BIO 219: Muscle Physiology (Part 2)

1. number of fibers activated
2. increased muscle size = ↑ muscle fiber diameter
3. ↑ frequency of stimulation
4. length-tension relationship

rarely

motor neuron & all muscle fibers it supplies (4 to 1000's)
• when motor neuron fires (action potential) → all muscle fibers it innervates contract

an increase in # of active motor units
• ↑ motor unit recruitment = ↑ force of contraction

↑ force of contraction

Motor unit X = 5 fibers → less force
Motor unit Y = 7 fibers → more force

fine control, less force per motor unit

course control, greater force per unit area

small

large

• the more tension it can develop
• Resistance exercise increases muscle force by causing muscle cells to hypertrophy (↑ size)

In general: an increase in muscle (organ) size is due to an increase in the diameter of the muscle fibers (cells) → rather than an increase in the number of muscle fibers

single
∙ a single contraction or twitch lasts ~ 7-100 msec

many repeated stimuli

graph of twitch tension development

Latent period, Contraction phase, and Relaxation phase

before contraction
• AP moves across sarcolemma causing Ca²+ release

Ca²+ binds to troponin → tension builds to peak

Ca²+ levels fall → active sites covered; tension falls to resting levels

More rapidly delivered stimuli result in wave summation or incomplete tetanus

If stimuli are quick enough → complete tetanus results

one muscle twitch

Muscle fiber contracts → then releases

• Increasing tension or summation of twitches
• Repeated stimulations before the end of relaxation phase
• Ca²+ remains in sarcoplasm
• Ap frequency exceed time of a single muscle twitch cycle

• Twitches reach plateau (of tension)
• If rapid stimulation continues and muscle fibers is not allowed to relax, twitches will reach a maximum level of tension

• If stimulation frequency is high enough, muscle fiber never beings to relax, and is in continuous contraction

generate maximum force

ideal-tension relationship
• muscle is slightly stretched
• thin and thick filaments overlap optimally

sarcomeres have an optimal resting length for developing maximum force
• number of cross bridges formed → depends on overlap of filaments
∙ more crossbridges = more tension (more people pulling in tug of war)

• however → too much or too little reduces efficiency

sarcomeres compressed; Z lines contact thick filaments; thin filaments overlap/interfere with one another

filaments do not overlap; myosin cannot bind to actin

"on" (producing tension); "off" (relaxed)

can't vary # of contracting sarcomeres within 1 muscle fiber

1) fiber's resting length (length-tension relationship)
2) frequency of stimulation

1) tension produced by stimulated muscle fibers
2) total number of muscle fibers stimulated (motor unit recruitment)

some motor units are always active within a skeletal muscle (muscles appear firm and defined)

Muscle Tone - normal tension & firmness of muscle at rest

Muscle units actively maintain body position, without motion

Asynchronous (motor units rotate) to avoid fatigue

varying # of active motor units
• during sustained contracted → motor units are activated on rotating basis
∙ some rest & recover while others actively contract

1) elastic forces
2) opposing muscle contraction
3) gravity

energy "spent" in contraction stretching tendons is recovered as they recoil or rebound to original length

reverse direction of original motion; antagonist skeletal muscle pairs

can take the place of opposing muscle contraction to return a muscle to its resting state

• ATP is only energy source used directly for contractile activity
• Muscles have limited ATP storage (enough for ~ 4-6 seconds of activity)
• ATP is regenerated within milliseconds by one or more of the following:
1) direct phosphorylation of ADP by creatine phosphate (CP)
2) anaerobic respiration (glycolysis)
3) aerobic respiration

Energy Source: CP
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provision: 15 seconds

Energy Source: glucose
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provision: 30-60 seconds

Energy Source: glucose; pyruvic acid; free fatty acids from adipose tissue; amino acids from protein catabolism
Oxygen use: Required
Products: 38 ATP per glucose, CO₂, H₂O
Duration of energy provision: Hours

• ~ 4-6 seconds of vigorous exercise → creatine phosphate (CP) is primary source of ATP
∙ creatine kinase → catalyzes reaction
• Stored ATP + CP provide maximum muscle power for ~ 16 seconds (100m dash)
• Reaction is reversible → CP is replenished after exercise

6 seconds: ATP stored in muscles is used first
10 seconds: ATP is formed from creatine phosphate and ADP.
30-40 seconds to End of exercise: Glycogen stored in muscles is broken down to glucose, which is oxidized to generate ATP.

