| View previous topic :: View next topic |
| Author |
Message |
M.C. Guest
|
Posted: Sun Apr 15, 2007 12:43 pm Post subject: Question 12 |
|
|
Dr. Ferdinand,
What is cross-bridge formation in muscles and how does it improves contractile power of the muscles?
I was wondering if it is the same as musle contraction?
Thanks |
|
| Back to top |
|
 |
Matthew Guest
|
Posted: Sun Apr 15, 2007 10:17 pm Post subject: |
|
|
| Cross bridges are where the actin filaments attach to the myosin heads. So when you are trying to understand how cross bridges generates force, think of a strong arm (connection) that can grab hold tightly to a muscle (myofibril). |
|
| Back to top |
|
 |
Matthew Guest
|
|
| Back to top |
|
 |
admin Site Admin
Joined: 08 Dec 2003 Posts: 2176
|
Posted: Tue Apr 17, 2007 3:45 am Post subject: |
|
|
To understand the levels of organization of muscle, pay special attention to the diagram http://upload.wikimedia.org/wikipedia/commons/c/c0/Skeletal_muscle.jpg or if you have the Gold Standard, BIO 5.2 has a full page schematic on muscle from the molecular level to the gross level.
Last edited by admin on Sat Jul 28, 2007 11:50 am; edited 1 time in total |
|
| Back to top |
|
 |
mvenus9292913
Joined: 08 Jan 2007 Posts: 23
|
Posted: Fri May 04, 2007 11:28 pm Post subject: |
|
|
| Also, though I'm not sure if it matters for the MCAT or not, but when you first move a muscle, only some of the cross bridges are used. To increase force, you increase the number of active cross bridges. This can be done by increasing the frequency or voltage of stimulation, or by increasing the number of neurons sending messages. |
|
| Back to top |
|
 |
anon3543
Joined: 12 May 2007 Posts: 16
|
Posted: Thu Jul 26, 2007 4:37 pm Post subject: |
|
|
From what I understood, the stretching of the heart actually decreases overlap between myosin and actin fibers (thus decreasing the amount of myosin head to actin bonds initially), giving it more room to slide back in resting position and thus exerting a greater contraction. In other words, there is some overlap between actin fibers in the middle of sarcomeres of the resting cell of the heart, which makes contracting anymore difficult. Stretching the sarcomere at first will increase the number of cross bridges by eliminating this actin overlap, but subsequent stretching (most of it) will start decreasing the number of cross bridges, but allowing more room to decrease back in length. Obviously even more stretching beyond some optimal overlap makes the contraction weaker, but I still think the bulk of the strength gathered from the increased heart contraction is from the actually less actin/myosin overlap (less cross bridges) because it allow more space to become small in length again. Ok, that was redundant...
12. Ventricles are able to increase their output only up to a certain point upon exposure to increased volume. Beyond that the output will drop. This is most likely explained by which of the following?
1. Increased volume is associated with the separation of actin and myosin molecules from each other up to a certain point. [x]
2. Increased volume causes formation of cross bridges between muscular myosin and actin molecules up to a certain point. [x]
3. Increased volume causes generation of new cardiac muscle fibers up to a certain point. [x]
4. Increased volume causes formation of lactic acid up to a certain point. [x]
INCORRECT:
Your Answer: A
Correct Answer: B |
|
| Back to top |
|
 |
admin Site Admin
Joined: 08 Dec 2003 Posts: 2176
|
Posted: Sat Jul 28, 2007 11:48 am Post subject: |
|
|
| Quote: | | With an increase in cardiac filling, ventricular volume increases and stretches the ventricular wall. Lengthening the resting muscle fibers increases the probability of actin-myosin cross bridge formation. Since force generated is proportional to the number of cross bridges forming per unit time per cross section of muscle, greater force develops in the pre-stretched muscle. As with skeletal muscle, stretch beyond an optimum length, decreases the active tension (pressure) the muscle develops. |
http://rfumsphysiology.pbwiki.com/Regulation+of+Cardiac+Contraction
Increased volume leads to "increased cross-bridge formation": http://findarticles.com/p/articles/mi_m0FSL/is_n4_v67/ai_20972813/pg_11
OK, let's put that aside and return to the MCAT which is based on first year, introductory level science. For advanced level info, we must rely on the passage. The passage states that "the higher the volume of returning blood, the higher the rate of ventricular contraction." So the question forces us to answer the following: what is the mechanism by which muscle (ie the ventricle) contracts?
The details in your questions and even the details in the links that I have provided are not necessary for the new MCAT. If you knew an equivalent amount of organic chem as you clearly have learned in bio, you'd be coming up with 10 different possible answers for every synthesis on the MCAT! Your first objective always is to keep it simple. It's first year stuff! |
|
| Back to top |
|
 |
quadalpha
Joined: 21 Feb 2010 Posts: 65
|
Posted: Tue Mar 23, 2010 4:04 pm Post subject: |
|
|
| So what explain the subsequent drop in output? |
|
| Back to top |
|
 |
addiaz2714087
Joined: 09 Mar 2010 Posts: 9
|
Posted: Wed May 19, 2010 11:35 am Post subject: |
|
|
Like anon3543, I also thought the answer was A.
First paragraph says
"....one of the major factors contributing to the force of contraction is the INITIAL LENGTH OF THE CARDIAC MUSCLE. The increased length (preload) is related to the volume of the cardiac ventricles right before contraction".
The sarcomere has an optimal operating length- once overstreched, the thin and thick filaments wont be able to overlap, and therefore sliding will not be able to occur.
The stretching of the muscle then is more relevant here than the formation of cross bridges. Actually I remember reading somewhere that only a fraction of potential cross bridges are formed at any given time. |
|
| Back to top |
|
 |
admin Site Admin
Joined: 08 Dec 2003 Posts: 2176
|
Posted: Wed Jun 09, 2010 3:59 pm Post subject: |
|
|
In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin and thick filaments; for smaller sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments.
As you said, “The sarcomere has an optimal operating length”.
Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For smaller sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. For larger sarcomere lengths, which is the case here, this is the result of less overlap of the thin and thick filaments; answer
choice B |
|
| Back to top |
|
 |
|