SNAB Topic 7 is the biology of exercise: how muscle contracts by the sliding filament mechanism, how respiration supplies the ATP, how the heart and lungs are controlled, and how negative feedback holds the body in dynamic equilibrium.
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A synovial joint (e.g. the elbow) has cartilage covering the bone ends to reduce friction and absorb shock, synovial fluid as a lubricant, a synovial membrane that secretes it, and a fibrous capsule.
Muscles can only pull, never push, so they work in antagonistic pairs. At the elbow the biceps is the flexor (it contracts to bend the arm) and the triceps is the extensor (it contracts to straighten it). While one contracts, the other relaxes.
A myofibril is made of repeating sarcomeres — thin actin filaments and thick myosin filaments. In contraction the filaments slide past one another: the sarcomere and the I band and H zone shorten, while the A band (the length of the myosin) stays the same. The filaments themselves do not shorten.
Two jobs for ATP: detaching the head, and re-cocking it. Also, ATP is needed for the active transport of Ca²⁺ back into the sarcoplasmic reticulum so the muscle can relax — which is exactly why rigor mortis occurs when ATP runs out.
Respiration is a many-stepped pathway, each step catalysed by a specific intracellular enzyme. Overall it splits the respiratory substrate, releasing CO₂ as waste, and reunites the hydrogen with atmospheric oxygen, releasing a great deal of energy.
Glycolysis (in the cytoplasm — and it is the same in aerobic and anaerobic respiration):
If oxygen is available, pyruvate is actively transported into the mitochondrial matrix.
Link reaction (per pyruvate): pyruvate is decarboxylated (losing CO₂) and dehydrogenated (reducing NAD), and the 2C acetyl group joins coenzyme A to form acetyl coenzyme A. This happens twice per glucose.
Krebs cycle (per turn): acetyl CoA (2C) combines with oxaloacetate (4C) to form citrate (6C). A series of decarboxylation and dehydrogenation reactions regenerates oxaloacetate, yielding:
Why in the mitochondrion? The matrix holds the enzymes of the link reaction and Krebs cycle, and the inner membrane holds the electron transport chain — so the reduced coenzymes are made right next to where their electrons are needed. Glycolysis needs none of that machinery, so it stays in the cytoplasm.
On the inner mitochondrial membrane (the cristae):
Anaerobic respiration (7.7): pyruvate accepts hydrogen from reduced NAD and is converted to lactate by lactate dehydrogenase. The point of this is to regenerate NAD so that glycolysis — and its small ATP yield — can keep going. Lactate lowers the pH and is toxic, causing fatigue. Afterwards, extra oxygen (the oxygen debt / EPOC) is used to oxidise some lactate back to pyruvate, while the liver converts the rest to glucose and glycogen.
Tap a stage, then tap where in the cell it occurs.
Cardiac muscle is myogenic — it contracts of its own accord, without any nervous stimulation. The rhythm is set by the sinoatrial node (SAN), the pacemaker, in the wall of the right atrium.
The ECG: the P wave = atrial depolarisation; the QRS complex = ventricular depolarisation; the T wave = ventricular repolarisation. Tachycardia = a resting rate above 100 bpm; bradycardia = below 60 bpm; fibrillation = a chaotic trace with no coordinated contraction; ectopic beats = extra beats.
Both are controlled by the medulla oblongata.
Cardiovascular control centre: during exercise, chemoreceptors in the aorta and carotid bodies detect a fall in blood pH (from dissolved CO₂), and stretch receptors in the muscles detect movement. Impulses go to the medulla, which sends more impulses down the sympathetic (accelerator) nerve to the SAN, increasing heart rate. When it is over, the parasympathetic (vagus) nerve slows it again. Baroreceptors detect blood pressure and correct it the same way.
Ventilation centre: the same rise in CO₂ increases the rate and depth of breathing, via impulses to the intercostal muscles and diaphragm.
Notice that the primary stimulus is the rise in carbon dioxide, not the fall in oxygen. CO₂ dissolves to form carbonic acid, so it changes blood pH — and pH is what the chemoreceptors are really monitoring.
Tap a feature on the left, then the fibre type it describes.
Homeostasis is the maintenance of a constant internal environment within narrow limits, despite changes outside. It works by negative feedback: a receptor detects a deviation from the set point, a coordinator (usually the hypothalamus) processes it, and effectors act to reverse the change.
Positive feedback does the opposite — it amplifies the change. It is rare and usually used to complete a process quickly: the opening of sodium voltage-gated channels in an action potential, or oxytocin release in childbirth.
Thermoregulation: the hypothalamus monitors blood temperature.
Precision matters: capillaries cannot dilate or constrict — they have no muscle. It is the arterioles (and the shunt vessels) that do the work.
Too little exercise increases the risk of obesity, CVD and type 2 diabetes. Too much causes wear and tear on joints (osteoarthritis) and suppresses the immune system — heavy endurance training temporarily lowers natural killer cell activity and levels of secretory antibodies, so infections are more common. In both cases the evidence is correlational, and you must be careful to distinguish correlation from cause.
Medical technology (7.14): keyhole surgery causes less tissue damage and speeds recovery; prostheses and hip replacements let people with injuries and disabilities take part in sport.
Performance-enhancing substances (7.15): anabolic steroids build muscle but cause liver damage, heart problems and aggression; erythropoietin (EPO) raises red blood cell count but thickens the blood and risks clots; creatine raises phosphocreatine stores. Arguments against use: it is unfair, it is coercive (others must dope to compete), and it is harmful. Arguments for: athletes are adults who consent; the line between a legal supplement and an illegal drug is arbitrary; bans are unevenly enforced.
7.16 — genes can be switched on and off by transcription factors, including hormones. A steroid hormone is lipid-soluble, so it diffuses straight through the membrane, binds a receptor in the cytoplasm, and the complex enters the nucleus and acts as a transcription factor, binding the promoter and increasing transcription of specific genes. That is precisely how anabolic steroids increase muscle protein synthesis.
Sliding filament: Ca²⁺ moves tropomyosin off the actin binding sites → myosin head binds → power stroke → ATP binds and detaches the head → ATP hydrolysis recocks it. Actin and myosin slide past each other; they do not shorten.
Glycolysis (cytoplasm): glucose → 2 pyruvate; net 2 ATP and 2 reduced NAD. Anaerobic and aerobic.
Link reaction (matrix): pyruvate → acetyl CoA + CO₂ + reduced NAD.
Krebs cycle (matrix): per turn — 2 CO₂, 3 reduced NAD, 1 reduced FAD, 1 ATP.
Oxidative phosphorylation (inner membrane/cristae): electrons from reduced NAD/FAD pass down the ETC; protons are pumped into the intermembrane space; chemiosmosis through ATP synthase makes ATP. Oxygen is the final electron acceptor, forming water.
Anaerobic: pyruvate + reduced NAD → lactate, which regenerates NAD so glycolysis can continue. Lactate is later oxidised or converted to glycogen in the liver — the oxygen debt.
Cardiac output = stroke volume × heart rate. The heart is myogenic: SAN → AVN (delay) → bundle of His → Purkyne fibres.
Homeostasis: negative feedback returns a factor to its set point; the hypothalamus controls thermoregulation (vasodilation/vasoconstriction, sweating, shivering).
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