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So we have two types of colors and two types of wings. We have the color gray, which is dominant over the color black and the color gray is given by uppercase uppercase g. The color black is given by lowercase g. By the same exact token, we have two types of wing types. We have normal wings and we have vestigial wings. Now, normal wings which are functional are given by uppercase N and vestigial wings, which are nonfunctional, are given by lowercase N. So in this example, in this experiment, we're basically mating a female individual that is homozygous dominant for the color trade and homozygous recessive for the wing trade with a male individual. So we're mating this with a male individual that is homozygous recessive for the color and homozygous dominant for the wing type. Now, in a what is the genotype of the f one generation offspring that is produced when we make these two individuals? | Gene Mapping, Percent Recombination and Map Units .txt |
Now, normal wings which are functional are given by uppercase N and vestigial wings, which are nonfunctional, are given by lowercase N. So in this example, in this experiment, we're basically mating a female individual that is homozygous dominant for the color trade and homozygous recessive for the wing trade with a male individual. So we're mating this with a male individual that is homozygous recessive for the color and homozygous dominant for the wing type. Now, in a what is the genotype of the f one generation offspring that is produced when we make these two individuals? To actually determine what the genotype is, we first have to answer the question what are the gametes produced? What are the gametes that are produced by these two types of individuals? So let's begin with our female individual. | Gene Mapping, Percent Recombination and Map Units .txt |
To actually determine what the genotype is, we first have to answer the question what are the gametes produced? What are the gametes that are produced by these two types of individuals? So let's begin with our female individual. So we have uppercase G, uppercase G, lower case and lowercase N. So uppercase G, uppercase G, lower case and lowercase N. And before they actually mates, they have to produce our gametes, the sex cells. And in this case, because we have female, these are going to be X cells. Now, because we're assuming these genes are linked, that means they're located on the same exact chromosome. | Gene Mapping, Percent Recombination and Map Units .txt |
So we have uppercase G, uppercase G, lower case and lowercase N. So uppercase G, uppercase G, lower case and lowercase N. And before they actually mates, they have to produce our gametes, the sex cells. And in this case, because we have female, these are going to be X cells. Now, because we're assuming these genes are linked, that means they're located on the same exact chromosome. And in this particular case, if you carry out the process of Meiosis, we only have one type of gamete that can actually form. And that gamete will have a chromosome that contains an upper case G, a lowercase N. So this is our X cell, and this is equivalent to basically redrawing it in the following diagram. So we have this chromosome that contains lowercase ng and uppercase G, lower case ng, an uppercase G gene. | Gene Mapping, Percent Recombination and Map Units .txt |
And in this particular case, if you carry out the process of Meiosis, we only have one type of gamete that can actually form. And that gamete will have a chromosome that contains an upper case G, a lowercase N. So this is our X cell, and this is equivalent to basically redrawing it in the following diagram. So we have this chromosome that contains lowercase ng and uppercase G, lower case ng, an uppercase G gene. And so 100% of our gametes will look like this. Okay? Now we're crossing it with a male that is lowercase G, lowercase G, uppercase and uppercase N. And likewise, by the same exact reasoning, if we carry out the process of Meiosis, we'll see that only one type of gamete can actually be formed in this particular case. | Gene Mapping, Percent Recombination and Map Units .txt |
And so 100% of our gametes will look like this. Okay? Now we're crossing it with a male that is lowercase G, lowercase G, uppercase and uppercase N. And likewise, by the same exact reasoning, if we carry out the process of Meiosis, we'll see that only one type of gamete can actually be formed in this particular case. In fact, 100% of the gametes will have this genotype, as shown. So lowercase g, uppercase n. So it's a sperm cell. So let's designate that with this squiggly line. | Gene Mapping, Percent Recombination and Map Units .txt |
In fact, 100% of the gametes will have this genotype, as shown. So lowercase g, uppercase n. So it's a sperm cell. So let's designate that with this squiggly line. So we can either designate it this way or by using the chromosome symbol. So we have lowercase G, uppercase N, okay? So 100% of these genes will basically look like this. | Gene Mapping, Percent Recombination and Map Units .txt |
So we can either designate it this way or by using the chromosome symbol. So we have lowercase G, uppercase N, okay? So 100% of these genes will basically look like this. So this produces this sperm cell. This produces this X cell. When they combine to form the Zygote, we basically form. | Gene Mapping, Percent Recombination and Map Units .txt |
So this produces this sperm cell. This produces this X cell. When they combine to form the Zygote, we basically form. So this chromosome combines with this chromosome, and we form the following Zygote that contains uppercase G, lowercase N. So uppercase G and lowercase N. And then we have lowercase G uppercase, and that comes from this, right? So we have lowercase N. So let's write that like so, sorry, uppercase N, then we have lowercase N here. So lowercase N, uppercase G that came from the female, and lowercase G that came from the male. | Gene Mapping, Percent Recombination and Map Units .txt |
So this chromosome combines with this chromosome, and we form the following Zygote that contains uppercase G, lowercase N. So uppercase G and lowercase N. And then we have lowercase G uppercase, and that comes from this, right? So we have lowercase N. So let's write that like so, sorry, uppercase N, then we have lowercase N here. So lowercase N, uppercase G that came from the female, and lowercase G that came from the male. And so this will be the genotype of all the offspring produced in the F one generation. So f one generation genotype. Okay, now let's move on to Part B. | Gene Mapping, Percent Recombination and Map Units .txt |
And so this will be the genotype of all the offspring produced in the F one generation. So f one generation genotype. Okay, now let's move on to Part B. In Part B, when we mate an F one generation female, so what that means is we take a female that has the same genotype as the f one generation. And what that basically means is this is the f one generation. So we have a female that has a genotype that is uppercase G, lower case G, uppercase N, lowercase N, and we make this with a homozygous recessive male that is homozygous recessive for both traits. | Gene Mapping, Percent Recombination and Map Units .txt |
In Part B, when we mate an F one generation female, so what that means is we take a female that has the same genotype as the f one generation. And what that basically means is this is the f one generation. So we have a female that has a genotype that is uppercase G, lower case G, uppercase N, lowercase N, and we make this with a homozygous recessive male that is homozygous recessive for both traits. So homozygous recessive for both traits means we have lowercase G, lowercase G, lowercase N, lowercase N. So when we mate or cross an F one generation female, this individual here with a homozygous recessive male, this individual here, we obtain 2000 offspring. So we have 2000 individual fruit flies. Now, if we assume that the traits, the color trait and this wing type trade are linked, that means they are located on the same chromosome, but we assume no crossing over actually took place. | Gene Mapping, Percent Recombination and Map Units .txt |
