Download E) Muscle Tone - TONE - amount a muscle is contracted. * Even at

E) Muscle Tone
- TONE - amount a muscle is contracted.
* Even at rest, a muscle is contracted slightly - never fully relaxed.
* Stabilize joints, maintain posture, etc.
- LOAD - amount of force exerted; measured as RESISTANCE (the amount of force the object puts on
the muscle).
- 2 kinds of contraction; difference = how the muscle works:
1) ISOTONIC (iso=”same”, tonic=”tone”)--tone of the muscle doesn’t change, but length does (it
shortens!).
*so, bones move around a joint
2) ISOMETRIC (iso=”same”, metric=”length”)--length of muscle doesn’t change, but the tone
does!
*”tensing” your muscles--joints don’t move!
F) Muscle Metabolism
- Metabolism - how cells cycle energy.
* ATP = immediate energy source for the cell.
* Muscle fibers use a lot of ATP, so this is a good place to study how cells make and use ATP.
This is an overview; we'll go into more detail later
Release globular head, SR needs to pump Ca++, Na-K pump. Most of the energy is
wasted (only about 20% is used).
* Fibers store some glucose in the form of glycogen, and some oxygen on the myoglobin
molecule.
** Red pigment - allows the cell to store some O2. Gives muscle its reddish color.
* Fibers store some ATP, but not much; 4-6 seconds worth. ATP must be regenerated; there are
3 ways to do this (see next section)
- Overview of the 3 mechanisms (and seeing how they are tied together):
The Metabolic Machine
Fate of lactic acid
1) DIRECT PHOSPHORYLIZATION OF ADP (PHOSPHORYLATION =”put on a phosphorus”)
Also known as Substrate-level phosphorylation.
- Directly attaching a phosphate (Pi) onto ADP. The phosphate comes (sometimes...especially in muscle
and brain tissue) from a molecule called Creatine Phosphate (CP). You need an enzyme called
Creatine Kinase (CK).
* recall: kinase = an enzyme that phosphorylates another molecule.
* Energy to put the Pi onto the ADP comes from CP.
* Good points: easy to make the enzyme creatine kinase.
* Bad points: NEEDS ENERGY! It takes ATP to re-make the
CP. Inefficient to use energy to make energy. Your body
can't run on this method, although we use it to fuel parts of the metabolic machine.
** This is why it’s hard to burn off your fat! But, processes that depend on this tend to use your
adipose more quickly.
Elevation of CK is an indication of damage to muscle. It is therefore indicative of injury,
rhabdomyolysis (sever breakdown of muscle), myocardial infarction, muscular dystrophy, and
others.
2) ANAEROBIC RESPIRATION (“breathing w/out oxygen”) . Also known as GLYCOLYSIS (“sugar
splitting”).
- Glucose is split into 2 identical smaller molecules: 2 pyruvic acids (a ketone molecule).
- Good points: FAST, no O2 required.
- Bad points: inefficient, not many ATPs/glucose. Also, pyruvic acid is converted into LACTIC
ACID, which builds up in blood stream.
3) AEROBIC RESPIRATION - (“oxygen breathing”): needs O2!
- Takes place in the Mitochondria. Needs O2 and Glucose (energy sources).
- Several chemical steps involved in the process called OXIDATIVE PHOSPHORYLATION
(“putting on a phosphorus by using oxygen”), where the chemical bonds of the fuel molecules (O2
and glucose) are broken, which releases energy that is then used to put a Pi on ADP to form
ATP.
** The CO2 must be gotten rid of thru the respiratory system.
- Good points: LOTS of ATP are formed (36 ATP/glucose molecule) = very efficient!
- Bad points: SLOW!!! Takes a long time to go through the process. Your cells do this during
slow sustained exercise, especially simple minute - to - minute muscle use to sustain posture.
Summary Table:
-so, when do we use one system or another?
* Low exertion: Aerobic Respiration; have time for the more efficient type.
* High exertion: Anaerobic Respiration (glycolysis) - IF OVER 70% OF MAXIMUM ACTIVITY.
**muscles bulge, which restricts blood flow (= availability of O2). This cues fibers to
switch to glycolysis.
1. At rest, muscle predominantly uses fatty acids. Good time to be burning your fat!
2. During high-intensity, isometric exercise, anaerobic glycolysis, and the creatine kinase
reaction, in which phosphocreatine is converted to adenosine triphosphate (ATP), are the
primary sources of energy. You are mostly using glucose.
