Read the section titled “Overview of Muscle Tissues” (pp. 280-281).

• This will be the only significant mention of cardiac muscle in A&P1; it’s covered in detail in A&P2.
• Pay attention to the muscle functions and functional characteristics.

Read the section on gross anatomy of skeletal muscle (pp. 281-284).

• The three connective sheaths that surround parts of the muscle are important. They come up on both lecture and lab exams.
• Make sure you know everything in Marieb Fig. 9.2.
• See Art-Labeling Activity for Marieb Fig. 9.2.
• See animation – Muscle Layers.
  • Note: some detail in this animation is addressed in the next section of the text.

Read the section on microscopic anatomy of skeletal muscle tissue (pp. 284-287).

• Terms that are important to know: sarcolemma; sarcoplasm; myofibrils; A bands; I bands; sarcomere; Z disk; thin and thick filaments; myosin; actin; sarcoplasmic reticulum; terminal cisternae.
• Terms that will mean more to you later: cross bridges; troponin; tropomyosin.
• Terms to ignore: H zone; M line; nebulin; elastic filaments; F and G actin; titin; triads.
  • The figures in this section are important, but Martini Fig. 10-3 is (in my opinion) a better figure than Marieb Fig. 9.5.
• The section on troponin and tropomyosin (p. 287) gets a little off-topic for my taste.
  • For now, just know that these two proteins are associated with actin and they control how actin functions.
  • You’ll see how they do this in a little bit.
• Don’t worry about the term triad (in my opinion, unnecessary vocabulary word).
  • You can also skip the paragraph on triad relationships (p. 287).
• See this website that illustrates a schematic of skeletal muscle.
• See InterActive Physiology module – Anatomy Review: Skeletal Muscle Tissue.
• See Art-Labeling Activities for Marieb Fig. 9.3a-b and Fig. 9.3c-d.
• See A&P Place Activity – Microscopic Anatomy of a Skeletal Muscle Fiber.
• See video clips and animations (I recommend you watch them in the order below):
  • Anatomy of a Skeletal Muscle Fiber
  • Sarcomeres
  • Muscle proteins
  • Myosin
  • Troponin

Read the paragraph on the sliding filament model of contraction (pp. 287-288).

• You’ll see how this sliding is accomplished later on in this chapter.
• Personally, I think the cartoon pictures in Marieb Fig. 9.6 are more helpful than the text. Look at the figure and notice how the thin and thick filaments slide past each other, shortening the sarcomere.
• See InterActive Physiology module – Sliding Filament Theory
• See animation – Sliding Filament Model of Contraction.
  • Note: this animation has some added detail that we'll get to in a week or so.

Read the section titled Physiology of a Skeletal Muscle Fiber (pp. 288-289).

• Pay special attention to Marieb Fig. 9.7 (especially Fig. 9.7a and 9.7b).
  • Make sure you understand the following items in the figure: motor neuron; axon (axonal) terminal; synaptic cleft; synaptic vesicles filled with ACh (green aspirins); ACh receptors (purple cylinders).
  • Just make sure you understand where these items are in relation to one another.
  • I suggest hand-drawing the figure yourself. That’s what I do in class and it helps.
  • Don’t worry about what the Na⁺ and K⁺ are doing. Again, that’s coming up below.
• Stop reading when you get to the “Homeostatic Imbalance” heading on p. 289.

The next section of this topic deals with muscle contraction. Why can a muscle fiber contract while an epithelial cell or a chondrocyte cannot?

Muscle tissue responds to neurotransmitters that are released from axon terminals. When the neurotransmitter binds to its receptor on the sarcolemma, it triggers an electrical signal called an action potential that travels along the surface of the muscle fiber and down into the T tubules. This electrical signal causes Ca⁺⁺ to be released from the terminal cisternae. This Ca⁺⁺ is critical for the myosin and actin to interact with each other, causing a muscle contraction.

Action potentials are also used by neurons (nerve cells) to communicate with each other; therefore, this concept will carry us through the remainder of the semester. Most textbooks (ours included) delay talking about action potentials until the chapters on the nervous system. I prefer to get them out of the way in muscle, so they’ll be somewhat familiar to you when we get to the nervous system.