So homozygous recessive for both traits means we have lowercase G, lowercase G, lowercase N, lowercase N. So when we mate or cross an F one generation female, this individual here with a homozygous recessive male, this individual here, we obtain 2000 offspring. So we have 2000 individual fruit flies. Now, if we assume that the traits, the color trait and this wing type trade are linked, that means they are located on the same chromosome, but we assume no crossing over actually took place. What will be the expected genotype distribution between those 2000 offspring that are produced? So basically, the entire point of Part B is to note that no genetic recombination actually takes place because no Crossing Over takes place. So once again, to determine what the genotypes of the offsprings are we have to find what the gametes that are produced are so we have two types of gametes in this particular case, the question is why? | Gene Mapping, Percent Recombination and Map Units .txt |
What will be the expected genotype distribution between those 2000 offspring that are produced? So basically, the entire point of Part B is to note that no genetic recombination actually takes place because no Crossing Over takes place. So once again, to determine what the genotypes of the offsprings are we have to find what the gametes that are produced are so we have two types of gametes in this particular case, the question is why? Well, because no crossing over actually took place. And what that basically means is the same two gametes that were combined to produce this f one offspring. So, namely, this gamete. | Gene Mapping, Percent Recombination and Map Units .txt |
Well, because no crossing over actually took place. And what that basically means is the same two gametes that were combined to produce this f one offspring. So, namely, this gamete. And this gamete will be produced in this particular case because no new recombinant gametes are actually formed because no crossing over actually took place. And so when Meiosis actually takes place so we replicate these, then they divide to form haploid cells. Those Haploid cells divide. | Gene Mapping, Percent Recombination and Map Units .txt |
And this gamete will be produced in this particular case because no new recombinant gametes are actually formed because no crossing over actually took place. And so when Meiosis actually takes place so we replicate these, then they divide to form haploid cells. Those Haploid cells divide. What we form are a gamete that contains uppercase g, lowercase M, and a gamete that contains a lowercase g, uppercase N. So one of these gametes will contain a chromosome that has uppercase g. So uppercase G, lowercase N, right? Why? Well, because this individual contains these two chromosomes meiosis takes place, separates them and so we have uppercase g, lower case N and then this one has the other one lowercase g, uppercase N so lowercase g, uppercase N and so 50% of the gametes will have this genotype and the other 50 will have that genotype. | Gene Mapping, Percent Recombination and Map Units .txt |
What we form are a gamete that contains uppercase g, lowercase M, and a gamete that contains a lowercase g, uppercase N. So one of these gametes will contain a chromosome that has uppercase g. So uppercase G, lowercase N, right? Why? Well, because this individual contains these two chromosomes meiosis takes place, separates them and so we have uppercase g, lower case N and then this one has the other one lowercase g, uppercase N so lowercase g, uppercase N and so 50% of the gametes will have this genotype and the other 50 will have that genotype. So 50% this, 50% that. Now, in this particular case, things are quite simple because we only we only form one type of sperm cell that contains uppercase g, lower case g, lower case N. So lowercase g, lower case N. And that is 100% of the offspring. And so this always forms this. | Gene Mapping, Percent Recombination and Map Units .txt |
So 50% this, 50% that. Now, in this particular case, things are quite simple because we only we only form one type of sperm cell that contains uppercase g, lower case g, lower case N. So lowercase g, lower case N. And that is 100% of the offspring. And so this always forms this. But this can form two. Now, if this combines with this, what we basically form is offspring number one that contains well, we basically have uppercase g, lowercase g, or it should be uppercase g with this green color and lowercase g with this green color and then lowercase and lowercase N. So lowercase N, lowercase N. The second type of offspring that is produced is so if this combines with this, we have lowercase g, lower case g, uppercase and lowercase N. And because this is 50% and 100%, so .5 times one gives us zero. Five. | Gene Mapping, Percent Recombination and Map Units .txt |
But this can form two. Now, if this combines with this, what we basically form is offspring number one that contains well, we basically have uppercase g, lowercase g, or it should be uppercase g with this green color and lowercase g with this green color and then lowercase and lowercase N. So lowercase N, lowercase N. The second type of offspring that is produced is so if this combines with this, we have lowercase g, lower case g, uppercase and lowercase N. And because this is 50% and 100%, so .5 times one gives us zero. Five. So a half of the 2000 or 1000 of the offspring will have this. And the other 1000 are going to have this genotype right over here. So 1000 of the offspring will have this genotype here. | Gene Mapping, Percent Recombination and Map Units .txt |
So a half of the 2000 or 1000 of the offspring will have this. And the other 1000 are going to have this genotype right over here. So 1000 of the offspring will have this genotype here. The other 1000 will have this genotype here. Now, what exactly is the phenotype of this? Well, upper case G is dominant over lowercase G, so that means we have gray wingless because we're going to have vestigial non functional wings. | Gene Mapping, Percent Recombination and Map Units .txt |
The other 1000 will have this genotype here. Now, what exactly is the phenotype of this? Well, upper case G is dominant over lowercase G, so that means we have gray wingless because we're going to have vestigial non functional wings. And then we have lowercase g. Lower case G is black and uppercase and lowercase N is normal wings because uppercase N is dominant over lowercase N. So we have functional wings. So 1000 are gray wingless. The other thousand are black and winged. | Gene Mapping, Percent Recombination and Map Units .txt |
And then we have lowercase g. Lower case G is black and uppercase and lowercase N is normal wings because uppercase N is dominant over lowercase N. So we have functional wings. So 1000 are gray wingless. The other thousand are black and winged. Now, this is if we assume that no Crossing Over took place. But crossing over does normally take place. And that's exactly what we discussed in part three. | Gene Mapping, Percent Recombination and Map Units .txt |
Now, this is if we assume that no Crossing Over took place. But crossing over does normally take place. And that's exactly what we discussed in part three. Suppose that the actual F two distribution was as follows instead of having this hypothetical distribution because crossing over does take place we produce this distribution. So notice that now not only do we have the gray and wingless and the black and winged as we have in this case we also have the gray winged and the black winged. And these two here are actually the recombinant offsprings and they are produced as a result of crossing over as a result of the production of recombinant chromosomes. | Gene Mapping, Percent Recombination and Map Units .txt |
