Topic 7 - Respiration, Muscles and the Internal Environment

Aerobic respiration transfers energy from glucose to ATP using oxygen, producing carbon dioxide and water. Glycolysis occurs in the cytoplasm; the link reaction and Krebs cycle occur in the mitochondrial matrix; oxidative phosphorylation occurs on the inner membrane.

Enzymes release energy in controlled steps rather than one burst. NAD and FAD carry hydrogen/electrons between stages, while ATP provides immediately usable energy for cellular work.

A defect in the inner membrane can disrupt electron transport and ATP synthase even if glycolysis in the cytoplasm continues for a time.

The word “energy” is not a product that floats free: it is transferred into ATP and heat. Keep substrate, ATP yield, location and oxygen requirement distinct.

Glycolysis takes place in the cytoplasm and does not require oxygen. Glucose is phosphorylated and split into triose phosphate; oxidation then produces two pyruvate, four ATP gross (two net) and two reduced NAD.

The initial ATP investment makes glucose more reactive. Reduced NAD carries hydrogen to later stages when oxygen is available, while pyruvate can enter fermentation when it is not.

Two ATP are used at the start and four are formed later, so the net gain is two ATP per glucose, not four.

Glycolysis is not the complete aerobic pathway and does not require mitochondria. A reduced-NAD molecule is not the same thing as ATP.

In the mitochondrial matrix, pyruvate is decarboxylated and dehydrogenated, forming acetyl CoA, carbon dioxide and reduced NAD. Acetyl CoA then joins oxaloacetate; the Krebs cycle releases CO₂, reduces NAD/FAD and makes ATP while regenerating oxaloacetate.

Each glucose produces two pyruvate, so the link reaction and cycle turn twice per glucose. The cycle is sustained because the acceptor molecule is regenerated.

One glucose gives two acetyl CoA, two CO₂ and two reduced NAD in the link reaction; two turns of the cycle then yield four CO₂, six reduced NAD, two reduced FAD and two ATP.

No ATP is made directly in the link reaction. The Krebs cycle is not “in the mitochondrion” generally; its matrix location and carbon accounting matter.

Reduced NAD and FAD donate electrons to the inner-membrane electron transport chain. Energy released pumps protons into the intermembrane space; their return through ATP synthase drives ADP phosphorylation.

Oxygen is the final electron acceptor, combining with electrons and protons to form water. Without oxygen, carriers remain reduced, proton pumping stops and oxidative ATP production collapses.

A proton gradient is like stored potential energy: blocking ATP synthase prevents its controlled use, while making the inner membrane leaky dissipates the gradient as heat.

Chemiosmosis is not direct phosphorylation by oxygen, and the exact ATP yield depends on the accounting convention. Keep proton gradient, ATP synthase and final acceptor separate.

When oxygen is limited, the electron transport chain and Krebs cycle cannot continue normally. Reduced NAD transfers hydrogen to pyruvate, forming lactate and regenerating NAD for glycolysis.

Anaerobic metabolism yields only the small net ATP gain from glycolysis, but it can maintain short-term ATP production. Lactate can later be oxidised to pyruvate or converted to glucose when oxygen is available.

After intense exercise, deeper breathing supplies extra oxygen for processing lactate; the increased ventilation is not evidence that anaerobic respiration itself produced more ATP.

Lactate formation does not make oxygen irrelevant and does not create a large ATP yield. Separate immediate fermentation from later oxygen debt recovery.

Respiratory quotient (RQ) is calculated as CO₂ produced divided by O₂ consumed during respiration. The value helps infer which respiratory substrate is being used, provided the measurements refer to the same time period.

Use gas volumes or moles under consistent conditions, then compare the result with the expected quotient for the substrate. Mixed substrates or anaerobic metabolism can make interpretation less direct.

For glucose under aerobic respiration, equal stoichiometric amounts of CO₂ and O₂ give RQ = 1. A lower value can indicate a lipid-rich substrate because proportionally more oxygen is required.

RQ is not a direct measurement of ATP yield, and a quotient from mixed or anaerobic respiration cannot be assigned to one pure substrate without qualification.

A respirometer measures oxygen uptake by a respiring organism. Soda lime or potassium hydroxide absorbs produced carbon dioxide, so the fall in gas volume reflects oxygen consumption.

Use a control with glass beads, keep temperature constant, measure capillary movement over time, reset between repeats and convert the movement using the capillary radius and distance.

If the manometer moves 2 cm in one minute and the capillary radius is r, the volume change is πr²h per minute; averaging repeats gives a more reliable rate.