We’ll address this topic in three big steps:

• First, you’ll learn about the concept of membrane potential.
  • The membranes of all of our cells are electrically polar. The inside surface is slightly negative compared to the outside surface. This electrical difference is called the cell’s membrane potential.
• Next, you’ll learn how the binding of a neurotransmitter (ACh, in this case) to its receptor causes a rapid change in the muscle fiber’s membrane potential.
  • This change in membrane potential will sweep across the muscle fiber. This “wave” is the action potential.
• Lastly, you’ll learn how myosin and actin interact, causing the muscle fiber to contract.
  • Muscle fiber contraction will depend on both Ca⁺⁺ and ATP.

In order to understand what’s about to happen, you need a good foundation in how molecules cross the plasma membrane.

• Anytime you see reference to a channel:
  • facilitated diffusion will take place
  • facilitated diffusion = movement of ions or molecules from areas of high concentration to areas of low concentration (along or down their concentration gradient)
  • this movement occurs through the channel
  • this movement does not cost chemical energy
• Anytime you see reference to a pump:
  • active transport will take place
  • active transport = movement of ions or molecules from areas of low concentration to areas of high concentration (against their concentration gradient)
  • this movement is actively created by the pump
  • this movement requires energy in the form of ATP
• If any of this is new to you, you need to spend some significant time studying your Biological Principles notes until you know this cold.
• There are lots of animations and video clips that should help with this information.
  • I’ve cobbled these together from various places over the years, so a few may repeat or overlap some material.
  • Also, many of the better clips are actually designed for use with the nervous system, so you may hear reference to things like “neurons” or “threshold.” Don’t worry about that; you’ll get to that later in the nervous system.

Read the section called “Generating and Maintaining a Resting Membrane Potential” (pp. 81-83 – yes, way back there).

• The book does a fairly nice job of explaining an abstract concept.
• There are two items that are important about membrane potential:
  1. Ions always cross the membrane through transport proteins (either channels or pumps). Ions are charged, so they can’t tolerate the neutral (uncharged) environment inside the phospholipid bilayer. Ions always move through channels (high to low) or pumps (low to high).
  2. The positive and negative charges that make up the membrane potential only exist right at the membrane. The entire cytoplasm isn’t negative, just the tiny layer of cytoplasm facing the membrane.
• See animation – Transmembrane Potentials.
• See InterActive Physiology module – Nervous I: Membrane Potential.

Read the section called “Generation of an Action Potential Across the Sarcolemma” (pp. 290-291).

• This is a lot of material in those three “half-columns” of text, and everything’s important.
• The graph in Marieb Fig. 9.9 is probably in the Top 5 Most Important Figures in this course.
  • Make sure you understand what’s happening in that figure COLD.
  • You’ll be asked to interpret graphs like this from now until the end of the course.
• There are three types of membrane transport proteins at work during an action potential.
  • ligand-gated ion channel
    • This is an ion channel that is opened when it binds to a ligand.
      • Ligand is a word you should have learned in Biological Principles. Look it up if you don’t know what it means.
    • In this case, the ACh receptor is the ligand-gated ion channel and the ligand is ACh.
    • When ACh binds, the channel opens and Na⁺ is conducted into the cell (high to low).
    • Note: The ACh itself doesn’t move through the channel; Na⁺ does. The ACh is like a key that opens the door to let Na⁺ into the cell.
    • See animation – Ligand-Gated Ion Channel.
      • Ignore the calcium, we’ll get to that later.
  • voltage-gated ion channels
    • These ion channels open when the cell’s membrane potential changes.
    • There are two types of voltage-gated ion channels at work during an action potential.
      • voltage-gated Na⁺ channel: allows Na⁺ into the cell (high to low) = this continues the depolarization wave
      • voltage-gated K⁺ channel: allows K⁺ out of the cell (high to low) = this causes the cell to repolarize and return to its resting membrane potential
      • See animation – Voltage-Gated Ion Channels.
      • Ignore the detail on the activation/inactivation gates and threshold.
  • Na⁺/K⁺ pump
    • Once the cell has returned to its resting membrane potential, the charges are back to where they should be (negative inside; positive outside).
    • However, there’s still Na⁺ inside the cell and K⁺ outside.
    • The Na⁺/K⁺ pump moves Na⁺ back to the outside (lo to hi) and K⁺ back to the inside (lo to hi).
    • See two animations that show the Na⁺/K⁺ pump in action
      • Clip 1
      • Clip 2
        • This second clip is more technically accurate, as the pump does in fact move three Na⁺ ions for every two K⁺ ions, but I don’t dwell on that.
• See InterActive Physiology module – Neuromuscular Junction.