Suppose that the actual F two distribution was as follows instead of having this hypothetical distribution because crossing over does take place we produce this distribution. So notice that now not only do we have the gray and wingless and the black and winged as we have in this case we also have the gray winged and the black winged. And these two here are actually the recombinant offsprings and they are produced as a result of crossing over as a result of the production of recombinant chromosomes. So we are given that eight, nine, five are gray wingless, 905 are black wing but 110 are gray wings and 90 are black wingless. To make a total of if we sum these up, we obtain 2000 offspring. So the question is what is the recombination frequency between the two traits the color traits and that wing type trait? | Gene Mapping, Percent Recombination and Map Units .txt |
So we are given that eight, nine, five are gray wingless, 905 are black wing but 110 are gray wings and 90 are black wingless. To make a total of if we sum these up, we obtain 2000 offspring. So the question is what is the recombination frequency between the two traits the color traits and that wing type trait? And to find the recombination frequency, also known as percent recombination what we basically do is we sum up all the offspring that are recombinant. So 110 plus 90. So 110 plus 90, this is the total number of offspring that are recombinant and we divide it by the total number of offspring. | Gene Mapping, Percent Recombination and Map Units .txt |
And to find the recombination frequency, also known as percent recombination what we basically do is we sum up all the offspring that are recombinant. So 110 plus 90. So 110 plus 90, this is the total number of offspring that are recombinant and we divide it by the total number of offspring. So 2000 offspring and what we get is 200 divided by 2000. And that gives us, once we reduce it to one 10th and that's equivalent to 0.1. Now, this is our recombination frequency. | Gene Mapping, Percent Recombination and Map Units .txt |
So 2000 offspring and what we get is 200 divided by 2000. And that gives us, once we reduce it to one 10th and that's equivalent to 0.1. Now, this is our recombination frequency. And to find the percent recombination we basically multiply 0.1. So we multiply zero. One times 100% and we get 10% is our percent recombination between those two genes. | Gene Mapping, Percent Recombination and Map Units .txt |
And to find the percent recombination we basically multiply 0.1. So we multiply zero. One times 100% and we get 10% is our percent recombination between those two genes. It basically tells us how many of those offspring are a result of the process of crossing over. Now, we can use this to calculate what the recombination units are or the mapping units. And to basically do that we have to remember that one Map unit or one recombination unit is equal to 1% recombination. | Gene Mapping, Percent Recombination and Map Units .txt |
So we know that the plasma membrane is a fluidlike structure. And what determines the fluidity is the relative movement of all the molecules, the phospholipids and proteins that exist within that membrane. So the more movement we have, the more fluid that membrane is. The less movement we have, the more rigid that membrane is. Now, if the fluidity is determined by the relative movement, what determines the relative movement itself? Well, the relative movement of the molecules within the membrane is determined by the strength of the attractions, the non covalent intermolecular bonds that exist between the phospholipids, the molecules in the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
The less movement we have, the more rigid that membrane is. Now, if the fluidity is determined by the relative movement, what determines the relative movement itself? Well, the relative movement of the molecules within the membrane is determined by the strength of the attractions, the non covalent intermolecular bonds that exist between the phospholipids, the molecules in the membrane. So you might imagine that in a membrane in which we have more fluidity, we have more movement. And what that means is the attractions are not very strong. But in a membrane in which the attractions between the molecules is strong, that means we're going to have less movement. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So you might imagine that in a membrane in which we have more fluidity, we have more movement. And what that means is the attractions are not very strong. But in a membrane in which the attractions between the molecules is strong, that means we're going to have less movement. And so the membrane will be more rigid. And so we see that the stronger the interactions between the molecules in the membrane, the stronger these intermolecular bonds are, the more rigid the membrane is. And conversely, the weaker the interactions are, the less rigid and more fluid that membrane actually is. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And so the membrane will be more rigid. And so we see that the stronger the interactions between the molecules in the membrane, the stronger these intermolecular bonds are, the more rigid the membrane is. And conversely, the weaker the interactions are, the less rigid and more fluid that membrane actually is. So let's take a look at the following graph. And let's imagine what happens to a membrane as we go from a low temperature to a high temperature. So as we increase the temperature of the environment in which the membrane is in, so the y axis is the fluidity of the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So let's take a look at the following graph. And let's imagine what happens to a membrane as we go from a low temperature to a high temperature. So as we increase the temperature of the environment in which the membrane is in, so the y axis is the fluidity of the membrane. As we go higher up along the y axis, the fluidity increases. As we go lower along that y axis, the rigidity increases. Now, the x axis is the temperature. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
As we go higher up along the y axis, the fluidity increases. As we go lower along that y axis, the rigidity increases. Now, the x axis is the temperature. So on this side, we have a low temperature. As we go along the x axis, the temperature increases until we get to a high temperature. So let's suppose we have a rigid structure, a rigid membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So on this side, we have a low temperature. As we go along the x axis, the temperature increases until we get to a high temperature. So let's suppose we have a rigid structure, a rigid membrane. So we're at a low temperature. What begins to happen as we actually increase that temperature? Well, as we increase the temperature, we're essentially transferring kinetic energy to the molecules, the lipids and the proteins within that membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So we're at a low temperature. What begins to happen as we actually increase that temperature? Well, as we increase the temperature, we're essentially transferring kinetic energy to the molecules, the lipids and the proteins within that membrane. And so these phospholipids basically move with a greater velocity. And because they move with a greater velocity, those intermolecular bonds that are holding that rigid structure, the well defined and order structure, basically cannot maintain that rigidity any longer. And eventually, what happens is at a specific temperature called the melting temperature, there's a phase transition that takes place. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And so these phospholipids basically move with a greater velocity. And because they move with a greater velocity, those intermolecular bonds that are holding that rigid structure, the well defined and order structure, basically cannot maintain that rigidity any longer. And eventually, what happens is at a specific temperature called the melting temperature, there's a phase transition that takes place. And the collapse of that well defined and order structure basically leads into that fluid state. So as the temperature is increased, there's a sharp transition from the rigid state here to the fluid state here. And this temperature, the melting temperature, is the temperature at which this phase transition actually takes place. