© Distribution of this video is restricted by its owner
Transcript ×
Auto highlight
Font-size
00:08 All right. Mm. I hate it's just loud. There we

00:18 Right about there. All right. , what you're looking at up here

00:21 the, uh, distribution for this . Um, so the average on

00:25 exam is 60 standard deviation, which talks about how wide it goes.

00:30 , we like it around a But, you know, this is

00:33 surprising for a lower level class, , high grade, 98 medium

00:38 60 minimum grade 16. So just , medium average can be up just

00:42 a little bit based on how many are on one side or the other

00:45 that. But this is just the exam again. I, I throw

00:49 at you or show this to you that you can see, you

00:52 that, you know, where everyone of took the exam and what I

00:55 to do here is just kind of through a couple of things. So

00:58 is comparing unit one through to unit . So it's just the grades associated

01:02 that unit. You can see almost all cases that, uh, everyone's

01:07 of moving up. So every area moving forward that one didn't. But

01:11 these up something has to go down again moving up, there's one that

01:16 down but moving up, moving moving up. So you're moving in

01:19 right direction, right? And so is, this is important, this

01:23 something that you can take with you , oh, ok, I am

01:27 and that's good because ultimately, what really concerned about is what is my

01:31 looking like. And if I had give you a grade today, I

01:34 use this scale and remember this does include any extra credit. So um

01:39 it excludes people who haven't taken exams . So it doesn't mess with the

01:44 , but you can kind of get sentence right down. A minus would

01:46 starting around an 87.5, which is for this class B minus around a

01:51 , uh C minus around 59.5 and bottom of the D range begins at

01:57 . If you find yourself in these things, you are not out of

02:01 . This is not the time to . This is the time to ask

02:03 question. What am I doing? ? And what am I doing

02:06 All right. Yeah. You the point is is that there is

02:11 , you can move yourself upwards and is already showing up here the day

02:17 drop. The class is like November . I mean, it's like two

02:20 after the third exam. It's, like crazy late. So, if

02:24 find yourself going, wait, I like I studied really, really hard

02:27 I didn't get the grade that I . It's not that you're not

02:31 it's that you're not working. It's like trying to paddle or peddle

02:35 bike by sitting on the handle Right. You can do it,

02:39 can get some place with it, you're not doing it efficiently and you're

02:41 going to do it well. And what you need to do is you

02:44 to learn how to ride the bike . And that's kind of what I'm

02:47 is you, if you're, if struggling with not getting it and your

02:51 are not what you're happy with, and talk to me. I

02:54 I sit in my office staring at ceiling most Tuesdays and Thursdays and I'm

02:59 sitting there going, where are my ? You know, and I know

03:01 you guys have been trained over the five years to avoid contact with

03:07 Right. Yeah, that's, that's it was. Right. But that's

03:11 of this is you need to start proactive about who you are and what

03:16 gonna do. All right. So not gonna yell at you and

03:19 oh, you're a bad student. on you. I mean, if

03:21 sitting in that range where it it, um, if you're sitting

03:24 here. I'm gonna, I'm, sympathetic. I understand. All

03:28 I'm not mad at you. You , I want you to achieve your

03:31 . That's my job is to help achieve your goals. I like to

03:35 for you. That's why I'm wearing shirt today. Right? I don't

03:38 wear shirts like this out in public on game days. Well, that's

03:43 true. I, I even have , I'm not gonna show you,

03:46 I'm wearing my swim dive shirt underneath . So, um, anyway,

03:50 , I'm, I'm, I'm I want you to achieve your

03:52 So if you're not happy, if not satisfied, it's not done.

03:56 not doomed. You're not, it's not the end of the

04:00 Let's get you moving in the direction want to go. All right,

04:04 ok to stumble and fall and scrape nose or scrape your knees or whatever

04:08 is. Get up, dust yourself . Ask how do I do things

04:11 ? Because if you keep doing the thing, what, what are you

04:13 get? Same thing? You're gonna the same result and that's not gonna

04:18 the thing that you want. let's come and talk to me.

04:21 right. And if I get a of students today, you know,

04:24 you're like, I can't do it , then come the next day,

04:27 Tuesday. You know, if you come during my office hours, email

04:31 and say I can't come during office . When would be a good day

04:34 come in and talk to you? right. So I'm happy to do

04:38 . Happy to walk you through So, um the exams will open

04:43 probably next Tuesday, extra credit uh the exam to do that self assess

04:48 open up next Tuesday. So just before and what I wanna do is

04:53 wanna start moving this into another And so really the second half of

04:58 MP is dealing with the nervous But before we get into the nervous

05:03 , we have to do a small of muscles. Ok. So what

05:07 really doing here is we're, we introduced the idea of electrical

05:11 cells that have electrical activity. And muscles are one of those cells.

05:15 so we're gonna spend some time talking how they use action potentials to create

05:21 . All right, we're gonna walk in depth the, the details of

05:25 this happens. Ok. So we're be working at the molecular level.

05:29 you want to learn the names of muscles, you need to be in

05:31 lab because there are a lot of . All right. So this is

05:36 we're gonna be start uh spending our today and in the next lecture and

05:39 after that, everything until the end the semester is all nervous system.

05:44 . So with that in mind, we ready? Anyone going to the

05:49 tonight or are you? I I'm looking around the room. I

05:52 like, yeah. Ok. Are gonna paint yourself up? Ok.

05:56 key. Uh you, we, gotta wake up and start doing some

06:00 painting here, right? You don't the big 12 unless you, you

06:04 yourself in red. Yeah, this true. When you go to track

06:09 field, when you go to when you go to volleyball, paint

06:12 red, go nuts. Be This is your only time in life

06:16 you can do that. Can you me painting myself and going to a

06:19 game? Would you guys just go sad and pathetic? Yeah, you

06:24 so see it's ok when you're a student, not OK after out of

06:28 of college. So tonight go out fun. Cheer on your fellow classmates

06:37 you have fellow classmates playing. All . So what we're gonna do is

06:42 gonna deal with muscle. And so I wanna do is I just want

06:44 briefly show you what is the function muscle and typically what we do is

06:48 think of muscle as movement and that the correct thing. All right,

06:51 is physical movement or what we refer as locomotion. I'm gonna get that

06:55 light off there. Come on, . There we go. Kind of

07:05 that reflection up there. But it's than just that. So we can

07:08 here. It actually holds your internal in place. It protects them.

07:12 we don't really think about that so , but your guts are actually held

07:16 place and protected by muscle itself. , posture. We don't think about

07:21 much, you know, unless your tells you to sit up straight,

07:24 know, at the dinner table, up straight. Um, but

07:27 the, the ability for us to up is really because our muscles are

07:31 a constant uh are in constant pulling and pushing to bring ourselves into

07:36 position that we want to be All right. Um They all stabilize

07:41 joints. Uh You're probably more familiar this idea that we do generate

07:45 Heat is a byproduct of muscle It's basically the result of inefficient a

07:51 uh production. And so when muscles working and contracting, they're, they're

07:57 heat as a byproduct of their And so when we generate heat,

08:02 doing so because of just how poorly bodies are designed. Um But it's

08:08 a benefit too, right? uh what we're gonna do is we

08:12 use that to heat ourselves when we cold. And so, shivering is

08:16 a series of very quick muscle contractions and over again to produce the heat

08:20 we need to keep us from freezing death. Right. And lastly,

08:24 it's very, very important uh in . And again, this is not

08:28 we really think about, but most our communication is done through facial

08:33 which is why texting is such a email is a terrible form of

08:38 Because how many times have you ever offended by, uh, an email

08:42 a text at someone since you? they, and they weren't being

08:45 They just, you just couldn't see tone was when someone sits there and

08:49 at you and tells you something. kind of know. Oh,

08:52 they're kidding around. But if someone frowning at you, you know,

08:56 kind of know this is serious, know, we have lots of muscles

08:59 our face to express emotion. We through our muscles. So gestures.

