Muscle Physiology & Dynamics of Work: How a Working Horse Works
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Muscle Physiology & Dynamics of Work
How a Working Horse Works
Lee Ann Swenson, MS, BSc, CEMMT
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Equine Muscle Physiology & Mechanics
Muscle Tissue Intro
Structure & Function
Muscle Microanatomy & Physiology
Dynamics of Work
Specific Muscle Fibers & Energy Substrates
Exercise & Effects on Muscle
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Muscle Tissue: Introduction
Muscles = Contraction
3 Types of Muscle
Visceral Muscles (Smooth Muscle) Involuntary GI Tract, Blood Vessels, Uterus, etc.
Cardiac Muscle Involuntary Heart
Skeletal Muscle (Striated Muscle) V oluntary
Movement of Joints, Limbs, etc.
± Explosive power
± Stamina
± Motor Control
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Skeletal Muscle: Structure & Function
Large part of body weight (up to 40% including H20)
Closely associated with the skeletal, nervous, and
circulatory systems
Manipulation impacts a range of tissues & systems Generates heat
Each muscle is a collection of fibers & associated tissues
Attached to bone via tendons & connective tissue
Least moveable attachment = origin
Most moveable attachment = insertion
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Microanatomy
& Physiology
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Muscle Fiber = Individual Muscle Cell
Multinucleated ± composed of fused cells Large cells
10 ± 100 µm diameter
Approx 20 cm in length
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Muscle Cells
Specialized to contract
Generate FORCE and MOVEMENT
Do not divide
Increased muscle size is due to Increased cell size
Key Qualities of Muscle Cells
Excitable
Conductive Contractile
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Muscle Cell Key Components
Membrane = Sarcolemma T-Tubules
Transmit Messages
Mitochondria
Generate Energy
Numerous
Myofibrils
2 Proteins in long strands
Heart of the contractile function
Sarcoplasmic Reticulum (Endoplasmic Reticulum)
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Muscle Cell & Associated Structures
As visible with a standard light microscope
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Skeletal Muscle
Electron Micrograph
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Dynamics of Work
Mechanism of Contraction
Stimulus of Contraction
Energy for Contraction
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Sarcomere = Smallest Unit of Contraction
Repeating Pattern of Striations
Thick and Thin Filaments
Actin (Thin) & Myosin (Thick)
Myofilaments arranged in a specific pattern
H-Zone
Z-Line
A-Band
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Actin & Myosin
2 Principal Muscle Proteins
Found in Myofibrils
Arranged in a Ring-like Structure
Usally 6 Actin strands around a Myosin fibril Run Parallel & Lengthwise
Myosin (Thick) has protrusions (Crossbridges)
Actin (Thin) is intertwined with thinner topomyosin and
troponin
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Mechanism of Contraction
1. Nerve Impulse Stimulation2. CA++ Released into Cytoplasm by Sarcoplasmic
Reticulum
3. CA++ Binds to Troponin, which Rotates
4. Tropomyosin Moves and Actin is Exposed to Myosin5. Myosin Crossbridge Binds to Actin
6. Crossbridge Drags Along Actin (Power Stroke)
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When all the crossbridges in a sarcomere act together,the whole sarcomere contracts
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Mechanism of Relaxation
7. Nerve Impulse Ends
8. SR Reabsorbs CA++
9. CA++ Dissociates from Troponin
10.ATP Binds to the Crossbridge
11.Crossbridge Disconnects from Actin
12.Actin Fibers Return to Previous Positions
13.Sarcomere Relaxes
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Contraction-Relaxation
A muscle cell may not go back to immediate completerelaxation
Contraction can continue through a series of stimulations
(Summation)
Summation increases the total force of contraction If the stimulus is great enough, many sarcomeres in
many fibers are recruited, and the muscle as a whole
contracts.
Allows for varying amounts of work
Muscle failure occurs when the maximum number of
fibers are stressed beyond their limits
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Stimulus of Contraction:Muscle Contraction is Controlled by Motor Nerves
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Interaction of Motor Nerves and Muscle Fibers
Each muscle is innervated by only one motor nerve
One nerve can innervate a number of muscles
Each nerve controls many fibers (motor units), the fewer
the fibers the more delicate the movement If nerve contact is lost, fibers shrink (atrophy)
The pattern of nerve activity determines the fiber type
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Feedback Loop
Feedback from the tendon and stretch receptorscontrols motor nerve activity
Motor nerve activity is also controlled by higher
centers (brain)
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Mechanism of Neuromuscular
Stimulation (Excitation)
1. Electrical depolarization occurs along the stimulated
nerve
2. Nerve end touching the muscle fiber releases a
neurotransmitter ( ACH)3. Depolarization of the muscle cell membrane ( Action
Potential)
4. T-tubules open in SR and Ca++ is released
5. Increased intracellular Ca++
allows actin and myosin tointeract and the crossbridge cycle starts
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Relaxation
When electrical activity stops, the calcium is removed
and contraction stops
Muscle must relax between each contraction by actively
pumping Ca back to SR Ion pumps in the cell membrane actively repolarize the
muscle cell membranes
All processes necessary for relaxation are active ±
require energy
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Energy for Contraction
Each crossbridge requires ATP Each myosin strand has dozens of crossbridges
Each muscle fiber has hundreds of myosin strands
Muscle Contraction Requires Significant Energy
Basic Unit of Energy = ATP
ATP ADP & Pi ENERGY
( ATP + H2O ADP + Pi +H+ + Energy)
ATP= adenosine triphosphate; ADP=adenosine diphosphate;
Pi=Inorganic phosphate
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F or a horse to maintain exercise for more than a few
seconds, ATP stores in muscle must be replenished at
an appropriate rate.