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And the collapse of that well defined and order structure basically leads into that fluid state. So as the temperature is increased, there's a sharp transition from the rigid state here to the fluid state here. And this temperature, the melting temperature, is the temperature at which this phase transition actually takes place. And if we look on the microscopic level, we see that as the temperature is raised, the kinetic energy of the lipids and other molecules increases. And as a result, the intermolecular non covalent bonds holding the lipids can no longer maintain a packed and well ordered, well defined structure. And so as a result of the collapse of this rigid structure, the well defined structure, we basically create a more fluid and less ordered structure. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And if we look on the microscopic level, we see that as the temperature is raised, the kinetic energy of the lipids and other molecules increases. And as a result, the intermolecular non covalent bonds holding the lipids can no longer maintain a packed and well ordered, well defined structure. And so as a result of the collapse of this rigid structure, the well defined structure, we basically create a more fluid and less ordered structure. So we go from the rigid state to that fluid state. So let's suppose we have two membranes, one membrane. In one membrane, we have strong intermodal interactions. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So we go from the rigid state to that fluid state. So let's suppose we have two membranes, one membrane. In one membrane, we have strong intermodal interactions. In the other membrane, we have weak intermolecular interactions. So how do you think the melting temperature of these two systems will compare? Well, in the membrane where we have stronger intermolecular interactions, that membrane will have a higher melting temperature. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
In the other membrane, we have weak intermolecular interactions. So how do you think the melting temperature of these two systems will compare? Well, in the membrane where we have stronger intermolecular interactions, that membrane will have a higher melting temperature. Why? Well, because a higher amount of energy. So high temperature must actually be used to actually get that well defined structure that exists due to those intermolecular interactions to actually collapse. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
Why? Well, because a higher amount of energy. So high temperature must actually be used to actually get that well defined structure that exists due to those intermolecular interactions to actually collapse. And so we conclude that a membrane with strong intermolecular interactions will have a higher melting temperature than a membrane with weaker ones. So again, a stronger or stronger interactions basically implies a more rigid, more well defined and ordered structure and that implies a higher melting temperature. Now, we know that membrane fluidity is determined by the relative movement of those lipids and the other molecules in the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And so we conclude that a membrane with strong intermolecular interactions will have a higher melting temperature than a membrane with weaker ones. So again, a stronger or stronger interactions basically implies a more rigid, more well defined and ordered structure and that implies a higher melting temperature. Now, we know that membrane fluidity is determined by the relative movement of those lipids and the other molecules in the membrane. And the relative movement is determined by the strength of those inter molecular interactions. But what determines the strength of those intermolecular interactions within the membrane? Well, three things. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And the relative movement is determined by the strength of those inter molecular interactions. But what determines the strength of those intermolecular interactions within the membrane? Well, three things. Number one is the length of fatty acid chains. Number two is degree of unsaturation. So how many double bonds we find in those hydrocarbon chains of the fatty acids and three, the concentration of cholesterol. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
Number one is the length of fatty acid chains. Number two is degree of unsaturation. So how many double bonds we find in those hydrocarbon chains of the fatty acids and three, the concentration of cholesterol. So let's discuss how each one of these actually affects the strength of the intermolecular interactions within the membrane. And let's begin with length of fatty acids. So let's compare these two adjacent fatty acids and these two adjacent fatty acids. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So let's discuss how each one of these actually affects the strength of the intermolecular interactions within the membrane. And let's begin with length of fatty acids. So let's compare these two adjacent fatty acids and these two adjacent fatty acids. So these one are clearly longer than this particular case. And because of the difference in length, we see that in this particular case we have many more interactions, intermolecular interactions. To be more specific, we have many more London dispersion forces that can potentially form in this case than in this case. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So these one are clearly longer than this particular case. And because of the difference in length, we see that in this particular case we have many more interactions, intermolecular interactions. To be more specific, we have many more London dispersion forces that can potentially form in this case than in this case. And what that means is if we have a membrane that consists of these fatty acids and one that consists of these fatty acids, the overall strength of the intermolecular interactions in this particular membrane will be greater than in this particular case. And so in such a case, the membrane will be more rigid and will have a higher melting temperature. So longer fatty acids can form more lung dispersion forces than shorter ones. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And what that means is if we have a membrane that consists of these fatty acids and one that consists of these fatty acids, the overall strength of the intermolecular interactions in this particular membrane will be greater than in this particular case. And so in such a case, the membrane will be more rigid and will have a higher melting temperature. So longer fatty acids can form more lung dispersion forces than shorter ones. Therefore, the presence of longer fatty acids decreases the fluidity, makes the membrane more rigid and increases the melting temperature because we have to input more energy to break those lung dispersion forces than in this particular case. Now, what about the double bonds? So let's compare. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
Therefore, the presence of longer fatty acids decreases the fluidity, makes the membrane more rigid and increases the melting temperature because we have to input more energy to break those lung dispersion forces than in this particular case. Now, what about the double bonds? So let's compare. We have this system in which we have four adjacent phospholipid molecules in which we don't have any double bonds. And such a system is said to be a saturated system. Now, let's suppose we compare this to this case in which we have these for phospholipids that have the same exact length. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
We have this system in which we have four adjacent phospholipid molecules in which we don't have any double bonds. And such a system is said to be a saturated system. Now, let's suppose we compare this to this case in which we have these for phospholipids that have the same exact length. But now we add CIS double bonds. So let's suppose we add a single CIS double bond into this molecule. How exactly will that determine or change the fluidity of the membrane? | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