09:08 a, I'm a gesticulated. My hates it because when I talk like

09:12 , my hands move all over the . She's afraid she's gonna get hit

09:15 the face. I'm sitting there doing . She was making fun of me

09:19 other day about that. Um All . So as I mentioned, there

09:24 tons and tons of muscles in your . I think there are pages that

09:27 kind of go through lists of muscles we don't have to bother with in

09:31 class. We're not going to do because that is something that you really

09:35 to sit there and walk through uh, a structure, a model

09:41 to be able to do that. me just pointing at pictures like I

09:43 the skeletal system is not helpful to . All right. So it's something

09:47 you do in the lab and I reserve that for the lab and leave

09:50 there. And so we're really kind dealing more with the physiology of muscle

09:53 than the, the different types of that make up your anatomy. There's

09:57 too many of them. And I think at your level, they

10:00 you learn somewhere around 100 and 50 , not all 600 because that would

10:05 a nightmare. Uh The good news in terms of nomenclature, muscles are

10:09 much a name for shape or what do. And so, uh even

10:14 they have these horribly scary names, you start seeing the pattern of how

10:17 name things, it's like, oh , it's not as hard as I

10:19 it is. All right. But we want to do is we want

10:22 kind of dive in anatomically to deal what do all muscles have. All

10:27 . And so our starting point is the connective tissue. And so in

10:30 little cartoon right here, you can the bone and what we've done is

10:32 separated out a muscle. So that be a named muscle. We refer

10:36 that portion of the muscle, the part as the belly. All

10:40 the muscle itself is connected by connective to the bone. So when a

10:44 contracts, it's pulling on the connective which is pulling on the bone to

10:49 the movement. But if you look we can do is we can keep

10:53 this down. This is basically a of cells. And so here is

10:57 cell and that cell is, is in connective tissue. And then those

11:03 are bundled together as a group of which is then wrapped in connective tissue

11:09 are then bundled in that whole muscle . All right. So we have

11:13 for the levels of connective tissue that gonna see. So the the suffix

11:18 gonna miss right? That, so just telling you this is the connective

11:21 that surrounds the muscle. The connective on the uh on the outside of

11:26 whole muscle is the epi the connective that arounds the bundles of cells is

11:32 the paramecium. And then the one nearest to the cell. So each

11:37 cell has its own connective tissue. the Endomysium. Now, the reason

11:41 wrap each individual cell with connective tissue because we feel like wasting connective tissue

11:47 now. It's actually because we're going be stimulating a cell, we don't

11:54 those ions that are moving to affect cells that we're not stimulating. So

11:59 wrapping each one individually, you're stimulating that one cell, it's like wrapping

12:04 copper wire in insulation. So that the current is flowing through it just

12:08 in a neuron, you're not going be exciting the other neurons you're not

12:12 to be exciting the other cells. these are the three concentric layers.

12:17 this one and this one and this , they all come together and converge

12:21 they extend beyond that muscle um structure become the tendon. All right.

12:28 this connective tissue isn't just there to . It actually is what ultimately forms

12:33 tendon and then that tendon is what to the bone. Um It can

12:38 attach to skin or can attach to muscles. But typically we just think

12:42 terms of bone to cause movement and um attached to on with, with

12:49 to the bone, it's gonna be the periosteum of the bone. All

12:54 . So, structurally, when you of a muscle, it's a bunch

12:58 cells that are bundled together when you inside an individual cell. So here

13:04 are, we're cutting away into the cell. If I go back to

13:06 picture, you can see here, looks like it's filled with stuff.

13:09 what they've done is they've pulled one . You can see that it's filled

13:12 a bunch of skeletal elements or cyto elements. Back, here's the individual

13:19 , they're pulling out the cytoskeleton bundles then they're pulling out individual fibers.

13:24 so we have names for all this . So the bundle of fibers is

13:27 the myofibril. The individual fibers themselves called the myo filaments. All

13:33 So those are just collective terms and can get a little confusing because you

13:36 see this is called the myocyte or myofiber myo fibri myofilament. So this

13:44 just like what we saw in um nervous system. When we talked about

13:49 , they had special names for They get kind of confusing. The

13:53 first started exploring the my muscles, naming everything my, my my or

14:00 so those prefixes just kind of Oh, we're in muscle. All

14:06 . So what you can see here's our picture. And you can

14:09 here, here's our myo fibros which within them, uh my filaments and

14:14 can see surrounding them are part of cells that we've already learned about or

14:20 some of the parts right now in little cartoon, we're, we're going

14:25 be looking here. See the yellow here goes, it starts, it

14:30 up on the surface and it basically works its way to the opposite side

14:33 the cell. So this is kind an open tube, kind of like

14:37 tunnel that kind of works its way the cell. All right. And

14:41 is called the transverse tubule. So a tube, tiny tube,

14:44 transverse crosses the whole thing. And in this case, what we're doing

14:48 we're bringing the surface of the cell to the cell, we're bringing it

14:54 to the middle of the cell and the blue stuff here. That's a

14:59 of endoplasm partum. It's a smooth partic that's been modified and you can

15:04 it's wrapped around each of these cytoskeleton and it's in close a opposition to

15:10 transverse tubule or the T tubule. right. So all the blue stuff

15:14 looks like a network, it's basically their way through. And that's just

15:18 sarcoplasm or sar sarcoplasm reticulum, that's name we give it and it's just

15:23 smooth endoplasm reticulum. Now its the sarcoplasm partum is to hold on

15:29 to sequester calcium, which means when is in the, uh what what

15:34 do is we pump calcium into this and this is kind of where it's

15:39 and it's held in place and then region, region of the sarcoplasm,

15:43 particular, nearest the transverse tubule broadens and widens up. And so we

15:50 them the terminal cerne. And so some reason, uh we decided to

15:55 it, keep it as it's kind its own designated structure. But

15:59 it's just an extension of the sarcoplasm . So you have sarcoplasm partum,

16:03 very tips are the transverse or the uh internal CIA and that sits

16:07 next to a transverse tubule, the tubule moving from one side of

16:11 of the next. And collectively, three structures are referred to as the

16:16 . All right. So skeletal muscle a triad when we look at cardiac

16:20 and a MP two, they don't a triad. They have a

16:24 so their terminal CIA aren't really They're tinier. And so that's why

16:28 refer to it as a dia, it's structurally it's very, very

16:33 So, when I have two things to each other, do you think

16:36 they interact? What do you Yeah. Ok. And if we

16:41 it a tribe, do you think they kind of work together as a

16:44 ? Yeah. So we have a here that is gonna work together as

16:48 group for some purpose, calcium being . But we're not telling you exactly

16:53 . Just yet, I want to deal with this microanatomy. All

16:56 So T tubule is a tube that through the whole thing. It sits

17:00 to the terminal cistern of the partic sarcoplasm partic holds on to

17:08 Now again, what we're gonna do we're looking now at this myofibril.

17:12 right. This is the structure that have now inside your muscle cell.

