Lecture 34 - Movement & Muscles IV

Lecture 34 - Movement & Muscles IV - Monday’s Class...

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Unformatted text preview: Monday’s Class MOVEMENT & MUSCLES IV Chapter 6 pp. 208-­‐243 Chapter 5 pp. 196-­‐235 Important Deadlines Problem Set #4 (Endocrine Systems and Movement & Muscles) – Available 5PM Monday May 22nd • Closes Monday May 29th, 11:59PM • ONE SUBMISSION ONLY (save and don’t submit until ready) • Answers will only be revealed after quiz closes • BE SURE TO SUBMIT YOUR ANSWERS BY DEADLINE! What you should be able to do by the end of today’s lecture MOVEMENT & MUSCLES IV • Compare modes of excitation-­‐contraction coupling in the vertebrate heart and skeletal muscle. • Know the terms used to distinguish types of muscles based on various parameters. • Explain the differences in the structure of numerous muscle types and how variation in molecular structure relates to contractile function. Excitation of Vertebrate Striated Muscle • Skeletal muscle and cardiac muscle differ in mechanism of excitation and excitation-­‐ contraction (EC) coupling • Differences include – Initial cause of depolarization – Time course of the change in membrane potential (action potential) – Propagation of the action potential along the sarcolemma (cell membrane of muscle) – Cellular origins of Ca2+ Ca2+ Channels & Transporters involved in EC coupling Figure 6.35 • Channels allow Ca2+ to enter cytoplasm – Ca2+ channels in cell membrane • Dihydropyridine receptor (DHPR) – Ca2+ channels in the SR membrane • Ryanodine receptor (RyR) • Transporters remove Ca2+ from cytoplasm – Ca2+ transporters in cell membrane • Ca2+ ATPase • Na+/Ca2+ exchanger (NaCaX) – Ca2+ transporters in SR membrane • Ca2+ ATPase (SERCA) Induction of Ca2+ release from SR Figure 6.35 • AP along sarcolemma conducted down T-­‐tubules – Depolarization opens DHPR – Ca2+ enters cell from extracellular fluid • In heart, ­ [Ca2+]i causes RyR to open, allowing release of Ca2+ from SR – “Ca2+ induced Ca2+ release” • In skeletal muscle, change in DHPR shape causes RyR to open, allowing release of Ca2+ from SR – “Depolarization induced Ca2+ release” Ca2+ induced Ca2+ Release (Cardiac Muscle) Figure 6.37 Depolarization Induced Ca2+ Release (Skeletal Muscle) Figure 6.36 Action Potential in motor neuron Action Potential in muscle fiber Muscles generate force by contraction Human Physiology by Silverthorn Increasing muscle tension by increasing neural stimulation frequency Human Physiology by Silverthorn Increasing muscle tension by increasing neural stimulation frequency Human Physiology by Silverthorn Increasing muscle tension by increasing neural stimulation frequency Human Physiology by Silverthorn Sustained high [Ca2+] in the cytoplasm permits summation and tetanus Human Physiology by Silverthorn Skeletal vs Cardiac Muscle Smooth Muscle Muscle cells first arose in cnidarians True muscle first arose in ctenophores (comb jellies) Smooth Muscle Smooth Muscle • Key differences from skeletal muscle – No sarcomeres (no striations) • Thick and thin filaments are scattered in the cell • Attached to cell membrane at adhesion plaques – No T-­‐tubules and minimal SR – Often connected by gap junctions • Function as a single unit – Contract in all dimensions – Different mechanism of EC coupling • Slow, prolonged contractions (Involuntary) • Often found in the wall of “tubes” in the body • Blood vessels, intestine, airway, etc. Figure 5.31 Control of Smooth Muscle Contraction • Regulated by nerves, hormones, and physical conditions (e.g., stretch) – At rest, the protein caldesmon is bound to actin and blocks myosin binding • Smooth muscle does not have troponin or tropomyosin – Stimulation of cell increases intracellular Ca2+ • Ca2+ enters through plasma membrane • (Ca2+ ATPase removes Ca2+ from cytoplasm) – Ca2+ binds to calmodulin • Calmodulin binds caldesmon and removes it from actin – Cross-­‐bridges form and contraction occurs • Calmodulin also causes phosphorylation of myosin – Increase in myosin ATPase activity Work potential = muscle area • Since muscle length is restricted by skeletal system, changes in muscle work capacity involve changes in cross-­‐sectional muscle area – evolutionary modification (e.g., Belgian Blue cattle) – acclimatization/training (e.g., the Governator) Genetic underpinnings of hypermyotrophy: Myostatin *myostatin inhibits muscle differentiation of myoblasts to muscle fibers (a negative regulator of muscle mass) Mice with myostatin mutations Myostatin inhibitor: Treatment for muscular dystrophy WT Myo-­‐ Myo-­‐/Myo-­‐ What you should be able to do by the end of today’s lecture GAS EXCHANGE • Explain how physical and chemical processes influence the design of respiratory systems. • Describe the evolutional diversity in respiratory tissues. • Discuss the fundamental differences in breathing air versus water. The Physics of Respiratory Systems • Diffusion of gases • Fick equation • When applied to gases, we typically think of the pressure gradient of gas, rather than the concentration gradient • To maximize diffusion respiratory surfaces are typically thin, with a large surface area Henry’s Law • Gas molecules in the air must first dissolve in liquid in order to diffuse into a cell • The concentration of gas in a liquid is proportional to its partial pressure & solubility of the gas • Henry’s law • [G] = concentration of the gas – [G] = Pgas ž Sgas • Pgas = partial pressure of the gas • Sgas = solubility of the gas Figure 9.2b Diffusion Rates • Graham’s law – Diffusion rate is proportional to solubility/ÖMW • Combining the Fick equation with Henry’s law and Graham’s law – Diffusion rate of a gas molecule is proportional to • D ´ A ´ DPgas ´ Sgas / X ´ ÖMW Tuesday’s Class OXYGEN & CARBON DIOXIDE PHYSIOLOGY II Chapter 11 pp. 442-­‐452 Chapter 9 pp. 410-­‐422 ...
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