LABORATORY REPORT Fundamental Mammalial Physiology Laboratory Practice III Muscle Contractile Property Lecture: Tepmanas Bupha-Intr (e-mail:

tepmanas.bup@mahidol.ac.th) Submission eadline! Monday February "#$ "%&' Student Name: Nguyn Triu iu Linh!!!! Student I : "ST#-BST$-%&'

ISC"SSI(N ') *+plain the mechanism used ,or communication -et.een somatic ner/e and s0eletal muscle The synapse -et.een somatic motor neurons and s0eletal muscle cells is 0no.n as the neuromuscular 1unction 2NM34) It5s a chemical synapse6 though its a special chemical synapse in se/eral respects) *lectric current comes in the somatic ner/e6 that means .e put the electrical charge changes -et.een intracellular and e+tracellular spaces) The ner/e -ecomes e+cita-le cell) Negati/e charges .ill -e the electrical signal and cause 7ction potential) Ner/e cell uses 7ction Potential to send the signal along the mem-rane) 7ction Potential acti/ates Ca$8 in,lu+ inducing e+ocytosis o, neurotransmitter) In Presynaptic terminal 2ner/e46 the Ca channel open and Ca $8 come in and acti/ate the chemicals 27cetylcholine4 release) Chemicals -ind to the receptors on postsynaptic terminal 2s0eletal muscle 9 e,,ector organs4 and acti/ate Na channel open the Na8 mo/e in 2 epolari:ation4 then ;8 mo/e out 2<epolari:ation4) Muscle uses 7ction Potential to acti/ate muscle contraction) $) *+plain .hy muscle contraction increases .hen .e increase electrical 2/olt4 stimulation) =orce o, s0eleton muscle contraction can -e a,,ected -y Motor unit summation) 7nd ' ner/e cell can stimulate more than ' s0eletal muscle ,i-er 2'-$% ,i-er4) >hen .e increase the /olt6 the num-er o, stimulated ner/e is higher6 and stimulated muscle increase as .ell) 7cti/ate more neuron .ill increase many muscle ,i-ers) Then the muscle contraction .ill increase)

&) *+plain t.o mechanisms that reduce muscle contraction .hen .e continuously stimulate the ner/e-muscle ,or a /ery long period o, time) The reducing o, muscle contraction in this case is the muscle ,atigue) T.o mechanisms are: - Neural =atigue: loss o, neurotransmitter 27cetylcholine4) In the peripheral ner/ous system6 acetylcholine acti/ates muscles6 and is a ma1or neurotransmitter in the autonomic ner/ous system) >hen acetylcholine -inds to acetylcholine receptors on s0eletal muscle ,i-ers6 it opens ligand-gated sodium channels in the cell mem-rane) Sodium ions then enter the muscle cell6 initiating a se?uence o, steps that ,inally produce muscle contraction) That means i, losing some o, 7ch6 the muscle contraction is lo.er) 7,ter a period o, ma+imum contraction6 the ner/e@s signal reduces in ,re?uency and the ,orce generated -y the contraction diminishes) It is this neural training that generate ma+imum contractions and the muscle reaches its physiological limit) Past this point6 training e,,ects increase muscular strength through myo,i-rilar or sarcoplasmic hypertrophy and meta-olic ,atigue -ecomes the ,actor limiting contractile ,orce) - Muscle =atigue: loss o, 7TP or 7ccumulation o, Lactic 7cid: 7TP -inds to the myosin head and causes the Aratchetting@ that results in contraction according to the sliding ,ilament model) Creatine phosphate stores energy so 7TP can -e rapidly regenerated .ithin the muscle cells ,rom adenosine diphosphate 27 P4 and inorganic phosphate ions6 allo.ing ,or sustained po.er,ul contractions that last -et.een B9C seconds) Dlycogen is the intramuscular storage ,orm o, glucose6 used to generate energy ?uic0ly once intramuscular creatine stores are e+hausted6 producing lactic acid as a meta-olic -yproduct) Besides6 i, .e continuously stimulate the ner/e-muscle ,or a /ery long period o, time6 time o, rela+ation .ill short6 the muscle ,i-er cannot come contraction ?uic0ly6 the energy stored .ill -e lo.er) No time ,or restore the energy) So the 7TP loss6 reducing muscle contraction)