(a) In a resting sarcomere, tropomyosin blocks binding sites on the actin filaments. (b) In the presence of calcium, troponin alters the position of tropomyosin to expose the binding sites.
It is important to remember that ATP is necessary for both muscle contraction and for muscle relaxation. The trigger for contraction is the increase in cytosolic calcium in response to stimulation by ACh from a motor neuron.
A few hours after death, the skeletal muscles partially contract, fixing the joints. This condition, called rigor mortis, may continue for seventy-two hours or more. It results from an increase in membrane permeability to calcium ions, which promotes cross-bridge attachment, and a decrease in availability of ATP in the muscle fibers, which prevents cross-bridge release from actin. Thus, the actin and myosin filaments of the muscle fibers remain linked until the muscles begin to decompose.
If acetylcholine receptors at the motor end plate are too few, or blocked, muscles cannot receive the signal to contract. This may occur as the result of a disease, such as myasthenia gravis, or a poison, such as nerve gas. A drug called pyridostigmine bromide is used to treat myasthenia gravis. The drug inhibits the enzyme (acetylcholinesterase) that normally breaks down acetylcholine, keeping the neurotransmitter around longer. It was given to veterans of the Persian Gulf War who complained of muscle aches in the months following their military service. Health officials reasoned that the drug's effect on myasthenia gravis might also help restore muscle function if the veterans' symptoms arose from exposure to nerve gas during the war. Acetylcholinesterase inhibitors are also used as insecticides. The buildup of acetylcholine causes an insect to twitch violently, then die.
U Describe a neuromuscular junction. Define motor unit.
List four proteins associated with myofibrils, and explain their structural and functional relationships.
Explain how the filaments of a myofibril interact during muscle contraction.
Explain how a motor nerve impulse can trigger a muscle contraction.
The energy used to power the interaction between actin and myosin filaments during muscle fiber contraction comes from ATP molecules. However, a muscle fiber has only enough ATP to contract briefly. Therefore, when a fiber is active, ATP must be regenerated.
The initial source of energy available to regenerate ATP from ADP and phosphate is creatine phosphate. Like ATP, creatine phosphate contains a high-energy phosphate bond, and it is actually four to six times more abundant in muscle fibers than ATP. Creatine phosphate, however, cannot directly supply energy to a cell's energy-utilizing reactions. Instead, it stores excess energy released from mitochondria. Thus, whenever sufficient ATP is present, an enzyme in the mitochondria (creatine phosphokinase) promotes the synthesis of creatine phosphate, which stores the excess energy in its phosphate bond (fig. 9.13).
As ATP is decomposed to ADP, the energy from creatine phosphate molecules is transferred to these ADP molecules, quickly converting them back into ATP. The amount of ATP and creatine phosphate in a skeletal muscle, however, is usually not sufficient to support maximal muscle activity for more than about ten seconds during an intense contraction. As a result, the muscle fibers in an active muscle soon depend upon cellular respiration of
IS III Major Events of Muscle Kflkll Contraction and Relaxation
Muscle Fiber Contraction
Muscle Fiber Relaxation
1. The distal end of a motor neuron releases acetylcholine.
Was this article helpful?