SNAB Biology Topic 7 - NEW

The chemical process of releasing energy from organic compounds such as glucose through oxidation, the energy released is used to combine ADP and Pi - ATP

Aerobic - requires oxygen, releases a lot of energy 

Anaerobic - the breakdown of molecules without oxygen, releasing much less energy

ATP hydrolysed, releasing a lot of energy on hydration by water (as the third phosphate group bond is weak). ATP is at a higher energy level than ADP and Pi, so is a form of storing energy and moving to where it is needed, enzyme ATPase catalyses this reaction and also the reformation of ATP

Aerobic respiration involves glycolysis + link reaction + Krebs cycle + ETC/oxidative phosphorylation

Energy is released by splitting glucose, mitochondria are vital

Respiration is a many-stepped process with each step controlled and catalysed by a specific intracellular enzyme

Occurs in the cytoplasm and makes pyruvate (3C) from glucose (6C), the first stage in both aerobic and anaerobic respiration, does not require oxygen

1. Glycogen from liver or muscle cells is converted into glucose

2. Glucose molecule phosphorylated by 2 ATPs producing 2 ADP and a reactive 6C compound, which turns into 2 phosphorylated 3C compounds 

3. Hydrogen is removed, which is taken up by NAD which is reduced, 2ATPs are made as phosphates are added to ADP (substrate-level phosphorylation), forming a molecule of pyruvate 3C - THIS HAPPENS TWICE

Overall 2 ATP used, 4 ATP produced from one molecule of glucose, 4H which are taken up by 2 NADs and 2 pyruvate molecules

Occurs if oxygen available, pyruvate passes into mitochondrial matrix and is completely oxidised, it is decarboxylated and then dehydrogenated (NAD takes this up), the resulting 2C compound combines with coenzyme A to form acetyl coenzyme A

The link reaction and Krebs cycle occur twice for every glucose molecule 

No ATP is produced 

Happens twice - De Na De Na A Fa Na

Occurs in matrix, where all the enzymes required are 

Energy lost in redox reactions by electrons gives energy for H+ ions to move into the intermembrane space, making it more positive, electrochemical gradient created, H+ ions diffuse back in through ATPase, producing ATP due to the energy released by protons, known as chemiosmosis 

Oxygen required as it is the final electron acceptor

NAD = 3 ATP and FAD = 2 ATP so total ATP = 38

Link reaction and Krebs cycle do not occur, and oxidative phosphorylation does not occur as no oxygen, glycolysis still continues, however, only 2 ATP per glucose produced (net)

Done by converting pyruvate to lactate, reduced NAD transfers H to pyruvate, thus forming lactate and reforming NAD for use again, lactate built up in muscles diffuses into blood, wherein solution it forms lactic acid which travels to the liver, where it is converted back to pyruvate, requiring oxygen - known as the oxygen debt 

Once oxygen is available again, oxygen uptake is greater than normal, some of the pyruvate is oxidised in the liver through the link reaction/Krebs cycle/ETC, some pyruvate is reconverted into glucose in the liver cells and released into the cells or converted into glycogen for storage 

Alcohol produced in anaerobic respiration of plants and yeast 

Immediate ATP is regenerated at the start of exercise using creatine phosphate, substance stored in muscles that can be hydrolysed to release energy, used to regenerate ATP from ADP and Pi, the Pi being provided by the creatine itself, broken down as exercise begins (triggered by formation of ADP)

Does not require oxygen and provide energy for 6-10 seconds - therefore used in bursts of intense activity, creatine regenerated when the body is at rest 

Creatine phosphate + ADP ---> Creatine + ATP 

Done using a respirometer, the temperature must be controlled 

Use energy released from ATP to contract, becoming shorter

Striated (skeletal/voluntary) muscles attach to bones by tendons, muscle fibres have many nuclei as cells are very long, mitochondria for ATP and sarcoplasmic reticulum (Ca2+), cell membrane = sarcolemma, sarcoplasm = cytoplasm, sarcolemma fold inwards producing fibules which help spread electrical impulses through the sarcoplasm

Muscle fibres made from myofibrils, which are made of sarcomeres, they contain myosin and actin which slide over each other to cause contraction