But now we add CIS double bonds. So let's suppose we add a single CIS double bond into this molecule. How exactly will that determine or change the fluidity of the membrane? Well, in this particular case, we have a well defined structure. And because of this well defined structure, the adjacent hydrocarbon chains of these adjacent phospholipid molecules can actually interact very well and form many of these London dispersion forests. But in this particular case, because of the CIS double bond, we have a kink, we essentially have this bend in the chain. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
Well, in this particular case, we have a well defined structure. And because of this well defined structure, the adjacent hydrocarbon chains of these adjacent phospholipid molecules can actually interact very well and form many of these London dispersion forests. But in this particular case, because of the CIS double bond, we have a kink, we essentially have this bend in the chain. And because of that bend, the interactions are not as strong and not as extensive as in this particular case. So we simply have less of these interactions taking place. And because of that, if we have less interactions taking place, what that basically means is the fluidity in this particular case will increase and the melting temperature will decrease. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And because of that bend, the interactions are not as strong and not as extensive as in this particular case. So we simply have less of these interactions taking place. And because of that, if we have less interactions taking place, what that basically means is the fluidity in this particular case will increase and the melting temperature will decrease. So we see that saturated fatty acids create a well structured arrangement of hydrocarbon chains. And these straight chain hydrocarbons can form stronger and more extensive intermolecular bonds with the nearby fatty acids. And this favors rigidity. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So we see that saturated fatty acids create a well structured arrangement of hydrocarbon chains. And these straight chain hydrocarbons can form stronger and more extensive intermolecular bonds with the nearby fatty acids. And this favors rigidity. It basically decreases fluidity and it raises the melting temperature. Now, a cyst double bond like the one shown here. So in systems that are unsaturated and contain a cyst double bond, we see that that bond creates a kink, a bend in that structure, and this interferes with the well defined structure of that membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
It basically decreases fluidity and it raises the melting temperature. Now, a cyst double bond like the one shown here. So in systems that are unsaturated and contain a cyst double bond, we see that that bond creates a kink, a bend in that structure, and this interferes with the well defined structure of that membrane. And so this favors membrane fluidity, it decreases the rigidity and lowers the melting temperature of that system. So we see that increasing the length of our fatty acid chains and removing those says double bonds basically makes the membrane more rigid and increases the melting temperature of that membrane. Now, in bacterial cells, bacterial cells tend to basically use these two factors to control and regulate the rigidity or fluidity of the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And so this favors membrane fluidity, it decreases the rigidity and lowers the melting temperature of that system. So we see that increasing the length of our fatty acid chains and removing those says double bonds basically makes the membrane more rigid and increases the melting temperature of that membrane. Now, in bacterial cells, bacterial cells tend to basically use these two factors to control and regulate the rigidity or fluidity of the membrane. So they usually increase the number or decrease the number of these double bonds. Now, in animal cells, we normally use cholesterol. So let's see how cholesterol can be used to basically regulate the rigidity of the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So they usually increase the number or decrease the number of these double bonds. Now, in animal cells, we normally use cholesterol. So let's see how cholesterol can be used to basically regulate the rigidity of the membrane. So remember, cholesterol molecules are steroid molecules. They contain four fused chains or four fused rings, as shown in the following diagram. So these are phospholipid molecules. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So remember, cholesterol molecules are steroid molecules. They contain four fused chains or four fused rings, as shown in the following diagram. So these are phospholipid molecules. These are glycophosolipids that contain these sugar components. These are cholesterol molecules, and this is some type of transmembrane integral protein. Now, when cholesterol fits into the structure of the membrane, it actually interferes with the structure of these fatty acids because of the difference in shape. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
These are glycophosolipids that contain these sugar components. These are cholesterol molecules, and this is some type of transmembrane integral protein. Now, when cholesterol fits into the structure of the membrane, it actually interferes with the structure of these fatty acids because of the difference in shape. So cholesterol interferes with the regular interactions of the fatty acids. However, because the cholesterol molecule, by being present inside that membrane, because it basically stimulates formation of complexes between the cholesterol molecules and these glycophosolipid molecules, like the one shown here, they basically are responsible for forming these very important structures we call lipid rafts. So what exactly is a lipid raft? | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So cholesterol interferes with the regular interactions of the fatty acids. However, because the cholesterol molecule, by being present inside that membrane, because it basically stimulates formation of complexes between the cholesterol molecules and these glycophosolipid molecules, like the one shown here, they basically are responsible for forming these very important structures we call lipid rafts. So what exactly is a lipid raft? Well, basically a lipid raft is a section of the membrane that contains a high concentration of cholesterol molecules as well as the glycophospholipids. And because we have a high concentration of these lipids within the area of the membrane, what that does is ultimately it increases the rigidity and makes that membrane less fluid. Because if in a given section, if we're in that lipid rack region, we have many more of these large molecules. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
Well, basically a lipid raft is a section of the membrane that contains a high concentration of cholesterol molecules as well as the glycophospholipids. And because we have a high concentration of these lipids within the area of the membrane, what that does is ultimately it increases the rigidity and makes that membrane less fluid. Because if in a given section, if we're in that lipid rack region, we have many more of these large molecules. So cholesterol molecules are relatively large, and these glycophosolipids are also very large, and they're packed densely to this region. That area will have a lower amount of movement. And so if we have lower movement, that means we have more of these interactions. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
