Skeletal Muscle Structure and Function

Overview of Muscle | Sarcomere Structure | Excitation-Contraction

Muscle Reflexes - Proprioceptors | Skeletal Muscle Fiber Types | Motor Unit Recruitment

Muscle Movements | Muscle Mechanics | Adaptations to Strength Training

Exercise-Induced Muscle Damage and Soreness

Overview of Muscle

Three types of muscles 

1. skeletal - striated
2. cardiac - striated
3. smooth - non-striated

All muscles require adenosine triphosphate (ATP) to produce movement thus, muscles are chemomechanical energy transducers. 

This slide is a cross-sectional slice of human skeletal muscle (X40) with shows muscle fibers surrounded by connective tissue.

This is a scanning electron myograph of human skeletal muscle (X20,000) showing horizontal rows of myofibrils. The Z-discs are the dark vertical lines in the middle of the wide, light-colored spaces. Pick out the myosin and actin filaments. The numerous small black dots are glycogen granules and there are a few triglycerides stores visible which are the large, round white areas lying between the myofibrils.

Sarcomere Structure

• each fiber is composed of myofibrils which is a series of repeating structural units called sarcomeres
• sarcomeres are composed of thick (myosin) and thin filaments 

Thick filament

• composed of numerous protein strands which are called myosin filaments
• each myosin filament is composed of a two twisted strands called the heavy chains and two other, but each different, pairs of twisted strands, called light chains. these light chains are found in the myosin heads
• myosin filament is flexible at the point of the myosin head, and the stacking of the myosin molecules leaves the myosin heads protruding from the filament at ~60°. this spacing maximizes chances for interaction with actin binding sites
• myosin ATPase is found in the myosin heads  

• another structural element, titin, as shown below, connects the ends of the myosin filaments to the Z-discs
• the M-region, centered in the middle of the myosin filaments and cross-links with other myosin, serves as structural support for the sarcomeres; a part of the M-region contains creatine phosphokinase (CPK or CK)

Thin filament

• actin exists as a polymer of repeating globular proteins called G-actin
• two actin filaments are twisted into a single stranded filament. these strands are anchored at one end to the Z-disk
• an ADP molecule on each G-actin molecule is thought to be the active or binding site on the actin filament
• lying in the groove formed by the actin filaments are a series of rod-shaped protein molecules called tropomyosin. each tropomyosin molecule is 6-7 G-actin molecules in length
• bound to the end of each tropomyosin is a third protein called troponin
• troponin consists as three small bound proteins molecules. one molecule is bound to the actin filament, one to the tropomyosin, and the third is available to bind with Ca²⁺

This represents a cross-sectional view of the myosin and actin filaments. The actin filaments (smaller dots) are positioned every 60º so that they are aligned with the myosin heads that protrude from the myosin filaments (larger dots). Thus, six actin filaments surround each myosin filament, moreover active sites from an actin filament are available to three different myosin filaments.

Sarcoplasmic reticulum (SR) (skeletal muscle only)

• serves as a storage depot for Ca²⁺
• SR is made up of the terminal cisternae and the longitudinal tubules
• in skeletal muscle, each sarcomere has two T-tubules which lie at junction of A- and I-bands
• abutting each side of a T-tubule (in skeletal muscle) is a terminal cisternae-collectively they are called a triad
• longitudinal tubules run parallel to the sarcomere and connect the terminal cisternae of each side
• as an AP passes down the T-tubule, it stimulates the terminal cisternae to release enough Ca²⁺ to saturate all the troponin in the sarcomere
• after an AP causes the release of Ca²⁺ into the sarcoplasm, a Ca²⁺ pump that is activated by cytoplasmic Ca²⁺ removes the Ca²⁺ back into the SR. in skeletal muscle, one calcium "pulse" lasts ~0.03 s

Excitation-Contraction

Much of what we currently know about muscle contraction was originally reported simultaneously by H.E. Huxley and A.F. Huxley (not related) in the 1950s and is referred to as Huxleys' sliding filament mechanism.

