Unit 5: Respiration, Internal Environment, Coordination and Gene Technology

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.

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.

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.

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.

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.

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.

1. Prepare equal yeast suspensions with the same strain, concentration and volume, plus equal glucose solution and indicator volumes.
2. Place tubes at five controlled temperatures within a safe range and allow all contents to equilibrate.
3. Add indicator or substrate in the same order, mix consistently and start the timer immediately.
4. Record time to the same defined colour endpoint, or measure absorbance continuously with a colorimeter.
5. Repeat each temperature, calculate mean time and compare rate as $1/\text{time}$ or calibrated absorbance change per unit time.

Keep pH, glucose concentration, yeast quantity, total volume, indicator concentration and oxygen availability constant. Include a no-yeast or heat-killed control to show that non-biological colour change is negligible.

1. Place equal masses of germinating seeds or approved small invertebrates in matched chambers, separated safely from any carbon-dioxide absorbent; use inert beads of equal displaced volume as a control.
2. Equilibrate in a constant-temperature water bath, close the system and set the marker fluid.
3. Measure distance moved in a fixed time and calculate gas volume as $V=\pi r^2l$.
4. Repeat, correct for control movement and divide by time and organism mass for respiration rate.
5. Run matched measurements with and without carbon-dioxide absorbent over the same interval.

Let $O$ be the volume decrease with carbon dioxide absorbed. Without absorbent, signed net gas change represents oxygen uptake minus carbon dioxide output; use the apparatus sign convention to obtain $C$, then calculate $RQ=C/O$. Check the mass balance rather than memorising a sign.

Keep temperature, time, organism mass, developmental stage and activity constant; test for leaks and keep absorbent from contacting organisms. Use the minimum number of organisms, prevent harmful temperature or oxygen conditions and follow approved end handling.

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.

A skeletal muscle fibre is a long multinucleate cell surrounded by a sarcolemma. Its sarcoplasm contains parallel myofibrils made of repeating sarcomeres with actin and myosin filaments. Sarcoplasmic reticulum stores calcium, transverse tubules carry excitation inward, and mitochondria and glycogen supply ATP.

Endurance activity benefits from oxygen delivery, myoglobin storage and many mitochondria in slow fibres. Sprinting and explosive movement benefit from rapid ATP supply and force in fast fibres. Most muscles contain a mixture recruited according to demand.

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.

1. The sinoatrial node (SAN) depolarises and spreads excitation across both atria, causing atrial systole.
2. Non-conducting tissue prevents direct spread to ventricles; the atrioventricular node (AVN) receives the wave and delays it so ventricles fill.
3. The bundle of His conducts down the septum.
4. Purkyne fibres carry excitation from the apex upward through ventricular walls, producing coordinated ventricular systole.

Cardiac output is blood volume pumped by one ventricle per minute: $\text{cardiac output}=\text{heart rate}\times\text{stroke volume}$. If heart rate is 120 beats min$^{-1}$ and stroke volume is 90 cm$^3$, output is 10 800 cm$^3$ min$^{-1}$ or 10.8 dm$^3$ min$^{-1}$.

During exercise, faster ventilation increases oxygen entry and carbon dioxide removal, while greater cardiac output transports these gases more rapidly between lungs and tissues. Both rate and depth of breathing, and both heart rate and stroke volume, can contribute.

Higher tissue respiration raises blood carbon dioxide and lowers pH. Chemoreceptor input reaches the ventilation and cardiovascular control centres in the medulla oblongata. The ventilation centre increases impulses to the diaphragm and intercostal muscles; the cardiovascular centre increases sympathetic and reduces parasympathetic signalling to the SAN, raising heart rate. Venous return and sympathetic action can also increase stroke volume.

As carbon dioxide and pH approach their normal range, negative feedback reduces the drive. Proprioceptor and anticipatory signals can accelerate the response at exercise onset before blood chemistry changes fully.

