Skeletal Muscle

I. Skeletal Muscle Anatomy

A. Skeletal muscle macroarchitecture

1. Sarcoplasm: muscle cell cytoplasm

2. Sarcolemma: muscle cell membrane

3. Endomysium: covers muscle cell

4. Fascicles: groups of fibers (cells)

5. Perimysium: covers fascicles

6. Epimysium: covers entire muscle

B. Muscle Cells components

1. Cell membrane = sarcolemma – ends of the sarcolemma fuse into the tendons

2. Cell cytoplasm = sarcoplasm – contains organelles, glycogen, fat, myoglobin etc.

3. T-tubles – extensions of the sarcolemma inside the cell – like tunnels (for signals, oxygen, nutrients) into the cell

4. SR – cytoplasmic reticulum – storage container for calcium

5. Myofibrils – the contractile elements, consist of sarcomeres in series

C. Skeletal muscle fiber microarchitecture

1. Myofibril: Longitudinal Axis

2. Sarcomere - functional unit of muscle

3. Skeletal muscle – striated muscle - striations caused by light/dark bands of different optical densities (note, cardiac muscle is also striated, smooth m is not)

4. Light = I band – actin, dark = A band – myosin, H-zone – no actin

5. Arrangement of actin & myosin

- Myofilaments

- Actin (“thin”) filament: composed of 3 protein complexes – actin, tropomyosin, troponin

- Myosin (“thick”) filament: myosin heavy chain (heads) and light chains (arms)

II. Sliding filament theory

A. Steps of actin-myosin interaction and contraction

1. Troponin binds Ca++

2. Tropomyosin moves, exposes binding site for myosin on the actin

3. Myosin heads bind actin, power stroke, ADP, Pi released, distance between Z lines is reduced

4. Power strokes are NOT synchronous - ~50% cross bridges at any given time

5. Ca++ reuptake and release from troponin

B. Series elastic elements – tendons

C. Excitation-Contraction Coupling

D. ATP & Muscle Contraction - Muscle contraction is absolutely dependent on ATP for 3 processes:

1. hydrolysis of ATP energizes the myosin head which begins the “power stroke” of the cross-bridge cycle

2. attachment of ATP to myosin facilitates the dissociation of the actomyosin complex

- allows for continued x-bridge cycling and further shortening

- each x-bridge cycle shortens the muscle 1% of its resting length

- no ATP = stiff muscles as in rigor mortis

3. Ca++ reuptake into the SR occurs through an ATP dependent pump

III. Muscle fiber types

1. Different types – I, IIa, IIb, characteristics of each type

2. Fiber type analysis

3. Fiber type differences between athletes

4. Effect of Resistance Training on Fiber Type

IV. Types of Contraction

A. Isometric (fixed-end)

1. External load = force generated

2. No change in fiber length

B. Concentric “miometric”

1. External load < force generated

2. Fiber shortens

C. Eccentric “pliometric”

1. External load > force generated

2. Fiber lengthens during contraction

V. Factors that affect Force of contraction

A. Speed of contraction

1. The maximum speed of muscle shortening (Vmax) can be measured by studying “twitch” characteristics of single muscle fibers in response to neural stimulation

2. Fast fibers have a faster Vmax than slow fibers due to:

- Quicker release of Ca++ from SR

- Higher ATPase activity (on myosin, and in SR)

B. Force Regulation in Muscle

1. The amount of force generated in a single muscle fiber is determined by the number of x-bridge formations

2. The amount of force exerted during muscle contraction of a group of muscles is dependent upon:

- number (cross sectional area) & types (I, IIa, IIb) of motor units recruited

- initial length of muscle fiber

- nature of the neural stimulation of motor units

3. Recruitment of additional motor units increases force

4. Recruitment of fast fibers increases force

C. Length-Tension Relationship

1. Optimum length for maximizing force = resting length

2. Related to optimum level of initial actin-myosin overlap

D. Force-Velocity, Power-Velocity Relationships

1. Force is maximized at the lowest shortening velocity (and velocity is highest at lowest force)

2. Fast fibers produce greater force and power for any given velocity

3. An optimum velocity exists to maximize power output

VI. Receptors in Muscle: Feedback to CNS

A. Feedback types

1. Chemical (i.e., O2, CO2, H+): chemoreceptors

2. Tension: Golgi Tendon Organs (GTO’s)

3. Muscle length: Muscle spindles

B. Muscle Spindle: Length Detectors

1. Functions as a length detector

2. Each spindle contains several thin muscle cells (intrafusal fibers) arranged in parallel with “normal” muscle cells (extrafusal fibers)

3. Two types of cells: a. nuclear bag – nuclei bunch in center of cell, b. nuclear chain – nuclei arranged in rows

4. Associated with sensory neurons (two types) that respond to passive and active stretch

5. Co-activated during contraction via gamma motor neuron stimulation

6. Muscles which require fine motor control contain many muscle spindles

7. When over-stretched, or with rapid stretch, stimulate reflex contraction (knee-jerk reflex)

C. GTO’s: Tension Detectors

1. Located in tendon

2. Monitor muscle tension via sensory neuron

3. Activation causes inhibition of alpha-motor neuron (via interneuron in CNS)

4. “Safety mechanism” against excessive force during contraction

VII. “Plasticity” of Skeletal Muscle

A. Adaptation to use and disuse – plasticity

1. Adaptations may include changes in muscle fiber size, mitochondrial size and number, type and quantity of biochemical machinery, with disuse – change in fiber number (?)

2. The types of adaptations which result are determined by the nature of the physical stimulus

3. Adaptations to chronic aerobic exercise or chronic electrical stimulation – fiber type shifts

B. Adaptation of muscle to disuse (NASA’s interest)

C. Aging and muscle

1. Loss of muscle mass (LBM) with age “sarcopenia”

2. Aging results in a reduction in innervation of skeletal muscle by large alpha motor neurons (innervate Type II fibers)

3. Selective loss of certain fiber types? Fiber type shifts with age?

4. Changes in rate of force development

5. “Trainability” of older muscle