MUSCULAR CONTROL

In this chapter, skeletal muscle contraction related to a stimulus- neglecting muscle metabolism is described. Muscle is an excitable tissue, meaning that it can be stimulated chemically, electrically, or mechanically to pro-duce a contraction. Calcium plays an important role as a cofactor to ATP, which is instrumental in the release of energy for muscular contraction.

5.1.1 Mechanics of Contraction (Sliding Filament Theory)

In Section 2.3, the basic structure of a muscle fiber and its composition are described (see Figure 2.5). Muscle contraction occurs by a sliding filament mechanism whereby the sarcomeres as the structural units of the myofi-brils shorten (the Z-lines come together, close to each other) by the action of the actin filaments sliding over the myosin filaments. A myosin filament head is large and looks like a golf ball. The force behind a muscle contrac-tion is the ratchet movement of the myosin heads toward the center of their sarcomere. In fact, the ratchet movement is the muscle contraction itself (Figure 5.1).

Two other proteins are part of the actin filaments, tropomyosin and troponin. During muscle contraction, Ca²⁺ and high-energy chemical compounds, such as ATP, ADP, and inorganic phosphate (P_i), have the leading role. ADP is produced when ATP is hydrolyzed (broken down)

and used as a substrate in reactions producing ATP. The transfer of the ATP, ADP, and Pi happens in the mitochondria. ATP binds to a myosin head and forms ADP and Pi. When ADP and Pi are released, the actin filament sliding motion occurs over the myosin. Below are the phases of muscle contraction:

1. ATP binds to a myosin head and forms ADP and P_i. The ADP and P_i remain attached to the myosin head.

Ca²⁺ discloses the binding sites on the actin filaments. Ca²⁺ binds to the troponin molecule causing tropomyosin to disclose its posi-tion on the actin filament for the attachment of the myosin head.

2. Cross bridges between myosin heads and actin filaments form.

3. ADP and P_i are released and the sliding movement of actin results.

The attachment of cross bridges between myosin and actin causes the release of ADP and P_i. The myosin head generates a sliding movement of the actin filaments toward the center of the sarcomere.

Z discs are pulled together, contracting the muscle fiber to produce a power stroke.

4. The new ATP arrives at the myosin head, the cross bridge between the actin and myosin breaks, returning the myosin head to its former unattached position. Then the process starts all over again.

Myosin filament

Titin I band ^{H zone}

A band Sarcomere Z disc Actin

filament M line

FIGURE 5.1 Structure of a myofibril and its function (sliding filament theory).

See also Section 2.3.

5.1.2 Action Potential

The quick change from the resting membrane potential (RMP) in electri-cal activity across a muscle cell or nerve cell membrane that generates an electrical current is called action potential. Any muscle or nerve cell has a potential electrical charge or resting potential, which is approximately

−70 millivolts (mV). This state of a neuron is called the polarized state.

Section 5.2 will describe in more detail the different states of polarity.

The action potential travels along the neuron until the end of the neuron.

A gap called a synaptic cleft or synapse separates the neuron from a muscle cell or another neuron. If a neuron stimulates the muscle, then the neuron is called the motor neuron or motoneuron and its synapse is called a neuro-muscular junction.

5.1.3 Excitation of Muscle Contraction

Muscle contraction is stimulated through the following steps:

1. The action potential generates the release of acetylcholine (ACh) from the excited neuron. The ACh is a neurotransmitter, which dif-fuses across the synaptic cleft.

The action potential is generated throughout the T tubules, which are arranged in a transverse direction throughout the muscle and also travel along the sarcolemma.

2. As a result of the action potential, sarcoplasmic reticulum releases Ca²⁺. 3. Myosin cross bridges form. The calcium released binds to troponin

molecules on the actin helix, directing tropomyosin molecules to expose binding sites for myosin cross bridge formation (see Figure 5.2).

When ATP is available, muscle contraction begins.

Actin

(a) (b)

Troponin

(binding site for Ca²⁺) Tropomyosin Myosin head

FIGURE 5.2 (a) The structure of actin (thin myofibril). (b) Myosin (thick myofibril) filaments. Some actin proteins have the binding sites for myosin (head) proteins.

5.1.4 Contributory Factors in Muscle Contraction

1. Frequency of excitation. Excitation can be singular or applied repeat-edly to a muscle fiber; in this case, the calcium may accumulate, espe-cially during long and repeated excitations. The muscle will have a stronger contraction. Depending upon the frequency of excitations, there are different kinds of effects.

• Staircase effect or treppe is produced if each successive excitation occurs after the relaxation period of the previous excitation. Each successive muscle contraction must be greater than the previous one. Some other factors can contribute to the treppe effect, such as changes in pH or temperature increase and others. Generally, this stage is the warm-up period of the athlete.

• Wave summation occurs when consecutive excitations are applied during the relaxation period of each preceding muscle contraction.

• Incomplete tetanus occurs when the frequency of the excitations increases. In this case, successive contractions appear to be a large muscular contraction.

• Complete tetanus occurs during a large muscular contraction.

2. Strength of excitation. More motor neurons excite more muscle fibers.

3. Length of muscle fiber contraction.

4. Type of contraction. Isotonic and isometric contraction.

5. Type of muscle fiber. Type I, Type IIA, and Type IIB.

6. Muscle tone.

7. Muscle fatigue.

5.2 NEUROLOGICAL CONTROL