3. With submaximal exercise, the type of substrate used by muscle is heavily dependent
upon the relative intensity of exercise.
(i) During low-intensity submaximal exercise (like walking or mild weight
training), the main sources of energy are blood glucose and free fatty acids.
(ii) With high-intensity submaximal exercise, the proportion of energy derived
from glycogen and glucose is increased, and glycogen becomes the main
source.
* So ... you burn your fat while your muscles are at REST. You exercise so you will
build muscle, and therefore burn more fat while you are resting!!
NOTE: Reading the available literature, it seems to me that whether or not your
muscles are burning fat has more to do with how long it has been since you've
eaten. We will discuss this in a later section.
**but, have a lactic acid build-up, which will increase the pH and damage muscle
proteins; how get rid of it? In the LIVER:
Lactic acid + O2
converted to
CO2 + H2O
OXYGEN DEBT: the amount of oxygen needed after exercise that it takes to get rid of lactic acid--this is
why you breathe hard after exercising!!!!!
-so, in summary:
ACTIVITY
REQUIREMENT
METABOLIC
PATHWAY
ENERGY
SOURCE
Fast burst exercise-Weightlifting,
diving, sprinting.
Other energy producing
pathways don’t have
time to start.
Phosphorylation of stored
CP & ADP to form ATP
Fatty Acids (some)
More sustained than
above--tennis, soccer,
100 meter swim.
Power is needed, but
must get rid of lactic
acid.
Anaerobic
Glucose (glycogen)
Prolonged Activities-marathon, jogging, etc.
Endurance needed.
Aerobic
Glucose (glycogen)
G) Muscle Fatigue, O2 Debt & Heat Production--Byproducts of Contraction
1) Fatigue: ATP production doesn’t keep up w/ ATP use--”THE WALL” = AN INABILITY TO CONTRACT.
*WRITERS CRAMP = CONTACTURES = rigor-mortis-like condition where cross bridges won’t
dislocate.
2) O2 Debt: require O2 to return to HOMEOSTASIS.
*heavy breathing triggered by high lactic acid levels in blood.
3) Heat Production: muscles only about 20-25% efficient; most energy lost as heat--used to maintain
body temperature
*if heat goes too high, putting proteins in danger, SWEATING begins to radiate heat from the
body.
F) Force, Velocity & Duration of Contraction
- Force is affected by:
(a) # fibers or motor units activated.
(b) Size of muscle; exercise leads to HYPERTROPHY (“big size”)
(c) Series-elastic elements-non-contractible elements w/in the cell (organelles, etc.) take tension
away from work. They help the cell regain shape after contraction has stopped.
(d) Degree of muscle stretch - how relaxed was the fiber in the first place?
- Velocity of contract (how fast?) is affected by:
(a) load-how much does it have to pull?
(b) fiber type--there are 3 types of muscle fibers:
(i) RED (or SLOW TWITCH) FIBERS -fatigue resistant because ATP is used slower, but also
contracts slower.
*red color = lots of oxyhemoglobin & mitochondria = aerobic, O2 dependant, fat is the major
energy supply. Low power generation, but doesn’t fatigue--use these fibers if standing a long
time.
(ii) WHITE (or FAST TWITCH) FIBERS--less mitochondria & oxyhemoglobin, anaerobic, fast,
high force, but fatigue fast.
* lots of glycogen reserves; lactic acid builds up fast.
* lg. diameter
have a lot of contractile elements for rapid, intense movements.
*You use these to move furniture.
(iii) INTERMEDIATE FIBERS - red or pink, intermediate in size. More like red fibers in that they
are O2 dependant; but, they can contract fast like white fibers. Intermediate fatigue resistance.
NOTE: most muscles are a combo of these 3 types.
- DISUSE ATROPHY - (atrophy = “lose shape”) degeneration of muscle mass if not used * Atrophy of muscles (muscle atrophy) and bones, with loss of mass and strength, can occur after
prolonged immobility, such as extended bedrest, or having a body part in a cast (living in
darkness for the eye, bedridden for the legs etc.). This type of atrophy can usually be reversed
with exercise unless severe. Astronauts in microgravity must exercise regularly to minimize
atrophy of their limb muscles.