Muscle action potential

• resting membrane potential is -90 mV
• duration of the action potential is 1-5 ms (about 5X that of a large myelinated nerve)
• velocity of conduction is 3-5 m•s^-1
• action potential spreads to interior of fiber through the T-tubules (which are in direct communication with the extracellular fluid)

Cross-bridge cycling

• ATPase of the actomyosin complex is stimulated by the combination of Ca²⁺ and Mg²⁺, but without Ca²⁺, Mg²⁺ inhibits myosin ATPase
• [ATP] affects ATPase-a high sarcoplasmic [ATP] inhibits actin/myosin interaction while a low [ATP] will stimulate interaction
• contraction is initiated when Ca²⁺ binds with troponin
• each cycle shortens the sarcomere ~10 nm

1. In the resting state, the myosin ATPase has partially hydrolyzed ATP. The ADP and Pi do not immediately dissociate, however a complex is formed in which ADP and Pi remain attached to the myosin head along with the stored energy.
2. When a binding site on the actin filament becomes available, the myosin head binds to the active site and a cross-bridge is formed (called an actomyosin complex).
3. The ADP and Pi are released to complete the energy release. This causes the myosin head to return to a position of lower energy by a "ratchet"-like movement, and shortens the sarcomere.
4. The actomyosin complex is severed when ATP binds to the myosin head.

Entire cycle takes 50 ms, although the myosin head is attached only 2 ms. A single myosin head will produce 3-4 pN.

Muscle Reflexes - Proprioceptors

Muscle spindles

• specialized muscle fibers which monitor rate and changes in muscle length
• interspersed among skeletal muscle fibers
• rapid stretching of muscle spindles causes reflex stimulation causing agonist muscle fibers to contract and resist stretch (stretch reflex)
• functions to oppose sudden changes in muscle length

Golgi tendon organs

• sensory receptors located in muscle tendons that respond to tension
• when stimulated, Golgi tendon organs cause inhibition of agonist muscles and stimulation of antagonist muscles
• function as an inhibitory reflex for injury prevention

Skeletal Muscle Fiber Types

Muscle fibers are usually classified based on histochemical criteria.

• originally, muscle fiber characteristics were related to whether they appeared red (from the iron-containing compounds) or white
• also classified based on metabolic capacities that reflect the activities of the glycolytic or oxidative characteristics
• slow-twitch (ST, Type I, red)
• fast-twitch a (FTa, FOG, fast oxidative glycolytic, Type IIa, white)
• fast-twitch b (FTb, FG, fast glycolytic, Type IIb, white) different muscles have different ratios of fiber types
• innervating nerve appear to be primary determinant of fiber type
• see Table 2.1, p 35; Table 2.2, p 36; and Figure 2.11, p 37; Table 2.3, p 38
• another commonly used method is to stain for the ATPase
• each muscle is a mixture of 3 general fiber types
• different muscles have different ratios of fiber types

Differences between fiber types

• nerve conduction velocity
• diameter
• maximal tension
• maximal contractile speed
• oxidative (aerobic) capacity
• glycolytic (anaerobic) capacity
• fatigability

Motor Unit Recruitment

• at low intensities, ST are primary fibers recruited
• as intensity increases, FTa fibers are also recruited
• at high and maximal intensities, FTb are also recruited
• some evidence suggests that for explosive, maximal intensities, ST fibers are de-recruited

This EMG recording of the biceps muscle reflects a subject performing six arm curls. The first three curls were made using an increasing weight and the last four curls were performed with the same weight. The subject paused momentarily between lifting the weight (concentric movement) and returning back to the starting (eccentric movement) position. Notice the difference in EMG activity between the increasing weight, and the difference between the concentric and eccentric movement. Be able to explain these phenomena.

