W.O.W. 1/12/14-The Amazing Power of Myokines

I apologize for the delay in posting, but my work schedule has been quite hectic.  I did the following WOW yesterday at UE after a busy ER shift.  Wendy and the kids met me and worked out also.

SuperSlow Systems Pulldown

Nautilus Pullover with SS retrofits

MedX Compound Row with SS retrofit fall-off cam

SuperSlow Systems Neck Extension

Barbell Deadlift

Wendy did her every 14th day workout.  She has reverted back to her Big 4, feeling that the rotating specialization routines did not offer her any advantage.  Her routine was (MedX chest press, SSS Pulldown, MedX overhead press and MedX leg press).  The kids both do a Big 3 routine of Leg Press, Chest Press and Pulldown.

Lately I have found myself hooked on the literature surrounding myokines.  I am amazed at the degree of endocrine activity and cross-talk with other tissues that is exhibited by skeletal muscle.  I have always had the sense that skeletal muscle and the activities that result in its activity and adaptations have always had health benefits that go way beyond strength or “gettin ‘swole”.  But as I delve into the literature on myokines, I must admit….I had no idea!  Marc P wanted to discuss strength training’s contribution to fat loss.  Myokines are where most of this action takes place.  There are mediators that enhance fatty acid oxidation in the mitochondria, others accelerate the mobilization of glycogen from the muscle while simultaneously up-regulating insulin receptors and lowering serum insulin levels (effectively reversing the obesogenic effects of the metabolic syndrome).  Myokines also directly oppose the inflammatory cytokines produced by adipose tissue and help to block uptake of fat into the adipocyte.  There are myokines that bind monocytes and T-cells that help to repair muscle damage, but also attack foreign invaders and trigger apoptosis of cancer cells.  In one of the studies listed, a specific myokine liberated from skeletal muscle during exercise was shown to halt the growth of breast cancer cells and even caused apoptosis (cell destruction) of breast cancer cells.  A perusal of this review article, along with the attached citations will show a virtual treasure-trove of benefits that are derived when skeletal muscle is engaged in a challenging way.

These articles also indicate that all fiber types secrete beneficial myokines and that slow twitch oxidative, intermediate and fast twitch fibers all secrete different myokines, each with their beneficial effect.  Despite the recent emphasis on the importance of the fast twitch fibers, it seems that all fiber types have something to contribute.  In my opinion, this means that endurance exercisers may show a different myokine profile from those that emphasize strength and power.  I suspect, however, that it is possible to have the best of all worlds with regard myokines if you participate in a combination of exercise routines that cover all fiber types or better yet…if you use an exercise protocol that results in sequential recruitment of all fiber types.

What is most evident to me is that what matters most is that the populace at large needs to participate in meaningful exercise.  My major concern about some of the heated debate that goes on here about what is “best” my make a “newbie” visiting the site decide to throw up their hands and not get started at all.  Sometimes our arguments can make this look way more complex than it needs to be for someone who needs nothing more than to get started.  So for any newcomers who have been intimidated by the technical verbiage and heated debates, please understand that ALL who participate here are deriving the amazing benefit of myokines and that the techincal discussion and debate is just icing on the cake that keeps us all interested and in the game.  Remember….Just. Lift. Weights.  Get started.  As you progress and experiment, then you can join the fray.  But rest assured, whether you are working out on state of the art RenEx machines under professional supervision, or if you are lifting an old barbell in your garage or basement you are part of an elite club that knows the amazing value of myokines.  I have attached the full-text article below.  Please read it and be proud of what we promote here.

Adipocyte. 2012 July 1; 1(3): 164–167.
PMCID: PMC3609091

Muscle-to-organ cross talk mediated by myokines


Cytokines and other peptides are secreted from skeletal muscles in response to exercise and function as hormones either locally within the muscle or by targeting distant organs. Such proteins are recognized as myokines, with the prototype myokine being IL-6. Several studies have established a role of these muscle-derived factors as important contributors of the beneficial effects of exercise, and the myokines are central to our understanding of the cross talk during and after exercise between skeletal muscles and other organs. In a study into the mechanisms of a newly defined myokine, CXCL-1, we found that CXCL-1 overexpression increases muscular fatty acid oxidation with concomitant attenuation of diet-induced fat accumulation in the adipose tissue. Clearly this study adds to the concept of myokines playing an important role in mediating the whole-body adaptive effects of exercise through the regulation of skeletal muscle metabolism. Yet, myokines also contribute to whole-body metabolism by directly signaling to distant organs, regulating metabolic processes in liver and adipose tissue. Thus accumulating data shows that myokines play an important role in restoring a healthy cellular environment, reducing low-grade inflammation and thereby preventing metabolic related diseases like insulin resistance and cancer.

