodents, as well as my remarks that - if we discard potential underdosing as a contributing factor - it would appear that the beneficial effects of CLA we see in rodent studies is highly species specific. Now, Headley et al. have published the results of a study that investigated the effects of 0.05% CLA enriched chow on horses. Similar to what we see in humans, the conjugated linoleic acid had no effect on the body composition of the animals. Interestingly though, the mixture of three CLA isomers used in the study (cis-9, trans-11 + trans-10, cis-12 + and trans-9, trans-11; usually we have only the latter two in significant amounts) led to a statistically significant reduction of the potentially pro-inflammatory arachidonic acid in the blood of the horses. This spiked the interest of Headley et al. as it could turn out that this would render CLA (this specific isomer mix, I should say) as an agent that could have beneficial effects on the progression of joint disease, which is - in parts - driven by C20:4 (chemical name for arachidonic acid).
  • Towards a better understanding of why fructose is making us fat - Using in-vitro studies and a genetically engineered Glut5 -/- mouse model (these mice lack the glut-5 receptor which is responsible for the uptake of fructose), Li Du and Anthony P. Heaney were able to show that the preferential expression of Glut5 in developing adipocytes and the corresponding adipogenic (=promoting the creating of new fat cells) effects of fructose could well explain why fructose, which can no longer be taken up by mature fat cells, has been shown time and again to be way more fattening than its pro-insulinogenic cousin glucose (Du. 2012). Put simply, you could say: Increased serum levels of fructose require a) the conversion of fructose to triglycerides of glucose in the liver or b) the proliferation of adipose tissue so that the developing new fat cells can take the superfluous fructose up. If you consume too much of so that your liver is already working overtime, it is no wonder that your healthy high-fructose corn-syrup fat-free breakfast cereals are making you fatter and fatter. 
  • Figure 3: Effects of incremental treadmill running on selected markers of immune activity before and after 2 weeks of sublingual treadmill running in 38 healthy young men nucleotid supplementation (Ostojic. 2012)
    Supplement with RNA and DNA building blocks protects from immune-suppressive effects of exercise - The effects Sergej M Ostojic and Milos Obrenovic observed in response to a 14-day sublingual nucleotide supplementation regimen were basically what common wisdom tells you, you should see as a result of glutamine supplementation (Ostojic. 2012): The RNA and DNA precursors did not just ameliorated the dreaded immune-suppressive effects of a standardized cardio workout on a treadmill, they effectively boosted natural killer cells count and cytotoxic activity as well as salivary immunoglobulins and lactoferrin (cf. figure 3); so profoundly, though, that I am not 100% sure this is a good thing - at least not for people with auto-immune issues.
  • Don't stress yourself if you want to recover as fast as possible! That's the take home message of a recently published study by two researchers from the Nothern Illiniois University and the University of Texas at Austin, who correlated measures of perceived psychological stress with physical data on exercise recovery and found a surprisingly linear relationship between perceived stress, on the one hand, and phyical recovery as measured by maximal isometric force, on the other hand, in 31 undergraduate resistance training students (Stults-Kolehmainen. 2012). So, mark my words: Don't overstress about making everything right (this includes having the optimal workout and nutrition plan and thinking about whether or not you should add in another 0.5g BCAA pre-workout or not), if you don't want to sabotage your training success.
References
  • Argilés JM, Meijsing SH, Pallarés-Trujillo J, Guirao X, López-Soriano FJ. Cancer cachexia: a therapeutic approach. Med Res Rev. 2001 Jan;21(1):83-101.
  • Brenner H, Arndt V, Bode G, Stegmaier C, Ziegler H, Stümer T. Risk of gastric cancer among smokers infected with Helicobacter pylori. Int J Cancer. 2002 Mar 20;98(3):446-9.
  • dos Santos RG, Viana ML, Generoso SV, Arantes RE, Davisson Correia MI, Cardoso VN. Glutamine supplementation decreases intestinal permeability and preserves gut mucosa integrity in an experimental mouse model. JPEN J Parenter Enteral Nutr. 2010 Jul-Aug;34(4):408-13.
  • Druesne-Pecollo N, Latino-Martel P, Norat T, Barrandon E, Bertrais S, Galan P, Hercberg S. Beta-carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials. Int J Cancer. 2010 Jul 1;127(1):172-84.
  • Du L, Heaney AP. Regulation of Adipose Differentiation by Fructose and GluT5. Mol Endocrinol. 2012 Jul 24.
  • Headley S, Coverdale JA, Jenkins TC, Klein CM, Sharp JL, Vernon KL. Dietary supplementation of CLA in horses increases plasma CLA and decreases plasma arachidonic acid, but does not alter body fat. J Anim Sci. 2012 Jul 24.
  • Jumpertz R, Guijarro A, Pratley RE, Mason CC, Piomelli , Krakoff J. Associations of Fatty Acids in Cerebrospinal Fluid with Peripheral Glucose Concentrations and Energy Metabolism. PLoS ONE 2012; 7(7): e41503.
  • Koshiol J, Flores R, Lam TK, Taylor PR, Weinstein SJ, Virtamo J, Albanes D, Perez-Perez G, Caporaso NE, Blaser MJ. Helicobacter pylori seropositivity and risk of lung cancer. PLoS One. 2012;7(2):e32106.
  • Miller E, Kaur G, Larsen A, Loh SP, Linderborg K, Weisinger HS, Turchini GM, Cameron-Smith D, Sinclair AJ. A short-term n-3 DPA supplementation study in humans. Eur J Nutr. 2012 Jun 23.
  • Mohamed Dugani A, Elhelawi A, Edrah A. Comparative effect of flaxseed oil and fish oil in acetic acid induced colitis in rats. The Libyan Journal of Pharmacy and Clinical Pharmacology LJPCP. 2012;1.
  • Ostojic SM, Obrenovic M. Sublingual nucleotides and immune response to exercise. Journal of the International Society of Sports Nutrition 2012, 9:31. 
  • Stults-Kolehmainen MA, Bartholomew JB. Psychological Stress Impairs Short-Term
    Muscular Recovery From Resistance Exercise. Med Sci Sports Exerc. 2012 Jun 8.
  • Sun Z, Lasson A, Olanders K, Deng X, Andersson R. Gut barrier permeability, reticuloendothelial system function and protease inhibitor levels following intestinal ischaemia and reperfusion--effects of pretreatment with N-acetyl-L-cysteine and indomethacin.
  • Touchberry CD, Gupte AA, Bomhoff GL, Graham ZA, Geiger PC, Gallagher PM. Acute heat stress prior to downhill running may enhance skeletal muscle remodeling. Cell Stress Chaperones. 2012 May 17.
  • van Wijck K, Lenaerts K, van Bijnen AA, Boonen B, van Loon LJ, Dejong CH, Buurman WA. Aggravation of Exercise-Induced Intestinal Injury by Ibuprofen in Athletes. Med Sci Sports Exerc. 2012 Jul 6.
  • Xue Y, Meadors EP, Wang W, Baybutt RC. Microarray Analysis reveals that Dietary Retinoic Acid Suppresses Cancer Related Gene Expression of the Lungs of Cigarette Smoke-Exposed Rats. J Nutr Food Sci 2012, S2.
  • Zhang JP, Chen XY, Li JS. Effects of all-trans-retinoic on human gastric cancer cells BGC-823. J Dig Dis. 2007 Feb;8(1):29-34.