1. Nerve impulse arrives at the neuromuscular junction, causing depolarisation                                2. Calcium ions released from sarcoplasmic reticulum and diffuse across the sarcoplasm                3. Calcium ions bind to troponin, displacing the tropomyosin, exposing myosin binding sites            4. Myosin head binds to actin filaments, forming cross-bridges                                                          5. ADP and Pi on myosin head are released                                                                                      6. Myosin head thus nods forward, pulling actin towards centre of the sarcomere                              7. ATP binds to myosin breaking the cross bridges, myosin head detaches                                        8. An ATPase molecule on myosin head hydrolyses ATP into ADP and Pi                                          9. Myosin head moves back to original upright position                                                                  10. Cycle repeats for as long as action potentials arrive 

Once the muscle is no longer being stimulated the calcium ions are actively transported back to the sarcoplasmic reticulum using ATP, troponin and tropomyosin return to original positions, myofilaments can no longer slide past each other, actin moves back to its respected position in the sarcomere

Muscles attached to bone by strong, inelastic tendons, which are made of collagen, when a muscle contracts it pulls on tendon

Bones join through ligaments, connected as joints (synovial), bones separated by synovial fluid which is a lubricant secreted by the synovial membrane, allowing free movement

Ligaments contain elastin, moreso than tendons, so can stretch more, ligaments control and restrict amount of movement in a joint 

Cartilage is firm and thick, protecting the bones within joints, it absorbs synovial fluid and acts as a shock absorber 

Bending at joint when contracting = flexors

Straightening at joint when contracting = extensors 

Muscles can only pull, so work in antagonistic muscle pairs, when one contracts the other relaxes

Increases arterial vasodilation which decreases BP, and so reduces risk of CVD

Increases levels of HDLs and reduces levels of LDLs

Decreases risk of obesity

Increased sensitivity of muscle cells to insulin

Increases bone density - slowing progress of osteoporosis 

Reduces risk of some cancers

Improves mental well-being 

Moderate exercise also increaes number of natural killer cells in blood and lymph

Increased risk of obesity

Higher BP

Higher risk of cancer

Higher risk of type II diabetes

Higher risk of osteoporosis

HIgher chance of CVD/CHD and stroke

Joints become abnormally worn, due to damage of ligaments and swelling of knees and synovial joints

Can make the immune system less effective (suppression) - more likely to suffer infections such as upper respiratory tract (especially in teams)

High levels decrease activity of lymphocytes

Psychological stress and physical stress cause secretion of hormones adrenaline and cortisol from adrenal glands above kidneys which suppress the immune system

Small incision, tendons or ligaments taken from elsewhere to repair the damaged cruciate ligament 

Only small incisions so less blood loss and scarring 

Less pain and recovery time - easier to return to normal activities 

Surgery does not take long - save money, resources and staff of hospitals 

Whole joint replaced with a prosthetic joint, can replace whole limbs or limb parts 

Make it possible for people with disabilities to participate in sport

Make it possible for people with injuries to play sport again 

Variations in design for specific activities 

However, are very expensive as they must be made from materials that:

Are unaffected by body fluids, can stand up to the high forces of the knee

Have the right combination of flexibility, strength and weight for movement and support

Anabolic steroids - increase strength, speed and stamina by increasing muscle size, allowing athletes to train harder and increase aggression (testosterone)

Stimulants - speed up reactions, reduce fatigue and increase aggression 

Narcotic analgesics - reduce pain so injuries don't affect performance 

Steroids increase protein synthesis so can increase muscle size and strength, erythropoietin increases the rate at which RBCs are produced, increasing oxygen carrying capacity of blood

Peptide hormones such as erythropoietin are protein chains, cannot pass through cell membranes as they are charged, instead, they bind to receptors on the membrane, activating a second messenger in the cytoplasm,  causing changes in gene transcription

Steroid hormones are formed from lipids and have ring structures, the hormone-receptor complex functions as a transcription factor, switching genes on and off

Against

Some are illegal and can have serious health risks such as high BP and heart problems 

Unfair, as they gain an advantage rather than through hard work, athletes may not be fully aware of health risks 

For 

Up to each individual, athletes have the right to make their own decisions 

Drug-free sport isn't fair regardless 

Hard to detect every drug, so hard to develop tech

No ban on nutritional substances such as vitamins 

Myogenic - contracts and relaxes automatically without nervous stimulation, made of cardiac muscle, rhythmic contraction of the muscle is coordinated through electrical impulses 

