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dr. frankenstein

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dr. frankenstein last won the day on March 19

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  1. . Nice paper Nutrition and Athletic Performance Medicine & Science in Sports & Exercise: March 2016 https://journals.lww.com/acsm-msse/Fulltext/2016/03000/Nutrition_and_Athletic_Performance.25.aspx?WT.mc_id=HPxADx20100319xMP . .
  2. . i like to think on grams per kilo ( X LBM weight) macros are (carb-pro-fat) get lean 1-2-1 1-3-1 growth (lean) 2-2-2 3-2-2 .
  3. interesting. breakfast, shake (you) or maybe, dinner, shake (me) thinking on watery essential aminos (on workout) .
  4. . ...maybe you were around 200 ......... .
  5. . Journal of Experimental Biology 2016 219: 235-242. Muscle memory and a new cellular model for muscle atrophy and hypertrophy http://jeb.biologists.org/content/219/2/235 "previously untrained fibres recruit myonuclei from activated satellite cells before hypertrophic growth. Even if subsequently subjected to grave atrophy, the higher number of myonuclei is retained, and the myonuclei seem to be protected against the elevated apoptotic activity observed in atrophying muscle tissue. Fibres that have acquired a higher number of myonuclei grow faster when subjected to overload exercise, thus the nuclei represent a functionally important ‘memory’ of previous strength". but the point is, there is no donation of myonuclei from satellite cells to adult muscle cells. .
  6. . . i am on 1.100 ng/dl at 55 years old (no TRT) muscle mass normal, libido sub-standard. more testorene does not mean necessarilly a better perfomance. "some conditions apply" .......... . .
  7. . 500-600 ng/dl American Urological Association J Urol. 2018 Aug;200(2):423-432. https://www.jurology.com/article/S0022-5347(18)42817-0 "The Panel recommends that clinicians use the minimal dosing necessary to drive testosterone levels to the normal physiologic range of 450-600 ng/dL" .
  8. . https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723165/ "The tryptophan-serotonin theory has been expanded from data obtained in animal studies by indication that 5-HT release and reuptake can affect central fatigue (Bequet et al. 2002). Moreover, some authors introduced the concept of the ratio of 5-HT to DA, and other neurotransmitters as more closely related variables with central fatigue" related from stendec Int J Sports Med. 1988 Oct;9(5):301-5. Effect of L-tryptophan supplementation on exercise performance. Segura R1, Ventura JL. The performance of strenuous physical exercise is associated with discomfort and pain, the tolerance for that being modulated by the activity of the endogenous opioid systems. As 5-hydroxy-tryptamine (5-HT) affects nociception through its effects on the enkephalin-endorphin system, we have analyzed the effects of a moderate supplementation with L-tryptophan, the immediate precursor of 5-HT, on endurance and sensation of effort. Twelve healthy sportsmen were subjected to a work load corresponding to 80% of their maximal oxygen uptake on two separate trials, after receiving a placebo and after receiving the same amount of L-tryptophan. The subjects ran on a treadmill until exhaustion. Total exercise time, perceived exertion rate, maximum heart rate, peak oxygen consumption, pulse recovery rate, and excess post-exercise oxygen consumption were determined during the two trials. The total exercise time was 49.4% greater after receiving L-tryptophan than after receiving the placebo. A lower rate of perceived exertion was exhibited by the group while on tryptophan although the differences from the control group were not statistically significant. No differences were observed in the other parameters between the two trials. The longer exercise time als well at the total work load performed could be due to an increased pain tolerance as a result of L-tryptophan ingestion. Int J Neurosci. 2010 May;120(5):319-27. doi: 10.3109/00207450903389404. L-tryptophan supplementation can decrease fatigue perception during an aerobic exercise with supramaximal intercalated anaerobic bouts in young healthy men. Javierre C1, Segura R, Ventura JL, Suárez A, Rosés JM. Physical exercise is often terminated not due to muscle fatigue but because of inadequate neural drive in the serotonergic system. Modifications in activity levels of the serotonergic system, induced by variations in the availability of L-tryptophan (a serotonin precursor) may alter neural drive. We examined the effect of L-tryptophan supplementation on physical performance by combining aerobic work with brief periods of supramaximal intensity that closely mimics the activity typical of team sports. Twenty healthy young sportsmen (mean age 21.2 +/- 0.7 years) performed a submaximal exercise on a cycle ergometer, with a workload corresponding to 50% of their respective VO(2) max for 10 min, followed by a maximal intensity exercise for 30 s. This sequence was repeated three times and, after the fourth series, each participant continued to exercise at the highest speed that he could sustain for 20 min. This protocol was performed twice: once with and finally without supplementation of L-tryptophan, in random order and double-blind. Peak power output, average anaerobic power output, and power output during the last 20 min of the trial were higher on the trials performed with L-tryptophan supplementation than on those performed with placebo. The distance covered during the last 20 min of the trial was 11,959 +/- 1,753 m on placebo and 12,526 +/- 1,617 m on L-tryptophan (p < .05). In conclusion, in some types of exercises, modification of the serotonergic system may improve the physical performance. .
