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A ciascuno il suo: a brief personal history in translational myology at turn of millennium Giorgio Fanò-Illic Free University of Alcatraz, Loc. Santa Cristina, 06020 Gubbio PG, Italy. E.mail: "Giorgio Fano'-Illic" <fano@unich.it> In 1940 and thanks to L.E. Heilbrunn 1 the scientific hypothesis on the possible role of calcium ion in muscle contraction was published. Nevertheless, Ca 2+ was not recognized as an indispensable factor of contraction up to the paper of A. Weber that appeared in 1959 and in which it was shown that Ca 2+ exerts its effect having the filament proteins as target; just a ionic concentration of 0.2 mM was capable to induce the muscle contraction. 2 The goal of the calcium ion on the filaments is a protein, troponin C, identified some years later by Ebashi and Kodama. 3 It is important to note that a few years earlier in 1954, at the same time and in the same issue of the Nature, AF Huxley and Niedergerke 4 and HE Huxley and Hanson, 5 published the hypothesis of "sliding filaments theory" on the mechanism of action of muscle contraction. Starting from the seventies of the last century, the studies on Ca2+ exploded (together with calcium related proteins or Calcium Binding Proteins or CBP) linked to the mechanisms of signal transduction with problems and surprises related to mechanisms of phosphorylation and de-phosphorylation of protein substrates. In particular, in skeletal muscle were identified: the principal proteins (Ryanodine receptor or RYR, Dhyidropiridine receptor or DHPR and Calsequestrin or CSQ) capable of coupling the electrical phenomena occurring in the sarcolemma with the release of Ca 2+ from the terminal cisternae of the sarcoplasmic reticulum. 6 To assure a precise coordination of Ca 2+ handling regulation during contraction of skeletal muscle, several different CBP, as well as S100, were proposed. 7 In striated muscle, S100 demonstrated highest expression in cardiac muscle, followed by slow twitch and fast twitch skeletal muscle, respectively. S100 binds specifically to a CaM binding site on RyR1 and enhances the Ca 2+ release flux resulting from coordinated opening of multiple RyR1s. 8 Muscle requires two cofactors to function: load and innervation. If both or one of the them are impaired, muscle becomes atrophic 25 through a mechanism of protein degradation that develops into proteasomes and lysosomes (autophagy). 9 However, the muscle is a surprising tissue because even when it seems to have almost disappeared, as a consequence of a long time denervation, it is able to regenerate, if exposed to daily cycles of functional electrical stimulation (FES). 10 Ageing of muscle tissue is a complex process (Sarcopenia) that is usually associated with a decrease in mass, strength, and velocity of contraction triggered by reactive oxygen species (ROS) that have accumulated throughout one's lifetime. Exercise as a method to prevent or at least delay sarcopenia has been discussed in many scientific reports. While on the one hand, it seems clear that exercise is effective in reducing the loss of muscle mass, on the other it appears that physical activity increases both the mechanical damage and the accumulation of free radicals as results of increase in the aerobic metabolism of the involved muscles. 11 How to take advantage of physical exercise, limiting the adverse effects, is the main goal for further successful managements of agerelated power decline. 1. Heilbrunn LV., 1940. Physiol. Zool. 13:88-94 2. Weber A. 1959 J. Biol. Chem. 234:2764-9; 3. Ebashi, S., and Kodama, A., 1965. J. Biochem., 58, 107 4. Huxley, AF, Niedergerke, R. 1954. Nature 173: 971-973 5. Huxley, SE Hanson J. 1954. Nature 173: 973-76 6. Franzini-Armstrong, C. 1970. J. Cell Biol.47:488-499 7. Dolcini C. 1970. Boll. Soc. Ital. Biol. Sper.46:1069-1970 8. Fanò G. et al. 1989 FEBS Lett. 255:381-384 9. Milan G et al. 2015 Nat Commun. 10;6:6670 10. Kern H, et al. 2004 J Neuropathol Exp Neurol. Sep;63(9):919-31. 11. Musarò A. et al. 2010 Curr Opin Clin Nutr Metab Care. May;13(3):236-42. The Epidemiology of Aging Stefania Maggi National Research Council, Institute of Neurosciences, Aging Section Padova, Italy. E-mail: stefania.maggi@in.cnr.it The marked fall in birth and mortality rates that has taken place over the last century has modified the demographic structure of the European Journal of Translational Myology eISSN 2037-7460 – BAM On-Line Interdepartmental Research Center of Myology IRCCS Fondazione Ospedale San Camillo, Venezia, Italy 26 Eur J Transl Myol Basic Appl Myol 2016; 26 (1):25-28 This article is distributed under the terms of the Creative Commons Attribution Noncommercial License (by-nc 3.0) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. 2016Spring PaduaMuscleDays: February 16 Myology Seminar Are deferrable the mobility impairments in older aging? Aula Guariento, Accademia Galileiana di Scienze Lettere ed Arti in Padova (Italia), 16 Febbraio 2016 Via Accademia, 7 – 35139 Padova Segreteria generale 049 655249 – e-mail: galileiana@libero.it – www.accademiagalileiana.it Organizzatori: Ugo Carraro, Stefano Masiero, Carlo Reggiani Italian population: there are now 13,220,000 persons over 65; they represent more than 21% of the population and make Italy the country with the highest percentage of elderly persons in Europe (it has been estimated that in 2050 persons over 65 will exceed 33% and those over 85 will make up approximately 8% of the

european journal of translational myology

Abstracts of the Myology Seminar: Are deferrable the mobility impairments in older aging? | Accademia Galileiana di Scienze Lettere ed Arti, Padua, Italy, February 16, 2016