Cachexia ("ka-kee-sha") or wasting syndrome is loss of weight, muscle atrophy, fatigue,
weakness, and significant loss of appetite in someone who is not actively trying to lose weight
(cancer, AIDS, MS, heart failure, renal failure, hormonal problem). The formal definition of
cachexia is the loss of body mass that cannot be reversed nutritionally: Even if the affected
patient eats more calories, lean body mass will be lost, indicating a primary pathology is in place.
- Flaccid paralysis: Loss of muscle tone due to a pathology (spinal injury, polio, curare, etc.). Lose
muscle mass (up to 5% per day)!
* muscle is replaced by fibrous connective tissue.
III. REVISIT SMOOTH MUSCLE TISSUE
NOTE: We have an entire chapter on Cardiac Muscle Tissue later.
A) Microscopic Structure
- Spindle-shaped cells, uninucleated, 1/1000 the size of skeletal muscle tissue.
- Very stretchable & elastic. Good for organs that need to expand and snap back.
* Location: walls of blood vessels, hollow organs, respiratory, digestive, urinary & reproductive
tracts.
- Exerts a lot of force when stretched.
- Organized in sheets that contract together.
- Usually, 2 layers present, w/fibers arranged in different orientations:
* One type of movement: Opposing layers leads to a squeezing effect = PERISTALTIC
CONTRACTIONS
- Neural control = AUTONOMIC (INVOLUNTARY).
B) Contraction of Smooth Muscle
- Slow, synchronized, peristaltic contractions.
- No striations. Why?
*less actin
*no sarcomeres; thick & thin myofilaments “spiral” from 1 end to other; force of contraction is
spread out over cell
- APS can move from 1 cell to another along junctions between cells. 1 cell acts as a PACEMAKER-exhibits SPONTANEOUS DEPOLARIZATION = has occasional APS w/out outside influence. These APs
then spread to other cells in the sheet. This coordinates their contraction.
- Contractions are slow, sustained, and resistant to fatigue.
C) Regulation of Smooth Muscle Contraction
- Use different neurotransmitters, WHICH MAY HAVE DIFFERENT EFFECT ON THE SMOOTH
MUSCLE OF DIFFERENT ORGANS.
* Difference: neurotransmitters can be
INHIBITORY or EXCITATORY,
depending on the type of receptors
found on the sarcolemma.
* INHIBITORY: sarcolemma has
spontaneous generation of action
potentials. Neurotransmitter act to turn
it off. Above example: Adrenaline is
INHIBITORY on organ “A”.
* EXCITATORY: like skeletal muscle,
neurotransmitter starts AP on
sarcolemma. Above example:
Adrenaline is EXCITATORY on organ
“B”.
D) Other Special Features
- HYPERPLASIA: cells divide to increase in #, especially in response to certain hormones. EXAMPLE:
growth of uterus at puberty.
- Have a secretory role -secrete elastin & collagen.
E) 2 Types of Smooth Muscle
1) VISCERAL or SINGLE UNIT
- more common; have gap junctions & rhythmic contractions w/ spontaneous generation of APs.
2) MULTI UNIT
- Lg. arteries, lungs, erector pili in the skin.
- No gap junctions, no spontaneous APs, do not have rhythmic contractions in sheets--independent of each other.
- Still have AUTONOMIC (involuntary) CONTROL.
IV. CLINICAL CONDITIONS
- MYOPATHY: any disease of muscle.
- MUSCULAR DYSTROPHY: a group of muscle-destroying diseases.
*muscles enlarge, fat & connective tissue deposits, fibers degenerate.
*inherited w/ female carriers & male expression.
*1 out of every 3500 births.
*most common form is DUCHENNE’S MUSCULAR DYSTROPHY- can’t make DYSTROPHIN, a
protein important in the sarcolemma. At 4-6 yrs. of age, they begin to lose balance, falling = first
signs. They do not live much past 25 yrs of age.
** Steroid Therapy with PREDNISONE, not curative, just slows it down.
- TETANUS: An anaerobic bacterium (bacteria that can’t live in the presence of oxygen) invades body,
usually through a deep wound. Causes a sustained firing of motor neurons
* LOCKJAW (inability to open jaw) one of first signs. Death occurs from respiratory failure.
- HERNIA: any protrusion of an organ thru the body cavity wall; often caused by heavy lifting or a
weakening of the muscle wall of the cavity thru obesity.
- CRAMP: sustained tetanic contraction caused by any number of conditions: low sugar or electrolyte
levels, dehydration, irritated motor neurons especially near spinal cord.