Muscle tissue is made up of highly specialised cells hat are able to use energy from the hydrolysis of ATP to make themselves shorter (contraction).
Muscle attached to the bones is called striated muscle because it looks striped through a microscope. The cells in striated muscle are highly specialised, and are called muscle fibres.
Each fibre contains many nuclei, many mitochondria, endoplasmic reticulum, and fibrils made from actin and myosin.
THE SLIDING FILAMENT THEORY
Muscles contract as the actin and myosin filaments slide between each other. this makes each sarcomere shorter, so the whole muscle fibre gets shorter.
- An action potential arrives at the cell surface membrane of a muscle fibre. It travels along the membranes of the sarcoplasmic reticulum, deep into the muscle fibre. This causes calcium ions (which were stored in the sarcoplasmic reticulum) to be released into the muscle fibre.
- In a relaxed myofibril, proteins called tropomyosin and troponin cover binding sites on the actin filaments. The calcium ions cause the tropomyosin and troponin to change shape which uncovers the binding sites.
- Myosin heads now bind with the actin filaments, forming 'bridges' between them.
- The myosin heads tilt, pushing the actin filaments along.
- ATP now binds with the myosin heads and is hydrolysed by ATPase, releasing energy. The energy causes the myosin heads to disconnect from the actin filaments.
- The disconnected myosin heads flip back to their original position, and bind with another exposed binding site on the actin filament. They tilt again, pushing the actin filament along again.
- This process repeats over and over, as long as action potentials keep arriving.
FAST AND SLOW TWITCH MUSCLE FIBRES
There are two types of muscle fibres in our striated muscle.
Fast twitch fibres are adapted for rapid contraction over and short time period.
Slow twitch fibres are adapted for slightly less rapid contraction over longer time periods.
- Use aerobic respiration to produce ATP.
- Have many mitochondria to carry out Krebs cycle and oxidative phosphorylation.
- Have large amounts of the protein myoglobin, which stores oxygen.
- Are relatively narrow, so oxygen can diffuse into their centres rapidly.
- Are supplied with oxygenated blood by many capillaries.
- Use anaerobic respiration to produce ATP.
- Have few mitochondria.
- Have much less myoglobin.
- Are relatively wide.
- Few capillaries supplying them.
TENDONS AND LIGAMENTS
These attach muscles to bone and are long fibres made of collagen and elastin. When a muscle contracts, it pulls on the tendons which transmit the force to a bone.
These connect your bones to other bones at joints. Like tendons, they contain collagen and elastin, but a much higher proportion of elastin which means they can stretch much more than tendons.
Muscles can only produce a force when the contract. When they relax, they stay in the same position unless something pulls them back into their original lengthened state.
Muscles work in antagonistic pairs - when one is contracted the other is relaxed.
At a joint such as the elbow some muscles pull in one direction when they contract and others pull in the opposite direction. The major muscle causing the elbow to bend is the biceps, this is the flexor muscle. The major muscle causing the arm to straighten when it contracts is the triceps, and this is the extensor muscle.
All cells obtain usable energy through respiration, which is the oxidation of energy containing organic molecules, such as glucose. These are known as respiratory substrates.
The energy released from this process is used to combine ADP with inorganic phosphate to make ATP (energy).
In aerobic respiration, oxygen is involved. Glucose is split to release carbon dioxide as a waste product. The hydrogen from the glucose is with atmospheric oxygen. This releases a large amount of energy, which is used to drive the synthesis of ATP.
Glycolysis is the first stage of respiration and takes place in the cytoplasm.
- A glucose molecule is phosphorylated, as two ATP's donate phosphate to it.
- This produces a hexose bisphosphate molecule, which splits into 2 triose phosphates.
- Each triose phosphate is converted to a pyruvate molecule. This involves the removal of hydrogen, which are taken up by a coenzyme called NAD. This produces reduced NAD. During this step the phosphate groups from the triose phosphates are added to ADP to make ATP.
- Overall two molecules of ATP are used and four are made during glycolysis of one glucose molecule, make a net gain of 2 ATP's per glucose.
The link reaction:
If oxygen is available, the pyruvate moves onto the mitochondrion, where the link reaction and the Krebs cycle take place. During these processes, the glucose is completely oxidised. Carbon dioxide is removed from the pyruvate. This carbon dioxide diffuses out of the mitochondrion and out of the cell. Hydrogen is also removed from the pyruvate, and is picked up by NAD, producing reduced NAD. This convert pyruvate into a two carbon compound. This immediately combines with coenzyme A to produce acetyl coenzyme A.
THE KREBS CYCLE
Acetyl coenzyme A has two carbon atoms. It combines with a four-carbon compound to produce a six carbon compound. This is gradually converted to the four carbon compound again through a series of enzyme-controlled steps.
These steps all take place in the matrix of the mitochondria.
During this process, more carbon dioxide is released and diffuses out o the mitochondrion and out of the cell. More hydrogens are released and picked up by the NAD and another coenzyme called FAD. This produces reduced NAD and reduced FAD. ATP is also produced.
The hydrogens picked up by NAD and FAD are now split into electrons and protons. The electrons are passed along the electron transport chain, on the inner membrane of the mitochondria.
