Chapter Seven Flashcards
Structure, Function, & Location: Skeletal Muscle
Covers the skeleton, giving the body its shape. Attached to the skeleton by strong, springy tendons or are directly connected to rough patches of bone. Under voluntary control. Almost all body movements caused by skeletal muscle contraction. Generates heat as a by-product of muscle activity. Heat is vital for maintaining the set point of body temperature
Describe the structure, function and location of the Cardiac muscle
This type of muscle only exists in the heart. Cardiac muscle never gets tired. It works automatically and constantly without pausing to rest. Cardiac muscle contracts to squeeze blood out of the heart, and relaxes to fill the heart with blood.
Describe the structure, function and location of the Smooth muscle
Found in the walls of hollow organs like the intestines and stomach. Smooth muscles are under involuntary control. Muscular walls of the intestines contract to push food through your body. Muscles in the bladder wall contract to expel urine from your body. Smooth muscles in a woman’s uterus help to push babies out of the body during childbirth
Identify in a drawing and describe the location of the connective tissue sheaths within a skeletal muscle like the biceps brachia:
SEE IMAGE
i. endomysium
ii. perimysium
iii. epimysium
Identify the structures of a skeletal muscle fiber on a model:
Identify sarcolemma, sarcoplasmic reticulum, myofibril, tropomyosin, myosin, troponin, actin, t-tubles
Describe the arrangement of actin and myosin within a muscle cell and describe how they are organized to form sarcomeres
Actin and myosin are two important proteins in forming sarcomeres. The enzyme myosin
has a long, fibrous tail and a globular head, which binds to actin through ATP, which is the source of energy for muscle movement. Myosin then releases actin, as ATP goes to ADP plus a phosphate group. This process cocks the myosin protein to high energy shape. At this point, the phosphate group releases from myosin, causing the myosin to push on the actin. This process plays itself out over and over, intertwining within the sarcomeres. When the sarcomeres receive action potential from neurons, the myosin crawl towards the actin and the tension from the process creates a muscle contraction
NOTE: sarco=flesh, myo=muscle
Context: A muscle cell from biceps may contain 100,000 sarcomeres
Explain the microscopic evidence that was used to support the sliding filament theory of muscle contraction
Sir Andrew Huxley in 1954 begun to develop the sliding filament theory of muscle contractions, where thick and thin filaments within the sarcomere slide past one another, shortening the entire length of the sarcomere. He synthesized his findings, and the work of colleagues into a detailed description of muscle structure and how muscle contraction occurs and generates force that he published in 1957. In 1963, Huxley won the 1963 Nobel Prize in Physiology or Medicine
Briefly describe the role of the nervous system in muscle contraction
Muscle contraction initiated or “communicated” from somewhere in the central nervous
system, either as voluntary activity from the brain or as reflex activity from the spinal cord.
Explain the details of muscle contraction including details of the cross bridge cycle and why and where calcium and ATP are used
Calcium ions flow into the cytoplasm, which is where the actin and myosin filaments are. Calcium ions bind to troponin-tropomyosin molecules located in the grooves of the actin filaments. Normally, the rod-like tropomyosin molecule covers the sites on actin where myosin can form cross bridges. Upon binding calcium ions, troponin changes shape and slides tropomyosin out of the groove, exposing the actin-myosin binding sites. Myosin interacts with actin by cycling cross bridges. The muscle thereby creates force, and shortens. After the action potential has passed, the calcium gates close, and calcium pumps located on the sarcoplasmic reticulum remove calcium from the cytoplasm. As the calcium gets pumped back into the sarcoplasmic reticulum, calcium ions come off the troponin
Explain how the following chemicals and diseases interfere with neuromuscular communication: Botulinum Toxin
Botox blocks neuromuscular transmission by impairing the calcium influx that normally accompanies nerve depolarization.
Explain how the following chemicals and diseases interfere with neuromuscular communication: Organophosphate Pesticides
Excess acetylcholine (ACh) present at different nerves and receptors in the body
because acetylcholinesterase (how’s that for a fifty cent word) is blocked causes
organophosphate poisoning. Accumulation of ACh at motor nerves causes
overstimulation of nicotinic expression at the neuromuscular junction.
Explain how the following chemicals and diseases interfere with neuromuscular communication: Lou Gherig’s disease
Causes damage to the nerve cells controlling voluntary muscle movement (motor neurons). Over time, individuals with ALS will lose movement in muscles throughout the body, including the muscles used in breathing.
Explain how these diseases interfere with muscle structure and function: Myotubular Dystrophy
Myotubular Dystrophy is a rare disease that primarily affects infant boys. Myotubular dystrophy causes muscle weakness, problems breathing, and problems swallowing when infants are feeding.
Explain how these diseases interfere with muscle structure and function: Duchenne muscular dystrophy
Rapidly progressive form of muscular dystrophy that occurs primarily in boys. It is
caused by an alteration (mutation) in a gene, called the DMD gene that can be inherited in families in an X-linked recessive fashion. Induviduals with DMD have progressive loss of muscle function and weakness, which begins in the lower limbs.!
Explain how these diseases interfere with muscle structure and function: Myostatin and Sports doping
Scientists have developed antibodies to myostatin and other molecules that can boost
lean muscle mass in animals by as much as 60 percent. It’s not yet clear how well myostatin inhibitors will work in humans. Clinical studies of two myostatin inhibitors are now under way for muscular dystrophy and other muscle-wasting diseases. They also are potentially the next wave in performance enhancing drugs as a result of their ability to grow muscle at an alarming rate.