Read the section titled “Excitation-Contraction Coupling” (pp. 291-293) and continue up through the section on rigor mortis on p. 294.

• “Excitation-contraction coupling” is the somewhat ridiculous name given to the molecular events that occur when the muscle fiber is excited by a neuron that lead to muscle contraction. Get it? Get it?!?
  • On the bright side, there are lots of videos….
• The book discusses the troponin complex with parts called TnC, TnI and TnT. Don’t worry about any of that. Just consider it as one protein called troponin.
• I consider Campbell Fig. 49-33 and Marieb Fig. 9.12 to be very important.
  • Frankly, Marieb Fig. 9.11 somewhat baffles me, but the gist of it is summed up in one sentence in the legend: “Calcium-activated troponin undergoes a conformational change (change in protein shape) that moves tropomyosin away from actin’s binding sites.”
• In terms of animations, I’m going to break them up into four sections:
  • Excitation-contraction coupling (entire process in three unrelated clips)
    • Clip 1
    • Clip 2
    • Clip 3
  • Contraction cycle
  • Regulation of troponin by calcium (two consecutive clips)
    • Clip 1
    • Clip 2
  • Detailed animation of a myosin head in action (lots of extra detail, but neat to see).
• As you read and think about this material, here are two questions that I often ask and that I’d like you to think about:
  • Question 1: What specifically is the function of Ca⁺⁺ during muscle contraction?
    • Hint: See Campbell Fig. 49-33.
  • Question 2: What specifically is the energy stored in the ATP molecule used for during a muscle contraction?
    • Hint: See Marieb Fig. 9.12.
• The section on rigor mortis is just for your general interest. I think it’s kind of neat.
• See InterActive Physiology module – Sliding Filament Theory

Read the section called “Contraction of a Skeletal Muscle” (pp. 295-300). Here are some things to think about, divided up by section:

• Introduction (pp. 295-296)
  • Make sure you know what’s meant by the terms muscle tension, load, and isotonic and isometric contractions.
  • Think up some examples of isotonic vs. isometric contractions.
• The Motor Unit (pp. 296-297)
  • Just make sure you understand what a motor unit is.
  • See InterActive Physiology module – Contraction of Motor Units
  • It’s also shown nicely on Martini Fig. 10-17. This is essentially the same as Marieb Fig. 9.13, but I think the colors on the Martini are better.
• The Muscle Twitch (p. 297)
  • A muscle twitch is a rapid contraction (followed by relaxation) that is triggered by a single action potential.
  • Sometimes, we experience muscle twitches around our eyes.
  • Make sure that you’re familiar with the three phases of the muscle twitch and what’s happening during each phase.
  • Marieb Fig. 9.14a is important, but pay attention to the Y-axis; this isn’t showing the same information as an action potential graph!
• Graded Muscle Contractions (pp. 297-299)
  • A graded contraction is one in which either the frequency or strength of the stimulus varies.
    • The purpose is to provide a smooth, steady movement.
  • Read how graded contractions are accomplished.
  • In class, I use a biologically incorrect metaphor to help describe this.
    • Imagine that you have isolated a muscle from a lab animal and you hook it up to an imaginary machine.
    • This machine delivers electrical “zaps” repeatedly to the muscle in order to stimulate it to contract.
    • This machine has two knobs on the front. One knob (the “A” knob) controls how fast the zaps occur (i.e., the frequency – how many zaps are delivered to the muscle per second). The other knob (“B”) controls how strong the zaps are (in volts).
    • These two knobs can be controlled independently of each other. For example, you can hold “A” steady at… let’s say, 20 stimulations/sec, while you turn “B” from 0 volts to 100 volts (see Marieb Fig. 9.16). This will increase the strength of the stimulation, but keep the frequency constant. On the other hand, you can keep “B” at a constant voltage (let’s say, 25 V), but you can change the frequency of the stimulation by turning “A” (see Marieb Fig. 9.15).
    • Your body can produce smooth, steady, strong contractions by “turning” these knobs either independently or together. We call these graded contractions.
    • The PhysioEx simulation that you’ll complete this week will demonstrate these principles.
  • As indicated above, Marieb Fig. 9.15 and Fig. 9.16 are both important, but please please please pay attention to the X and Y axes.
    • I like Fig. 9.16, but it may make more sense to me that it does to you (there’s a lot of looking back and forth, and it helps to have some background when looking at it).
    • In class, I draw this graph on the board that may be a little easier to digest.
  • Also read about treppe, which is a phenomenon wherein additional stimulations in a series result in increasing muscle tension.
  • See InterActive Physiology module – Contraction of Whole Muscle
• Muscle Tone (p. 300)
  • Just to refresh your memory; we covered this initially back in articulations.
• Isotonic and Isometric Contractions (p. 300)
  • Just remember what the difference is between them.
  • Don’t worry about the figures or about the concentric and eccentric contractions.