Electrical Stimulation Improves Clearance of Lactic Acid After Anaerobic Activity in Collegiate Athletes. EMS Turns Out to Be as Effective as 'Traditional' Massage Therapy.

Image 1: The EU-940 EMS device the
scientists used in their study to activate
the vastus medialis and lateralis (high-
lighted in the image) of their subjects, is
very different from the average EMS based
"abdominal toner" advertised on TV.
Even here, at the SuppVersity, news on ergogenics, i.e. things that improve (athletic) performance, are usually about a pill, a fancy plant extract or another 'superfood'. Today's news, however is about a much more "physical" means to improve anaerobic exercise performance, decrease lactate accumulation and improve regeneration: Electrical Muscle Stimulation (EMS).

EMS? Now, many of you will probably remember those TV spots, where you were told that "Abmaster" & Co would transform your pot-belly into a "six-packed" attractant for the opposite sex, if you did not miss this "unique" opportunity and bought one of those electro-shockers no sane fitness professionals would voluntarily substitute his/her good old sit-ups and leg raises for. Yet, while these battery-powered torture instruments did, or I should say, were intended to electrically stimulate muscles (in fact in many of the obese buyers of these products, the abs were probably covered by a layer of fat that was way too thick for actually "stimulation" of the abdominal muscles to occur), both the devices, as well as the EMS protocol Seo et al. (Seo. 2011) employed in their double-blind randomized controlled trial at the Sports Science Research Laboratory of Kyungwoon University in Korea were a little more sophisticated.
Did you know? The fatigue index is a concept used in the study of fatigue during anaerobic activities. It is the ratio of power decline to the length of the time interval in seconds between peak power and minimum power. This means lower fatigue indexes equate lower declines of exercise intensity per time unit. When looking at the data in figure 1, you may want to keep in mind that higher starting values / greater overall workloads will entail greater declines in anaerobic power per time unit and thus present with higher fatigue indexes
During and after 3 all out intervals on an ergometer (resistance: 0.8 x body weight Nm; active rest between intervals: 10 seconds) verbal feedback on perceived fatigue, fatigue indexes in W/s, mean power/weight, total work and lactic acid values (from serum drawn before, after and at 15 min and 25 min post exercise) were recorded in a group of 24 randomly selected collegiate Taekwando athletes (age: 19.8yrs, height; 177cm; weight: 66kg, training experience: 5yrs; mean values with non-significant differences between groups).
Figure 1: Fatigue index, mean power (primary axis) and total workload (secondary axis) during Wingate ergometer test
(data adapted from Seo. 2011)
Immediately after the exercise bout, eight athletes, each, received one of the following treatments:
    Table 1: Outline of the massage
    protocol the  athletes in the massage
    group received after having performed
    an exhaustive anaerobic Wingate
    ergometer test (according to Lee. 1998)
  • The control group received no regenerative treatment at all. 
  • The massage group was subjected to a massage protocol which had been shown to effectively improve exercise recovery in a previous study by the same authors (Lee. 1998).
  • The EMS group was attached to an interferential current unit (EU-940, ITO CO., LTD, Tokyo, Japan), which applied an interferential current with a carrier frequency of 4kHz and a pulse duration of 125µs via four vacuum electrodes (vacuum pressure: 60ppm) to the vastus medialis and the vastus lateralis of the subjects.*
    * "The current  intensity was set within the range of the minimum visible contraction of the quadriceps femoris muscle", so that the muscle of the quadriceps were maximally stimulated, while the current was not so intense that cross-over effects to neighboring muscle groups would occur.
Seo and his colleagues found "significant differences in the lactic acid concentrations in the blood among the three groups [...] at 15 min and 25 min after exercise".
Figure 2: Relative reduction in lactic acid concentration after a wingate performance test followed by massage or EMS therapy compared to untreated control (data adapted from Seo. 2011)
As the data in figure 1 shows, massage and EMS promote the clearance of lactic acid to a similar degree (+17-18% vs. control). So, if you are a professional athlete you should either make good use of your already existing six pack and attract a significant other who is a massage therapist or save some bucks and get yourself a reasonably professional EMS device, in case you intend to be a gold medalist at the 2012 Olympics in London ;-)

