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Chapter 10, Part 2 – Muscle
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Chapter 10!Muscle Tissue - Part 2!Pages 308 - 324!!
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SECTION 10-5 !Sarcomere shortening and muscle fiber stimulation produce tension!
Chapter 10, Part 2 – Muscle
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More active cross-bridges → more tension produced
1. Fiber length at time of stimulation!• Affects overlap between actin and myosin!
2. Frequency of stimulation!• Affects duration of high [Ca2+]!
3. Fiber diameter!• Affects amount of actin and myosin available!
Tension Production - MUSCLE FIBER!
All-or-none principle: !For a given “dose” of Ca2+, all sarcomeres within a muscle fiber contract together!
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Tension Production – WHOLE MUSCLE!
More tension produced by individual fibers and more fibers contracting → stronger whole muscle contraction
Factors:!1. Internal and external tension!• Series Elastic Component (stretch in CT)!
2. Recruitment!• Number of active motor units!
3. Muscle size!• Number of muscle fibers present!
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Tension Production in Muscle FIBER!
Fiber length affects overlap between actin and myosin!
• There is an optimal length for a fiber at which force generation is maximal.!
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Effect of Sarcomere Length on Tension!Figure 10-14!
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Effects of Stimulation Frequency!
1. Single stimulus!• Simple twitch!
2. Multiple stimuli!• Treppe!• Summation (wave summation)!• Incomplete tetanus!• Complete tetanus!
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Latent period• Ca2+ release from SR!• “Slack” taken out of system ! Called Series Elastic Component:! - Contractile elements! - Tendons in whole muscle!
Contraction period• Tension increases!
The Simple Twitch Figure 10-15!
Relaxation period• Tension decreases!• Passive process follows pumping of Ca2+ back into SR!• Relaxation is a passive process!
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Treppe Figure 10-16a!
Also called “warm up effect”!• Gradual increase in
strength of contraction with the same stimulus
Factors:!1. Increased Ca2+ available !• Not time to pump it all back into SR!
2. Muscle fiber warms up!• Enzymes more efficient at higher temp.!
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Repeated stimulation before relaxation phase has been completed → stronger contraction!• Wave summation: one twitch is added to
another!• Incomplete tetanus: muscle/cell doesn’t
relax completely!• Complete tetanus: muscle/cell doesn’t relax
at all. Relaxation phase is eliminated – maximum contraction strength
Summation!
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Summation Mechanism!
Stronger contractions (summation) probably due to:!• Prolonged presence of Ca2+!• Action potential (AP) duration vs. contraction
duration:!ü AP is short (1 - 2 msec)!ü Contraction is longer (to 100 msec)!ü So another AP can stimulate the
muscle before the contraction phase has ended!
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Effects of Repeated Stimulations Figure 10-16a,b!
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Effects of Repeated Stimulations Figure 10-16c,d!
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Tension Production - WHOLE MUSCLE!
Factors:!1. Internal and external tension!• Series elastic component (stretch in CT)!
2. Recruitment!• Number of active motor units
3. Muscle size!• Number of muscle fibers present!
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Internal tension!• Tension generated inside contracting
muscle!• Myosin pulling on actin in sarcomere!
External tension!• Tension generated on extracellular fibers!• Endo-, peri-, and epimysium form
tendons!• Tendons stretch
Series elastic component !
Internal and External Tension - Series Elastic Component!
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Internal and External Tension (not in text)!
SEC
Simple twitch TetanusSEC = Series Elastic Component = e.g. the rope
stretching before the car moves up the hill!
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Motor Units and Tension Production!
Motor units!• Motor unit = a motor neuron and all of the
muscle fibers that it innervates!!Recruitment!• Stimulating more motor units!• More motor units → more active muscle
fibers → stronger contraction!
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Motor Units in a Skeletal Muscle Figure 10-17!
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Muscle Tone!
At least some of the motor units of a muscle are active at any one time, even at rest.!• Which motor units are active varies!• Does not produce movement, but generates
muscle toneMuscle tone:!• Stabilizes bones and joints!• Maintains body position!• Allows more rapid activation of whole muscle
(don’t need to start the car, just “step on the gas and go”)!
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1. Isotonic: means “same tension”!• Whole muscle’s length changes!a. Concentric contraction!• Tension > load!• Muscle shortens!
b. Eccentric contraction!• Tension < load !• Muscle lengthens (stretches) while
contracting!2. Isometric contraction: means “same length”!• Muscle’s length does not change, but
individual fiber lengths do shorten!
Contraction Types!
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Isotonic Concentric Contraction Figure 10-18a!
Muscle capable of 4kg peak tension!Tension produced > load, muscle shortens!
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Isotonic Eccentric Contraction Figure 10-18b!
Muscle capable of 4 kg peak tension, but…!Support removed as contraction begins: !
Tension produced < load, muscle elongates!
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Isometric Contraction Figure 10-18c!
Muscle capable of 4 kg peak tension!Contraction begins, tension NOT greater than
load, muscle length stays same!