So cholesterol molecules are relatively large, and these glycophosolipids are also very large, and they're packed densely to this region. That area will have a lower amount of movement. And so if we have lower movement, that means we have more of these interactions. And so that will increase, make that membrane more rigid. Now, on top of that, even though the membrane is more rigid in the presence of cholesterol, what these lipid wraps also do, and what cholesterol does in general, is it basically increases the resistance of the membrane to this transition transition phase that we spoke of earlier. So instead of having this steep slope, the slope is slightly flatter. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And so that will increase, make that membrane more rigid. Now, on top of that, even though the membrane is more rigid in the presence of cholesterol, what these lipid wraps also do, and what cholesterol does in general, is it basically increases the resistance of the membrane to this transition transition phase that we spoke of earlier. So instead of having this steep slope, the slope is slightly flatter. And what that means is the membrane is able to resist these transition phases. So we see that cholesterol, even though it interferes with the regular interactions of fatty acids, because cholesterol seems to actually form complexes with glycos single lipids, a type of glyco phospholipid. We see that because they form these complexes. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
And what that means is the membrane is able to resist these transition phases. So we see that cholesterol, even though it interferes with the regular interactions of fatty acids, because cholesterol seems to actually form complexes with glycos single lipids, a type of glyco phospholipid. We see that because they form these complexes. These complexes, in turn, form these lipid ramps. And what that does is it makes the membrane slightly less fluid, so more rigid, but at the same time, it makes it much more resistant to actually phase transitions. And so when there's a change in temperature taking place, that membrane is less likely to actually transition between these two stages. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
These complexes, in turn, form these lipid ramps. And what that does is it makes the membrane slightly less fluid, so more rigid, but at the same time, it makes it much more resistant to actually phase transitions. And so when there's a change in temperature taking place, that membrane is less likely to actually transition between these two stages. And that's very important to maintaining homeostasis inside the cells of our body. So cholesterol is basically used in animal cells, in our own cells to regulate the fluidity of the membrane and is also used to basically regulate the transition from the rigid state to the fluid state or vice versa. So we conclude that there are three different things that basically allow the that basically influence the fluidity of the membrane. | Cholesterol and Fatty Acids Regulate membrane Fluidity .txt |
When we break down amino acids inside our liver, we essentially remove that alpha amino group. And what we have left over is a carbon skeleton. So in this lecture and the next several lectures, what I'd like to focus on is the fate of that carbon skeleton. So when we metabolize amino acids and we form that carbon skeleton by removing that alpha amino group, one exactly happens to that carbon skeleton. So all the carbon skeletons that we form, when we metabolize the 20 different types of amino acids inside our liver cells, all those carbon skeletons lead to one of seven different molecules. And all these seven molecules are intermediates of the metabolic pathway, the metabolic system that allows us to generate high energy ATP molecules. | Introduction to glucogenic and ketogenic amino acids .txt |
So when we metabolize amino acids and we form that carbon skeleton by removing that alpha amino group, one exactly happens to that carbon skeleton. So all the carbon skeletons that we form, when we metabolize the 20 different types of amino acids inside our liver cells, all those carbon skeletons lead to one of seven different molecules. And all these seven molecules are intermediates of the metabolic pathway, the metabolic system that allows us to generate high energy ATP molecules. So let's recall some basic facts about metabolic pathways. Let's begin with the citric acid cycle. So this is our citric acid cycle. | Introduction to glucogenic and ketogenic amino acids .txt |
So let's recall some basic facts about metabolic pathways. Let's begin with the citric acid cycle. So this is our citric acid cycle. And inside our liver, the point of the citric acid cycle is to help us generate oxyloacetate. Why? Because oxalo acetate is ultimately the starting material to produce glucose via gluconeogenesis as it takes place inside our liver cell. | Introduction to glucogenic and ketogenic amino acids .txt |
And inside our liver, the point of the citric acid cycle is to help us generate oxyloacetate. Why? Because oxalo acetate is ultimately the starting material to produce glucose via gluconeogenesis as it takes place inside our liver cell. So if we can form any one of these intermediate molecules, that can ultimately help us form oxalo acetate, and that can lead to glucose production. Now, inside our liver, we can actually use Pyruvate to basically form oxalo acetate. And this pathway is catalyzed by the enzyme Pyruvate carboxylase. | Introduction to glucogenic and ketogenic amino acids .txt |
So if we can form any one of these intermediate molecules, that can ultimately help us form oxalo acetate, and that can lead to glucose production. Now, inside our liver, we can actually use Pyruvate to basically form oxalo acetate. And this pathway is catalyzed by the enzyme Pyruvate carboxylase. And so what that means is we can use Pyruvate to actually help us generate glucose, because if we transform Pyruvate to oxaloacetate, we can then use this in gluconeogenesis to help us form glucose. Now, what about this pathway here? So, if we take pyruvate, the second fate of Pyruvate is to undergo decarboxylation. | Introduction to glucogenic and ketogenic amino acids .txt |
And so what that means is we can use Pyruvate to actually help us generate glucose, because if we transform Pyruvate to oxaloacetate, we can then use this in gluconeogenesis to help us form glucose. Now, what about this pathway here? So, if we take pyruvate, the second fate of Pyruvate is to undergo decarboxylation. So the enzyme pyruvate carboxylase transforms pyruvate into acetylcoenzyme a. Now, what happens to acetylco enzyme A? Well, we can use acetylcoenzyme A to help us generate fatty acids, but we can also use acetylcoenzyme A to help us generate ketone bodies. | Introduction to glucogenic and ketogenic amino acids .txt |
So the enzyme pyruvate carboxylase transforms pyruvate into acetylcoenzyme a. Now, what happens to acetylco enzyme A? Well, we can use acetylcoenzyme A to help us generate fatty acids, but we can also use acetylcoenzyme A to help us generate ketone bodies. So by transforming acetyl coenzyme A to acetoacetalco enzyme A, this ultimately can be transformed into ketone bodies. Now, one fact that you have to remember is acetylco enzyme A cannot be used, at least inside humans, to actually generate glucose molecules. And what that means is, even though it seems like we can use acetyl coenzyme A, transform it into the citric acid cycle, ultimately form oxalo acetate, and then form glucose via glucoinogenesis, that is not actually true. | Introduction to glucogenic and ketogenic amino acids .txt |
So by transforming acetyl coenzyme A to acetoacetalco enzyme A, this ultimately can be transformed into ketone bodies. Now, one fact that you have to remember is acetylco enzyme A cannot be used, at least inside humans, to actually generate glucose molecules. And what that means is, even though it seems like we can use acetyl coenzyme A, transform it into the citric acid cycle, ultimately form oxalo acetate, and then form glucose via glucoinogenesis, that is not actually true. And the reason is the following. When we use acetyl coenzyme A and we feed it into the citric acid cycle, we actually use up a single oxalo acetate. So we use a single oxylacetate combined with acetytl coenzyme A, and we form citrates. | Introduction to glucogenic and ketogenic amino acids .txt |