Edit (26 July): The lactate & Lactic acid confusion

After I posted this piece of information an interesting discussion around the physiological role of lactic acid broke lose on Facebook and I do not want to deny you the great information my buddy Sean Casey from CasePerformance brought to the table. So, here is what he had to say:
Lactic Acid is an interesting thing....During the 1970-1980’s various studies found lactic acid impaired strength and contraction velocity in samples of isolated muscle tissue (1). Based off these early findings, many researchers evaluated ...post workout recovery modalities on their ability to remove lactate from muscle tissue post workout. Similarly, coaches and athletes started employing post workout techniques aimed at removing lactate from muscular tissue. For instance, our high school track coach used to have us lie on our backs and rest our legs on an elevated surface w/ respect to our body. Usually we'd lie on the floor next to a wall & place legs on wall. The theory was that acid would “drain” out of our muscle tissue, allowing our legs to be fresher for the following day’s workout. (I know, a very bro-science approach; , but mentally felt good and you'd always get a cool tingly sensation when you set your legs down and the blood rushed back into them!)

Interestingly, it turns out that lactic acid may not be the best form of measurement with respect to evaluating the effectiveness of a PWRM [post workout recovery measures]. As pointed out by Cairns SP, it may have a much smaller effect on muscle fatigue than was previously hypothesized(1). Thanks to advances in technology, scientists are now able to study muscle tissue closer to physiological temperatures (old studies were completed at muscle tissue held at cooler temperatures, 50-68ºF). As shown by Westerblad et al., acid had little effect on contraction velocity when completed on muscle tissue held at 89ºF (2). On the other hand, a 2006 study by Knuth et al. did indicate that lactic acid decreased muscle contractile power even at warmer temperatures(3). 

Although the lactate question is still being debated amongst scientist, athletes must ask themselves if the research is even applicable to their post training recovery protocol. Although lactate may induce muscular fatigue, its quickly metabolized within the body (1/2 life: muscle- 9.5 minutes; blood- 15 minutes), and eliminated from our system 90 minutes after an exercise session has been completed (4)(5). Thus, exercise induced lactic acid from one workout is likely not even present during a subsequent workout depending on when you complete it.

All this being said, don't misinterpret my comments and think that I'm trying to put down the role of EMS. I've had to use one a fair amount due to various issues and have found it to be effective. Anything that can get a muscle contracting and increase blood flow is always a good thing ;-) 

References

1 Cairns SP. Lactic acid and exercise performance: culprit or friend? Sports Med. 2006;36(4):279-91.

2 Westerblad H, Bruton JD, Lännergren J. The effect of intracellular pH on contractile function of intact, single fibres of mouse muscle declines with increasing temperature. J Physiol. 1997 Apr 1;500 ( Pt 1):193-204.

3 Knuth ST, Dave H, Peters JR, Fitts RH. Low cell pH depresses peak power in rat skeletal muscle fibres at both 30 degrees C and 15 degrees C: implications for muscle fatigue. J Physiol. 2006 Sep 15;575(Pt 3):887-99. Epub 2006 Jun 29.

4 Karlsson J, Saltin B. Oxygen deficit and muscle metabolites in intermittent exercise. Acta Physiol Scand 1971; 82: 115-22.

5 Barnett A. Using recovery modalities between training sessions in elite athletes: does it help? Sports Med. 2006;36(9):781-96.
The only thing I would like to add to Sean's insightful dissertation is a criticism of the indiscriminate use of lactate, which is sort of 'recycled' muscle fuel, and lactic acid, which is its ugly 'degraded' relative. With the ever increasing H+ levels as they can be observed in the course of a long distance race, for example, more and more lactate gets degraded into lactic acid and thus works like a buffer similar to the beta-alanine derived intramuscular H+ buffer carnosine. Now it is no wonder that with H+ release being a measure of muscular exertion and lactic acid being a measure of H+ buffering, Faude et al. (Faude. 2009) found in what is one of the most recent reviews on the role of lactate in exercise metabolism that
[t]hirty-two studies evaluated the relationship of LTs with performance in (partly simulated) endurance events. The overwhelming majority of those studies reported strong linear correlations, particularly for running events, suggesting a high percentage of common variance between LT and endurance performance.
And, after all, it does not really matter in how far the established performance increases from massages and EMG therapy are related to their ability to accelerate lactate clearance, or more generally to their ability to increase blood flow and thus nutrient delivery and waste clearance in the respective tissue - does it?