17:17 have hundreds to thousands of these. right. And so that's why when

17:22 look at this picture, they're trying demonstrate, oh, look how full

17:25 is. All right. So these cytoskeleton. All right. So when

17:29 talk about the intermediate filaments and we about the my uh we talked about

17:33 micro filaments and the myo tube and uh microtubules, we're talking about

17:39 these cyto skeletal structures. And so all related to what we're seeing

17:44 These are all have uh uh uh relationship and, but what we are

17:48 at here is something that's highly, organized, they're bundled together. There's

17:53 relationship between the filaments that make up mild fibros. Now, the other

17:59 that we're going to see in there I guess I just missed is the

18:02 . I forgot to mention that. that's just the cytoplasm inside the muscle

18:06 . There's lots and lots of Myoglobin is related to hemoglobin. Hemoglobin

18:12 the molecule that carries blood or oxygen your blood. And so myoglobin does

18:16 same thing, it binds up and oxygen. Do you think your muscles

18:21 oxygen to do their job? Do you wanna wait for your respiratory

18:25 to catch up when you start running do you just want the oxygen already

18:29 ? You want the oxygen there? . So that's what the muscles are

18:32 is they're basically holding onto oxygen nearby they can, they can start doing

18:36 work and then when the respiratory system up, they can deliver the oxygen

18:40 replace what they've used up. All , lots of mitochondria. So they're

18:45 to show you mitochondria, mitochondria, cells that have lots of mitochondria are

18:49 indicator that there is lots of energy made. So lots of a TP

18:52 made. So this is not The other thing that's really weird about

18:57 is that they're multinucleate. Uh when were being developed, you had these

19:02 tiny cells, myoblast cells. Um little itsy bitsy, tiny, tiny

19:07 . And what they do is they other myoblast cells and say,

19:10 let's make a um actual skeletal muscle . So they start fusing together.

19:14 so you get these really, really muscle cells and so you can think

19:18 a muscle, it goes the length the entire structure. So all those

19:22 are basically one length. So, know, my bicep, which is

19:28 here to here is basically the cells that bicep are that long. All

19:34 . And the longer the muscle, longer those cells. And it's just

19:38 these cells fuse together and because they together, they don't lose their

19:43 they stay inside the cells. So why they are multi nucleated. All

19:48 , cardiac muscle cells and smooth muscle do not have this feature. This

19:52 unique to skeletal muscle. Anyway, down on the mile fibro. Uh

19:57 are highly, highly organized. Um extend the entire length of the cell

20:02 like the cells can be long. you're gonna have these structures that go

20:06 entire lengths. And ultimately, what are is they're an arrangement of these

20:10 different mile filaments, what we call thick and the thin filament. And

20:13 you've taken an anatomy or biology at point where they talk about muscles.

20:17 probably already learned about the thick and thin filament, the thick filament is

20:21 made up of my, all And it actually has this kind of

20:25 organization. Uh This picture doesn't uh it very well, but basically,

20:29 a series of mayas and structures that bundled together. And my looks like

20:34 , a golf club. Lack of better term. It has this uh

20:38 , this globular head that kind of like so and has this really,

20:42 long tail and there's actually two heads they, they work like this.

20:47 right. And it's this head that it to interact with the thin

20:52 And so you can take bundles and and bundles of these structures that are

20:56 thicker and more dense than what you're at in this picture up here.

21:00 what they're gonna do is they're gonna to interact with the acting in the

21:04 filament. All right, there's a portion, that hinge portion has an

21:11 P A activity. It's actually in head, but it allows for the

21:15 in that hinge so that when the P is available, it will actually

21:21 movement and we'll talk about how that because it's a little bit backwards to

21:25 you might think. The other thing you have in that head is you

21:29 a binding site that active. All . And so if acting is

21:35 it wants to buy. And that's you'll see in my thin filaments.

21:42 the other hand, are a little more complex. So we do say

21:45 , acting is the primary we're interested . And the interactive on acting,

21:51 is a binding site. But if get my act together, you're gonna

21:55 them to interact and get the, want to separate. So you don't

21:59 them to do that, you only them to interact when you want to

22:01 a contraction. So right now, have relaxed muscles in those relaxed

22:06 you do not have an interaction between and Mycin right now. So something

22:10 to get in between them, And so in the thin filament,

22:14 have this molecule that's being shown here green. See, it kind of

22:18 around that is called troy. It's to my, it has a small

22:24 to this my binding site on act it kind of sits in the

22:28 right? It basically blocks or prevents from binding. But if it's

22:34 it's causing a problem because when I to act or interact with acting,

22:39 in the way. So I need have a way to remove it to

22:41 it out of the way. And why we have a third molecule there

22:44 called troponin. And it's represented by little tiny purple blueberries. All

22:49 And here this molecule has three parts it. One part is attached to

22:54 , one part is attached to the and then the third part binds up

23:00 . All right. And when calcium available, what it'll do is it

23:04 take and change shape and it will the trope of myo out of the

23:08 , making the acting binding site or the myo binding site on acting available

23:14 my. So when my sees that or that my binding site, it

23:19 itself to it and now we can a contraction. OK. So thick

23:24 thin filaments are in close opposition, they can't interact because on the thin

23:29 , we have something blocking since calcium what allows us to pull the thing

23:34 because of the other part of the filament. The troponin. Just remember

23:41 is like min and it hides the site. Troponin is the hinge that

23:48 to the calcium to cause the And Acton is doing the interesting part

23:53 is interacting with Myson. Now, is probably what you guys learned when

24:00 looked at muscle. The first time , oh, let's learn about the

24:04 and the different bands and the bands confusing and scary. And you're

24:07 oh no, I don't want to this stuff. Do you remember

24:11 Did you guys do that? I'm seeing some heads nod.

24:15 All right. All right. So you look what we're looking at up

24:22 is we're looking at the, my , remember. So now this,

24:24 is showing you how dense those myo are inside that skeletal muscle. And

24:29 we take a slice through and look a microscope, this is what we're

24:34 to see. And this is exactly the scientists thought without knowing what they're

24:38 at. They're like, wow, a pattern. What I see is

24:40 see this, this dark pattern and I see a light pattern and then

24:44 see a dark pattern, but then see kind of this lighter pattern,

24:46 then there's a dark band in the and then a lighter pattern that's darker

24:51 this, but it just kind of itself and they kind of watched this

24:54 and said, OK, what we're to do is we're going to name

24:56 and we're going to give them letters I don't know what the letters

24:59 Honestly, they don't match up necessarily acting and my right. So don't

25:04 say a equals act and that is app, you will go horribly wrong

25:08 that's what you do. All But what we do is we

25:11 all right, what we have here we're going to start with a line

25:14 that sits all by itself and we're to call this the Z line.

25:19 , the Z line, what you're is you're looking at something from this

25:22 . If you looked at my hand had to describe my hand is my

25:25 have three dimensions or does it look a line to you looks like a

25:29 ? Right? They look like a . Yeah. Right. But really

25:33 we have is we have a three structure. It's a lattice work.

25:36 so what you'd see is if you at it, we were able to

25:39 the cross section through it and actually , you'd see that it's really a

25:42 of proteins that are cross linked to other that serve as the boundary to

25:48 acting uh filaments are actually bound up . In other words, the thin

25:52 originate at the Z lines. And so we see a Z

25:57 we see a Z line and there's be another one and another one.

26:00 they repeat themselves. And so what said is oh with this little tiny

26:04 line that we don't have any we're gonna call this the structure of

26:08 . Because what we do is when observe and stimulate these muscle cells,

26:12 two Z lines get closer together. so that's why they established this as

26:17 unit of function of the muscle, called it the sarcomere. All

26:23 So when you contract a muscle, Z line here is being pulled to

26:27 Z line there. And this E and that Z line are being pulled

26:30 . And that's why you're getting a contraction. But what's interesting is that

26:35 not getting every line, every, structure in this changing shape. All

26:43 . And so what we did is explored and explore, finally figured out

26:46 all the things are and they represent overlapping of these micro filaments or these

26:52 filaments that we described earlier. So we have is we have the Z

26:57 , the Z line is the point the thin filaments are projecting outward.