Keywords: cancer, diabetes, exercise, myokine, physical activity

Exercise is associated with many beneficial metabolic and health effects. Today it is known that during exercise, cytokines and other peptides are secreted by the working muscles with the potential to act locally within the muscle tissue or in an endocrine manner by targeting distant organs. Although they are not exclusively secreted by the muscle cells, such proteins are classified as “myokines” within the context of skeletal muscle physiology.1 Emerging evidence suggests that these muscle-derived cytokines play an important role in mediating both acute exercise-associated metabolic changes, as well as the metabolic changes following training adaptation.2 Increased insulin responsiveness, glucose uptake and fatty acid oxidation within skeletal muscles are some of the anticipated beneficial effects of regular exercise, all of which have been shown in part to be mediated by myokines. Likewise, systemic effects of myokines released in response to muscle contractions are involved in various immediate and long-term metabolic regulatory mechanisms in distant organs like the adipose tissue.3 Thus myokines are central to our understanding of the cross talk during and after exercise between skeletal muscles and other organs (Fig. 1). In view of that, further insight into the effect and regulation of potential myokines is of major importance.

figure adip-1-164-g1

Figure 1. Muscle-organ cross talk mediated by myokines. In response to muscle contraction skeletal muscle expresses and releases myokines into the circulation. The myokines mediate effects locally within the muscle in an autocrine or paracrine

The first myokine identified was interleukin 6 (IL-6),4 which is now recognized as the prototype myokine, exerting both local muscular effects as well as endocrine effects on distant organs.5 Since the discovery of IL-6, it has been recognized that skeletal muscle has the capacity to express a large range of myokines. Today the list of verified myokines includes IL-6, IL-8, IL-15, brain-derived neurotrophic factor (BDNF), leukemia inhibitory factor (LIF), fibroblast growth factor 21 (FGF21) and follistatin-like-1.3 In addition, recent proteomic studies have predicted that the list of myokines may include more than 600 candidates belonging to distinctly different protein families.6 Recently we and others reported that an acute bout of exercise in mice induced a 6-fold increase in skeletal muscle mRNA and a 2.4-fold increase in serum concentration of the chemokine CXC motif ligand-1 (CXCL-1) also known as KC (keratinocyte-derived chemokine), suggesting that CXCL-1 acts as an exercise-induced myokine.7,8Murine CXCL-1 is often mentioned as the functional homolog to human IL-8, which previously was identified as a myokine in humans.9 However, murine CXCL-1 shares the highest sequence homology (90% homology in conserved regions) with human CXCL-1, also named GROα (growth-related oncogene, α).10 CXCL-1 belongs to the glutamate-leucine-arginine (ELR)-containing CXC chemokine family and has primarily received attention for its role in inflammation, chemotaxis and angiogenesis,11,12 its neuro-protective effects13 and as a regulator of tumor growth14,15 whereas its role in metabolism remains to be clarified.

In line with the involvement of myokines in regulation of skeletal muscle metabolism, we went on to characterize the role of CXCL-1 in the exercise-associated adaptations in oxidative capacity in the muscle.16 To this end, we used a mouse model of in vivo electrotransfer-mediated overexpression of CXCL-1 in the tibialis cranialis muscle. The resulting increases in muscle CXCL-1 mRNA and serum CXCL-1 in this model are within the normo-physiological range and comparable to levels observed in response to a single bout of exercise.7,8 Importantly this model reflects the long-term effects of regular exercise-induced peaks in CXCL-1 rather than an occasional acute exercise effect. As assessed by MR scanning, DEXA scanning and weight of dissected organs, this long-term overexpression model revealed a CXCL-1-dependent reduction in the diet-induced fat accumulation in adipose tissue. In fact, after three months of high-fat feeding, CXCL-1 transfected animals had a significantly lower visceral fat mass (1277.5 ± 107.2 mg) compared with control mice (1889.5 ± 147.1 mg, p < 0.01). Likewise, did these mice have lower subcutaneous fat mass (494.8 ± 51.2 mg) compared with control mice (637.2 ± 40.8 mg, p < 0.05). Chow-fed mice also had lower levels of adipose tissue. As determined by DEXA scanning eight weeks after the transfection, the CXCL-1 transfected mice had significantly lower proportion of total body fat (13.2 ± 1.6%) compared with chow-fed control mice (19.8 ± 1.5%, p < 0.01). Similar results were found by MR scanning. Interestingly, the reduced accumulation of fat in the CXCL-1 transfected animals was associated with increased fatty acid oxidation in the muscles, as measured both directly and indirectly through upregulation of rate-limiting oxidative enzymes. Furthermore, the CXCL-1-dependent reduction adipose tissue mass was accompanied by whole-body improvements in glucose tolerance and insulin sensitivity. Clearly this study shows that by influencing metabolism locally in the muscles, the myokines are likely to be involved in the whole-body metabolic adaptive changes that occur in response to regular exercise like, for example, attenuation of fat accumulation.