And the reason is the following. When we use acetyl coenzyme A and we feed it into the citric acid cycle, we actually use up a single oxalo acetate. So we use a single oxylacetate combined with acetytl coenzyme A, and we form citrates. And so ultimately, even though we do form oxalo acetate at the end, we use up one oxalo acetate at the beginning, and the net result is zero. So what that means is we cannot use acetylco enzyme A to help us form glucose in our liver. Now, let's focus on all these different amino acids. | Introduction to glucogenic and ketogenic amino acids .txt |
And so ultimately, even though we do form oxalo acetate at the end, we use up one oxalo acetate at the beginning, and the net result is zero. So what that means is we cannot use acetylco enzyme A to help us form glucose in our liver. Now, let's focus on all these different amino acids. So basically, if we metabolize an amino acid, and the carbon skeleton of that amino acid is used to form any one of these intermediates here, or Pyruvate, these are known as glucogenic. So glucogenic amino acids are those amino acids that, when metabolized, help us form intermediates that ultimately lead to the production of glucose. So that includes all these, these and these. | Introduction to glucogenic and ketogenic amino acids .txt |
So basically, if we metabolize an amino acid, and the carbon skeleton of that amino acid is used to form any one of these intermediates here, or Pyruvate, these are known as glucogenic. So glucogenic amino acids are those amino acids that, when metabolized, help us form intermediates that ultimately lead to the production of glucose. So that includes all these, these and these. So, for example, let's take tryptophan. Tryptophan, if it follows a specific pathway, that will ultimately lead to the production of pyruvate. Now, Pyruvate basically goes this way via the pyruvate carboxylase enzyme that forms oxalo acetate, and that then helps to form glucose via glucomgenesis. | Introduction to glucogenic and ketogenic amino acids .txt |
So, for example, let's take tryptophan. Tryptophan, if it follows a specific pathway, that will ultimately lead to the production of pyruvate. Now, Pyruvate basically goes this way via the pyruvate carboxylase enzyme that forms oxalo acetate, and that then helps to form glucose via glucomgenesis. Now, if we look at aspartate, for example, aspartate can be transformed into oxalo acetate, and we actually looked at this example in a previous lecture, and then the oxylacetade goes on to form glucose via glucaniogenesis. So all of these amino acids are known as glucogenic. Now, if we look at these, these and these ultimately helps us form these two molecules. | Introduction to glucogenic and ketogenic amino acids .txt |
Now, if we look at aspartate, for example, aspartate can be transformed into oxalo acetate, and we actually looked at this example in a previous lecture, and then the oxylacetade goes on to form glucose via glucaniogenesis. So all of these amino acids are known as glucogenic. Now, if we look at these, these and these ultimately helps us form these two molecules. And so these can then be used to form ketone bodies. So these are known as ketogenic. So all of these are ketogenic. | Introduction to glucogenic and ketogenic amino acids .txt |
And so these can then be used to form ketone bodies. So these are known as ketogenic. So all of these are ketogenic. Now, the only ones that are solely strictly ketogenic are actually leucine and lysine. Why? Well, because tryptophan, if it follows one pathway, we can form acetylco enzyme A, in which case it's ketogenic. | Introduction to glucogenic and ketogenic amino acids .txt |
Now, the only ones that are solely strictly ketogenic are actually leucine and lysine. Why? Well, because tryptophan, if it follows one pathway, we can form acetylco enzyme A, in which case it's ketogenic. In a different pathway, it can form acetoacetalco enzyme A. Again, it's ketogenic. But in this pathway, it helps us form pyruvate. | Introduction to glucogenic and ketogenic amino acids .txt |
In a different pathway, it can form acetoacetalco enzyme A. Again, it's ketogenic. But in this pathway, it helps us form pyruvate. And Pyruvate goes this way to help us form glucose. Now, we can also go this way, of course, and this will be ketogenic. But if we look strictly on this pathway, this pathway is glucogenic. | Introduction to glucogenic and ketogenic amino acids .txt |
And Pyruvate goes this way to help us form glucose. Now, we can also go this way, of course, and this will be ketogenic. But if we look strictly on this pathway, this pathway is glucogenic. So tryptophan is both glucogenic and ketogenic. So the only ones which are only ketogenic are leucine and lysine. This is the list of all the glucogenic. | Introduction to glucogenic and ketogenic amino acids .txt |
So tryptophan is both glucogenic and ketogenic. So the only ones which are only ketogenic are leucine and lysine. This is the list of all the glucogenic. Only we have 14. And this is the list of both ketogenic and glucogenic. So as we saw earlier, we have tryptophan, but we also have isolucine, phenylalanine and tyrosine. | Introduction to glucogenic and ketogenic amino acids .txt |
Only we have 14. And this is the list of both ketogenic and glucogenic. So as we saw earlier, we have tryptophan, but we also have isolucine, phenylalanine and tyrosine. So my suggestion, if you're going to memorize these, memorize these two and these four, but don't memorize this, because if you memorize these two, the other 14, which essentially must be glucogenic only. Now, one caveat, however, is the way I've listed is I have 14 glucogenic and four under both. Sometimes you're going to see three anine listed under both. | Introduction to glucogenic and ketogenic amino acids .txt |
So my suggestion, if you're going to memorize these, memorize these two and these four, but don't memorize this, because if you memorize these two, the other 14, which essentially must be glucogenic only. Now, one caveat, however, is the way I've listed is I have 14 glucogenic and four under both. Sometimes you're going to see three anine listed under both. So that means we have 13 here, not including three anine, and five here, including three anine. And that's simply because of the way you define glucogenic. So if you define glucogenic one way, the three anine ends up being here. | Introduction to glucogenic and ketogenic amino acids .txt |
So that means we have 13 here, not including three anine, and five here, including three anine. And that's simply because of the way you define glucogenic. So if you define glucogenic one way, the three anine ends up being here. If you define a different way, the three ane ends up being here. Now, that's really not too important. What's important here is to notice that the majority of the amino acids that are metabolized inside our liver actually end up being metabolized into glucose, because 14, or in some cases 13, essentially end up being transformed into glucose, and then that glucose can be used to help our cells generate high energy ATP molecule. | Introduction to glucogenic and ketogenic amino acids .txt |
Previously we discussed our somatic system and we said that the somatic nervous system consists of two divisions. We have the sensory division and the motor division. And in the same exact way, the autonomic nervous system system also consists of the sensory division and the motor division. But in the case of the autonomic nervous system the motor division is even further subdivided into two. We have the sympathetic and the parasympathetic systems. Now before we actually discuss these two individual systems, let's discuss what the difference is between our somatic and autonomic nervous system. | Autonomic Nervous System .txt |
