Flashcards in Muscle Tissue Histo Deck (47)
Cytoplasm = Sarcoplasm
Smooth Endoplasmic Reticulum = Sarcoplasmic Reticulum
Plasma Membrane or Plasmalemma
Muscle Fiber or Myofiber
Special Characteristics of Muscle Tissue
Excitability (or Irritability)
Functions of Muscle Tissue:
Generating Heat (i.e. Thermogenesis)
Strong, quick contractions
Large, elongated, cylindrical, syncytial (multinucleated) cells
Peripheral, oval nuclei
Strong, quick contractions
Centrally located nucleus
Elongated and branched cells joined by intercalated discs
Weak, slow contractions
Uninucleated, fusiform cells
Centrally located nucleus
Type I Skeletal
Slow, Red Oxidative Fibers
Many mitochondria and lots of myoglobin (dark red color)
Derive energy primarily from aerobic oxidative phosphorylation of fatty acids
Adapted for slow, continuous contractions over long periods
Fast, Intermediate Oxidative-Glycolytic Fibers
Many mitochondria, and lots of myoglobin and glycogen (intermediate)
Utilize both oxidative metabolism and anaerobic glycolysis to produce energy
Adapted for rapid contractions and short bursts of activity
Fast, White Glycolytic Fibers
Fewer mitochondria and myoglobin, but LOTS of glycogen (pale color)
Derive energy primarily via anaerobic glycolysis
Adapted for rapid contractions, but fatigue quickly
In the middle.
all of myosin
1/2 of I band X2, all of A band.
Neuromuscular Junction (Motor End Plate)
A neuromuscular junction (motor end plate) is a chemical synapse between a motor (efferent) neuron and a skeletal muscle fiber (cell).
A motor unit is defined as the motor (efferent) neuron and all the muscle fibers (cells) it innervates.
A skeletal muscle (i.e. the organ) contains
Skeletal Muscle Tissue
Vessels (arteries, capillaries, veins, lymph vessels)
Connective tissue sheaths associated with skeletal muscle (i.e. the organ):
FA = fascia adherens
links actin (thin) filaments
D = desmosome
links intermediate filaments
N = gap junction
Muscle develops from
Ability of tissue to be stretched or extended - passive process
Requires presence of ATP. refers to the capacity of muscle to contract or shorten forcefully
is the ability of your muscles to extend in an activity and resume their contracted position. Optimize strong, safe, graceful movement by stretching to increase the elasticity of your muscles.
Cells 10 to 100 microm in diameter. In terms of length, they could be a few mm long to 1+ m in length (sartorius).
Cardiac muscle (this muscle only has 1 nucleus- found centrally). Where one cell connects to another. Specialized junctions help cells communicate and hold them together.
Cardiac muscle cells
15 microm in diameter, 85 to 100 microm in length.
Nuclei in the center - fusiform (wide in center, narrow at end). Cells are 20microm in length in blood vessels, can be upwards of 500 microm in a pregnant uterus.
If you fix smooth msucle in contracted state, the way that actin/myosin sets up causes it to twist – twisting the nucleus with it.
Sarcomeres - build together to form myofibers.
1 microm in length, 8 nm in width. 1 end attaches into Z disc, while other end extends into A band.
wall/edge of sarcomere.
Sliding filament hypothesis
Why contraction with shortening causes changes in sarcomere. Muscle contraction w/shortening occurs because rod-like myosin has globular heads. These have actin binding sites, and grab them to walk along them. This produces tension and potential shortening.
A band stays the same length - I band shrinks and disappears with full contraction. H zone goes away as well.
each myosin interacts with
6 actin filaments. This is hexagonal in shape.
central thick filament that is made up of myosin protein. Has tail of interwoven peptide chains, with two globular heads. Heads have binding sites for ATP and Actin, and ATPase activity.
G actin - polymerize to form f-actin (fibrous actin). What you see is that each thin filament has 2 f-actin chains. Each g-actin subunit has a myosin binding site.
Has 3 subunits - found at regular intervals along each tropomyosin. TnT, TnC, TnI subunits. TnI inhibits, TnC where you have calcium being able to bind. TnT makes sure that troponin is stuck to tropomyosin.
Calcium ions are
the final trigger for contraction. It signals for contraction, nerve signals this, T-tubules (extensions of sarcoplasmic reticulum in the cell) - transverse tubules - extensions of PM into cells, these fingerlike extensions in skeletal muscle come in twice at each sarcomere- at A/I band junctions. On either side of T-tubules, you have enlargements of Smooth ER called terminal* cisternae. Creates a triad- T-tubule, 2 terminal cisternae. When cell gets signal, action potential goes along membrane, down t-tubules, terminal cisternae, releases calcium.
**while this is happening, cell is "pulling" calcium back in**
Muscle nerve NT. Exocytosis releases these into cleft between axon terminal and motor neuron. Bind ligand gated channels, cause difference in voltage that causes action potential to begin.
blocks myosin binding. When calcium comes in binds to TnC, it moves tropomyosin away.
Myosin has been waiting for Ca to show up. Once actin and myosin bind, myosin goes from high energy to low energy state. Creates tension, potentially movement. When ATP binds to myosin head, myosin lets go after ATP is hydrolyzed putting myosin back into the high energy state.
Calcium floods cytoplasm - one of the first things that happens - comes from outside of cell, or from sarcoplasmic reticulum breaking down a bit.
Cardiac muscle- Diads
Diad (SR) at each Z disc - not as elaborate as in skeletal musle.
The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single T-tubule paired with a terminal cisterna of the sarcoplasmic reticulum.