Anatomy & Physiology - Muscle Contraction
Anatomy & Physiology - Muscle Contraction 80197 - BIOL 2220 - 001
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80197 - BIOL 2220 - 001
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This 6 page Class Notes was uploaded by Courtney Luber on Tuesday October 18, 2016. The Class Notes belongs to 80197 - BIOL 2220 - 001 at Clemson University taught by John R Cummings in Fall 2016. Since its upload, it has received 6 views. For similar materials see Human Anatomy and Physiology I in Biology at Clemson University.
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Date Created: 10/18/16
Muscle Contraction Myogram o Y axis = muscle tension o X axis = time o Latent period – period of time between stimulation and beginning of activity ACh causing channels to open o Then, contraction phase o Then, relaxation phase o Refractory period – period of time in which a second stimulus will not evoke a second response Types of contraction o Twitch – single muscle contraction in response to a single stimulus o Tetanus – second contraction due to a second stimulation before complete relaxation Has to come after refractory period has ended Comes during relaxation phase Two types: Partial relaxation (incomplete tetanus) – relaxes some No relaxation (complete tetanus) – stimulus tendency equals refractory period Wave summation – when second stimulus applied before complete relaxation; eventually cannot get any stronger; reaches a maximum o Treppe – muscle completely relaxes and then it is stimulated again o Isotonic – effort exceeds load; muscle changes shape; i.e. bend arm – feel bicep get shorter o Isometric – load exceeds muscle; stays the same shape Energy for contraction o First energy used is the stored energy – one power stroke o Direct phosphorylation – o Anaerobic respiration – no oxygen present o Aerobic respiration – when oxygen is present Phosphorylation o Occurs in cytoplasm of cell o Creatine phosphate couples with ADP to produce ATP o Muscle stores creatine phosphate gives us immediate energy o Can power muscle for up to 15 seconds o CP reserves replenished during periods of inactivity Anaerobic respiration o Glycolysis breaks down glucose into pyruvate o Glucose from glycosomes in muscle o Also in blood sugar o Pyruvic acid converted to lactic acid o Shuts off production of ATP o Can power muscle up to 1 minute o Lactic acid diffuses into bloodstream Aerobic Respiration o Glycolysis breaks down glucose o Pyruvic acid enters mitochondria for complete breakdown o This produces lots of ATPs – 30’s vs 2 for anaerobic respiration o Takes more time Muscle Fatigue o Inability to contract o Stimuli still go through muscle, but the muscle can’t respond o Myosin stays attached to actin o ATP is required to separate them o ATP use exceeds ATP production o Excessive accumulation of lactic acid changes pH of muscle cell denatures enzymes that are involved in making ATP o Ionic imbalances Esp. potassium Leads to cramps o Muscle is cramping because it is staying contracted & when it continues to pull, it sends pain receptors to brain Requirements for resting state o Oxygen reserves must be replenished Restock myoglobin o Lactic acid must be converted to pyruvic acid, glucose or glycogen Stores in glycosomes o Glycogen stores must be replaced Comes from our diet or stored glycogen in liver o ATP reserve must be resynthesized o Creatine phosphate reserve must be resynthesized Force of contraction o Number of fibers stimulated to contract More fibers, stronger contraction Number of motor units o Relative size of fibers We change size of fibers by increasing number of proteins, store more myoglobin, and store more creatine Larger fiber greater strength of contraction o Frequency of stimulation Faster frequency stronger contraction o Degree of stretch No contraction if muscle is stretched too far No contraction if muscle is already contracted as much as it can be When thin just barely overlaps thick (minimal), the greatest force of contraction occurs Types of muscle fibers - based on speed of contraction and how ATP is produced o Slow oxidative fibers Slow; oxygen present Produce a lot of ATP because oxygen and it is split slowly Fatigue-resistant “long distance runner” o Fast oxidative fibers Fast; oxygen present Produce a lot of ATP and split it quickly Tendency to maybe run