Muscle Flashcards
What is the difference between red and white skeletal muscle fibres?
White skeletal muscle has less mitochondria and is poorly vascularised. It is specialised for faster and stronger contraction. It is found in fingers and extra ocular muscles.
What is myoglobin?
Red protein containing haem that is structurally similar to harm but takes oxygen when pH is lowered, from haemoglobin.
How does muscle hypertrophy make it more efficient at performing work?
More contractile proteins: hence, increase in fibre diameter
Metabolic changes: increased - enzyme activity for glycolysis, mitochondria, stored glycogen, blood flow
How are troponin assays used in clinical practice?
Troponin (esp. I & T forms) used as a marker for cardiac ischaemia. The smallest changes in troponin levels in the blood are indicative of cardiac muscle damage. Must measure within 20 minutes of cardiac ischaemic damage.
However quantity of troponin is not necessarily proportional to the degree of damage.
Used by emergency units as the assay of choice, superseding muscle enzyme assays.
What is creatine kinase?
CK used to be measured to diagnose heart attacks (MIs), enzyme increase being largely proportional to infarct size, but has been largely superseded by troponin assay.
CK is an enzyme that is also released into the blood by damaged skeletal muscle and brain.
A rise in plasma CK can result from: • intramuscular injection, • vigorous physical exercise, • a fall (especially in the elderly), • rhabdomyolysis (severe muscle breakdown), • muscular dystrophy, and • acute kidney injury.
What is the sliding filament theory of muscle contraction?
1) Rigor Conformation
2) Uncoupling when ATP binds myosin head
3) ATP hydrolysis causing myosin head to advance shortly and bind weakly
4) Weak binding until organic phosphate released and power stroke occurs. This returns myosin to its former position
5) ATP binds myosin head again and causes uncoupling
6) Myosin head binds tightly again, and cycle repeats.
Movement as different myosin heads bind at different times.
What is the role of calcium in sliding filament theory?
Calcium binding to Tnc causes conformational change making tropomyosin move away from actin binding site. Displacement allows myosin heads to bind actin.
What is excitation-contraction coupling?
- Initiation: nerve impulse along motor neuron
axon arrives at neuromuscular junction. - Impulse prompts release of acetylcholine
(Ach) into synaptic cleft causing local depolarization of sarcolemma. - Voltage-gated Na+ channels open; Na+
enters cell. - General depolarization spreads over
sarcolemma and into T tubules. - Voltage sensor proteins of T tubule
membrane change their conformation. - Gated Ca2+ -release channels of adjacent
terminal cisternae are activated by 5. - Ca2+ is rapidly released from the terminal
cisternae into the sarcoplasm. - Ca2+ binds to the TnC subunit of troponin.
- The contraction cycle is initiated and Ca2+
is returned to the terminal cisternae of sarcoplasmic reticulum.
What are natriuretic peptides?
Natriuretic peptides are peptide hormones that are synthesized by the heart, brain and other organs. The release of these peptides by the heart is stimulated by atrial and ventricular distension, usually in response to heart failure.
The main physiological actions of natriuretic peptides is to reduce arterial pressure by decreasing blood volume and systemic vascular resistance. Normal hearts secrete extremely small amounts of ANP, but elevated levels are found in patients with left ventricular (LV) hypertrophy and mitral valve disease.
Natriuretic peptides serve as a counter-regulatory system for the renin-angiotensin-aldosterone system
What is ANP?
Atrial natriuretic peptide (ANP) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension (amongst other stimulations). Therefore, elevated levels of ANP are found during hypervolemic states (elevated blood volume), which occur in congestive heart failure (CHF).
What is BNP?
A second natriuretic peptide (brain-type natriuretic peptide; BNP) is a 32-amino acid peptide that is synthesized largely by the ventricles (as well as in the brain where it was first identified).
BNP is released by the same mechanisms that release ANP, and it has similar physiological actions. Proteolysis of pro-BNP (108 amino acids) results in BNP (32 amino acids) and the N-terminal piece of pro-BNP (NT-pro-BNP; 76 amino acids).
Both BNP and NT-pro-BNP are sensitive, diagnostic markers for heart failure in patients (for instance, of increased LV filling pressures and dysfunction).
A rapid 15 minute immunoassay is possible.
Describe skeletal muscle repair
Skeletal muscle cells cannot divide but the tissue can regenerate by mitotic activity of satellite cells, so that hyperplasia follows muscle injury. Satellite cells can also fuse with existing muscle cells to increase mass (skeletal muscle hypertrophy).
Describe cardiac muscle repair
Cardiac muscle is incapable of regeneration. Following damage, fibroblasts invade, divide, and lay down scar tissue.
Describe smooth muscle repair
Smooth muscle cells retain their mitotic activity and can form new smooth muscle cells. This ability is particularly evident in the pregnant uterus where the muscle wall becomes thicker by hypertrophy (swelling) and by hyperplasia (mitosis) of individual cells.