Read the section on muscle metabolism (pp. 300-302).

• Most of this should be review from Biological Principles.
  • This material is scantly reviewed in Marieb Fig. 9.20, but you’ll need to rely on your Biological Principles background for the details.
• Muscle fibers can make ATP via three mechanisms:
  • aerobic respiration (requires O₂) -- slow, but makes the most ATP per molecule of glucose
    • Why does this type of respiration require oxygen? What’s the oxygen used for?
  • creatine kinase (does not require O₂) -- transfers a phosphate from creatine phosphate to ADP to make ATP
    • This can be seen in this video clip.
  • lactic acid fermentation (does not require O₂) -- couples a fermentation step with glycolysis
  • both of these generate small amounts of ATP through substrate-level phosphorylation
  • See InterActive Physiology module – Muscle Metabolism
    • Only concern yourself with pp. 1-23.
• Skip over the section on energy systems used during sports (pp. 302-303).
• Read the section on muscle fatigue (pp. 303-304).
  • Just know that muscle fatigue occurs when the muscle can’t make enough ATP to keep up with demand.
  • This causes the muscle to eventually lose tension.
  • It’s most commonly observed following complete tetanus.
• Read the section on oxygen debt (p. 304).
  • Oxygen debt is the amount of oxygen that you have to take in following vigorous exercise to replenish your oxygen stores.
  • It’s why you breathe heavily after sprinting, etc.
• Read the paragraph on heat generation (p. 304).
  • Muscles generate heat as a byproduct of cellular respiration.
  • Converting glucose to ATP and then using ATP for movement isn’t 100% efficient, so you give off waste energy as heat.
  • Your car does the same thing, when it converts gas (potential energy) into movement (kinetic energy). That’s why your car generates heat as you drive.

Read the section on the force of contraction (pp. 304-305).

• I think this is fairly self-evident. It's nicely summarized in Marieb Fig. 9.22, which you should consider an important figure.
• The part of this that will come back in the future is the section on how the degree of muscle stretch affects how much tension the fibers can generate.
  • Imagine performing a bicep curl when you’re sitting comfortably vs. when you’re hanging from a pull-up bar.
  • When your muscles are stretched, the thin and thick filaments overlap less, and therefore it becomes difficult for them to generate muscle tension.
  • This becomes very important in A&P2 when you learn about cardiac muscle.
    • As you’ll hear in A&P2, cardiac muscle fibers in the walls of the heart are normally understretched when the heart is empty. As the heart fills with blood, the walls stretch, pulling the thin and thick filaments into optimal alignment and allowing the muscle to contract with maximal force.

Read the section on the microscopic structure of smooth muscle fibers (pp. 309-311).

• Things you should know about smooth muscle:
  • Smooth muscle fibers do have thin and thick filaments, but they’re arranged differently than in skeletal muscle -- no visible striations.
  • Smooth muscle is found in the walls of hollow organs where it helps the contents of the organ move (i.e., blood and food).
    • This movement is called peristalsis.
  • Smooth muscle is usually arranged in two layers: the circular and the longitudinal layers (Marieb Fig. 9.24).
  • Smooth muscle fibers are innervated by varicosities rather than by motor units (Marieb Fig. 9.25).
  • Each smooth muscle fiber is wrapped in a net of intermediate filaments that transmits the fiber’s contraction to the surrounding tissue (Marieb Fig. 9.26).
    • Hmm! Intermediate filaments used as reinforcing fibers to anchor cells together? Where have we seen something like that before? Cough, cough

Lastly, read the section on the mechanism and characteristics of smooth muscle contraction (pp. 311-312).

• In class, I usually spend some time discussing the role of calmodulin and how the Ca⁺⁺ can also enter the smooth muscle fiber from the extracellular fluid (rather than just from the sarcoplasmic reticulum).
  • Calmodulin is covered very superficially here, but it is a fairly important intracellular protein to cell biologists. It controls the activity of many cytosolic enzymes in the presence of calcium ions.
• The rest of the section on smooth muscle is interesting, but it will probably be more important in hindsight after taking A&P2.