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Energy for Contraction
Fuels
Intramuscular Triglycerides & Glycogen
Extracellular FFAs from Adipose Deposits and Glucose from the
Liver
Total amount of fuel stored in a 1,000 lb horse
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AEROBIC
ANAEROBIC
Two Main Pathways For Energy Metabolism
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Aerobic Metabolism
Occurs in Mitochondria
For low energy demands of slow speed exercise
Primary pathway for endurance exercise
Gallop speeds < 18sec/200m can usually be met byaerobic metabolism in fit horses
Training can increase capacity to generate energyaerobically
Enhanced oxygen delivery to muscle Increased mitochondrial density
Increased enzyme concentrations
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Aerobic Metabolism
Oxidative Phosphorylation Fats & CHO oxidized to produce ATP
Fats ± stored in depots around body
CHO ± stored as glycogen in liver & muscle
(glycogen metabolizes to glucose)
Aerobically metabolized approx 2x as fast as fat
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Aerobic Metabolism
Limitations
Primarily limited by availability of oxygen in working
muscles
Upper airway obstructions Cardiovascular system impairment
Hemoglobin concentration
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Anaerobic Metabolism
High intensity exercise of short duration (2-3 min in
horses)
At start of fast exercise, O2 delivery does not
immediately reach the level required to support aerobicmetabolism
Approx 30-45 seconds of exercise is required before maximal
rate of oxygen use is achieved
During this time, anaerobic metabolism supplies energy
Fast Exercise not totally anaerobic; makes up the deficit Horse galloping over 1200 m, aerobic metabolism provides
approximately 70% of energy
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Anaerobic Metabolism
Glycolysis = Degradation of muscle glycogento lactate
Results in increases in lactate, hydrogen ions
and Pi in the cells
Lactic acid accumulation and fatigue developas muscle pH falls
At pH < 6.4 glycolysis and contraction are
inhibited
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Different Muscles have Fibers with
Different PropertiesType I & Type IIA
High Oxidative Capacity
Store Triglycerides & Glycogen
Standing and posture: Slow contracting fibers that are well suppliedwith oxygen ± example stay apparatus
Type I aka ³Slow Twitch´ Fibers ³Red Fibers´
Type IIB
Low Aerobic Capacity
Store Glycogen
Athletic Movements: Muscles that generate rapid movement containfast fibers and can work for short periods without oxygen
Type II aka ³White´ Fibers, ³Fast Twitch´ Fibers
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Walking Primarily Type I Fibers
primarily aerobic energy, primary substrate is fat
Transition from Walk to Trot and Cancer Type IIA Fibers Recruited
Primarily aerobic energy, substrate is both fat and glycogen
Transition to Gallop Type IIB Fibers Recruited
Energy no longer purely aerobic,
Fiber Type Recruitment Based on Energy
Requirements
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Exercise
Concentric Exercise
Isometric ± constant length
Isotonic ± constant force
Or a mixture of the two
Eccentric Exercise
Lengthening contractions
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Effects of Exercise on Muscle
Lack of exercise leads to fiber atrophy
Gentle exercise maintains muscle mass & flexibility
Moderate long term activity increases fatigue resistance
High load exercise leads to muscle fiber hypertrophy
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Muscle Fatigue
Prolonged and/or strong contraction > Fatigue
Inability of contractile and metabolic processes to
continue supplying the same work output
Nerve sends electric stimulation, NMJ transmits, actionpotentials spread over muscle fibers
However contraction becomes progressively weaker due
to reduced ATP in the muscle fibers
Interruption of blood flow through a contracting muscle
leads to almost complete fatigue in less than a minute
due to loss of nutrient supply
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Muscle Fatigue
Endurance Horses
Most often due to glycogen depletion, as most work is
performed aerobically
Race Horses
Most often due to lactic acid accumulation
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Lactic Acid or Lactate
By product of anaerobic glycolysis
A potential cause of late onset muscle soreness 24 ± 48
hours after intense exercise
Sent from muscle to blood and removed via liver
Removal requires oxygen and is hastened by light work
during recovery
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Muscle Atrophy
Results anytime a muscle is not used or used only for
weak contractions
Denervated muscle begins immediate atrophy
Example: Sweeney Injury to Suprascapular N causing atrophy in supraspinatus &
infraspinatus
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Muscle Hypertrophy
Diameter of individual muscle fibers increase
Sarcoplasm increases
Fibers gain in nutrient and intermediary metabolic
substances ( ATP, creatine phosphate, glycogen,intracellular lipids, additional mitochondria)
Myofibrils may also increase in size
Hypertrophy increases both power of the muscle and the
nutrient mechanisms to maintain that power
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Conclusion
Muscle Microanatomy & Physiology
Dynamics of Work
Specific Muscle Fibers & Energy
Substrates
Together IMPACT> Exercise &
Its Effects on Muscle