Induction of other myokines, in particular IL-6, has been involved in similar metabolic adaptations. By signaling through the gp130Rβ/IL-6Rα receptor, causing subsequent activation of the AMPK and/or phosphatidylinositol 3-kinase (PI3-kinase) pathways, IL-6 acts within the muscle to increase glucose uptake and fatty acid oxidation.1 Upon receptor activation, IL-6 signals through either the Janus kinase/signal transducer and activator of transcription (STAT) pathway or a Ras/ERK/CAAT enhancer binding protein (C/EBP) β pathway.17

In addition to the local muscular effects that indirectly affect whole body metabolism, myokines have also been shown to act directly on distant organs when released into the systemic circulation. Again IL-6 can be used as an example. Following release from both type I and type II muscle fibers in response to muscle contractions circulating IL-6 works in an endocrine fashion.1 In adipose tissue IL-6 has been shown to increase lipolysis and fatty acid oxidation,18 likely through the induction of AMPK phosphorylation.19 In further support of IL-6 affecting accumulation of fat in adipose tissue, IL-6 knockout mice have been found to develop late-onset obesity.20 In the liver, muscle-derived IL-6 is suggested to enhance hepatic glucose production during exercise21 and has been reported to directly upregulate gluconeogenic genes, i.e., phosphoenolpyruvate carboxykinase (PEPCK) and 6-phosphatase (G6Pase), leading to increased hepatic glucose production.22 Interestingly, IL-6 is also thought to affect pancreatic function, and secretory products from skeletal muscles have directly been shown to increase proliferation and glucose-stimulated insulin secretion from primary β-cells.23,24 In addition, injection of IL-6 as well as elevated levels of IL-6 induced by exercise have recently been demonstrated to stimulate GLP-1 secretion from intestinal L cells and pancreatic α cells, leading to improvements in insulin secretion and glycemia.25 Thus, skeletal muscle and the pancreas act in a synergistic manner to monitor systemic glucose homeostasis and these results demonstrate a role of myokines in mediating cross talk between insulin sensitive tissues.

In line with this, plasma IL-6 is not only directly correlated with exercise intensity, but is also inversely related to plasma glucose level.26 With this, it is thought that IL-6 works as a sensor of carbohydrate availability.18,22,27 Thus, contracting muscle fibers produce and release IL-6 in an endocrine manner to facilitate substrate mobilization from liver and adipose tissue. More recently it was also reported that muscle-derived IL-6 induces expression of CXCL-1 in the liver and that IL-6 is directly essential for the peaks in liver CXCL-1 expression that occurs in response to exercise. These observations further suggest that IL-6 is involved in muscle-to-liver cross talk during exercise.8 Also, an exercise-induced and PGC1-a (transcriptional co-activator PPAR-γ co-activator-1 α) dependent myokine named Irisin was recently reported to replicate some of the positive effects of exercise and diet. It increases energy expenditure likely through stimulation of UCP-1 and brown-fat-like development and was found to improve glucose tolerance in obese animals.28

Definitely the communication network between muscles and other tissues define a physiological concept of muscle-to-organ cross talk. Common for many of the identified myokines are a direct or indirect effect on adipose tissue. Importantly, visceral fat is known as a source of systemic chronic low-grade inflammation, which in turn is involved in the pathogenesis of various disorders like insulin resistance, atherosclerosis and cancer.5 The attenuating effect of myokines on accumulation visceral adipose tissue either by acting directly on the adipose tissue itself or by improving fatty acid metabolism in the muscle is therefore of major importance in describing why inactivity is a strong risk factor for development of various diseases induced by low-grade inflammation like type 2 diabetes and cancer.5 With this, the myokines could in theory be therapeutic for human metabolic disease and other kind of disorders that normally are improved with regular exercise.