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Resistance and Speed of Contraction!
Contraction velocity is inversely proportional to resistance.!!High resistance (heavy weight) leads to slow contraction speed.!!Fairly obvious from everyday life!!!Each muscle has optimum combination of speed and load.!
Figure 10-19!
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SECTION 10-6 !ATP provides energy for muscle contraction!
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Energy-producing systems in muscle:!• Phosphagen system (ATP and CP reserves)!• Glycolysis (Glycogen-lactic acid system)!• Aerobic system!
Muscle Contraction Requires Lots of ATP!
?!
? : Heading says, “Utilization process.” But recall that these are reversible reactions.!
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Phosphagen System!
• Found only in muscle cells!• Involves creatine phosphate (CP) and ATP!• A FAST, SHORT-TERM method of ATP
generation!ü Involves only 1 enzyme (creatine
phosphokinase), not a long pathway!CP + ADP + H+ ↔ creatine + ATP !
• Total is enough for maximal burst of about 15 sec.!
Allows time for other systems to “kick in.”!
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Glycolysis!
Used after phosphagen system during burst activity!• Is first part of aerobic pathway, but…!• Does not require oxygen (anaerobic)!
Anaerobic metabolism leads to H+ buildup!• Decreases muscle cell pH!• Affects enzyme function!
Can provide maximal burst of energy for about 2 min.!
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Aerobic System!
Requires oxygen delivery to mitochondria!• Involves a multi-enzyme pathway (Chapter 25)!
Resting muscle!• Use fatty acids as substrate!
Active muscle!• Use pyruvate from glycolysis as substrate!
Glycogen → glucose → [GLYCOLYSIS]→ pyruvate!Pyruvate → [MITOCHONDRIA]→ aerobic ATP
generation!• Provides energy for long-term exercise!
Marathon run = almost all aerobic!
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Energy Use and Level of Muscular Activity!
Resting muscle!• Low ATP demand!• Lots of O2 available to mitochondria!
Surplus ATP → CP!Surplus glucose → glycogen!
• Use fatty acids from blood for energy production!
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Resting Muscle Figure 10-20a!
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Moderate Activity!
During what is defined as Moderate Activity:!• Increased demand for ATP!• Increased demand for O2, but O2 delivery still
matching O2 demand by mitochondria• Aerobic metabolism still active!
Muscle glycogen → glucose → pyruvate → ATP!- OR -!
Also use fatty acids (and amino acids)!• No surplus ATP so no new CP is produced!
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Moderate Activity Figure 10-20b!
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Peak Exercise!
O2 deliver cannot meet O2 demand• Mitochondrial ATP production very low (about
1/3 of total needed)!• ATP production is via glycolysis!
ü Decreased cellular pH helps limit exercise duration!
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Peak Activity Figure 10-20c!
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Muscle Fatigue (1 of 3)!
Normal function requires:!1. Energy reserves (e.g. glycogen) for ATP!2. Blood supply!• Deliver O2, nutrients!• Carry away wastes (CO2, H+, heat, etc.)!
Factors leading to muscle fatigue:!1. ↓ energy reserves (↓ substrate)!2. ↓ pH effects: !
a) Changes in enzyme activity!b) H+ displaces Ca2+ from troponin!c) H+ interferes with hemoglobin reoxygenation!
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Muscle Fatigue (2 of 3)!
3. Central fatigue (“I’m tired.”)!• pH effects on brain!• Pain effects on brain!
Recover faster when performing a “diverting” mental activity (Setchenov phenomenon)!
4. Other factors:!• Sarcolemma, SR damage !
(slower Ca2+ uptake + release)!• ↑↑ [ADP] - interferes with cross-bridge
formation!
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Muscle Fatigue (3 of 3)!
5. Neuromuscular junction fatigue??!• Probably not important. (Merton, 1954)!Experiment testing this: !• Work muscle to fatigue - can’t contract any
longer!• Stimulate nerve leading to muscle!• He observed an action potential on the
muscle, but no muscle contraction.i.e. muscle receiving stimulus at neuromuscular junction, but is not contracting !
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Recovery After Exercise!
Recovery after exercise!• Return muscle cell conditions to resting
levels!• Return oxygen consumption rate to resting
levels!Recovery mechanisms include:!• Lactic acid removal/recycling!• Excess postexercise oxygen consumption
(EPOC)!• Heat loss: e.g. sweating, vasodilation!
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Lactic Acid Removal/Recycling!
Fate of lactic acid depends upon severity of exercise!
1. Moderate exercise!• Glycogen stores and blood glucose not
severely depleted!• Lactate → pyruvate → mitochondria → energy
for recovery from exercise!• This is the usual fate of lactate!
2. Severe, prolonged exercise!• Glycogen and blood glucose are depleted!• Lactate to liver; converted to glucose → muscle
cells → glycogen (Cori cycle)!
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Excess Postexercise Oxygen Consumption!
Oxygen consumption does not return to resting levels immediately after exercise. Some reasons:!