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.

Calibrate volume and time axes, obtain a stable resting trace, apply a standardised safe exercise workload, then record recovery traces at defined times. Calculate each quantity over several breaths, repeat participants or trials and compare like time windows. Check the apparatus for leaks and use a fresh mouthpiece and approved soda-lime arrangement.

A tidal volume of 1.2 dm$^3$ and breathing rate of 30 min$^{-1}$ gives minute ventilation of 36 dm$^3$ min$^{-1}$. If the oxygen baseline falls 1.5 dm$^3$ in 3 min, consumption is 0.50 dm$^3$ min$^{-1}$.

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.

Thermoreceptors in skin and the hypothalamus detect temperature change; the hypothalamus compares input with the regulated range and coordinates effectors. If core temperature rises, skin arterioles dilate and sweat secretion increases. Evaporation removes latent heat. If temperature falls, vasoconstriction, shivering and increased metabolic heat production respond.

During exercise, blood flow is redistributed, ventilation and cardiac output rise, and thermoregulation prevents metabolic heat from pushing enzymes and membranes outside effective conditions. Responses continually adjust as production and loss change—this is dynamic equilibrium.

Each kidney has a fibrous capsule, outer cortex and inner medulla arranged in pyramids. Urine drains through collecting ducts into the renal pelvis and ureter. The renal artery supplies blood; the renal vein returns it after filtration and adjustment.

Blood flows renal artery → afferent arteriole → glomerulus → efferent arteriole → peritubular capillaries/vasa recta → renal vein. Filtrate flows capsule → proximal tubule → loop → distal tubule → collecting duct → pelvis → ureter.

Excess amino acids cannot be stored. In liver cells their amino group is removed by deamination, producing toxic ammonia; ammonia is converted to less toxic, soluble urea without requiring details of the ornithine cycle. The remaining carbon skeleton can enter respiration or other metabolism.

Urea travels in plasma to the kidney. The afferent arteriole is wider than the efferent arteriole, helping create high glomerular hydrostatic pressure. Water and small solutes cross fenestrated capillary endothelium, basement membrane and podocyte filtration slits into Bowman's capsule; cells and most large plasma proteins remain in blood.

Urea enters filtrate by ultrafiltration. Water and useful solutes are subsequently reabsorbed, while much urea remains for excretion in urine, so its concentration can change as water is removed.

Proximal-tubule cells have microvilli, basal infoldings and many mitochondria. Na$^+$/K$^+$ pumps lower intracellular sodium; sodium then enters from filtrate through co-transporters carrying glucose or amino acids. These solutes move into capillaries, and water follows by osmosis. Normally all filtered glucose is recovered below the transport maximum.

Filtrate flows in opposite directions through adjacent limbs. A small transverse salt gradient is repeated along the loop, multiplying into a steep cortex-to-medulla water-potential gradient. The vasa recta helps preserve it, and collecting-duct water can then leave osmotically when ADH makes the duct permeable.

When plasma water potential falls or effective blood volume falls, hypothalamic osmoreceptors change activity. Neurosecretory cells cause more ADH to be released from the posterior pituitary. ADH binds collecting-duct cell receptors, activates signalling and inserts aquaporin channels into the luminal membrane, increasing water reabsorption into the medulla and blood.

When plasma becomes too dilute, osmoreceptor stimulation and ADH release fall. Fewer aquaporins make collecting ducts less permeable, so less water is reabsorbed and a larger volume of dilute urine is produced.

The response restores plasma concentration and supports blood volume; as the deviation decreases, the original ADH signal decreases. Thirst and circulatory pressure signals can work alongside osmotic control when volume is threatened.

Changed transcription alters mRNA abundance, then protein synthesis and cell behaviour. Steroid action is often slower to begin because it depends on transcription and translation, while peptide signalling can also change existing proteins rapidly before later gene effects.