As they move along the chain they lose energy. This energy is used to actively transport hydrogen ions from the matrix of the mitochondrion, across the inner membrane and into the space between the inner and outer membrane. This builds up a high concentration of hydrogen ions in this space.
The hydrogen ions are allowed to diffuse back into the matrix through special channel proteins that work as ATPases. The movement of the hydrogen ions through the ATPases provides energy to cause ADP and Pi to combine to make ATP.
The active transport and subsequent diffusion of the hydrogen ions across the inner membrane of the mitochondrial membrane is known as chemiosmosis.
At the end of the chain the elections reunite with protons. They combine with oxygen to produce water. This is why oxygen is required for aerobic respiration, if the supply of oxygen stops then the Krebs cycle stops.
Is oxygen is not available the Krebs cycle and the link reaction come to a halt. However glycolysis can still continue as long as the pyruvate made can be removed and the reduced NAD can be converted back to NAD. In animals this is done by converting the pyruvate to lactate.
The lactate that is produced (usually in muscles) diffuses intot he blood and is carried in solution in the blood plasma to the liver. Here, liver cells convert it back to pyruvate.
This requires oxygen, so extra oxygen required after exercise has finished, this is known as the oxygen debt.
When the exercise is finished and the oxygen is available again, some of the pyruvate in the liver cells is oxidised through the link reaction, the Krebs cycle and the electron transport chain. Some of the pyruvate is reconverted to glucose in the liver cells and this may be released into the blood or converted into glycogen and stored.
ACTIVITY OF THE HEART
The heart is myogenic - this means it contracts and relaxes automatically without the need for stimulation from nerves.
In the wall of the right atrium there is a patch of muscle tissue called the sinoatrial node (SAN). This has an intrinsic rate of contraction a little higher than that of the reat of the heart muscle.
As the cells of the SAN contract, they send out a wave of depolarisation along the wall of the left and right atria, causing them to contract. This is atrial systole.
When the wave of depolarisation reaches the atrioventricular node (AVN) in the septum it is delayed briefly. It then continues down the septum between the ventricles, along fibres called the bundle of His and then up through the ventricle walls. This causes the ventricle to contract and is known as ventricular systole.
There is then a short delay before the next wave of depolarisation is generated in the SAN. During this time the muscles contract and this stage is known as diastole.
The electrical activity taking place in the heart can be monitored and recorded by an ECG.
Abnormal ECGs can be used to diagnose problems with the heart. For example:
- an unusually long delay between the P and R waves can mean that electrical impulses cannot pass from the atria to the ventricles, perhaps because of damage to the bundles of His.
- a flat T wave can indicate lack of blood flow to cardiac muscle in the heart wall, so that it does not have energy for the contraction. This could be an indication of cardiovascular disease (CVD).
PHYSIOLOGICAL EFFECTS OF EXERCISE
Exercise involves the contraction of muscle. Muscles obtain energy from ATP which is produced by respiration. Exercise therefore requires increased rate of respiration in muscles which requires more oxygen. This is achieved through:
- faster and deeper breathing, which increases the rate at which oxygen enters the blood in the lungs and carbon dioxide leaves it.
- faster and stronger heart beat, which increases the rate at which blood moves through the blood vessels, delivering oxygen to muscle tissues nd removing carbon dioxide and lactate from them.
CONTROL OF HEART RATE
The cardiac output is the volume of blood leaving the left ventricle with each beat multiplied by the number of beats per minute. Cardiac output can be increased by increasing the strength of contraction or by increasing the number of beats per minute. Usually, both occur.
Just before and during exercise:
- Adrenaline is secreted from the adrenal glands stimulating the SAN to increase its rate of contraction.
- Action potentials are sent along the motor neurone from the cardiovascular control centre in the brain, to the SAN. The neurone releases noradrenaline when it reaches the SAN, causing the SAN to increase its rate of contraction. This may happen if there is too much carbon dioxide in the blood. This decreases the pH of the blood which stimulates the cardiac centre to generate a higher frequency of action potentials in the sympathetic nerve.
- When oxygen concentration falls in muscles, the walls of blood vessels secrete nitric oxide. This makes muscles relax so arterioles dilate and carry more blood. This increases the rate at which blood is returned to the right atrium of the heart.
CONTROL OF VENTILATION RATE
- During normal breathing, rhythmic patterns of nerve impulses are sent from the ventilation centre in the medulla oblongata in the brain to the muscles in the diaphragm which respond by contracting rhythmically.
- Stretch receptors in the lungs are stimulated during breathing in and send impulses to the ventilation centre, which uses this information to help regulate breathing rate.
- During exercise chemoreceptors in ventilation centre sense a fall in pH, caused by increased carbon dioxide in the blood.
- Carbon dioxide concentration is also sensed by receptors in a patch of tissue in the wall of the aorta, called the aortic body.
- Another set of chemoreceptors in the walls of the carotid arteries, called carotid bodies, sense concentration, as well as carbon dioxide concentration in the blood.