27:04 then so the region next to it just the area where we have only

27:09 filament. All right. And so call this the I band. So

27:13 is I band. Now, on side, that's half the I band

27:17 the other side, that's the other . So in a mirror, you

27:20 off with a half an eye band on the other side, you end

27:22 half an eye band, does that of makes sense. So here's a

27:26 an IAND, there's the other half an I band. But you can

27:29 that both sides of the Z line I bands sticking out from either

27:33 OK. Then we get really, dark and what this really, really

27:39 represents is an overlapping, thick And so if you go further

27:44 you'll see that it lightens up and it gets dark again. And so

27:47 middle line that's divides the uh sarcomere in half, that's the M line

27:52 just like the Z line, it's bunch of proteins that are crossing

27:56 turned it and standing out. All . So what we have is on

28:02 side, we have a Z I'm a Z line and I have

28:05 filaments and over here, I'm an line in the middle and I have

28:08 filaments going out and then where the overlap, that's where it gets

28:13 really dark. And so where they to overlap, we call that the

28:17 band and the A band continues from they begin to overlap and where they

28:22 overlapping. So see it crosses over M line. So basically, it's

28:27 there is thick filament overlapping, that's to be a band and then there's

28:32 to be a point where there is overlap. And so it's slightly

28:35 And so that's going to be the zone. All right. Now,

28:40 you're not seeing this, I'm going demonstrate this right now because I'm gonna

28:44 out my special helper who's always stuck in the front row and he gets

28:47 , damn it, I have to this again. So he's gonna stand

28:50 here and he's gonna help me show . All right. This is how

28:56 get great grades. All right. he is going to be an M

29:00 . And what he's going to do he has thick filaments that extend from

29:03 M line. So make your thick . All right. Do you see

29:06 ? So, what we have is have that thick filament. I'm a

29:09 line. Right. And I have thin filaments. Right. And you

29:13 how they're overlapping. So, here here to here that's I starting here

29:19 going all the way over here, would be a OK. And then

29:26 inside the A, that would be H zone. And then he's the

29:30 line. Does that make sense? , do you see that?

29:34 you don't see that. All let's try it again. I am

29:38 , say I am the Z from to here where it's thin, it's

29:45 beginning here where the thick and the filament overlap that is, and then

29:51 the, where the thin filament but you still have thick, you

29:55 H and then he is the M then you just repeat on the other

29:58 just going the opposite way. Do see that? And then you just

30:03 it? We've got a whole bunch us. You could see it's

30:06 oh, it just repeats and you'd there's hundreds of these things and that's

30:09 it's so thick up there. All . Thank you so much. All

30:15 . Yeah. Yeah. Now we're see how these go through when we

30:22 a contraction, how they change because thick and thin filaments have a specific

30:28 to them. If I stick my out, does it change the

30:32 Can I change the length of my ? No, those So those you

30:40 , but a muscle contracts, the get closer together. So we're gonna

30:45 the question, how, how does happen if this can't get shorter?

30:49 does the sarcomere get shorter? All . But we're just dealing with structure

30:54 now. Now, there are other involved here. Uh We have a

31:00 that's nebula. This is the thing um helps to make the uh acting

31:05 go straight. So we want all active filaments to be uh parallel to

31:10 other. We don't want them going way and that way. And so

31:13 the middle of them, we have other molecule called nebula that says,

31:17 , this is the direction you And so it keeps it nice and

31:20 and stiff with a mo a molecule Titin. What it is is this

31:26 tiny uh spring looking structure that you here in light blue from right

31:32 It's, it basically behave like a . It's a, it's a protein

31:36 that when you shrink. Uh so to stay strong. All right,

31:42 actually serves as a bounce it back to the original shape. So,

31:47 result when returned back to the original . That's the purpose of the,

31:55 have a molecule called dystrophin. So you start getting towards the edge of

31:59 cell, um you're gonna have things don't allow for injury. In other

32:04 , there's no, there's no uh and there's no acting. And so

32:08 want to keep these things still going . And so these kind of serve

32:12 an anchor to ensure that the myo are doing what they're supposed to

32:16 All right. And finally, we this other molecule which is even less

32:20 . Uh A alba 10 is basically molecule that takes and binds act to

32:25 molecule. All right. But really key one here, the most important

32:31 the um and the nebula because without um your thick and thin filaments would

32:37 out of alignment. And when they out of alignment, you wouldn't be

32:40 to get the contraction that gotta watch these things when they fall off.

32:51 right. So the thing we're interested is something called a motor unit.

32:59 individual cell is not particularly strong. so typically, what we do is

33:04 going to bundle muscles cells together to a stronger contractile unit. A motor

33:13 simply consists of a single alpha neuron the cells that are associated with

33:19 Now, I'm gonna do a, simple demonstration here. All right.

33:24 you can laugh and say how stupid was later. All right. So

33:27 I wanted to curl this, how do you think that weighs couple of

33:33 ? Do you think I can curl ? No, you don't think I

33:36 . Some person they know have a bit of faith, right? Can

33:42 curl this? Yeah. It doesn't a lot of work. Do I

33:45 to use a lot of muscle to this structure? No. All

33:50 Now someone left their bottle. Do think the bottle weighs more than a

33:56 tiny pointer? Do you think I curl it? Thank you for your

34:00 in me. I'm making sure So, uh, do I have

34:05 use, do more work to curl heavier bottle? Yes. Ok.

34:11 you think I can curl the Thank you for your faith and I

34:19 . All right. Do I need use more muscle fibers? It's the

34:22 movement. Do I have to do ? Yeah. Do you think I

34:27 curl the table? You're wise cause cannot, that is too big and

34:32 too bulky and too heavy. I'm attempt it. I think I've done

34:36 in classes before and it's like, , it's not gonna happen, you

34:39 , even this one is just yeah, I couldn't lift the whole

34:44 . All right. The point here that for the same movement for different

34:50 . All right. So load would the, the thing I'm trying to

34:53 . I am going to have to more uh tension to bear that

34:59 And so what each of the motor represent is a portion of tension that

35:04 can produce. All right. So I'm trying to do a job,

35:08 only gonna recruit the cells that I to do the job. In other

35:12 , for me to lift that it , I'm just gonna make up a

35:15 , let's say it was 10 times motor units to do than that.

35:19 not gonna recruit all 10 times the units to curl that I might hurt

35:25 . And that's, and it's a of energy. So a motor unit

35:30 the, the group of cells that need to recruit to create a certain

35:34 of tension and the more tension I to produce the more motor units I'm

35:38 recruit into that activity in order to that. All right. Now,

35:44 are the features of this? And we're just kind of look at the

35:47 up here. So you can see we have two different motor units represented

35:51 that's blue and one that's red. right, that's the motor unit.

35:54 motor unit two. You can see they are not of equal size.

35:57 don't have to be of equal right? So you can see here

36:01 one has two, this one has . So this one has more cells

36:04 are involved. So it produces more than the one that has two.

36:07 second thing that is a feature of units is that they're not going to

36:10 clustered together. Now, the artist have the space to do this.