Ask Dr. Andro: Does the Deer Velvet Antler Spray NFL Fullback Heath Evans is Supposed to Have (Ab-)Used Work? Does it Contain IGF-1 & Can IGF-1 Be Taken Orally?

Question from Lerner: "Dr. Andro, check out the following link. It's about deer antler (which I didn't find being discussed in a search of suppversity) -- and how that supposedly contains IGF-1. I don't watch NFL football, but they do get paid big money and that motivates them to try different things for sure. Still, does it work, or is it just placebo effect?"

Image 1: Legal growth hormone
supplements in the NFL? How legit is
the deer velvet antler extract containing
'The Ultimate Spray'  (image source
official SWATS homepage)
Answer from Dr. Andro: Initially, I wanted to dismiss this one all together, because I remembered out of my head one of two peer-reviewed studies on the use of deer antler, which was not able to find any effect of elk velvet antler extract at a daily dose 560mg on exercise performance or endocrine parameters in 25 male and female rowers (Syrotuik. 2005). How on earth would the hilariously labeled The Ultimate Spray, Heath Evans is supposed to have taken, then make a difference for a high level NFL fullback?

Well, after "pubmeding" (make sure you remember this neologism of mine, it is like "googling" for smart people ;-) the missing study by Sleivert et al. (Sleivert. 2003), in which at least some of the 38 active males, who had received deer antler velvet extract in powder form concomitantly to a 10-week strength training protocol, actually gained twice as much isokinetic knee-extensor strength and endurance than the placebo group, Mr. Lerner's question suddenly had my full attention...


What is The Ultimate Spray?

A closer look at The Ultimate Spray then revealed that, other than I had expected, it was no Patrick Arnold style transdermal, but an oral preparation. Well, to be precise this is only my interpretation of the information, if you would like to call it such, on the website, of the producer SWATS, where it says, I quote:
"sparyed into the moutn, where the phospholipid spheres easily penetrate the mucosal layers of the moutn and go directly into the blood stream." [my emphasis]
So if to "spary" something "into the moutn" means to spray it into your mouth and not to smear it onto the next best mountain, I would assume that the undisclosed amount of "liposomal encapsulated" (sounds funky, no?) velvet antler extract, one serving contains, is supposed to be taken up orally - in that, I exclude sublingual delivery because a) it says that you got to spray it "into" your "moutn" and not under the tongue and b) the liposomal encapsulation would make little sense if the IGF-1, which is supposed to be in the product, would not even reach the digestive juices and enzymes of the stomach, from which the encapsulation in turn is supposed to protect it. Note: The amilase and lipase in the saliva would not harm the protein based IGF-1 peptides, anyway.

How is the product supposed to work?

Now that we know that The Ultimate Spray is a liposomally encapsulated extract from deer antler velvet that is to be taken orally as a spray, the next question we would have to answer is: How on earth does this product make Evans feel improvements in "some rest and recovery aspects" and what is the "sleep of a deeper nature" the New Orleans Saints fullback mentions all about?

A look at the purported ingredients of the product could help, but as a matter of fact, without appropriate lab analysis, we have no clue how much, if any, IGF-1, collagen, amino acids, epidermal growth factor (EGF), chondroitin sulphate, erythropoietin, glycosphingolipids, prostoglandins, phospholipids and monoamine-oxidase inhibitors The Ultimate Spray ultimately contains. What we can say for sure, however, is that IGF-1 is not "a precursor for the production of growth hormone (HGH)", as SWATS tries to tell you. It is rather a hormone whose molecular structure is very similar to insulin and which plays an important role in childhood and - you guessed it - deer antler growth.

If we leave the "amino acids", "collagen","phospholipids" and "monoamine-oxidase inhibitors" aside (you could get these in much higher concentrations from food or way cheaper supplements, anyway) IGF-1, EGF, the unspecified prostaglandines and last, but not least, every cyclist's favorite blood building 'supplement', erythropoietin, are the most likely candidates on the ingredient list which could be responsible for the beneficial effects Evans claims to have noticed. So let's see...
  • Erythropoietin, commonly known as EPO, is in fact a naturally occurring glycoprotein hormone which does - as its name suggests - control erythropoiesis, or red blood cell production. The usual dosage that is used for doping purposes is 100IU/kg three times per week for the first 8 weeks, to increase red blood cell count, followed by 25-50IU/kg to maintain stable erythrocyte counts. According to Jelkmann, 1mg of pure synthetic EPO has a standardized efficiacy of 130.000 IU, while EPO from human urine has meager ~2IU/mg (Jelkmann. 2009). It stands out of question that there will be at least trace amounts of erythropoietin in the extract, since the antler of deer is supplied with blood, but even if it had an efficiacy of 50% of the purified rDNA-derived human EPO, a man like Evans who certainly weighs >160 pounds would have to get >3.500 IU or 18mg per day right into his blood stream to get the desired effects. This is something that probably is not going to happen, as the previously cited study by Sleivert et al. (Sleivert. 2003) shows that notwithstanding inconsistent beneficial effects on strength and endurance, the antler extract did not raise red cell mass or VO2max, parameters which should have been affected, if the amount of EPO in the supplement would have been adequate to elicit physiological effects.
  • Prostaglandins are, in contrast to what SWATS claims not generally anti-inflammatory. The function of these locally acting messenger molecules are diverse and the blatant statement on their "anti-inflammatory" character, the producer makes here, is not worth the webspace it occupies. Whether or not Evans could have felt their effects would really depend on which kind of prostaglandins the product contains, but I bet that this is something even the SWATS team does not know.
  • Epidermal growth factor (EGF) does play a role in the regulation of cell growth. Thus it is no wonder that it can be found in a constantly regrowing tissue, like deer antler (Ko. 2004 & Barling. 2005). Yet, even if it was retained in the extract, I have my doubts that it plays a major role in the ergogenic effects Evans has been talking about.
This leaves us with what the original Yahoo article on the subject also dealt with: IGF-1, a basic peptide hormone composed of 70 amino acids, which - and this has been shown by Gu et al. - is "only detectable in osteoblasts around the bone in the mid and base parts" (Gu. 2007) of deer antler. So, if the extract SWATS uses in their The Ultimate Spray was made from whole deer antler, it will in fact have IGF-1 in it. Whether this would be enough to elicit physiological effects cannot be decided without running an ELISA or HPLC test on the product to find out how much IGF-1 actually is in one serving of The Ultimate Spray (cf. Liu. 2011). But wait... being a large peptide, would the IGF-1 be able to be absorbed into circulation, even if - as the producer promises - it is protected from digestive enzymes by liposomal micro-encapsulation?