Oestrogen can enter a responsive cell, bind its receptor, and the complex can promote transcription of proteins involved in cell division. A peptide hormone stays extracellular and relays its message through a membrane receptor.

Schwann cells wrap repeatedly around peripheral axons to form a lipid-rich myelin sheath. Gaps between cells are nodes of Ranvier, where ion channels allow action potentials to be regenerated. Myelin insulates internodes and enables faster saltatory conduction.

The basic pathway is stimulus → receptor → sensory neurone → CNS → motor neurone → effector. The CNS integrates information and the effector produces a response through muscle contraction or gland secretion.

Bright light activates retinal receptors; impulses reach the CNS and motor neurones stimulate circular iris muscles so the pupil constricts. In low light, radial muscles contract and the pupil dilates.

Antagonistic effectors allow opposite outcomes, while a rapid neural pathway limits exposure to harmful conditions.

The spinal cord has central butterfly-shaped grey matter containing neurone cell bodies, dendrites and many synapses. Surrounding white matter contains bundles of myelinated axons running up and down the cord. Sensory axons enter through a dorsal route and motor axons leave through a ventral route.

In a withdrawal reflex, a pain receptor activates a sensory neurone, a relay neurone excites the flexor motor neurone and an inhibitory pathway relaxes the antagonist extensor. Information also ascends through white matter so pain can be perceived after the response begins.

When membrane depolarisation reaches threshold, voltage-gated sodium channels open and sodium ions enter. Potassium ions then leave to repolarise the membrane; the signal propagates as neighbouring sections reach threshold.

The all-or-nothing action potential is regenerated along the axon, so its amplitude does not fade with distance. Refractory periods help maintain one-way transmission.

A stronger stimulus is represented by more frequent action potentials, not a larger action potential, once threshold has been crossed.

In a myelinated axon, the sheath insulates the membrane between nodes of Ranvier. Depolarisation is regenerated at the nodes, so the impulse appears to jump along the axon by saltatory conduction.

The insulation reduces ion leakage and increases conduction speed compared with a non-myelinated axon, where the membrane is activated continuously.

Damage to myelin can slow or disrupt signalling even when the axon and its cell body remain present, because the normal node-to-node pattern is lost.

An arriving action potential opens presynaptic voltage-gated Ca$^{2+}$ channels. Calcium entry triggers acetylcholine-containing vesicles to fuse with the membrane. Acetylcholine diffuses across the cleft, binds complementary postsynaptic receptors and opens ion channels; sufficient depolarisation triggers a new action potential. Acetylcholinesterase hydrolyses acetylcholine so stimulation is brief.

Vesicles and release machinery are presynaptic, while receptors are postsynaptic, making chemical transmission one-way. Synaptic delay, summation and inhibition allow integration rather than simple electrical continuity.

In darkness, rhodopsin is intact and cGMP-gated cation channels remain open. Sodium and other cations enter the rod outer segment, keeping the cell relatively depolarised and causing continuous neurotransmitter release onto bipolar cells.

A photon absorbed by rhodopsin changes retinal and separates/activates the opsin component. The signalling cascade lowers cGMP, so cation channels close. Sodium entry falls while potassium loss continues, hyperpolarising the rod and reducing neurotransmitter release.

The change in transmitter alters bipolar-cell activity and then ganglion-cell firing. Ganglion-cell axons form the optic nerve, where information is carried as action potentials; the rod itself signals mainly by graded membrane-potential change.

Many rods converge onto shared pathways, giving high sensitivity in dim light but lower spatial resolution and no colour discrimination compared with cones.

Habituation occurs when repeated harmless stimulation produces a smaller response. The animal saves energy because fewer calcium ions enter the presynaptic neurone, less neurotransmitter is released and the postsynaptic cell is less likely to reach threshold.

A snail may take less time to re-emerge after repeated gentle touches. If the sound or touch becomes stronger, the response can return because the stimulus is no longer identical.

