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Anatomy & Physiology - Muscle Contraction

by: Courtney Luber

Anatomy & Physiology - Muscle Contraction 80197 - BIOL 2220 - 001

Marketplace > Clemson University > Biology > 80197 - BIOL 2220 - 001 > Anatomy Physiology Muscle Contraction
Courtney Luber

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About this Document

These are the notes we covered in class over the muscle contraction lectures.
Human Anatomy and Physiology I
John R Cummings
Class Notes
anatomy, Physiology
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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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