36:14 you can imagine if I cluster all motor units together, I'm not going

36:17 be able to pull the same way time. The purpose of each muscle

36:22 to create a very specific movement of bone. And so what you want

36:27 you want your motor units to be out so that you can repeat that

36:32 movement, even though you're recruiting in and greater tension or greater and greater

36:37 units when you're trying to produce more more tension, right? So this

36:41 here is the same movement I did the chair, right? And so

36:45 motor units are all spread out through bicep to allow me to do

36:49 And so when I'm recruiting, I'm recruiting throughout the entire muscle, not

36:54 in one place, otherwise that would the muscle to pull us a weird

37:01 . Um um And the other thing has to do with delicate versus uh

37:05 activity. Uh What if you had think of something that would be a

37:09 activity? What would be an easy for us all to kind of visualize

37:12 would be a delicate activity that you daily? Now walking, I heard

37:20 , writing and I'm, I'm sitting looking at someone holding their stylists,

37:24 ? Writing when you do that kind movement, that's a real delicate

37:28 And so there's a fine motor skill is going along with it. And

37:32 when you're doing that, what you're use is you're gonna recruit lots and

37:37 , very small motor units to get kind of activity. Now, a

37:42 activity would be something like walking. . What do I have to do

37:46 I walk? I lift my foot , I fall forward, I catch

37:49 . There's not a lot of work a lot of fine detail that goes

37:53 that. Right. So, when dealing with course activity, you might

37:58 lots and lots of muscle cells associated that motor unit, right? Because

38:03 trying to create tension quickly. Another to think about this is think about

38:12 like your ipod or your, your whatever you listen to your music

38:16 , right? Uh If you look the volume on that, what is

38:19 volume scale? Is it like 1 100 or is like 1 to 10

38:24 1 to 10? Right? So if you have 1 to 10,

38:27 basically, you're going each time you a button up, you're increasing the

38:31 , 10% right? But if you a volume scale that went 1 to

38:35 each time you click the button, only increasing the volume 1%. So

38:39 having more detail, you can fine , you know, the volume.

38:44 so that's what uh you know, delicate activities want. They want very

38:49 motor units. So I can make adjustments rather than going, you

38:54 oh no difference between that and that wanna, you know, create this

39:00 movement. So motor unit size dictates type of activity that you're going to

39:07 doing or how much tension you're going be producing and what kind of activity

39:10 gonna be using. And I don't if the volume thing really connected with

39:14 lot of, a lot of but that's how I think about it

39:17 if I want to fine tune something I want in a very simple

39:23 Now, the key feature here, what we said is that each cell

39:27 wrapped by its own connective tissue and it each has its own neuron,

39:32 ? So a motor unit like this has four neurons, but each of

39:35 has their own, it's one neuron divides and so each of them has

39:38 own connection and this connection is what refer to as the neuromuscular junction.

39:44 , that's just a fancy word for the interaction between a neuron and a

39:48 . This is no different than a that we've seen previously. All

39:52 So if you learned about the synapse you understood the synapse from the last

39:56 , you're already good to go. just gonna put some new words around

39:59 . OK. So the neuromuscular junction simply the point of contact between the

40:05 and the muscle fiber. So we're give you some special names. All

40:10 . So we're going to have the that underlies the neuron, we're going

40:15 call that the motor end plate. right. And at the motor in

40:20 , what we're gonna do is we're see a whole bunch of receptors for

40:22 neurotransmitter that's being released by the the alpha neuron. So, the

40:29 that we're gonna use. Always, , always, no exception to the

40:32 . This is the one time I'm tell you is a set of

40:35 All right. So it's always a of Colling and it's always,

40:39 always, always, always excitatory. , if I create a contraction,

40:45 releasing neurotransmitter, it excites, it the contraction. When I stop the

40:50 , I stop sending a signal and causes the muscle to return back to

40:54 original shape. Right? You don't to tell it to relax. It

40:59 does. So because of the titan , remember it causing it to go

41:04 to the original shape. All So, um we have Aceto

41:11 So again, what we'll see is see an travel down opens up calcium

41:15 , calcium binds to the vesicles, up, the vesicles releases the Aceto

41:20 Aceto coin crosses the synaptic cleft. what it'll do is it'll bind to

41:24 Aceto coline receptors at the motor in and it will open up, allow

41:28 to come into the cell. And thing that it's going to produce is

41:31 greater potential that we call them. All right. Now, this is

41:36 same thing as an Epsp. All . And, but here, the

41:41 is an in plate potential. So just defining, oh, this is

41:44 at the neuromuscular junction. Now, we learned about the neurons, we

41:48 , oh, we have to add things together to get a strong,

41:52 response in the in the downstream right? So we have to do

41:57 additive, some sort of summation in muscle cell. The PP is big

42:03 that one ep oh look, I out of battery. Good news.

42:08 One Epp results in one action All right. So it's a 1

42:14 1 ratio. You don't do anything . It just does. There we

42:30 . Oh And this one's dead The other one's dead. I wonder

42:36 much has been missing. You're like ? But everything is now recording

43:29 All right. So we have an one Epp is equivalent or strong enough

43:38 produce a single action potential in the cell. All right. And remember

43:44 is an action potential? It's simply signal that travels along the surface of

43:47 cell to cause something to happen in neuron. What was it causing?

43:51 was causing the release of neurotransmitter, ? In a muscle cell? What

43:55 you think an action potential is responsible causing the contraction? Right? So

44:01 act potential is not a contraction, action potential is a signal to create

44:06 contraction. OK. So this is of what you're doing now, the

44:15 that we're producing, we have a name for it. We call it

44:18 twitch. All right. A twitch not what you're used to. It's

44:22 this. So people are asleep and look up but they missed it.

44:27 I do it again? All That's not a twitch. I

44:31 it is, but it's not the that we're producing. You cannot visually

44:36 the twitch in a muscle. All , you can measure it. You

44:40 , you can put in a probe you can see a ha I'm seeing

44:44 contraction at the level of you the micro level, but you cannot

44:50 see a twitch. In fact, moving my muscle like that, that's

44:53 actual larger contraction that's called uh all or all right. Now, what

45:00 is showing you here in this once all this is talking about is

45:04 gonna, we're gonna connect those three together. We have an action potential

45:08 coming down the neuron. We have action potential in the muscle cell and

45:12 creating our twitch. So this is it's showing you and notice the timing

45:16 . So we have the action potential the neuron precedes the action potential in

45:20 fiber. Does that make sense if sending a signal to you, do

45:25 expect to respond before at the same or after I send you the signal

45:31 ? And so that's what we're They're very, very close together because

45:34 signaling is very, very quick, ? But one proceeds the other.

45:39 the uh a pen neuron results in action potential in the muscle fiber.

45:45 what we said is that the ax is not the contraction. The ax

45:49 is the signal that causes the In fact, where the ax potential

45:55 precedes the contraction by a large And again, these are in

46:01 So large is a relative term, ? So in other words, what

46:05 do is we go a potential action and then we get contraction.

46:11 That's how quick it is. And this period of time where the a

46:14 is taking place prior to the contraction referred to the late as is referred

46:19 as the latency period. So it's you got the signal and then you

46:25 and you go through a contraction phase then you go through a relaxation

46:29 which is what you see here. , then relaxation. And as I

46:34 this twitch, this contraction that you're here isn't big. You can't visually

46:40 it, it doesn't produce any sort tension to do anything. If you

46:43 to get something to happen, you to get a lot of these twitches

46:46 add up together. So the additive in a muscle is in the

46:52 All right, we don't have the potentials to add up here, which

46:56 be a signal. We, we the action potential. So what we're

47:00 do is we're gonna use action potentials the frequency of the action potentials to

47:05 lots and lots of contractions that add . So twitches are added through something

47:12 called wave summation. And so what looking at here in this little graph

47:17 the little red arrows up here represent potentials. They're saying here's the

47:23 here's the stimulus, here's the here's the stimulus. And then what

47:26 doing is we're looking at the amount tension that's being produced. So if

47:29 get an ax potential, I get small wave, there's contraction relaxation.

47:33 if my stimulus is before I get full relaxation, then I start the

47:39 one and I go up a little higher and I come down and I

47:42 my next action potential. I go again a little bit higher.