In continuation of this, regular exercise is clearly associated with reduced cancer development and progression in large epidemiological studies29,30 and a few animal studies report that exercise is associated with decreased tumor growth and metastatic dissemination.31 The protective effect of exercise is applicable on a diverse array of neoplastic diseases, indicating that the mechanism behind this protection is not limited by specific oncogenic mutations but likely caused by more general mechanisms. We have recently shown that myokines, in addition to the reduction of low-grade inflammation, also play a direct role in the tumor-suppressing effect of exercise. By incubating breast cancer cells with serum taken immediately after an exercise bout, we found that the exercise-conditioned serum could reduce cancer cell viability and induce apoptosis through caspase activation.32 This study identified Oncostatin M as an exercise-induced myokine with anti-proliferative effects on the breast cancer cells. Likely the protection of exercise on tumor development and progression occurs through a variety of exercise-related changes like improved inflammatory fitness, immune function, growth factor signaling, sex hormones and improved metabolic status some of which are affected by the myokines. Knowing the mechanisms behind the beneficial anti-cancer effect of exercise will serve as foundation for public health guide with regard to exercise and likely facilitate the improvement of current anti-cancer strategies

Taken together, with the identified pleiotropic effects of myokines on multiple tissues, leading to fine-tuning of fuel utilization and energy homeostasis in these tissues, we believe that these secreted myokines are able to restore a healthy cellular environment, reduce low-grade inflammation and thereby prevent metabolic related diseases like insulin resistance and cancer.


The Centre of Inflammation and Metabolism (CIM) is supported by a grant from the Danish National Research Foundation (02-512-55). This study was further supported by the Danish Medical Research Council, the Commission of the European Communities (grant agreement 223576-MYOAGE) and by grant from The Novo Scholarship Program 2010.


Pedersen L, Olsen CH, Pedersen BK, Hojman P. Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle Am J Physiol Endocrinol Metab 2012 302 E831 40 doi: 10.1152/ajpendo.00339.2011.