  9. . i mean, more ARs -> more hypertrophy ? ...but, androgens (supaphysyological) upregulate ARs, on everybody ?... Muscle Androgen Receptor Content but Not Systemic Hormones Is Associated With Resistance Training-Induced Skeletal Muscle Hypertrophy https://www.frontiersin.org/articles/10.3389/fphys.2018.01373/full ...This study, in conjunction with others (Bamman et al., 2007; Petrella et al., 2008; Davidsen et al., 2011; Eynon et al., 2013), provides evidence that the relative increase in skeletal muscle mass following RET is underpinned by local intramuscular factors and not systemic hormonal concentrations... .
  10. . then, what are satellite cells for ?? on adult cells... Myogenic Progenitor Cells Control Extracellular Matrix Production by Fibroblasts during Skeletal Muscle Hypertrophy https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(16)30304-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1934590916303046%3Fshowall%3Dtrue "shows MPC-mediated regulation of the muscle extracellular matrix during remodeling, and the mechanism of this interaction with fibrogenic cells" Myonuclear Domain Flexibility Challenges Rigid Assumptions on Satellite Cell Contribution to Skeletal Muscle Fiber Hypertrophy https://www.frontiersin.org/articles/10.3389/fphys.2018.00635/full "satellite cell proliferation with loading, particularly in early phases but potentially throughout training, is likely for the purposes of supporting muscle repair and extracellular matrix remodeling" Starring or Supporting Role? Satellite Cells and Skeletal Muscle Fiber Size Regulation https://www.physiology.org/doi/full/10.1152/physiol.00019.2017?url_ver=Z39.88-2003&amp;rfr_id=ori%3Arid%3Acrossref.org&amp;rfr_dat=cr_pub%3Dpubmed "an exosome-mediated mechanism by which satellite cells remodel the ECM" .
  11. https://dreams.ucsc.edu/Library/domhoff_2000d.html "On the other hand, and contrary to the claim that the method is free of any suggestive influence by the psychoanalyst, there is experimental evidence that subtle suggestions from an experimenter-therapist can falsely convince many people on the basis of dream interpretations that they were once lost or abandoned as young children (Mazzoni & Loftus, 1998; Mazzoni, Loftus, Seitz, & Lynn, 1999). These and many other findings on the power of suggestion in a therapeutic context (Ofshe & Watters, 1994) take on greater importance when Freud's (1900) several mentions of arguments with patients concerning the wishful and infantile basis of their dreams are added to the picture. What Freud saw as overcoming "resistance" can be understood from the vantage point of social psychology as a process of persuasion and conversion within the context of great respect for an authority figure who is seen as offering relief from suffering. As can be seen from this brief overview of the relevant scientific literature on dreams, there is no reason to believe any of Freud's specific claims about dreams and their purposes. It is as likely that social influence processes led to Freud's "discoveries" as it is that free association uncovers the latent content of dreams. Moreover, the all-important wish theory is refuted by the dreams of post-traumatic stress disorder and the blandness of young children's dreams. The idea of dreams as guardians of sleep is contradicted by both the regularity of dreaming and the absence of dreaming in children and brain-lesioned patients. The lack of evidence for the processes called the dream-work suggests that they are at best forms of figurative thought familiar to us through jokes and slang (Hall, 1953a). Since there are many dreams without day residue, it cannot be the case that all dreams contain a reference to events from the previous day or two. These stark conclusions leave us with nothing that is explicitly "Freudian" in the search for a general psychological theory of dreams except that at least some dreams have psychological meaning" "However, none of these ideas implies that dreams have any "purpose" or adaptive function, and least of all the functions proposed for them by Freud and Jung (Antrobus, 1993; Foulkes, 1993). Dreams are too rarely remembered or related to daily events, and too infrequently contain even the hint of solutions to problems, to have any use to the waking mind in any evolutionary sense, and there is no evidence that dreaming has any adaptive purpose during sleep. Dreaming may well be the accidental by-product of two important adaptations, thinking and sleeping (Foulkes, 1985; Foulkes, 1993; Foulkes, 1999)"
  12. . Psychoanalysis? Is That Still Around? .
  13. . ...well, I did not know where to post this remembering endless discussions on the role of satellite cells in hypertrophy at mindandmuscle.net Starring or Supporting Role? Satellite Cells and Skeletal Muscle Fiber Size Regulation https://www.physiology.org/doi/abs/10.1152/physiol.00019.2017?fbclid=IwAR2G09SBA2IneSSynQzuuFQ3ZXHJDb0h4ufoHEFEodm5cpLo3Ig4g7bk_18&amp;journalCode=physiologyonline "INCREASED baseline SATELLITE CELL density in adult mice DOES NOT result in LARGER muscle fibers, indicating that satellite cells themselves DO NOT DRIVE ADULT MUSCLE FIBER GROWTH" then, what drives hypertrophy ?? increase in cytoplasmic volume and nucleus growth ....not more myonuclei Turn Up the Volume: Uncovering Nucleus Size Control Mechanisms https://www.physiology.org/doi/abs/10.1152/physiol.00019.2017?fbclid=IwAR2G09SBA2IneSSynQzuuFQ3ZXHJDb0h4ufoHEFEodm5cpLo3Ig4g7bk_18&amp;journalCode=physiologyonline "nucleus growth is regulated by the volume of cytoplasm in the immediate vicinity of the nucleus...the authors demonstrated that cytoplasmic volume is sufficient to increase nucleus growth". .
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