47:45 this is not good. This is uh acceptable in terms of a muscle

47:51 , right? What these are too apart to really do anything. And

47:54 we get this incomplete test tetanus and , it's not a functional way to

47:59 a contraction. So instead what we is when we are trying to create

48:03 contraction in any muscle is we're getting series of action potentials that are

48:07 really close together. In other you're never letting the contraction find a

48:13 of relaxation. So when I'm moving arm up, what I'm doing is

48:17 going a potential potential is really, fast like this. And so I'm

48:21 creating a sustained contraction or a smooth contraction that ultimately results in a sustained

48:29 . So I reach muscle tension at maximum level for that motor unit when

48:34 happens. All right. And so muscle contracts and stays contracted to do

48:39 job. And then when I'm done action potentials the muscle relaxes. So

48:46 I did this, it's just a of motor units, but they're going

48:49 a sustained tetanus. And when I , the technique is finished. All

48:56 , when I lift up the I'm recruiting more cells, more motor

49:01 , but they're all going through the pattern with a lot of action

49:06 that kind of makes sense. So actual potential is not the contraction.

49:11 , it's the signal if I want sustain contraction and something that actually can

49:16 work, I increase the rate at the action potentials are arriving. So

49:21 can imagine any sort of movement you're , whether it's wiggling your feet,

49:25 it's blinking your eyes, breathing. are a series of action potentials that

49:29 going very, very quickly, they're the muscle to contract and then you

49:33 it and then it causes the muscle relax. Ok. But we still

49:38 said how does this all happen so ? Are you guys with me back

49:44 the back with me? All right over here. Oh, I like

49:48 double thumbs up. That's even Who? Ok, just making sure

49:59 a meme the other day. It basically Jason's hunting for somebody,

50:04 inside a house. And so the is cowering behind the door and

50:08 how to find a Cougar. And goes whose house and from the other

50:13 s house, like know your I guess. So, what this

50:23 is basically doing is it's showing you we do this recruitment. This idea

50:31 what we're gonna do is we're going , if we have a small

50:35 we're just gonna have a single group a single motor unit involved. And

50:40 we increase our activity, we're this, this motor unit has a

50:45 tension that it can produce. So I need to create greater tension,

50:49 is when I recruit in another uh of motor units and then if I

50:53 to create more tension, more tension going to be produced as a result

50:58 more recruitment. And so it's a effect of all of these muscle cells

51:05 through that sustained contraction that we just over here. The other thing is

51:11 these cells have only a certain amount energy that they can produce. So

51:17 is a maximum amount of tension and tension can only last a certain amount

51:21 time. This is what we refer as fatigue. Now, if you're

51:26 doing a lot of work. So example, if I was, if

51:29 told me, hey, um, need to hold this out to your

51:32 forever now or we're gonna shoot you the head. Do you think I

51:36 do that? Do you think I hold this like this with the threat

51:39 being shot in the head? probably. Right. Because what I'm

51:43 do is when those motor units that , that I'm using to hold my

51:47 up, become tired, I can them by other motor units,

51:51 So I can recycle and go through a process of recruiting different motor units

51:58 letting the motor units rest if I it with this chair. However,

52:04 you think I could hold this chair to the side for more than 30

52:09 ? You know, I don't with a gun in my head,

52:13 don't know this is already tiring. what's happening here is because I recruited

52:18 motor units, they're all fatiguing At the same time, there's nothing

52:22 replace the fatiguing motor units. So begin to fail, they have to

52:27 because they run out of energy, run out of oxygen. So what

52:32 do is what we, what we this is asynchronous um recruitment,

52:38 So the idea is, is, , when I don't have a lot

52:41 motor units, I'm just going to kind of recycling through and keep going

52:43 and recruiting different ones and I can the activity for long periods of

52:47 But if I don't have a lot motor units that I can replace tired

52:51 with, then I start experiencing the and I can no longer produce the

52:56 necessary to do the function that I'm to accomplish or the job that I'm

53:00 to accomplish. All right. typically, what we do is we're

53:07 to recruit the fatigue, fatigued, , the fatigue resistant muscles first and

53:14 bring in the fatigable muscles last. . So the idea is your muscles

53:19 know what type of job they're They're just being told to do

53:22 And so they're going to, they're designed, prede designed to say,

53:25 deal with the, the, the stuff first and we're just gonna kind

53:29 be resistance, but then when they out, then we'll bring in those

53:33 ditch that those last little muscles that just gonna try to hold out for

53:37 last little bit and hopefully the job be done here. All right.

53:41 there's a pattern to which they'll be . All right back to the beef

53:46 and the cheesecake, um, muscle . Now, muscle tone is simply

53:54 continuous or passive partial contraction. And I throw these two models up here

53:59 they both demonstrate muscle tone. All . So this person isn't doing any

54:04 . They're just standing there and they're pretty good. This one's not doing

54:08 work other than the big smile, has her muscles and she's looking pretty

54:13 . Now, why is this Well, when your muscles are,

54:17 , are toned, what they they're being sustained in a partial

54:22 which is represented on the surface because the presence or lack of body

54:27 we all have muscle tone. So if you have tons of body fat

54:30 it's hiding all your muscle tone, muscles do have tone to them.

54:34 what we're seeing here in these because they have less fat, we

54:37 actually visually see it on the And so because of the way that

54:40 muscles are wrapped in their connective tissue the shape that they're formed in,

54:44 give us this appearance on the purpose on the surface. All right,

54:49 typically, uh you, if you less body fat, that doesn't mean

54:54 don't have muscle tone. I in other words, what I was

54:58 to get here is saying is that fat and less body fat have no

55:01 on your muscle tone. It's how work your muscles do, how much

55:06 allow them to, how much you've them. So they sustain a contraction

55:12 of the of the amount of work they're expected to do. Um So

55:18 muscle tone is usually associated with strength power because they're constantly being used in

55:23 way. Um Generally speaking, when say you have muscle tone, it's

55:30 more motor units that are in the state rather than a total relaxed state

55:34 kind of what we're getting at And really what I want, why

55:37 bring all this stuff up is because themselves, each individual muscle has a

55:43 length associated with them. And I think I really ever ask a question

55:49 about this. So you, you kind of just take this in as

55:53 , OK, so a muscle becomes when it gets out of its op

55:57 length. And I'll just explain why I stretch a muscle too far,

56:02 fibers themselves are no longer overlapping. , and so it takes more work

56:07 them to get to the point where can produce the tension that they're designed

56:10 produce. But if I push them , in other words, if I

56:14 a AAA deeper contraction, the muscles no place to go. You

56:19 if the fibers are running up against Z lines, they can't go past

56:23 Z lines. And so there's a range in which a resting muscle

56:28 so that it can do the work it does. And so they're not

56:33 in a relaxed state, they're in partial contracted state, but it's enough

56:38 them to be able to go either . Yes. All right. So

56:46 we're gonna do now is we're gonna our mouse trap. Remember we've talked

56:50 mouse traps as no step. A . B step C step D,

56:54 doing the same thing with the muscle everything is going to fall into

56:58 Uh, one year I had to this without a computer. My computer

57:01 in the middle of class. And like, all right. Well,

57:04 do I do this? And I done it on a chalkboard. And

57:06 I've just spent how much time um an hour laying the foundation for something

57:15 gonna take five minutes to explain. , you're like, well, why

57:19 you just do the five minutes? , because you need the other words

57:23 understand what we're talking about here. this literally is what happens first.

57:27 happens, second, what happens? type stuff and it's going to those

57:30 that we just learned, we're gonna them together. So the first thing

57:33 we're gonna see when we're dealing with muscle contraction is excitation, followed by

57:37 happening at the triad. And then , uh how do we get this

57:42 bridges formed? What is this, interaction between these mild filaments? All

57:48 . So our first step here is to be this at the neuromuscular

57:51 what's really going on there? All . So we have an, a

57:56 active potential is gonna go down through synaptic knob of the alpha neuron.