Movement is not automatically oxygen volume unless CO₂ is absorbed and pressure/temperature are controlled. Living organisms require humane handling.

A respirometer can estimate oxygen consumption; respiratory quotient compares CO₂ produced with O₂ consumed. Both are rates or ratios that require the same time interval and controlled conditions.

Use a control, repeat measurements, absorb CO₂ only when the design requires oxygen uptake, and keep organism mass, temperature and activity comparable. Calculate RQ from gas volumes or moles.

A rise in oxygen uptake after warming may reflect faster respiration, but if temperature also changes gas pressure the apparent rate is confounded unless the control corrects it.

RQ from mixed substrates or anaerobic metabolism is not a clean substrate fingerprint. Separate instrument movement, oxygen consumption and the final quotient.

Muscles generate pulling force; bones resist bending and act as levers. Tendons connect muscle to bone and transmit force, while ligaments connect bone to bone and stabilise joints.

Because a muscle cannot push, opposing muscles work antagonistically around a joint. One contracts while its partner relaxes to reverse the movement.

To flex the elbow, biceps contract and triceps relax; to extend it, triceps contract and biceps relax. The bone provides the rigid structure being pulled.

Tendons are not ligaments, and a relaxed antagonist is not necessarily inactive in every movement. Identify the joint action and force direction.

Fast-twitch fibres contract rapidly and suit short, high-intensity activity; slow-twitch fibres contract more slowly and resist fatigue during sustained activity. Their structure and metabolism support those roles.

Fast fibres rely more on anaerobic ATP supply and have fewer capillaries and less myoglobin; slow fibres have greater aerobic capacity, blood supply and oxygen storage.

A sprint uses fast fibres for rapid force, whereas prolonged walking recruits more slow fibres. A muscle usually contains a mixture rather than only one fibre type.

“Fast” does not mean stronger in every task, and fibre type alone does not determine performance. Link the claim to ATP pathway, fatigue and activity duration.

An action potential releases calcium from the sarcoplasmic reticulum. Calcium binds troponin, moves tropomyosin away from actin sites, and allows myosin heads to form cross-bridges and pull actin towards the sarcomere centre.

ATP lets a myosin head detach and its hydrolysis resets the head for another power stroke. Repeated cycles bring Z discs closer; when calcium is pumped back, binding sites are blocked and relaxation follows.

The filaments remain the same length while the sarcomere shortens. Without ATP, myosin cannot detach, explaining rigor mortis after death.

ATP is needed for detachment as well as the recovery stroke, and calcium exposes binding sites rather than directly pulling actin.

The sinoatrial node initiates a myogenic wave; the atria depolarise and contract, the atrioventricular node delays transmission, and Purkyne tissue spreads excitation through the ventricles from the apex.

On an ECG, the P wave reflects atrial depolarisation, the QRS complex ventricular depolarisation and the T wave ventricular repolarisation. Wave timing and rhythm reveal coordination, not blood pressure directly.

A prolonged interval or irregular rhythm can suggest conduction or fibrillation problems, while a low resting rate in a trained athlete may be normal bradycardia.

An ECG is an electrical trace, not a direct image of contraction force or a diagnosis by itself. Interpret the wave, interval and clinical context together.

Cardiac output is the volume pumped by a ventricle per minute: cardiac output = heart rate × stroke volume. It rises during exercise so working cells receive more oxygen and substrates.

Keep units consistent, convert cycle time into beats per minute, then rearrange the equation when heart rate or stroke volume is unknown.

If one cardiac cycle lasts 1.2 s, heart rate is 60 ÷ 1.2 = 50 bpm. With stroke volume 75 cm³, cardiac output is 3,750 cm³ min⁻¹ or 3.75 dm³ min⁻¹.

A higher heart rate does not always mean a higher cardiac output if stroke volume falls. Cardiac output is a volume per time, not the blood pressure itself.

Adrenaline is released during acute stress and prepares the body for rapid action. It increases heart rate and ventilation, redirects blood toward skeletal muscle and raises blood glucose availability.

The response is coordinated by receptors and effectors: more cardiac output and ventilation deliver oxygen, while glycogen breakdown supplies respiratory substrate. It is rapid and short-term rather than a complete long-term adaptation.

A sudden threat can cause heart rate to rise before movement begins, increasing cardiac output; the same response can be unnecessary or costly if stress is prolonged.

Adrenaline does not directly create ATP and “fight-or-flight” is not a single switch. Identify the target tissue and physiological effect.