Image 1: Parts of the small intestine,
relevant for IGF-1 absorption in the
rat model used by Kimura et al.
Can IGF-1 be taken orally?

The surprising answer is: "Yes, it can." After digging through the archives of various pharmacological journals I eventually came up with a 14-year-old study by Kimura et al. (Kimura. 1997), who, in 1997, investigated the bioavailability of orally administered recombinant human insulin-like growth factor I (rhIGF-1) [the attribute "recombinant" indicates that this is synthetic human IGF-1] in adult rats (I deliberately underlined the "adult", here because in various neonatal or new-born / very young mammals the intestinal permeability is elevated to allow for the absorption of larger peptides from the mother's milk). The results of this study (cf. figure 1), I must admit, did really surprise me. If you add up (note: if you think I miscalculated, you probably just added up the percentages from figure 1 and forgot that when you absorb 35% there is obviously less IGF-1 left, of which, in a second step. another 17% will be absorbed, etc.) the amounts of IGF-1 that reached circulation (i.e. became "bioavailable") via the three different parts of the digestive tracts of the rats, the critters ended up with roughly 50% of the orally administered radio-labeled 125I-rhIGF1 actually getting into their blood stream:
Figure 1: Bioavailability of orally administered rhIGF-1 with and without peptidase inhibitors.
(data adapted from Kimura. 1997)
As you can see, even without the addition of a peptidase inhibitor (peptidase = protease; enzyme that breaks down peptides its individual constituents and would thus "degrade" the IGF-1 before it could even be absorbed) the orally administered dose of 1.0mg/kg (human equivalent: 0.16mg/kg or 13mg for an 80kg adult human being) was absorbed at rates of ~35%, 17% and ~6% in the jejunum (middle section of the small intestine), the ileum (final section of the small intestine) and the large intestine, respectively.

This is not yet the "95% absorption" SWATS promises for a product they advertise as being "by far the best supplement for sports performance", but it is still adds up to a respectable amount of IGF-1 actually reaching circulation. To be precise, plasma concentrations peaked roughly 3 hours after administration at ~50ng/ml, ~180ng/ml and 375ng/ml for the no peptidase, the aprotinin and the casein groups, respectively. In both, the no peptidase and the casein groups, levels stayed constant for another 3h, after which they declined linearly.

I don't know about you, but when I hear about casein improving the absorption of IGF-1, I suddenly forget about dubious deer antler sprays and start thinking of colostrum - well, but I guess this would be a topic for another week ;-)


So what, Dr. Andro? Does it work?

As much as I would like to provide you with a definite answer, the only thing I can tell you for sure are the following facts:
  1. there is IGF-1 in whole deer antler
  2. IGF-1 survives passage through the intestines of rats even if it is not micro-encapsulated
  3. non-micro-encapsulated IGF-1 can be taken up in the jejunum, the ileum and the large intestine at surprisingly high rates
  4. protease inhibitors, above all, the readily available and reasonably priced peptidase inhibitor casein can improve bioavailability even further
I would yet have to speculate on
  1. whether or not the deer velvet antler extract used in The Ultimate Spray was derived from parts of the antler that actually contain more than trace amounts of IGF-1,
  2. how much IGF-1 actually is in one serving,
  3. how effective the "natural" and probably partly bound (to IGF1 binding globulins) form of IGF-1 in the product is compared to synthetic, free rhIGF-1,
  4. if the liposomal encapsulation does in fact improve and not maybe even hinder absorption,
  5. and, last but not least, if the amount of IGF-1 reaching the bloodstream would aactually be able to produce physiological effects
in order to answer Lerner's question. So, now that you got the facts, its up to you, students of the SuppVersity, to make up your mind on whether or not there is more behind this lurid yahoo news-story than just a clever marketing stunt.