1. Pedersen BK, Febbraio MA. Muscle as an endocrine organ: focus on muscle-derived interleukin-6.Physiol Rev. 2008;88:1379–406. doi: 10.1152/physrev.90100.2007. [PubMed] [Cross Ref]
2. Pedersen BK, Akerström TC, Nielsen AR, Fischer CP. Role of myokines in exercise and metabolism. J Appl Physiol. 2007;103:1093–8. doi: 10.1152/japplphysiol.00080.2007. [PubMed] [Cross Ref]
3. Brandt C, Pedersen BK. The role of exercise-induced myokines in muscle homeostasis and the defense against chronic diseases. J Biomed Biotechnol. 2010;2010:520258. doi: 10.1155/2010/520258.[PMC free article] [PubMed] [Cross Ref]
4. Steensberg A, van Hall G, Osada T, Sacchetti M, Saltin B, Klarlund Pedersen B. Production of interleukin-6 in contracting human skeletal muscles can account for the exercise-induced increase in plasma interleukin-6. J Physiol. 2000;529:237–42. doi: 10.1111/j.1469-7793.2000.00237.x.[PMC free article] [PubMed] [Cross Ref]
5. Pedersen BK. Muscles and their myokines. J Exp Biol. 2011;214:337–46. doi: 10.1242/jeb.048074.[PubMed] [Cross Ref]
6. Henningsen J, Rigbolt KT, Blagoev B, Pedersen BK, Kratchmarova I. Dynamics of the skeletal muscle secretome during myoblast differentiation. Mol Cell Proteomics. 2010;9:2482–96. doi: 10.1074/mcp.M110.002113. [PMC free article] [PubMed] [Cross Ref]
7. Nedachi T, Fujita H, Kanzaki M. Contractile C2C12 myotube model for studying exercise-inducible responses in skeletal muscle. Am J Physiol Endocrinol Metab. 2008;295:E1191–204. doi: 10.1152/ajpendo.90280.2008. [PubMed] [Cross Ref]
8. Pedersen L, Pilegaard H, Hansen J, Brandt C, Adser H, Hidalgo J, et al. Exercise-induced liver chemokine CXCL-1 expression is linked to muscle-derived interleukin-6 expression. J Physiol.2011;589:1409–20. doi: 10.1113/jphysiol.2010.200733. [PMC free article] [PubMed] [Cross Ref]
9. Rubio N, Sanz-Rodriguez F. Induction of the CXCL1 (KC) chemokine in mouse astrocytes by infection with the murine encephalomyelitis virus of Theiler. Virology. 2007;358:98–108. doi: 10.1016/j.virol.2006.08.003. [PubMed] [Cross Ref]
10. Oquendo P, Alberta J, Wen DZ, Graycar JL, Derynck R, Stiles CD. The platelet-derived growth factor-inducible KC gene encodes a secretory protein related to platelet alpha-granule proteins. J Biol Chem. 1989;264:4133–7. [PubMed]
11. Lira SA, Zalamea P, Heinrich JN, Fuentes ME, Carrasco D, Lewin AC, et al. Expression of the chemokine N51/KC in the thymus and epidermis of transgenic mice results in marked infiltration of a single class of inflammatory cells. J Exp Med. 1994;180:2039–48. doi: 10.1084/jem.180.6.2039.[PMC free article] [PubMed] [Cross Ref]
12. Scapini P, Morini M, Tecchio C, Minghelli S, Di Carlo E, Tanghetti E, et al. CXCL1/macrophage inflammatory protein-2-induced angiogenesis in vivo is mediated by neutrophil-derived vascular endothelial growth factor-A. J Immunol. 2004;172:5034–40. [PubMed]
13. Parachikova A, Nichol KE, Cotman CW. Short-term exercise in aged Tg2576 mice alters neuroinflammation and improves cognition. Neurobiol Dis. 2008;30:121–9. doi: 10.1016/j.nbd.2007.12.008. [PMC free article] [PubMed] [Cross Ref]
14. Dhawan P, Richmond A. Role of CXCL1 in tumorigenesis of melanoma. J Leukoc Biol. 2002;72:9–18. [PMC free article] [PubMed]
15. Feng G, Ohmori Y, Chang PL. Production of chemokine CXCL1/KC by okadaic acid through the nuclear factor-kappaB pathway. Carcinogenesis. 2006;27:43–52. doi: 10.1093/carcin/bgi174. [PubMed][Cross Ref]
16. Pedersen L, Olsen CH, Pedersen BK, Hojman P. Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle. Am J Physiol Endocrinol Metab. 2012;302:E831–40. doi: 10.1152/ajpendo.00339.2011. [PubMed] [Cross Ref]
17. Kamimura D, Ishihara K, Hirano T. IL-6 signal transduction and its physiological roles: the signal orchestration model. Rev Physiol Biochem Pharmacol. 2003;149:1–38. doi: 10.1007/s10254-003-0012-2.[PubMed] [Cross Ref]