58:00 gonna open up those calcium channels, pours into the neuron. Calcium binds

58:04 the vesicles causes the vesicles to open and release Aceto coline cyto colon goes

58:09 the synaptic cleft binds up to the coline receptors that creates an Epp in

58:16 muscle cell at the in play. Epp results in an action potential that

58:20 then travel along the surface of the . So far, anything sound hard

58:25 interesting. No stuff we've already seen . Now we talked about the t

58:31 , the T tubules are an extension the surface, right? So the

58:36 is along the outside of the But because now I have a tube

58:39 goes through the cell, that surface in through that cell. And so

58:45 attrition are gonna start working down through tubes uh as they also go along

58:49 surface. And it's this signal that important because those t tubules are associated

58:58 what you the terminal cistern, they're of the triad, right? And

59:10 here as the a pension goes down , nearest the T tubule, those

59:17 the terminal cyn of the sarcoplasm All right. On those terminal cni

59:24 a receptor called the rio receptor in T tubule associated with those rio receptors

59:30 the DH P receptor. Now, is complex and what I'm just describing

59:35 , this relationship. But basically, two molecules that are shaking hands.

59:40 I stimulate one molecule, it's going stimulate the other molecule. And so

59:44 the purpose of the action potential is do is to activate the DH P

59:49 , right. So they're just like vated sodium channels. They're not,

59:53 they're like that. So when the comes along, it causes the DH

59:57 receptor to become activated. And because associated with this other receptor that's found

60:03 the terminal end over here, the cni you're going to activate that one

60:08 well. So I open up these receptors and when the rine receptor is

60:14 up, what's gonna happen is the that I stored up in my sarcoplasm

60:18 curriculum begins flowing out into the cytoplasm the muscle cell. So calcium starts

60:24 outward, flooding the inside of the . So far. Are you with

60:30 ? So a potential results in a , a potential travels down, activates

60:34 receptor DH P which results in the of another receptor Rryr which is rine

60:40 which causes calcium to enter into the . So the key thing here,

60:44 is entering in the cell as a of an action potential. Ok.

60:50 does calcium come from? Does it from the outside? No, it

60:54 from the sarcoplasm partum, right? what we're saying. So here from

61:00 the outflow, so calcium from the partic goes out into the cytoplasm.

61:08 we said calcium is important. Why it important? Here we are my

61:18 we are thin filament. This is min head. This is a thin

61:22 . So remember the thin filament had parts thin filament consisted of Ain,

61:27 does the fun stuff, a blocking called troy. And another molecule that

61:32 a hinge that was called troponin, ? How do I make the troponin

61:37 calcium? Right? Ends up And that's what this picture is showing

61:41 . There is a lot of detail another textbook. Don't worry about all

61:43 detail, but basically it says, , I can't interact with my

61:47 What do I do? I add Callum, it causes that to move

61:50 of the way. What can I do I can interact with my

61:53 So what calcium does is it pulls troponin out of the way so that

61:58 can interact. So our mouse trap from the beginning, I'm just going

62:03 keep doing this over and over again we get an ax potential down the

62:06 cause the release of the neurotransmitter co causes an Epp which results in an

62:12 potential that travels along the surface of muscle cell goes down through the T

62:16 , opens up the DP receptors which the rio on receptors to open

62:20 which releases calcium from the sarcoplasm Calcium binds to the thin filament,

62:27 troponin troponin changes the shape pulls troy of the way. And now I

62:34 get actinomycin to interact and when they , I'm going to get a cross

62:39 , that is the term when they with each other crossbridge, when they

62:43 with each other, one pulls the . So the the floppy head pulls

62:49 the acting molecule and brings it towards M line. Now, the cross

62:58 when we're doing the polling results in we call the power stroke.

63:04 you've been trained to believe your entire that energy is important for muscle

63:09 right? And it is, but what's causing the interaction. Is it

63:14 TP that causes the interaction? Go to slide. Does a TP cause

63:19 interaction? What causes the interaction? ? A TP is doing something but

63:25 not causing the interaction. So what a TP doing? Well, it

63:29 an important role in the power stroke it's not the way you think it

63:33 . All right. So you can anywhere on this cycle here,

63:38 And, and because it's a circle you can be correct. But

63:41 what I wanna do is I want point out here, let's just say

63:44 we've already had the interaction, calcium along. We already had the cross

63:48 bridge formed and we pulled on the molecule. What a TP does is

63:54 breaks the interaction between the acting and mycin. And then when I break

64:00 A TP and remove the energy, I'm doing is I'm resetting and rec

64:06 the mayas and head so that it interact again. All right. So

64:12 T P's job is to break the and reset the head. Now,

64:18 the way you can remember it. right. When somebody dies, what

64:24 we say happens to the body? does it do? It gets,

64:28 gets stiff, doesn't it? And do we call that stiffness? Rigor

64:34 ? All right. So what is mortis? Well, it's based on

64:37 going on here. Every cell in body has a certain amount of A

64:41 . That's, that's being made always . It's a very small amount,

64:45 it's there. And that's what keeps cells alive when your cell dies,

64:49 A P is available for use to cell until it runs out. And

64:53 you can imagine I have nothing holding calcium anymore. So the calcium begins

64:59 out of the sarcoplasm medicum inside a cell and it starts doing what it

65:04 because this is just a chemical And so it makes available the interaction

65:08 mice and an act in. So get the power stroke and then what

65:12 do is you have a TP to the bond and reset and power repet

65:16 reset, power stroke reset. And there's no A TP and you're now

65:21 in a sustained contraction and that's rigor because I can't break the bond.

65:27 rigor mortis is stiffness as a Now, I get to tell you

65:32 story my grandfather told me I do know if this is true. You

65:36 how grandfathers like to make up stories he was, y'all's age. He

65:41 a job in a mortuary and he a night watchman. He said so

65:46 my, my ears are perked and , this is really true.

65:49 you know, when you're 10 years , it's like he said, he

65:52 going through the morgue and a body the table sat up. Yeah.

65:59 then he said he just dropped the and never went back. Now.

66:02 don't know if that's true. But mean, but that's what can

66:05 That's rigor mortis. It's basically the going into that sustained contraction and staying

66:10 . And then what happens over time eventually the body begins breaking down and

66:14 those fibers break down and the body again. So, but that's how

66:20 remember a TP. What it does it causes the breaking of the bond

66:25 the Actinomycin. And then when you the A TP, that's when you

66:30 the power stroke and you just repeat over and over again. So as

66:34 as a TP is available, you're be able to do power strokes,

66:37 you can't have a power stroke unless is there in the first place,

66:43 ? So those are the differences, allows for the interaction of the cross

66:49 . A TP allows the power Alright. So the whole process,

67:01 pencil in the neuron releases neurotransmitter, Coline causes an Epp at the end

67:08 results in an A pencil. A travels down through the T tubule opens

67:14 the DH P receptors which opens up iodine receptors on the terminal cistern.

67:18 sarcoplasm partum causes calcium to outflow that the AX and the my and interact

67:23 a TP available. What I can is I can go through a series

67:26 power strokes to ensure that a contraction so far. So good,

67:32 So what is a contraction? Well, it's not the shortening of

67:37 fibers themselves. What we have is have fibers sliding over each other.

67:42 right, this is what is called sliding filament theory. Can I see

67:45 again? Yeah. All right. remember he was the M line,

67:50 ? And as the M line, had what type of fibers thick,

67:55 ? So look at his thick Now he doesn't move. Remember we

67:58 with the score we had Z lines either side. And so you can

68:02 there's this interaction here between the thin the thick filament. And so what

68:06 is the my and the act are . So his fingers are pulling on

68:10 . And what happens is I pull in. Now notice did his arm

68:16 , did my arm shorten. But there was another Zon on the other

68:19 , did we get closer together? . So what we're seeing here is

68:23 seeing the sliding of the thin and thick filaments over each other. And

68:27 what we're seeing is we're seeing a of the eye band, right?