Speed Up Your Regeneration and Propel Your Gains by Taking a HOT Bath Bath 2-Days Before Arduous Workouts

Image 1: Are women tougher than men, because bathe more often? If you define toughness by your muscles resistance to eccentric exercise damage, the answer could be "YES!"
If you listened to Brooks, Carl and me on Super Human Radio, yesterday (download the podcast), you may remember me stating that 48h appears to be a good rule of thumb, as far as the rest periods between workouts for individual body parts are concerned (this assumes that you are young, healthy, reasonably conditioned and lift heavy). A recently published paper by Chad D. Touchberry  does now suggest that there may be another 48h window before your workout (Touchberry. 2012). One you would use a priori to improve your recovery a posteriori - preconditioning in a hot bath for 20 min at 41°C, 48h before a hard workout or competition!

Eccentric treadmill running = maximum muscle damage

At least in a rodent model, those 20 min of heat exposure in 41°C warm water lead to statistically highly significant decreases in exercise induced muscle damage, improved and accelerated the recovery process and, contrary to what could be assumed based on previous research on the expression of heat proteins (Frier. 2007), did not hamper, but promote muscle gains in response to an exercise protocol consisting that consisted of running at 18m/min down a -16% grade for 5 min. This protocol has been used as a model for injurious exercise repeatedly in the past and constitutes one of the standard tests in rodent, but also in human studies (e.g. Pumpa. 2011).
Figure 1: Creatine kinase (CK) activity and immune cell infiltration after eccentric exercise with (EE+HS) and without (EE) preconditioning via hot bath 48h before (data calculated based on Touchberry. 2012)
As the data in figure 1 goes to show, the hot bath (EE+HS) had significant ameliorative effects on both the muscle damage (indicated by CK and the black sections in the H&E-stained soleus muscle cross-sections in figure 1, right), of which the researchers state that, despite the fact that "the mechanism by which heat shock protects skeletal muscle from damage is currently unknown", the protection of skeletal muscle against damage in mice overexpresssing HSP70 (McArdle. 2004a) as well as the differential HSP72 elevation in the HS group 2h and 48 h following exercise collectively
[...] suggest that HSP72 or another heat sensitive protein (i.e.,alphaB-crystallin) may play a role in mediating cytoprotection of skeletal muscle cells.
Moreover, Touchberry et al. explain the existing discrepancies between their own results and previous results by Mc.Ardle et al. (Mc. Ardle. 2004b), who did not find reduced muscle damage after pre-treatment with hsp-inducing concentric exercise 10h prior to the (in my humble opinion questionable) in-vitro application of eccentric strain to skeletal muscle tissue, with the "greater time for HSP accumulation prior to the exercise stressor" in their (48h) vs. the Mc.Ardle study (10h), which is obviously yet another indicator that rest is one of the most under-appreciated determiners of workout efficiency (cf. my words on SHR ;-)

Regeneration is one thing, but are muscle gains another?

Now, I am well aware that one of the main reasons regeneration isn't sexy, is that it does not trigger the phosphorylation of Akt, m-TOR and all the rest of the sciency terms with which laymen are bombarded by the supplement industry these days.
Figure 2: Total protein, new myosin heavy chain (MHCNEO) content and p-Akt expression in soleus muscle 2h and 48h after the eccentric exercise bout (data calculated based on Touchberry. 2012)
The study at hand does even show that heat pre-treatment will actually reduce, not promote the phosphorylation of AKT 48h after the exercise bout (cf. figure 2). If you do yet take into account that the total protein concentration and MHCneo (novel myosin-heavy-chain motor proteins) content in the soleus muscle of the rodents was increased profoundly, I guess you will have to agree that it is unlikely that less damage, a faster regeneration, and as a consequence less need for protein to be recruited via p-AKT only to repair the damage is going to propel, not diminish your gains!

Practical implications & open questions

Once again, the obvious message of this study is: Not he who trains the most, but he who regenerates and rebuilds the best, gains the most! And adequate rest aside, preconditioning in a hot (not a "cold thermogenic" bath ;-) can help dampen the exercise induced damage and accelerate your recovery.
Note: In February 2012, Bayley et al. published a paper that shows that the application of passive heat in form of a 42°C hot water bath for 40min immediately prior to a bout of HIT leg extensor exercises reduced the time to fatigue in seven healthy men by a whopping -36%  (Bayley. 2012). Impatience, or rather the unwillingness to grant your body the time it needs to recover is thus detrimental even if the stressor is "just" a hot bath!
Whether the same would be true if you train today and do the hot water immersion immediately, 2h, 10h or 12h post and thus 48h, 46h, 38h or 36h before your next workout is yet about as questionable, as whether or not similar effects could be elicited by switching back and forth between light and heavy days every 48h.  Both may appear likely, but aside form the fact that the optimal timing or workout intensity will still have to be elucidated, are still in the state of an interesting research hypothesis, not more, but also not less.

Update - Suggested reading: Since there have been questions pertaining to the usefulness of hydrotherapy post-workout, i.e. as a means of "classic" re- and not "precovery", I thought I rather refer you directly to my buddy Sean's E-book on the issue. Here is a snippet from the book
Image 2: Don't miss Sean's free e-book on classic hydrotherapy
Quick Hit Summary Water therapy is a common modality to enhance muscle recovery post workout. Sitting in chest high thermoneutral water for 20-30 minutes may accelerate waste removal while increasing blood flow to working muscles. Cold, hot and contrast water temps are also commonly used to assist recovery. The goal of cold water therapy is to reduce inflammation whereas hot water purportedly increases muscle blood flow. Contrast water therapy involves alternating between hot and cold water baths to induce a vaso-pumping effect. Current evidence does not support the theory behind these latter 2 therapies simply because the heat (from the water) is incapable of penetrating more than a couple centimeters into the skin. Thus, there is no stimulus to increase muscle blood flow
You can get this e-book alongside two other books for free if you register for Sean's newsletter, which is, take my word on it (!), not a weekly advertisement piece!
 