18. van Hall G, Steensberg A, Sacchetti M, Fischer C, Keller C, Schjerling P, et al. Interleukin-6 stimulates lipolysis and fat oxidation in humans. J Clin Endocrinol Metab. 2003;88:3005–10. doi: 10.1210/jc.2002-021687. [PubMed] [Cross Ref]
19. Kelly M, Keller C, Avilucea PR, Keller P, Luo Z, Xiang X, et al. AMPK activity is diminished in tissues of IL-6 knockout mice: the effect of exercise. Biochem Biophys Res Commun. 2004;320:449–54. doi: 10.1016/j.bbrc.2004.05.188. [PubMed] [Cross Ref]
20. Wallenius V, Wallenius K, Ahrén B, Rudling M, Carlsten H, Dickson SL, et al. Interleukin-6-deficient mice develop mature-onset obesity. Nat Med. 2002;8:75–9. doi: 10.1038/nm0102-75. [PubMed][Cross Ref]
21. Febbraio MA, Hiscock N, Sacchetti M, Fischer CP, Pedersen BK. Interleukin-6 is a novel factor mediating glucose homeostasis during skeletal muscle contraction. Diabetes. 2004;53:1643–8. doi: 10.2337/diabetes.53.7.1643. [PubMed] [Cross Ref]
22. Banzet S, Koulmann N, Simler N, Sanchez H, Chapot R, Serrurier B, et al. Control of gluconeogenic genes during intense/prolonged exercise: hormone-independent effect of muscle-derived IL-6 on hepatic tissue and PEPCK mRNA. J Appl Physiol. 2009;107:1830–9. doi: 10.1152/japplphysiol.00739.2009. [PubMed] [Cross Ref]
23. Bouzakri K, Plomgaard P, Berney T, Donath MY, Pedersen BK, Halban PA. Bimodal effect on pancreatic β-cells of secretory products from normal or insulin-resistant human skeletal muscle.Diabetes. 2011;60:1111–21. doi: 10.2337/db10-1178. [PMC free article] [PubMed] [Cross Ref]
24. Gopurappilly R, Bhonde R. Can multiple intramuscular injections of mesenchymal stromal cells overcome insulin resistance offering an alternative mode of cell therapy for type 2 diabetes? Med Hypotheses. 2012;78:393–5. doi: 10.1016/j.mehy.2011.11.021. [PubMed] [Cross Ref]
25. Ellingsgaard H, Hauselmann I, Schuler B, Habib AM, Baggio LL, Meier DT, et al. Interleukin-6 enhances insulin secretion by increasing glucagon-like peptide-1 secretion from L cells and alpha cells.Nat Med. 2011;17:1481–9. doi: 10.1038/nm.2513. [PubMed] [Cross Ref]
26. Nehlsen-Cannarella SL, Fagoaga OR, Nieman DC, Henson DA, Butterworth DE, Schmitt RL, et al. Carbohydrate and the cytokine response to 2.5 h of running. J Appl Physiol. 1997;82:1662–7. [PubMed]
27. Pedersen BK, Steensberg A, Fischer C, Keller C, Keller P, Plomgaard P, et al. Searching for the exercise factor: is IL-6 a candidate? J Muscle Res Cell Motil. 2003;24:113–9. doi: 10.1023/A:1026070911202. [PubMed] [Cross Ref]
28. Boström P, Wu J, Jedrychowski MP, Korde A, Ye L, Lo JC, et al. A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature. 2012;481:463–8. doi: 10.1038/nature10777. [PMC free article] [PubMed] [Cross Ref]
29. Friedenreich CM, Orenstein MR. Physical activity and cancer prevention: etiologic evidence and biological mechanisms. J Nutr. 2002;132(Suppl):3456S–64S. [PubMed]
30. Holick CN, Newcomb PA, Trentham-Dietz A, Titus-Ernstoff L, Bersch AJ, Stampfer MJ, et al. Physical activity and survival after diagnosis of invasive breast cancer. Cancer Epidemiol Biomarkers Prev. 2008;17:379–86. doi: 10.1158/1055-9965.EPI-07-0771. [PubMed] [Cross Ref]
31. Jones LW, Viglianti BL, Tashjian JA, Kothadia SM, Keir ST, Freedland SJ, et al. Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer. J Appl Physiol.2010;108:343–8. doi: 10.1152/japplphysiol.00424.2009. [PMC free article] [PubMed] [Cross Ref]
32. Hojman P, Dethlefsen C, Brandt C, Hansen J, Pedersen L, Pedersen BK. Exercise-induced muscle-derived cytokines inhibit mammary cancer cell growth. Am J Physiol Endocrinol Metab. 2011;301:E504–10. doi: 10.1152/ajpendo.00520.2010. [PubMed] [Cross Ref]

