The three types of muscle are skeletal, cardiac, and smooth. The contractile ability of muscle derives from interactions between actin and myosin filaments. Contraction depends on control by Ca2+ in the sarcoplasm. Tropomyosin and troponin are controlling elements in skeletal and cardiac muscle. Calmodulin is the controlling element in smooth muscle.
learning outcomes
You should be able to:
Predict changes in sarcomere structure and appearance as muscle contraction occurs.
Describe the molecular events underlying the sliding filament model of muscle contraction.
Explain how ATP is involved in muscle contraction.
Beginning with an action potential in a motor neuron, describe the sequence of events at the molecular level that leads to skeletal muscle contraction.
Justify the need for gap junctions in cardiac and smooth muscle but not in skeletal muscle.
In terms of the arrangement of actin and myosin filaments in the sarcomere, why do the H zone and I band get smaller when the skeletal muscle contracts, and why does the A band stay the same?
A sarcomere is bounded by the Z lines and consists of overlapping actin and myosin filaments. The actin filaments are anchored on the Z lines and do not extend all the way to the middle of the sarcomere. The myosin filaments are anchored on the M band at the center of the sarcomere but do not extend all the way to the Z lines. Thus there are regions where the actin and myosin filaments do not overlap (i.e., the I band and the H zone). When the muscle, hence the sarcomere, contracts, the myosin filaments move along the actin filaments toward the Z lines. As a result, the I band gets narrower. At the same time, the actin filaments move closer to the M band, so the H zone gets narrower.
What roles do the three subunits of troponin play in the control of skeletal muscle contraction?
One subunit of troponin anchors it to tropomyosin filaments. One subunit of troponin binds to the actin filament. One subunit binds Ca2+. When Ca2+ binds to the troponin subunit, it causes a conformational change in the troponin, resulting in the tropomyosin filament pulling away from the myosin-
Why does rigor mortis—
Rigor mortis is due to the loss of ATP that is required to break actin-
The insecticide Malathion destroys the enzyme acetylcholinesterase. Accidental exposure can cause extreme rigid muscle paralysis. Why?
By destroying acetylcholinesterase, Malathione prevents the breakdown of acetylcholine released at the motor end plates, and as a result there is continuous and extreme activation of the muscle cell motor endplates. Action potentials continue to be fired in the muscle cell membranes resulting in tonic release of Ca2+ into the sarcoplasm and sustained activation of actin/myosin cross bridge formation.
Why are gap junctions important to the function of cardiac and smooth muscle, but not skeletal muscle?
Gap junctions enable sheets of cardiac or smooth muscle to contract as a unit. That makes it possible for cardiac muscle cells to work together to pump blood or smooth muscle cells to exert a unified function such moving food through the gut. The individual control over skeletal muscle fibers enables fine control over complex movements.
Now that you understand how muscles generate force, let’s look at what determines the characteristics of a muscle, its performance, and how individual muscles can change their characteristics with regular use and conditioning.