References:
  1. Bailey SJ, Wilkerson DP, Fulford J, Jones AM. Influence of passive lower-body heating on muscle metabolic perturbation and high-intensity exercise tolerance in humans. Eur J Appl Physiol. 2012 Feb 10.
  2. Briese E. Normal body temperature of rats: the setpoint controversy. Neurosci Biobehav Rev. 1998 May;22(3):427-36. Review. 
  3. Frier BC, Locke M. Heat stress inhibits skeletal muscle hypertrophy. Cell Stress Chaperones. 2007 Summer;12(2):132-41. 
  4. McArdle A, Dillmann WH, Mestril R, Faulkner JA, Jackson MJ. Overexpression of HSP70 in mouse skeletal muscle protects against muscle damage and age-related muscle dysfunction. FASEB J. 2004a Feb;18(2):355-7.
  5. McArdle F, Spiers S, Aldemir H, Vasilaki A, Beaver A, Iwanejko L, McArdle A, Jackson MJ. Preconditioning of skeletal muscle against contraction-induced damage: the role of adaptations to oxidants in mice. J Physiol. 2004b Nov 15;561(Pt 1):233-44. Epub 2004 Aug 26.
  6. Pumpa KL, Fallon KE, Bensoussan A, Papalia S. The effects of Lyprinol(®) on delayed onset muscle soreness and muscle damage in well trained athletes: a double-blind randomised controlled trial. Complement Ther Med. 2011 Dec;19(6):311-8.
  7. Touchberry CD, Gupte AA, Bomhoff GL, Graham ZA, Geiger PC, Gallagher PM. Acute heat stress prior to downhill running may enhance skeletal muscle remodeling. Cell Stress Chaperones. 2012 May 17. [Epub ahead of print]

Shock Your Calves to Grow Stronger & Recover Faster: $650 Electromyostimulation Device Works, But Is It Worth It?

You will have heard about "calf shocker" routines, but would you have imagined that it takes electro shocks?
I don't know how often I've been writing about the truth and fallacy of the good old saying "no pain, no gain", here at the SuppVersity. And while it certainly has its merit for the faint-hearted, the notion that "pain" will entail "gain" is fallacious, also because it suggests that allowing for adequate recovery would be inferior to digging a deep black "hole of pain" (suggested read: "The SuppVersity Athlete's Triad Series").

And while I know that you know that this ain't the way to go, I am also honest enough to admit that I often catch myself pondering the incorporation of intensity techniques, additional exercises or some fat burning minutes of HIIT, but rarely thinks about the undeniable benefits of things like the hot baths for pre-regeneration and other means to speed up recovery (learn more) ...

Recovery, ceratinly not the #1 topic for gym-conversations

I am not sure, whether or not today's SuppVersity article on the surprising benefits of electrical muscle stimulation (EMS) during the recovery period is going to change that, but it certainly adds another interesting option to my toolbox. After all, the improvements in strength and the researchers from the Quincy College the University of Texas at San Antonio, the Hospital  of the University of Pennsylvania, the National Strength and Conditioning Association and the University of Florida present in their most recent paper in the April issue of Official Research Journal of the American Society of Exercise Physiologists would suggest that it will not just allow me to return to the gym earlier, but will also make me stronger.
The "Marc Pro(TM)" is not just the $650 device used in the study, it is also one of most frequently used words in the study at hand... what? No, there is no conflict of interest declared, but I believe the Journal of the American Society of Exercise Physiologists does not even require that.
The study of which I'd better tell you in advance that is has a slight smack of "product pimping", because it mentions the specific EMS device, the Marc Pro(TM) not just in the methods section, but also in the title (Westcott. 2013), involved two trials with comparably large groups (n=43 / n=62) of male and female subjects in their best years (mean age: 61.3 / 61.7 years).

10 weeks 2x per week full body + 4x per week EMS

Suggested read: "Fast Paced High-Resistant Explosive Circuit Training Burns More Fat and Builds More Muscle Than Classical Weight Training. Trainees Dropped 1.5% Body Fat and Gained 3 Pounds of Lean Mass in 8 Weeks." - Don't discard the value of a fast paced full body resistance training (read more).
During both 10-week trials all participants trained twice a week for 60 minutes. The training comprised a medium-paced circuit training on 13 Nautilus machines including leg extension, leg curl, leg press, hip abduction/adduction, chest press, seated row, shoulder press, lat pull down, low back extension, abdominal flexion, torso rotation, neck flexion/extension and calf press. Each exercise was performed only once and the weight was progressively increased by 1% whenever the subjects were able to perform more than the prescribed number of 8-12 reps at a well-controlled pace of 3s for both the concentric and eccentric portion of the exercise. In addition to the standard strength workout, the subjects performed ~20 min of recumbent cycling at 70 to 80% of predicted maximum heart rate) and ~5 min of major muscle group stretching exercises towards the end of each workout. 