Hours: ATP is generated by breakdown of several nutrient energy fuels by aerobic pathway. This pathway uses oxygen released from myoglobin or delivered in the blood by hemoglobin. When it ends, the oxygen deficit is paid back.

more ATP is made via:
• breakdown (catabolism) of glucose
∙ glucose from blood or glycogen stored in muscle

initial phase of glucose breakdown

broken down into 2 pyretic acid
• O₂ not used
• 2 ATP produced

• bulging muscles compress BV = ↓ blood flow & O₂ delivery
• pyretic acid converted into lactic acid (= anaerobic respiration)

diffuses into blood
• converted into pyretic acid by liver or recycled for energy

• produces less ATP than aerobic
∙ but produces ATP 2 ½ times faster
• therefore used for short periods of strenuous exercise

ATP comes from aerobic respiration
• occurs in mitochondria
• requires oxygen

Glucose + O₂ → CO₂ + H₂O + ATP

• First 30 minutes - energy comes from:
∙ muscle glycogen, plasma glucose, free fatty acids
• After ~ 30 minutes
∙ fatty acids are a major energy source

~ 32 ATP (vs. anaerobic respiration = 2 ATP)

muscle is physiologically unable to contract

• Ionic imbalance (K+, Pi, Ca²+) interfere with E-C coupling
• SR damage - interferes with Ca²+ regulation & release

possibly locally occurs (writer's cramp)

long been assumed to cause fatigue
• likely more related to "psychological fatigue" (muscle can still "go", but we feel too tired)
• lactic acid = ↑ [H+] ICF causes muscle ache (alters contractile proteins)
• but likely not cause of "physiological fatigue"

Time required after exertion for muscles to return to normal
• Oxygen becomes available
• Mitochondrial activity resumes
• The Cori Cycle - removal and recycling of lactic acid by the liver
• Liver converts lactic acid to pyretic acid
• Glucose is released to recharge muscle glycogen reserves

Vigorous exercise causes dramatic changes in muscle chemistry

• oxygen reserves must be replenished
• lactic acid must be converted to pyretic acid
• glycogen stores must be replaced
• ATP and CP reserves must be re-synthesized

extra amount of O₂ needed for above restorative processes resulting in heavy breathing

1) speed of contraction - speed of shortening (how fast myosin ATPases split ATP + electrical activity of motor neurons)
• slow fibers
• fast fibers
2) major pathway of ATP formation
• oxidative fibers - rely on aerobic pathway
• glycolytic fibers - rely on anaerobic glycolysis

rely on aerobic pathway

rely on anaerobic glycolysis

1. Slow oxidative (SO)
2. Fast oxidative (FO)
3. Fast glycolytic (FG)

("red muscle") - slow to contract, flow to fatigue
• small diameter
• many mitochondria (aerobic respiration)
• high oxygen supply
• contain large quantities of myoglobin (red pigment, binds oxygen)

structurally related to hemoglobin; reversibly binds O₂ acts as a storage reserve of O₂

(intermediate)
• mid-sized, mid-speed
• low myoglobin
• more capillaries than fast fiber (aerobic), slower to fatigue

("white muscle") - contracts quickly
• large diameter (densely packed myofibrils)
• large glycogen reserves
• few mitochondria (mostly anaerobic)
• strong/high powered contractions, fatigue quickly

• Muscle capillaries
• Number of mitochondria
• Myoglobin synthesis

Results in greater endurance, strength, and resistance to fatigue
-May convert fast glycolytic fibers into fast oxidative fibers

• Muscle hypertrophy (due to increase in muscle fiber size)
• Increased mitochondria, myofilaments, glycogen stores, and CT

• Lacks straitions and sarcomeres (unlike skeletal & cardiac tissue)
∙ thick & thin filaments arranged obliquely
• contraction occurs by cross bridge formation between thick & thin filaments
∙ activated by graded potential or action potential

1. Smooth muscle cell depolarizes
2. Ca²+ enters cell from ECF via V-G Ca²+ channels &/or sarcoplasmic reticulum (via ryanodine receptor Ca²+ channels)
3. Ca²+ binds to calmodulin (Ca-calmodulin)
4. Ca-calmodulin activates myosin light chain kinase
5. Myosin light chain kinase is phosphorylated
6. Crossbridge cycling/contraction
7. Myosin light chain kinase dephosphorylated → relaxation