Skeletal Muscle Questions. I know that many of you are waiting to look at much of this material for this weekend as last weekend was so intense, so please feel free to send me your questions as you gather them this weekend and I will post another posting early next week to cover those!
First today a supportive resource from one of your classmates. As an action potential and charge movement junky myself, I think this is REALLY cool:
Wondering if you have ever seen this video, it is Hodgkin
himself recreating the action potential experiments. Very groovy, very old school. You can find it in the link below. I saw it a few years ago in a school and was
blown away by it. Thinking of seeing the
first action potential ever definitely gave me goosebumps.
Now here are your questions:
1. In class you briefly mentioned that muscle soreness,
after exercise, is due to lactic acid. A few years ago my undergrad physiology
professor (Dr. Linton from the University of Utah) taught us that recent
research indicated that this theory was incorrect, and that current thought is
that muscle soreness is caused by microabrasions. I was wondering if could
clarify. Thanks.
This is a great question and point that has come up the last few semesters. Indeed, recent research HAS demonstrated that much of the long-term muscle soreness, however, that part of the story does not entirely eliminate the contribution of lactic acid. It appears that initial soreness and fatigue certainly has some lactic acid contribution, but the delayed muscle soreness is more due to the micro and macro tears of the muscle fibers usually associated with eccentric isotonic contractions. Per one of your peers last semester who also did research in this area (and researched it in the literature for you) prior to coming to RUSM:
Lactic
acid build up in muscle during activity is part of the bodys natural defense
mechanism to prevent permanent damage...ie micro tears leading to macro tears.
The soreness/burning felt during activity is from lactic acid build up.
Soreness 2-3days later (Delayed Onset Muscle Soreness) is not do to Lactic acid but rather the
tears/damage inflicted on the muscle from the strenuous activity. Further, the
Cori cycle is important but can only happen once the body has slowed down and
more oxygen is present so the body can continue pyruvate down the energy
generating path.
2. I had a question regarding muscle fatigue more precisely
in relation to cross-bridge cycle inhibition. could you please elaborate more
on how the rise in ADP and Pi would lead to muscle fatigue.
ADP + Pi release form the myosin head leads to the power
stroke movement. so would it mean that an high level of ADP and Pi will lead to
maximum contraction that is sustained for a long period of time?
this will then cascade the other effects of fatigue
(Conduction failure as well as Increase pH)?
Yes and no. It appears through the research that the rise in concentration of ADP and Pi simply makes the biochemical reaction NOT favor the release MORE ADP and Pi into the system and that allow causes the failure of continued cross-bridge cycling. However, could this build up also work with the other causes of muscle fatigue, it would appear yes. More research in this area, however, is CERTAINLY needed and may be a fellowship with your name on it just waiting to be explored!
Yes!
In the skeletal muscle lecture, it was mentioned that each motor neuron controls muscle "fibers" (5-1000). Two questions here: Q1 Is it it 5-1000 motor units or 5-1000 muscle fibers? Q2 How does this idea of each motor neuron controlling more than 1 muscle fiber relate to the 1:1 ratio mentioned above?
What Dr. Yin was talking about is that each motor unit can contain one motor neuron which can control 5-1000 individual muscle fibers (or muscle cells). Therefore, if an action potential is sent out of the central nervous system down one motor neuron, it will activate an action potential (and subsequent contraction) of all of the muscle fibers within its motor unit causing them all to contract.
4. I have a question in relation to
hyperplasia/hypertrophy and the relationship between Force and velocity.
for the force and velocity we can think about it as the
number of muscles fibers remaining and able to do work, after isometric tension
has been reached.
the lighter the load-> the less muscle fibers are
required to hold the hold the object in place --> thus the more fibers are
available to do work and the velocity of that muscle to contract and bring the load up would be much greater than
for a heavier load.
Yes. Keep in mind, however, those specific graphs are referring to a SINGLE muscle fiber and so we would be talking about cross-bridge interactions available rather than fibers, but the idea is still the same. However, as fibers are not all in parallel or series with each other the confusion you present below could present.
if the same muscle undergoes hyperplasia or hypertrophy
thus an increase in the number of muscle fibers (all parallel to each other)
wouldn't the velocity of the muscle increase even more? (assuming that the same
load is being lifted).
so to lift the same load as before would require the same
amount of muscle fibers thus leaving a greater amount of muscle fibers that are
able to do work.
wouldn't that cause the velocity of the new muscle to be
even faster?
No. As I implied above, you need to consider the sarcomeres within a SINGLE muscle fiber. Please refer to slide 69 in the Skeletal Muscle lecture for guidance. When you increase the number of sarcomeres in parallel, they simply work together at the same speed to move an object, not faster. Think of it as stretching a very thick rubber band. If the sarcomeres were in series, then to get to the same location it wold have to move faster, so the velocity of shortening the muscle would increase (stretching a large rubber band).
Depending on what field in medicine you choose to go into you may need to know many things about synaptotagmin. For my purposes, however, I point out that protein because you know that Ca2+ influxing into the presynaptic neuron causes the vesicles to fuse with the membrane releasing whatever neurotransmitter is within them. There are a number of proteins involved in this process, but the one protein that bind to Ca2+ (and is therefore the initial protein involve) is synaptotagmin. That
And one more question that was asked of Dr. Yin and her response:
6. I'm still a little confused about the structure of myosin II.
So I understand that there are two heavy chains and 4 light chains.
The light chains wrap around the necks of the globular heads that are
made from heavy chains. Are these globular heads the same heads that are
involved in the power stroke? If not, what do they do?
They are the same heads that are involved in the power stroke.
Dr. Yin
Indeed,
please see slide 27 of the skeletal muscle lecture. The S1 portion of
the myosin molecule is what I refer to as the myosin head group.
Alternatively, the part of the spoon you eat off of in Dr. Yin's model
would be the myosin head groups.
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