During exercise, ventilation increases to bring in more oxygen and remove more carbon dioxide. A spirometer can record breathing volume over time so rate, tidal volume and total ventilation can be compared.

Calibrate the apparatus, keep posture and workload consistent, collect repeated traces and distinguish breathing rate from depth. Use a control or resting trace for comparison.

A person may increase ventilation by breathing deeper, faster or both. A larger trace area does not automatically mean a higher oxygen uptake unless the gas measurement is calibrated.

Spirometry measures air movement, not directly ATP production. Leaks, mouthpiece position and exercise intensity can distort the trace.

A homeostatic control system detects deviation from a set point and coordinates effectors. Negative feedback opposes the deviation and returns the variable toward its normal range; positive feedback reinforces a change until a defined endpoint.

Thermoregulation increases heat loss when body temperature rises, whereas clotting can amplify activation until a wound is sealed.

Homeostasis is dynamic equilibrium, not a perfectly fixed value. Do not label every response negative or assume positive feedback is automatically unstable.

When body temperature rises, vasodilation and sweating increase heat loss; when it falls, vasoconstriction, shivering and raised metabolic rate reduce heat loss or generate heat. Receptors and effectors maintain a narrow operating range for enzymes.

Vasoconstriction reduces heat loss rather than directly warming the blood. Sweating works by evaporation, so humidity changes its effectiveness.

In humid air, sweat may remain on the skin while evaporation slows; in cold air, vasoconstriction diverts blood from surface capillaries and shivering raises respiration.

Thermoregulation is not a single “set temperature” response and skin redness does not itself mean core temperature is safe.

The mammalian kidney maintains water and solute balance by filtration at the glomerulus, selective reabsorption along the nephron and controlled water permeability in the collecting duct.

Small molecules enter the filtrate under pressure, but cells and large proteins remain in the blood. Useful glucose, ions and water are reabsorbed according to body needs; hormones such as ADH alter collecting-duct permeability.

When blood water potential falls, more ADH increases aquaporins in collecting-duct membranes, so more water returns to the blood and urine becomes concentrated.

Filtration is not the same as excretion, and urine concentration is not controlled by “the kidney” as one undifferentiated organ. Separate nephron region, substance and hormone.

Amino-acid deamination produces ammonia, which is toxic. In the liver, the urea cycle converts ammonia into urea, a less toxic soluble compound transported in the blood to the kidneys.

Urea can be filtered and excreted in urine, allowing nitrogen from excess amino acids to leave the body without ammonia accumulating in tissues.

After a high-protein meal, more amino acids may be deaminated; increased urea production reflects nitrogen disposal, not direct protein storage.

Deamination is not the same as digestion, and urea is not formed in the nephron. Keep liver conversion, blood transport and kidney excretion separate.

High pressure forces water and small solutes from glomerular blood into Bowman’s capsule. Cells and large proteins remain in the blood; useful substances are then selectively reabsorbed along the nephron.

The loop of Henle establishes a medullary water-potential gradient, allowing the collecting duct to reabsorb water when hormone signals make it permeable.

Glucose is normally reabsorbed early in the nephron, while water reabsorption varies with body water status. A substance in filtrate is not automatically destined for urine.

Ultrafiltration is pressure-driven, whereas selective reabsorption is transport-based. Do not call every nephron segment equally permeable or equally responsible for concentration.

Osmoreceptors detect blood water potential and the hypothalamus/pituitary adjusts ADH release. ADH increases aquaporins in collecting-duct membranes, so more water returns to the blood and urine becomes concentrated.

When blood is dilute, less ADH leaves the collecting duct less permeable and more dilute urine is produced. The response is negative feedback around a regulated water balance.

After dehydration, high ADH increases water reabsorption even though the filtered load may be similar; the final urine changes because permeability changed.

ADH does not “add water” to urine and does not act equally on every nephron segment. Separate sensor, hormone, membrane change and final urine effect.

A transcription factor is a protein that binds a regulatory DNA sequence and changes whether RNA polymerase can transcribe a gene. Hormone receptors can act as transcription factors when a lipid-soluble hormone enters a cell and binds them.

Changing transcription changes mRNA production, which can change protein amount and therefore cell behaviour. Different cells respond differently because they express different receptors and target genes.

A steroid hormone–receptor complex can enter the nucleus, bind DNA and increase transcription of a target gene; a peptide hormone usually signals through a membrane receptor instead.

A transcription factor does not translate mRNA or guarantee a phenotype. Distinguish receptor location, DNA binding, transcription and downstream protein function.