In the right atrium wall lies the SAN which acts as a pacemaker, has an intrinsic rate of contraction a little higher than the rest of the heart muscle, as SAN contract they generate APs, sending a wave of depolarisation along the right atria wall, causing them to contract, when it reaches the AVN it is first delayed, allowing atria to fully contract and for the blood to enter the ventricles, the depolarisation then continues down between the ventricles, along Purkyne fibres in the bundle of His and upto the ventricle walls, causing ventricles to contract from the bottom up (apex), slightly after the atria

There is then a short delay before the next wave of depolarisation in the SAN, allowing the heart to relax and repolarise, also for the atria and ventricles start to fill with blood again - diastole 

Differences in resting heart rate due to: different size, genetic factors, gender, lifestyle 

Larger heart usually has lower resting heart rate, expels more blood in one contraction so does not need to beat as frequently, endurance training causes larger, muscular hearts to be produced 

P wave = contraction (depolarisation) of the atria

QRS complex = contraction (depolarisation) of the ventricles

T wave – relaxation/recovery (repolarisation) of the ventricles                                   

PR interval – time for impulses to be conducted from SAN across the atria to the ventricles, through the AVN

Abnormal ECGs can be used to diagnose heart problems. Doctors compare patient’s ECGs with a normal trace to diagnose problems with the heart rhythm such as CVD

Tachycardia – increased heart rate of more than 100bpm – sign of heart failure – cannot pump blood efficiently – can increase risk of heart attack
Bradycardia – heart rate of less than 60pbp
Fibrillation – irregular heartbeat – atria and ventricles have lost their rhythm. Atrial fibrillation – chest pains, fainting and increased risk of stroke. Ventricular fibrillation – heart attack
Ischaemia – heart muscle does not receive blood due to atherosclerosis causing blockage of coronary arteries – disrupts normal electrical activity and rhythm, arrhythmias is caused (irregular heart beat)

A longer delay between the P and R waves – electrical impulses cannot pass easily from the atria to the ventricles – e.g. damage to the bundles of His

A flat T wave – indicate lack of blood flow to cardiac muscle in the heart wall – no energy for contraction – could be an indication of CVD

Problems with AVN – atria are contracting but ventricles are not – some P waves not followed by a QRS complex

Therefore, ECGs can provide info on irregular heartbeats, areas of damage and inadequate blood flow 

The maintenance of a steady internal state in the body almost regardless of changes in either the external or internal conditions.

Core body temp must be maintained at around 37 degrees, for cells to function and stop enzymes denaturing - a dynamic equilibrium is set up, matching supply of oxygen and glucose to demands, while expelling carbon dioxide, each condition has a norm value that the mechanism maintains

Involves coordination and control, changes in the body detected by a sensor/receptor, sending messages to effectors which reverse or increase the change, negative feedback = do opposite of change and restore equilibrium, positive feedback = effectors increase effect which triggered the response 

Communication in a feedback system can be hormones or nerve impulses

Heart controlled by CVCC in the medulla, chemical and stretch receptors in blood vessels and heart walls send nerve impulses to the medulla and CVCC

Two types of nerves of the autonomic system then carry impulses to the heart 

Sympathetic - usually excitatory - speeds heart rate - releases adrenaline and noradrenaline when released 

Parasympathetic - usually inhibitory - slows heart rate - releases acetylcholine when stimulated 

Nerve impulses travelling down the sympathetic nerve from the CVCC stimulate the SAN, increasing the frequency of signals from the pacemaker, so the heart rate increases, from parasympathetic the SAN activity is inhibited and so the heart rate slows 

Adrenaline is secreted from the adrenal glands above the kidneys during fear, shock or excitement, stimulating the SAN to increase its rate of contraction. This speeds the frequency of excitation, supplying extra oxygen and glucose for the muscles and brain in a fight or flight response. Adrenaline also causes dilation of the arterioles supplying skeletal muscles and constriction of arterioles going to the digestive system and other non-essential organs. This maximises blood flow to the active muscles. Adrenaline also causes an anticipatory increase in heart rate before exercise.

Stretch receptors in the muscle walls of the heart send nerve impulses to the cardiovascular control centre. This sends more impulses along the sympathetic nerve to the SAN, increasing the heart rate. The increased stretching of the heart atrial muscle also makes the muscles contract harder, increasing the volume of blood expelled at each stroke.