- Nerve impulses are sent from the aortic body and carotid bodies to the ventilation centre, and this then sends impulses to the breathing muscles, causing them to contract harder and faster. This increases the rate and depth of breathing.
Whenever energy is transferred from one place to another, some is always lost as heat. Respiration therefore produces heat, as does muscle contraction. During vigorous exercise, considerable quantities of heat are generated in muscles and this causes the temperature of the blood to rise.
It's important that core temperature remains constant, around 37.8C as if it rises much above this then enzyme molecules become denatured, and normal metabolic reactions can't take place and cells may be damaged. The regulation of core body temperature is part of homeostasis.
IF CORE TEMPERATURE CHANGES
A change in core temperature is detected by thermoreceptors in the hypothalamus in the brain. The hypothalamus receives inputs from temperature receptors in the skin.
When temperature rises:
- Vasodilation. This is where the arterioles delivering blood to the skin dilate so a greater volume of blood flows into the surface capillaries. This allows heat to be lost by radiation from the blood through the skin surface.
- Sweat glands activate. Sweat flows up the sweat ducts onto the surface of the skin, where the water in it evaporates. This takes heat from the skin.
- Erector muscles attached to hairs relax to let hairs lie flat so they don't trap a layer of insulating air.
When temperature falls:
- Arterioles constrict so less heat is lost.
- Sweat glands secrete little or no sweat.
- Erector muscles contract pulling hairs up on end. This traps a later of insulating air next to the skin.
- Certain muscles contract and relax rapidly (shivering), generating extra heat which increases blood temperature.
This mechanism of temperature regulation is an example of a negative feedback mechanism.
In negative feedback, a receptor detects a change in the normal state of a system. If it detects an increase, it triggers events which bring about a decrease. If it detects a decrease, it triggers events which bring about an increase. The change is then detected by the receptor, which once again acts accordingly. The process is ongoing.
There is a slight time lag between the sensor detecting a change and the effectors responding, therefore in temperature regulation for example, the core temperature does rise and fall a little. However it rarely fluctuates far from the norm, this is called dynamic equilibrium.
Long term temperature regulation:
If a person spends a few days in a very cold environment, the hypothalamus releases more of the hormone TRH, which stimulate the anterior pituitary gland to secrete TSH. This stimulates the thyroid gland to secrete more thyroxine.
Thyroxine travels in the blood to it's target cells where it diffuses through the cell surface membrane and into the nucleus. Here it switches on several genes which are responsible for encoding respiratory enzymes, especially cytochrome oxidase and ATPase. It also causes more mitochondria to be produced. This increases the rate of aerobic respiration in cells, generating more heat.
DNA TRANSCRIPTION FACTORS
Thyroxine affects protein synthesis in a cell by binding to transcription factors in the nucleus of a cell. The activated transcription factors bind to a specific region of DNA and change the ability of RNA polymerase to attach to the dNA and catalyse the production of a complementary strand of mRNA from that gene.
This may increase the transcription of a particular gene, called up-regulating, or it may decrease transcription, called down-regulating. Most steroid hormones, such as oestrogen and testosterone, act in this way.
Transcription factors may bind with a large number of different areas of DNA, so they can switch many genes on or off. Thyroxine, for example, is known to affect the expression of at least 20 genes.
EXERCISE AND HEALTH
Regular exercise increases fitness:
- It decreases the risk of obesity as it increases metabolic rate during exercise. There is often a temporary increase for some time after the exercise has finished.
- Type 2 diabetes is caused by a decrease in the sensitivity of live and muscle cells to insulin. This means that high blood glucose levels are not returned to normals as fast as they should be. this can damage cells in all parts of the body.
- Coronary heart disease (CHD) is more likely to develop in people who do not exercise.
However people who exercise too much run the risk of causing damage to the body:
- Joints may become abnormally worn.
- There is evidence that very strenuous exercise taken over long periods of time can cause the immune system to become less effective.
TREATING INJURIES TO JOINTS
A relatively common injury in footballers is a torn anterior cruciate ligament. This ligament helps to support the bones at the knee joint. This is normally treated with keyhole surgery, which greatly reduces the recovery time compared with normal surgery.
If a knee joint is very badly damaged then the whole knee joint has to be replaced with a prosthetic joint. There are many different types of these but all are expensive as they have to be made of high-quality materials that:
- are unaffected by body fluids
- can stand up to the high forces experienced by the knee
- have the right combination of flexibility and strength to allow free movement yet support the whole body weight
USING DRUGS IN SPORT
Many performance enhancing drugs are now banned from sport.
Arguments for preventing the use of drugs in sport include:
- Many of these substances can cause damage to the athletes health, especially if used over a long period of time. They may causeliver damage and in some cases are thought to have caused the early death of an athlete, often by causing heart attacks.
- Athletes who use drugs may have a competitive advantage over those who do not, making it an unfair competition.
On the other hand some people think they should be allowed:
- It is impossible to detect every performance-enhancing drug that can be used in sport. New drugs are always being tried, and it is difficult for regulators to develop new tests quickly enough to keep up with these developments.
- There is no ban on nutritional supplements such as vitamins - so where do we draw the line between an illegal performance-enhancing drugs and a legal vitamin supplement?