1. ATP required to:!• Restore CP levels!• Lactate → glucose → glycogen!
2. Sweat glands active (using ATP)!3. Effects of exercise on mitochondria:!• Mitochondria less efficient at using O2 for ATP
production!• Ca2+ leaks into mitochondrion, must be pumped
out!
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EPOC (2)!
4. Myoglobin must be reoxygenated!5. Epinephrine causes leakage of Na+ into and K+
out of cells!• Must be pumped back out or in!
6. Increased body temperature → increased reaction rates → increased ATP consumption!
Others?!!
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SECTION 10-7 !Muscle fiber type and physical conditioning determine muscle performance capabilities!
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• Slow fibers (“dark meat”)!Also called: Type I, red, S (slow), slow-twitch,
SO (slow oxidative)!• Intermediate fibers
Also called: Type II-A, FR (fast resistant, fast-twitch oxidative)!
• Fast fibers (“white meat”)!Also called: Type II-B, white, FF (fast fatigue),
fast-twitch glycolytic
Types of Skeletal Muscle Fibers!
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Fast and Slow Fibers Figure 10-21!
Know the differences between these fiber types as shown on the next slide.!
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Skeletal Muscle Fiber Types (after Table 10-2)!Slow Oxidative Fast Oxidative/ Fast Glycolytic
GlycolyticStructural featuresFiber diameter Smallest Intermediate Largest
Myoglobin content Largest amount Small amount Smallest amount
Mitochondria Many Intermediate Few
Capillary density Many Intermediate Few
Color Red Red to pink WhiteFunctional FeaturesATP production Aerobic Aerobic/glycolytic Glycolytic
Substrates for ATP production Lipids, amino acids, carbohydrates (aerobic)
Primarily carbohydrates (anaerobic)
Carbohydrates (anaerobic)
ATP hydrolysis rate Slow Fast Fast
Contraction velocity Slow Fast Fast
Fatigue resistance High Intermediate Low
Glycogen content Low Intermediate High
Recruitment order First Second Third
Primary activities Posture, Walking, Rapid, short-marathon run sprinting duration movements
Weight lifting
*
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Percentages of Fast and Slow fibers are genetically determined. Training can cause:!• Fast fibers ↔ Intermediate fibers or…!• Slow fibers ↔ Intermediate fibers!
!Anaerobic enduranceLimited by:!• ATP/CP availability!• Glycogen availability!• Tolerance for acidosis (isozymes)!
Physical Conditioning (1 of 2)!
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Physical Conditioning (2 of 2)!
Aerobic enduranceLimited by:!• Oxygen delivery to mitochondria!
Cardiac output!Capillary density!
• Number of mitochondria!• Aerobic substrate availability!
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SECTION 10-8 !Cardiac Muscle Tissue!
This topic will be covered in chapter 20.!
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SECTION 10-9 !Smooth muscle tissue differs structurally and functionally from skeletal and cardiac muscle tissue!
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• No striations:!• No sarcomeres• Moderately developed sarcoplasmic
reticulum so no myofibrils !• No T-tubules (have caveoli = “dents” in
membrane)!Myosin !• Scattered within sarcoplasm!• Has more heads than in skeletal muscle!
Actin!• Attached to dense bodies
Smooth Muscle Structural Features (1 of 2)!
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Smooth Muscle Structural Features (2 of 2)!
Dense bodies – α-actinin (remember Z-lines?)!• Attached to actin!• Some anchored to cell membrane!• Some held in place by intermediate
filaments!• Some anchor one cell to another!• Analogous to Z-line in skeletal muscle!
Intermediate filaments!• Composed of protein, desmin and vimentin!• “Scaffolding” between dense bodies!
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Smooth Muscle Tissue Figure 10-23!
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Smooth Muscle Contraction (1 of 2)!
Contraction is slower, longer-lasting than in skeletal muscle
Stimulation → Ca2+ release from SR and entry from ECF!• 4 calcium ions bind calmodulin!• Calmodulin-Ca2+ activates myosin light chain
kinase!• Myosin light chain kinase activates
(phosphorylates) myosin!• Myosin pulls on actin!
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Smooth Muscle Contraction (2 of 2)!
Length-tension relationship demonstrates “plasticity”!• Stretch muscle: muscle adapts → can
contract again!• Range of lengths over which contraction can
occur is 4X that of skeletal muscle!Actin and myosin scattered, not organized
into sarcomeres. !Mechanism not completely understood
(next slide)!
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Types of Smooth Muscle!
Multi-unit smooth muscle!• Receives stimulus from nerves!• Precisely controlled!• e.g. iris, large arteries, arrector pili!
Single-unit (visceral) smooth muscle!• Contains pacesetter cells (like heart)!• Nervous stimulation not required!• Cells have gap junctions - contract in a
wave!• e.g. G.I. Tract walls, urinary bladder!
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Comparison of Skeletal and Smooth Muscle!Table 10-3!
Don’t worry about cardiac muscle for now.!