Baroreceptors in the aorta and carotid arteries are stretched as blood pressure increases after exercise. They send nerve impulses to the parasympathetic system to slow the heart rate and cause vasodilation. This lowers the blood pressure. The reverse happens when exercise starts – the blood vessels dilate in response to adrenaline and blood pressure falls, reducing the stretch of the baroreceptors. When the baroreceptors do not stimulate the cardiovascular control centre it sends signals along the sympathetic nerve to stimulate the heart rate and increase blood pressure. Negative feedback to prevent excessive blood pressure rise

Minute ventilation - volume of air taken into the lungs in a minute (VR x TV)

Tidal volume is the volume of air in a normal breath (about 0.4dm3)

Breathing rate is how many breaths are taken in a minute 

Vital capacity is the maximum volume of air we can inhale and exhale

Volume of blood pumped by the heart in one minute (SV x HR)

Stroke volume - volume of blood pumped out of the left ventricle each time it contracts 

Heart rate - the number of times the heart beats per minute 

During exercise, there are greater muscle contractions so more blood returns to the heart (venous return) – in diastole the heart fills with a larger volume of blood – the heart muscle is stretched more, increasing stroke volume and cardiac output.

Aerobic capacity is the ability to take in, transport and use oxygen

Long periods of strenuous exercise depends on maintaining a constant ATP supply, this depends on aerobic capacity.

VO2 is the volume of oxygen we consume per minute

VO2 max is the maximum amount of oxygen we can consume per minute

Spirometers can be used to measure tidal volume and breathing rate and can also be used to investigate the effects of exercise. A spirometer is a machine with an enclosed chamber containing oxygen, lying over water.  By counting the number of traces over a known period of time, breaths per minute can be calculated.

1. A person breathes through a mouthpiece/tube
2. As they breathe in, the lid moves 
3. As they breathe out, it moves up
4. These movements are recorded by a pen attached to the chamber lid, drawing on a rotating drum, creating a spirometer trace
5. The soda lime in the tube absorbs carbon dioxide breathed out during respiration – only oxygen is in the chamber to inhale from – total volume decreases.

The medulla controls breathing rate. Rhythmic patterns of nerve impulses are sent from the ventilation centre in the medulla to the muscles in the diaphragm and intercostal muscles, which respond by contracting rhythmically. There are two ventilation centres:

• Inspiratory centre – controls breathing in – sends nerve impulses to intercostal and diaphragm muscles to make them contract – increases volume and decreases pressure in lungs. These impulses inhibit the action of the expiratory centre. As the lungs inflate, stretch receptors are stimulated and send nerve impulses back to the medulla, inhibiting the action of the inspiratory centre.
• Expiratory centre – controls breathing out – no longer inhibited, sends nerve impulses to the diaphragm and intercostal muscles to relax – lungs deflate, expelling air. The stretch receptors become inactive then the cycle repeats

During exercise, there is an increase in carbon dioxide in the blood and a decrease in blood pH. This is detected by chemoreceptors in the medulla, aorta and carotid bodies which then send nerve impulses to the respiratory/ventilation centre. Impulses are sent to the breathing muscles (effectors) – intercostal muscles and diaphragm to change the breathing rate in a negative feedback system, removing the extra carbon dioxide and increasing oxygen uptake. The muscles contract harder and faster, increasing the rate and depth of breathing.

Changes in core temperature are detected by thermoreceptors in the skin and sent to the hypothalamus in the brain. The hypothalamus then sends nerve impulses to effectors which respond:

When temperature rises:

• Vasodilation: Smooth muscle in the arteriole walls delivering blood to the skin dilate so a greater volume of blood flows into the surface capillaries – 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 skin surface, where the water in it evaporates – takes heat from the skin
• Erector pili muscles attached to hairs relax to let hairs lie flat so they do not trap a layer of insulating air.

When temperature falls:

• Vasoconstriction: Arterioles constrict so less heat is lost from the skin surface, blood is diverted beneath the insulating fat layer beneath the skin
• Sweat glands secrete little or no sweat
• Erector pili muscles contract, pilling hairs up – traps a layer of insulating air next to the skin
• Certain muscles contract and relax rapidly (shivering), generating heat which increases blood temperature

A receptor detects a change in the normal state of a system – triggers events to reverse the change. However, temperature does fluctuate because of the lag time between the sensory (hypothalamus) detecting the change and the effectors respond to it.