68:31 here's the eye band to start off . And then when I moved

68:34 the IAND got shorter, the A get change length. No, because

68:41 the A band represents is where there's . So whether I'm here or whether

68:44 there, his arms stay the same . So the A band stays the

68:48 length. But when I move so here the I band got

68:51 Did the H band get shorter? , it did look. So,

68:55 I am, there's that H Now, when I get over

68:59 did the A band get or the get shorter? Yeah. So the

69:03 and the eighth shrink, the A the same side, the whole score

69:06 shorter. All right. Thank Obviously, when I contract a

69:25 I want to be able to relax the contraction, right? So each

69:30 is a contraction and relaxation. So do I relax? Well, I

69:35 need to make sure that the muscles or the thin, the thick filaments

69:39 interact. So how do I do ? Well, just get rid of

69:42 calcium. All right. If there's calcium, there's no calcium to bind

69:47 the troponin, no troponin, that Troy can't be moved out of the

69:51 that can't be moved out of the . Then the thick, the thick

69:54 the thin dome can interact. So we gotta do is just get rid

69:59 all the calcium. And so that's relaxation is. So in essence,

70:04 when we release the Aceto Coline, is a enzyme Aceta Colin Aster,

70:08 there to chew up all the Aceto . So it's already there. So

70:12 we're doing is we're terminating the signal we describe that in one of the

70:16 lectures in the last unit, That's how we terminate. So,

70:19 there is no Aceto Cole, there's Aceto Cole to bind to the aceto

70:23 receptors. If there's no Aceto Cole bind the aceto coin receptors, you

70:27 get in plate potential. If I get an in plate potential, I

70:31 get an action potential. If I get an action potential, I don't

70:35 up the DH P receptors. If don't open up the DH P

70:38 I don't open up the iodine If I don't open up the rio

70:41 receptors, I don't have any calcium the cytoplasm. So this is why

70:47 important to kind of walk through your . All right. All right.

70:51 , how do I get the calcium ? I've released all the calcium.

70:54 do I get it back in to sarcoplasm reticulum? Well, there's

70:58 These pumps are called circus. Do have it up there? I don't

71:02 , yeah, I do called All right. Circa is short for

71:06 endoplasm, reticulum, calcium pump. where the name comes from. All

71:11 . But the circuit pumps are always and they're pumping at a constant

71:15 But when I open up the right receptors, more calcium leads and gets

71:19 in. So that's why we end with more calcium. But if I

71:21 have right iron receptors open, then pumps are just pumping and they remove

71:25 calcium. And so the calcium goes the sarcoplasm and that's why we end

71:29 with no calcium in the side is right. So that's as simple as

71:35 is. That's what relaxation is. action potentials, no calcium, no

71:41 , no contraction, it just goes to its original shape. So how's

71:47 ? Was that hard? Some of , yes. Could you, could

71:53 walk through the seven steps? I , create some sort of cadence for

71:58 . Yeah, I think you Now we did say a TP is

72:05 and the reason it's essential is because allows for the power stroking. Um

72:10 we have a limited store and so we do is we define where that

72:14 TP comes from. So um A can be broken down into three different

72:20 . We have, what is it the immediate supply? It's, this

72:22 gonna be through something called the phospho or what we can do is we

72:27 make it through anaerobic cell, uh respiration or we can use aerobic cellular

72:32 . And what these last three slides , two slides are just describing those

72:36 things for y'all. All right. the phospho system is just a fancy

72:40 for saying. Look, um I a P and so what I'm gonna

72:45 is I'm gonna break it and I make in our AD P and organic

72:48 and release energy. And so this what we're doing through this process.

72:53 if I run out of this is there another source for A P

72:57 I can go to immediately to make A TP? And so one way

73:01 we can use Myo. So what does, it says, look um

73:04 Patp and its friend A A MP just basically this, this Ribo sugar

73:10 just has different numbering of phosphates on . So A TP S3, ad

73:15 has two A MP has one. the T the D the M is

73:20 die mono, that's where it comes . And the P is phosphate.

73:24 so if I have a AD P I take another AD P, I

73:28 steal one of the phosphates here to and add it to this so I

73:33 get a TP. And that's basically Myo does. And this will give

73:37 a little bit of energy. So start off about 56 seconds worth of

73:41 just in what's in storage. And I can add another two if I

73:46 this byproduct and add it to and it through myo, this is part

73:51 my uh the foy system. The thing I can do is a little

73:55 more complex. This is creatine phosphate . What I'm doing is I'm storing

74:00 energy in another molecule. And so I'm doing is I am taking energy

74:08 the form of A TP and I'm the phosphate to make AD P.

74:13 what I'm doing is I'm taking that and storing it on creatine to make

74:16 new molecule called crete phosphate. Now just going to make these numbers

74:20 But let's just say I have 100 of A P that I can keep

74:23 the cell. But I also have molecules of creatine. That means I

74:27 take a phosphate from each of those PS and put it onto the creatine

74:31 make 100 creatine phosphates. And then can add a phosphate to that ad

74:35 that I have left over. And I have another 100 A P.

74:38 in essence, what I'm doing is doubling how much A TP I have

74:42 that reaction that I'm doing here is . I could take crete phosphate,

74:46 the phosphate from it, add it here and make a TP there and

74:50 just use it in that reaction. it's just a way of shifting energy

74:56 so that I can increase my That kind of make sense. Let

75:01 put it another way. Let's say want to hold 100 jelly beans.

75:05 want to eat 100 jelly beans, each hand can only hold 50.

75:08 . What do I do? I put the jelly beans someplace else.

75:12 about my pocket? Right. Does change that? It's a jelly bean

75:16 I can get to later. but it's no longer a hand jelly

75:19 . It's a pocket jelly bean, ? So I have to go through

75:24 hand jelly beans first, but then can reach in my pockets and now

75:27 have hand jelly beans again. All . Do you distinguish between your jelly

75:32 , whether they're hidden or pocket jelly ? Ok. That's an easy way

75:35 do that. All right. So this is, is just shifting where

75:38 energy is. So they might require step to get to it, but

75:42 still there. So it's a form storage. And so this is another

75:45 or 15 seconds of energy before I to actually start making energy from

75:51 The other forms are making energy from and we're not going to go through

75:55 process. We don't have to do the steps, we're not going to

75:58 metabolism. What I want to get in terms of understanding these two things

76:03 simply that one requires oxygen. That's long term. That's the aerobic and

76:08 requires multiple steps. You've all learned at one point because of biology.

76:12 may not remember all the steps, we had glycolysis. We had um

76:16 the pyruvate steps, we had the acid cycle and then we had the

76:21 um uh the electron transport chain. through all these multiple steps, you

76:27 get a lot of energy as long you have oxygen available to receive the

76:31 . So what you're doing is you're electrons around to, to create this

76:35 TP. All right, you can a whole bunch and so we store

76:39 the oxygen to make this happen so we can actually produce this energy.

76:43 if you don't have oxygen available and still need to do work. If

76:48 can't do the work, you're going die. And so what we can

76:51 is we can shortcut this and all right, we're going to ignore

76:53 oxygen. We're just going to use first couple of steps and we're

76:57 we're gonna kind of bypass all this stuff, but we're only going to

77:00 a little bit of energy. And the anaerobic, the short term quick

77:06 energy thing only produces a small amount energy. So this is not a

77:10 term solution. It's a last Your body wants to do this.

77:16 just as an example, if you're sprinter, do you need to wait

77:19 make all that energy? No, want to use something quick and

77:23 So you're gonna use short term you're gonna use the glycolysis. If

77:27 , if you're a long distance runner a long distance swimmer, whatever,

77:31 are you gonna do? You're gonna this because you can sustain activity for

77:36 long period of time. All guys, there is a football

77:40 Go to it tonight, find your , show up, make a loud

77:45 . We got a cage. Let's those mountaineers wish they didn't show up

77:49 campus. We do so we better a good today. All right,

77:58 over

-
+