But in the case of the autonomic nervous system the motor division is even further subdivided into two. We have the sympathetic and the parasympathetic systems. Now before we actually discuss these two individual systems, let's discuss what the difference is between our somatic and autonomic nervous system. Now the somatic nervous system basically innervates skeletal muscle, skeletal tissue. And that means our somatic nervous system is responsible for our voluntary movement. So what allows me to move my arm back and forth is the fact that inside my arm I have skeletal tissue that is innovated by our somatic nervous system, our skeletal muscle. | Autonomic Nervous System .txt |
Now the somatic nervous system basically innervates skeletal muscle, skeletal tissue. And that means our somatic nervous system is responsible for our voluntary movement. So what allows me to move my arm back and forth is the fact that inside my arm I have skeletal tissue that is innovated by our somatic nervous system, our skeletal muscle. And that's exactly what allows me to move my hand back and forth. Now what about the autonomic nervous system? Well, the autonomic nervous system innervates cardiac muscle and smooth muscle and then also innervates different types of glands found inside our body. | Autonomic Nervous System .txt |
And that's exactly what allows me to move my hand back and forth. Now what about the autonomic nervous system? Well, the autonomic nervous system innervates cardiac muscle and smooth muscle and then also innervates different types of glands found inside our body. So that means the autonomic nervous system controls the race, the beating of the heart and also controls, for example, the dilation and constriction of our blood vessels. So it's the autonomic nervous system that controls all our involuntary movement, movement that we cannot actually control. Now the somatic nervous system consists of our electrical pathways that only have one neuron. | Autonomic Nervous System .txt |
So that means the autonomic nervous system controls the race, the beating of the heart and also controls, for example, the dilation and constriction of our blood vessels. So it's the autonomic nervous system that controls all our involuntary movement, movement that we cannot actually control. Now the somatic nervous system consists of our electrical pathways that only have one neuron. But in the case of the autonomic we usually have two neurons in our electrical pathway. We have a pre ganglionic neuron and a post ganglionic neuron. Now in the case of the somatic system we only use the cetylcholine neurotransmitter. | Autonomic Nervous System .txt |
But in the case of the autonomic we usually have two neurons in our electrical pathway. We have a pre ganglionic neuron and a post ganglionic neuron. Now in the case of the somatic system we only use the cetylcholine neurotransmitter. In the autonomous case we use acetylcholine as well as in some cases epinephrine and norepinephrine. So now let's discuss the sympathetic and the parasympathetic divisions of the autonomic nervous system. Now let's begin with our sympathetic case. | Autonomic Nervous System .txt |
In the autonomous case we use acetylcholine as well as in some cases epinephrine and norepinephrine. So now let's discuss the sympathetic and the parasympathetic divisions of the autonomic nervous system. Now let's begin with our sympathetic case. Let's suppose we're casually walking in the park and all of a sudden we have a dog that begins to chase us. Now, if we choose to run away from that dog or if we choose to fight that dog off, in either case it's the sympathetic nervous system that actually kicks in. So let's suppose we decide to run away. | Autonomic Nervous System .txt |
Let's suppose we're casually walking in the park and all of a sudden we have a dog that begins to chase us. Now, if we choose to run away from that dog or if we choose to fight that dog off, in either case it's the sympathetic nervous system that actually kicks in. So let's suppose we decide to run away. Now as we begin to run, what begins to happen is more blood begins to pump to our skeletal muscles so that we can run away. And as more blood is being pumped to our muscle, those muscles are basically using more energy creating more ATP molecules and they need more oxygen. And so the rate of our respiration increases as well as the rate of our heart. | Autonomic Nervous System .txt |
Now as we begin to run, what begins to happen is more blood begins to pump to our skeletal muscles so that we can run away. And as more blood is being pumped to our muscle, those muscles are basically using more energy creating more ATP molecules and they need more oxygen. And so the rate of our respiration increases as well as the rate of our heart. Now as we begin to run, we have to see where we're going. And so that means our pupils increase, they dilate so that more light gets into our eye and we can better see where we're actually running to. So we see that our sympathetic nervous system this is the division of the autonomic nervous system that is responsible for the fight or flight response. | Autonomic Nervous System .txt |
Now as we begin to run, we have to see where we're going. And so that means our pupils increase, they dilate so that more light gets into our eye and we can better see where we're actually running to. So we see that our sympathetic nervous system this is the division of the autonomic nervous system that is responsible for the fight or flight response. This includes dilating our pupils, increasing the heart as well as our breathing rate and increasing the mouth that we sweat. So that's because when we sweat we're basically expelling the byproduct our energy. So as we produce more ATP in our muscles, that creates more energy, more thermal energy as a byproduct. | Autonomic Nervous System .txt |
This includes dilating our pupils, increasing the heart as well as our breathing rate and increasing the mouth that we sweat. So that's because when we sweat we're basically expelling the byproduct our energy. So as we produce more ATP in our muscles, that creates more energy, more thermal energy as a byproduct. And to keep our temperature of the body at the same temperature, we have to expel that energy. And we do that by the process of sweating. Now, when we're running, we don't have to worry about digestion. | Autonomic Nervous System .txt |
And to keep our temperature of the body at the same temperature, we have to expel that energy. And we do that by the process of sweating. Now, when we're running, we don't have to worry about digestion. We don't want to have to worry about digestion because our body basically needs to use the majority of the energy to basically run instead of digest. And so what happens is that decreases our digestive rate and at the same time, it inhibits peristalsis because parastosis is the movement of our food products through our small intestine for the process of absorption. So when we essentially begin to run, we don't want to worry about digestion or peristalsis. | Autonomic Nervous System .txt |
We don't want to have to worry about digestion because our body basically needs to use the majority of the energy to basically run instead of digest. And so what happens is that decreases our digestive rate and at the same time, it inhibits peristalsis because parastosis is the movement of our food products through our small intestine for the process of absorption. So when we essentially begin to run, we don't want to worry about digestion or peristalsis. So the sympathetic nervous system shuts down these processes. It decreases their rate. So the overall effect of our sympathetic nervous system is to basically increase the blood flow to our heart, to our cardiac muscle, as well as to our skeletal muscle. | Autonomic Nervous System .txt |
So the sympathetic nervous system shuts down these processes. It decreases their rate. So the overall effect of our sympathetic nervous system is to basically increase the blood flow to our heart, to our cardiac muscle, as well as to our skeletal muscle. So the blood vessels that carry the blood to our cardiac and skeletal muscle increase in size. They dilate. But the blood vessels that carry the blood to our digestive tract basically decrease in size. | Autonomic Nervous System .txt |
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