While all subjects underwent the same supervised workout program, only 50% of them were assigned to the EMS group, and instructed to self-administer 1h of electrical muscle stimulation to the calf muscles of both legs four times a week. With the two obligatory exercise sessions, this allowed for two "recovery sessions" in-between workouts.
Figure 1: Changes (rel. to baseline) in the EMS and control groups after 10-weeks of training (Westcott. 2013)
As the data from the pre- and post strength 3-RM tests and the results of the fatigue questionnaire, a 9-point rating scale with anchors of 1 (never experience feelings of calf muscle fatigue) and 9 (always experience feelings of calf muscle fatigue) in figure 1 goes to show you this routine was surprisingly effective in both increasing the effective gains in calf muscle strength and decreasing the workout induced fatigue.

So what's the mechanism here?

It is not exactly likely that the medium intensity EMS targets the IGF-1 + muscle growth promoting PGC-1 a4 isoform (learn more)
The exact mechanism for the benefits, the researchers observed in both experiments, is not fully understood, they stand in line with previous research mostly by members of the same research group (Parker. 2003; Kemmler. 2010; Wescott. 2012; DiNubile. 2011; Girold. 2012) which suggests that the application of electical muscle stimulation "causes positive cellular responses such as nitric oxide (NO) production, fluid shifts, protein clearance, and angiogenesis" and allow for the hypothesis that additional, isokinetic contractive stimulus has the potential to induce mRNA transcriptional proteins such as PPAR gamma co-activator (PGC)-1 alpha (learn more) and the vascular endothelial growth factor VEGF.

Against that background, the scientists assumption that [...]the enhanced muscle recovery associated with [...] electrical stimulation may be due to increased microcirculation, muscle loading, and angiogenesis." (my emphasis in Westcott. 2013) appears reasonable and would warrant their conclusion that EMS which is hitherto used mainly by professional athletes (esp. football players) "may also be beneficial for less fit individuals who experience  prolonged periods of recovery or uncomfortable levels of muscle fatigue after exercising." (Westcott. 2013)




I openly admit: Hot baths are still not a part or my "pre-recovery" routine, but I like some cheap and effective walking on an incline on the day after a leg workout.
Bottom line: Depite the overall promosing results of the study at hand, I'd still have a few questions as far as (a) the usefulness, (b) the alternatives and (c) the superiority of EMS therapy as a means to accelerate recovery and adaptation actually is. A handful of studies, a shiny website and the argument that it does works in recreational, or as the scientists write "less fit" trainees, as well as in pro-athletes won't make me pay approx. $650 for an "electro shocker".  This is all the more true in view of the fact that regular aerobic exercise and HIIT (learn how to set up a routine) will also promote PGC1-alpha and VEGF and could - appropriately dosed - probably elicit similar effects.

Apropos "effects" you should not forget that the parameters the scientists measured are actually both performance parameters. Regardless of the fact that the latter is called "fatigue", the fatigue after a standardized workout is mainly determined by your central and peripheral conditioning. It is thus obvious that you should be able to reduce the post-workout fatigue by any means of additional exercise that does not overtax the system - this may also involve enhanced recovery, but the enhancement is a function of physiological adaptations and not externally applied electrical stimuli.

Against that background, the only advantage of EMS over "conscious", i.e. brain-controlled contractions such as a 3x3min (x2 for each leg) session of single-legged body-weight calf-raises or even a simple walk in the park with a deliberate emphasis on calf-involvement would produce, appears to be that it would ease the burden on the central nervous system. Whether that's essentially necessary for the average trainee is however questionable; and though I would probably be slightly irritated, if you called me "an average trainee", I for my part will stick to some recuperative walking on an incline to promote calf-recovery.

References:
  • DiNubile N, Westcott W, Reinl G, et al. The Marc  Pro TM device is a novel paradigm shift in muscle conditioning, recovery and performance:  Induction of nitric oxide (NO) dependent enhanced microcirculation coupled with angiogenesis mechanisms. JEPonline. 2011;14(5): 10-19.
  • Girold S, Jalab C, Bernard O, et al. Dry-land strength training vs. electrical stimulation in sprint swimming performance. J Strength Cond Res. 2012;26(2):497-505.
  • Kemmler W, Schliffka R, Mayhew JL, von Stengel S.  Effects of whole-body electromyostimulation on resting metabolic rate, body composition, and maximum strength in postmenopausal women:  The training and electrostimulation  trial. J Strength Cond Res. 2010;24(7):1880-1887.
  • Parker MG, Bennett MJ, Hieb MA, et al. Strength response in human femoris muscle during 2 neuromuscular electrical stimulation programs.  J Orthop Sports PhysTher. 2003:33(12): 719-726.
  • Westcott WL, Chen T, Neric FB, et al.  The Marc Pro TM device improves muscle performance and recovery from concentric and eccentric exercise in duced muscle fatigue in humans: A pilot study.  JEPonline. 2011;14(2):55-67. 
  • Westcott W, Han D, DiNubile N, Neric F, Loud RLR, Whitehead S, Blum K. Effects of Electrical Stimulation Using the Marc Pro(TM) Device during the Recovery Period on Calf Muscle Strength and Fatigue in Adult Fitness Participants. JEPOnline. April 2013; 16(2): 40-49.