out “sprinters” o Fast glycolytic fibers Split ATP quickly but do not produce a lot of energy Anaerobic Very prone to fatigue Gives a big burst of contraction “weightlifter” Effects of exercise o Aerobic exercise Works out slow oxidative fibers Running, rowing machines, aerobics, etc. Result is to increase endurance Produce new blood vessels (angiogenesis) Increases mitochondria vis demand for ATP Increases myoglobin o Resistance exercise Works with fast glycolytic fibers Naturally stop breathing for a second Increases strength Causes hypertrophy of the muscle fibers (increases size) o Disuse atrophy If you stop exercising, muscle sizes get smaller Therapists bend muscles for stroke patients to keep them in movement Begins the minute you stop exercising If you don’t use a muscle for a long time, it loses its ability to contract – muscle tissue turn into dense irregular connective tissue Elderly people who don’t use muscles as much lose strength because of disuse Cardiac muscle o Tends to contract as a unit o Pretty much the same as skeletal muscle Smooth muscle Microscopic anatomy o Fibers smaller than skeletal o Lack connective tissue sheaths Only tissue sheath is endomysium o Organized into sheets Longitudinal layer – end view; flat Circular layer – runs around intestine, so when it contracts, it squeezes intestine o Unstructured neuromuscular junction Autonomic nerve activates smooth muscle This comes from unconscious part of our brain we can’t control involuntary No change in sarcolemma when it attaches Instead, bulbous like swellings called varicosities that hold neurotransmitters (not ACh) Some neurotransmitters are excitatory and others are inhibitory Neuromuscular junction Varicosities release neurotransmitter into diffuse junctions No motor end place; still a synapse o Less developed sarcoplasmic reticulum touches sarcolemma at a number of places but no organized pattern o No real pattern to the myofilaments Smooth muscle SR o No sarcomeres o No pattern to myofilaments o No T tubules Instead have caveoli – pouch-like enfoldings of sarcolemma Concentrate calcium Have a bunch of Ca channels in them Myofilament arrangement o Contains both thick and thin myofilaments o 10-15 thin myofilaments for each long thick myofilament o Myosin heads found along entire length of thick myofilament o Tropomyosin associated with thin myofilament, but no troponin o Myofilaments arranged diagonally within fibers o Contain intermediate filaments Non-contractile filaments in cytoskeleton Attach to dense bodies, and stretch from one another Dense bodies attached to sarcolemma Types of smooth muscle o Visceral Contracts rhythmically as a unit Peristalsis – rhythmic, wave-like contraction of smooth muscle Cells are coupled with gap junctions We find this in the walls of internal, hollow organs Help regulate blood flow via blood vessels o Multiunit No gap junctions More like skeletal muscle than visceral is Arrector pili muscle, muscles that control size of our pupils, walls of large arteries, etc. Smooth muscle contraction o Neurotransmitter stimulates production of action potential Neurotransmitter released by autonomic neuron o Calcium is released by caveoli More importantly is taken in from extracellular space o Calcium binds to calmodulin Not attached to tropomyosin or actin – it is a separate protein inside the muscle & its role is to bind to Ca Calmodulin is activated when it attaches to Ca o Activated calmodulin activates myosin light chain kinase (ATPase) Splits ATP o Activated kinase charges myosin cross bridges o Actin and myosin interact to shorten fibers Regulation of contraction o Autonomic nerves release different neurotransmitters Excitatory and inhibitory neurotransmitters ACh is always excitatory o Chemical factors Hormones, histamine (allergic response), lack of oxygen, excessive carbon dioxide, change sin pH Development of muscle o Mesodermal origin Mesodermal cells are called myoblasts o Skeletal myoblasts fuse cardiac and smooth do not fuse they develop gap junctions though all myoblasts have neurotransmitter receptors over the entire sarcolemma o Agrin clusters and maintains ACh receptors Creates neuromuscular junction Makes motor end plate Causes junctional folds Causes ACh receptors to remain at site Rest of cell w/o agrin will lose ACh receptors
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