Articles from Adipocyte are provided here courtesy of Landes Bioscience


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168 thoughts on “W.O.W. 1/12/14-The Amazing Power of Myokines”

  1. Marc,

    US News and World Report? Who do you think they would side with? A panel of government experts or a bottom-up, spontaneously organized dietary movement? If you ever want a real laugh, find a 5 year old copy of UNSAWR. They pretty much predict and get everything wrong (as does Time and Newsweek). These bozos are not reporting news, they are trying to help program what we think.

    I was discussing EMG potentials as they relate to muscular fatigue at the motor end plate with Bo Railey today. He is in school getting an exercise physiology degree and may doing some research in this area as part of his degree.

    WRT TSC vs powerlifting, I do not advocate that such a slow build up would benefit a powerlifter. Producing a maximal force against and immovable object IS A DIFFERENT ANIMAL than overcoming gravity applied to a large mass. Gravity, I believe, is the defining difference.

    WRT “The Rock”…my son follows him on instagram. Over the past two years his personality has morphed along with his physique. Much more self-aggrandizement, narcissism and profanity from a once humble guy. He also played truly nice characters in the movies until recently. Ever since “Pain and Gain” things have not seemed right.

  2. Mark, although nowhere close to his league, I was a competitive Olympic-style lifter during the waning years of Bill March’s career. Re-connected with him 7 or 8 years ago. In many ways the fact that he is now considered the poster boy for early steroid use is still an open, psychological wound. Don’t know how long he still believed this, but Bob Hoffman initially had him believing the little pink pills were some kind of “special vitamin.” By the time he knew differently, he was hooked on the gains. But Bill would have been an animal with or without steroids. One example of his degree of “giftedness”: after 1972, when they removed the press from Olympic lifts, he quit all weight-training — forever! EXCEPT to go down to the local “Y” once a year, on his birthday, and see if he could still clean and press a pair of 100 lb. dumbells. He continued to still be able to do this all through his sixties. He is now
    75 or 76 and about six years ago I made the mistake, during one of our phone conversations, of pushing too hard on the subject of him starting to work out again.
    He started ducking my calls, and I finally got the message. Another Olympian, Fred Lowe, who is a close friend, tells me that Bill, a 198 pounder, now weighs over 300, so I guess I hit upon a sore subject and lost a phone friend.

  3. Dr. McGuff,

    I do not know who is to be believed anymore on the subject of diet. Everybody seems to be slant information in order to promote their latest diet. FWIW, I have very few problems with a modified Paleo diet. What I don’t believe in is a diet based on a hunter/gatherer fantasy paradigm. I’m not trying to find out who is wrong, but rather what works for ME! I’m sure sensitive feelings may be touched by my remarks at times, but would we rather not explore all avenues of factual information. I would think not. FWIW, I believe very little of what the government states as fact. As you well know, government self interests have all but destroyed efficient and productive healthcare.

    Dr Ziegler’s Isotron machine is eye-opening. Mike Mentzer knew about this machine also. For sure, isometrics and training without going to failure can drastically increase recovery ability.

    Question: Dr. McGuff

    In an article written by Eric Cressey, he has stated: “In scientific jargon, super-slow training doesn’t work due to a phenomenon called ‘asynchronous recruitment.'”

    The article is entitled: “Five Resistance Training Myths in the Running World”

    www (dot)performbetter.com/webapp/wcs/stores/servlet/PBOnePieceView?storeId=10151&catalogId=10751&languageId=-1&pagename=195

    I find this article disturbing and potentially damaging to BBS protocol. I sure that I don’t understand this article completely. Could you perhaps shed some light on asynchronous recruitment in regards to Superslow for all of us?

  4. Marc,

    I too do not like the hunter/gatherer fantasy paradigm. Evolution should guide or thinking but not romanticize it. This tendency is why there is such a draw toward “functional” training and the thought that using a machine or advanced technology is not “natural”. A zebra being eaten alive from the hind quarters up by a lion is natural…but not something I want to replicate.

    I will have to look into Eric Cressey’s criticism to respond. If an article written for runners and lay people cannot be understood by a pharmacist, then it makes me wonder if he is just churning to make the water muddy. If something is true, I find that it is easy to represent clearly.

  5. Marc,
    That article wasn’t all bad but Cressey seems to have a poor understanding of skill training vs strength training.

    The following quote in particular troubled me.
    “In layman’s terms, if you train an athlete slowly, that athlete will be slow in competition”
    Any type of weight training, (slow, fast, plyometrics, resistance band etc.), that makes a muscle stronger will enable that muscle to move a given load faster than it could before.

    The section on free weights vs machines was also pure hogwash along with the comments about stabilizer muscles for all the reasons clearly outlined in Body by Science.

    By the way, just finished the Body by Science Question and Answer Book and was very pleased with it for anyone who is considering buying it. Well worth the asking price and really illuminated some of the concepts in the Body by Science book for me.


  6. Abe,

    I doubt Mr. Cressey has much experience with Superslow. I would think there would be sequential recruitment of some fast twitch fibers during even a long TUT Superslow set. The optimal way to train fast twitch fibers will always be first through the slow twitch fibers and through the alactic energy system. Fatigue is the enemy of strength. I’ve done it so many times, but when I lift heavy weights for multiple sets of low reps, my high reps set goes up. On the other hand, high reps have never made my max go up. This is because maximum resistance recruits new muscle fibers. Light weights, slow rep speeds, long TUT’s, and high reps do not from my personal experience.

  7. Marc,

    Could we be talking about skill specificity though?