Muscle Movements

• isometric (static) contraction-muscle develops tension but does not change in length
• isotonic (dynamic) movement-muscle develops tension and either lengthens or shortens
• eccentric movement-muscle lengthens as it develops tension
• concentric movement-muscle shortens as it develops tension
• isokinetic movement--requires a special machine which varies the resistance across the range of motion so that muscle tension is equal through entire movement

Muscle Mechanics

Force development by a muscle is dependent upon:

• number of motor units recruited
• angle of pull
• length of muscle fiber
• velocity of muscle shortening

Length-tension (force) relationship

• when the sarcomere is stretched beyond its resting length, number of active sites within reach of myosin heads is decreased reducing tension development
• when the sarcomere is shortened beyond its resting length, actin strands begin to overlap which covers up available active sites which reduces tension development
• there is a passive stretch on the connective tissue at longer sarcomere lengths that resists further lengthening; this results in an added force to the tension development at longer sarcomere lengths
• a stretch reflex can be initiated as a result of pre-stretching the muscle (e.g. plyometrics); this increases the tension development
• the length-tension curve is higher for FT fibers than ST fibers

Force-velocity relationship (see Figure 2.15, p 41)

• there is an inverse relationship between force and velocity of shortening
• V_max is the maximum speed of shortening-occurs when the load is zero
• Po is the maximal force that a muscle can develop-occurs when the muscle is stationary (maximal isometric contraction)
• V_max is thought to reflect the maximal rate of ATP splitting
• force-velocity relationship for eccentric movement is a mirror image of concentric movement-greater velocity of shortening is achieved with greater force as speed of sarcomere shortening increases, the force decreases in exponential fashion (for concentric movements only)
• force-velocity curve is higher for FT fibers than ST fibers

Power-load relationship

• there is an optimal load (~40% of max) which allows for the greatest power development-any load less than or greater than this decreases power output

Summary of force, power, and velocity relationships

After integrating the force-velocity and load-power relationships, power and shortening velocity are maximized at a load of ~20% of maximal.

Adaptations to Strength Training

• training specificity determines adaptations
• strength is dependent upon neural, biomechanical, and physiological factors

Neural adaptations

• increased motor unit recruitment
• decreased neural inhibitions of motor units
• increased neural coordination

Muscular adaptations

• increased fiber size by hypertrophy (1°) and hyperplasia (2°)
• increased size in both fibers types although Type II fibers increase more
• (Olympic) power lifting training may shift some myosin isoforms toward Type FTb
• bodybuilding training may shift some myosin isoforms toward Type ST
• higher testosterone levels in males only partially explains larger muscle mass

Comparison of strength between sexes

• both sexes increase strength similarly during short-term training programs
• males have greater absolute strength than females because of greater muscle mass
• when compared on relative basis of kilogram of lean body mass, males are slightly stronger in upper-body strength but females are equal to males in lower-body strength

Suggested Reading:

SSE #53: Training for Improved Vertical Jump by W.J. Kraemer, 1994. This is one of Gatorade's Sports Science Exchange articles. http://www.gssiweb.com (you must apply for a free, on-line membership with Gatorade to access their publications).

Exercise-Induced Muscular Damage and Soreness

Eccentric movement, generating equal force to a concentric movement, utilizes fewer motor units as fibers develop greater tension while lengthening than shortening. Thus, the tension per fiber is greater during eccentric movements.

Unaccustomed exercise, primarily eccentric, causes a sequence of events that:

• diminishes performance,
• causes ultrastructural damage,
• initiates an inflammatory reaction, and
• causes delayed-onset muscular damage (DOMS).

Stages of Exercise-Induced Muscle Damage and Soreness

1. During exercise:

• mechanical factors (i.e. high stress) that result in:

-sarcolemma damage

-sarcoplasmic reticulum damage

-myofibrillar damage

• metabolic factors which cause damage that result from:

-free oxygen radical production

-excessive temperature

-decreased pH

2. 0-3 days postexercise:

• Ca²⁺ influx from the SR and outside the muscle cell initiate many of the inflammatory reactions
• production of phagocytic components (i.e. monocytes, neutrophils) to clear damaged and healthy tissue
• myofibrillar damage continues for 3-d postexercise
• cause(s) of DOMS may be:

-swelling

-release of stimulants

-hypersensitivity

-spasm

Time Frames for Peak Response to Injury

• performance - immediate postexercise
• soreness - 24-48-hr postexercise
• ultrastructural damage - 3-d postexercise

Effects on performance

• diminished strength/force for one to several days with peak at immediate postexercise

Ultrastructural damage

• damage occurs to myofibrils and connective tissue
• caused by mechanical stress from exercise and by metabolic factors from inflammatory response