    For example, to train a deadlift using lighter weights, longer TUT, slow rep speeds may not increase your max (significantly) because doing a deadlift with heavy weights for multiple sets of low reps “trains that particular skill”. And there can be no dispute that a lighter deadlift is a different skill than a heavy deadlift due to weight distribution being different. But if doing the deadlift with the lighter weight and slow rep speed does indeed build muscle and is also significantly safer, then who cares if it increases your max by any significant amount? Unless of course that is one of your goals ( to increase your max.)

    The question then becomes does working out with lighter weights, longer TUT, slow rep speeds build muscle or just improve that skill set? Thats a loaded question and probably very individual in nature.

  8. @#49

    The government endorsed approaches?? yeah there is no conflict of interest there….eating real food with little or no processed food is surely not safe. Follow the $$$ trail, it is obvious.

    I call it the real food diet. Who can argue with that?

  9. Abe,

    In my personal experience…the practical answer is no.

    It is true perfect practice makes for perfect skill. Practice increases skill, no doubt at all. Perfect practice increases skill, which in turn allows one to train harder and safer. This is the other side of that coin. I’m sure other styles of training increase strength to a degree….but Behm & Sale states it is the INTENT to move fast is the salient point overall. That takes “focused practice” on a few lifts to perfect safe and effective exercise. Find your favorite push, pull, and squatting exercises and perfect them. This will facilitate perfect exercise technique for safety, and ultimate strength gains. Nothing else is possible.

  10. I’ve tried Paleo and had absolutely no appetite… now I’m just avoiding gluten and processed foods… seems to be working really well! No more headaches and mental fog, feel lighter too (even though I weigh the same).

  11. My own experience suggests Marc has a point (at least as far as barbell training is concerned).
    If I train with low reps my high rep max (a different skill) goes up. However training with high reps drops my low rep weights considerably.
    The ‘skill’ argument should work in both directions?.

  12. Interesting Note: Yesterday in my “Work Out,” I tried an Unrestricted (relatively) Speed of Movement in my Leg Press. (BTW – I am Not recommending this) The Fatigue was kind of overwhelming to the point where when I tried to stand up as I normally might, I couldn’t. I have a Cybex Eagle (Modern Prototype) Leg Press and it is smooth as Hell! So, on this particular apparatus “you can get away with it.” The Lesson here that continues is that the Body is a Genius at adapting to sequence and certain set speeds. So, variation is a must from my end (but “you” can do what you want). Again, I do not recommend this, but there is something to learn here……..

  13. If you can squat 300lbs for a 1 rep max, and 200 lbs for 15 reps, will the max stay 300lbs (or go down) if the 15 rep squat weight goes up to 250? Nope.

  14. Hi Doug,

    I had a couple of questions about the exercise form that is shown in your book. For the squat, the picture showing the bottom position shows the guy in a full squat with his butt touching his calfs while his tip toes. The description says to have knees at 90 degrees and I’m pretty sure you shouldn’t be on your tip toes. His knees are at a 30 degree bend. For the leg press, the description says to start with thighs perpendicular to the ceiling. In the picture his things start at 45 degrees to the ceiling. So I’m just wondering if you noticed this discrepancy and if you would lean someone toward the picture or the description. I was also wondering if you had heard of Foundation Training and what you think of it?

    Thank you for your help. Keep up the good work.


    William Motley

  15. 1) myokines are excellent. I am now 63, and before meeting my new wife, was playing 10-14 hours of volleyball alternate weekends, plus some weight training, and I row indoors and scull on the water. Bypass surgery 10 years ago, and supposed to be 6 feet under 7 years ago.

    A favorite author for me is body builder Bill Pearl. He advocates staying with the same weight for 6-8 reps until 2-3 more are possible. No training to failure. The improvement can take two or three weeks. Then go up 5% in weight. Reps will drop again. With 5% increase every 3 weeks or so, in theory one can double their strength in a year.

    I do some sport specific work for rowing, archery, volleyball, and cardio for my heart.
    My max heart rate is somewhere over 170, for minutes at a time, and not breatless, and rarely breathing hard.

    I avoid fatigue, watching for cardiac drift as a warning sign. By the way, playing volleyball, I am known for my hustle. Among people half my age and very athletic themselves. They have me on skill, I have them on energy.

    I do weighted step ups. They are slow. They increase my vertical leap for blocking in vb, a quickness activity.

    Don’t stop exercising. Keep up a brisk walking speed. The Grim Reaper only walks up to 3.0 mph.

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