The change is in synaptic transmission, not a loss of all sensory ability. The animal can still respond when the stimulus becomes relevant.

The central nervous system (CNS) is the brain and spinal cord; the peripheral nervous system (PNS) carries information between the CNS and receptors or effectors. Sensory and motor pathways connect the two.

This division separates integration from transmission. A receptor detects a stimulus, the CNS coordinates a response, and motor neurones carry the output to muscles or glands.

A skin receptor sends an impulse through a sensory neurone in the PNS to the spinal cord; a motor pathway then activates an effector.

In a shoot lit from one side, more auxin action on the shaded side promotes greater elongation, bending the shoot toward light. In a germinating cereal, embryo gibberellin reaches aleurone cells and induces transcription of amylase genes, mobilising endosperm starch.

1. Surface-sterilise cereal grains using the approved aseptic procedure and cut them to separate embryo-containing and endosperm portions.
2. Soak matched portions in the same gibberellin concentration; soak equivalent portions in sterile water as negative controls.
3. Place cut faces onto sterile starch-agar plates, with equal spacing and labelled positions.
4. Incubate sealed plates at a fixed safe temperature for 24–48 hours.
5. Add iodine according to the approved method and measure clear-zone diameter or area around each portion.
6. Repeat grains and compare means with spread.

Independent variables may be tissue type and gibberellin treatment. Control grain variety/age, portion size, solution volume/concentration, agar depth, incubation time and temperature. A known amylase positive control can confirm that the starch-iodine detection works.

Nervous control uses rapid electrical impulses and targeted neurotransmitter release; hormonal control uses chemicals carried in blood, usually with slower onset and longer-lasting, broader effects. Both use receptors, coordination centres and effectors.

A reflex can move a hand away quickly, while adrenaline or thyroxine changes metabolism across several tissues. The best system depends on speed, duration and distribution.

The systems can interact: neural signals can trigger hormone release, and hormones can alter the sensitivity or activity of nervous tissues.

Compare a patient with reference data or the same person across conditions. Increased fMRI or PET signal supports involvement or altered metabolism, not that one region alone causes the behaviour. Diagnosis combines imaging with clinical evidence.

Some disorders are associated with altered neurotransmitter levels or signalling. Parkinson’s involves reduced dopamine from lost neurones; antidepressant drugs can increase serotonin or noradrenaline signalling.

A drug may mimic a transmitter, supply a precursor, block breakdown or inhibit reuptake. These mechanisms change synaptic transmission, but symptoms usually involve networks and multiple contributing factors.

L-dopa is converted into dopamine in the brain, while an SSRI reduces serotonin reuptake so more remains in the synaptic cleft.

Recombinant bacteria can produce human insulin; a suitable promoter drives expression, fermenter conditions are controlled, and insulin is purified rather than administering the organism itself.

Recombinant DNA is formed when DNA from different sources is joined. A restriction enzyme cuts the desired gene and vector, complementary ends pair, and DNA ligase seals the sugar-phosphate backbone.

PCR can amplify the target before insertion, while a plasmid provides replication or expression signals in the host. The construct must be introduced into cells and selected or screened.

A gene coding for insulin can be joined to a bacterial plasmid; the plasmid is then transferred into bacteria where the gene may be expressed.

Use a selectable or screenable marker to identify candidate cells, then PCR or another DNA test to verify the construct. Measure RNA or protein to show expression, because vector entry and marker survival alone do not prove a functional therapeutic product.

A microarray uses labelled nucleic acids from samples to measure which genes are expressed relative to a reference. Complementary binding at spots produces a pattern that can be compared between tissues or conditions.

The result is a relative expression profile, not a direct measurement of every protein or a guaranteed cause. Controls, normalisation and probe specificity determine how confidently differences can be interpreted.

A gene spot with stronger signal in diseased tissue suggests higher transcript abundance, but follow-up experiments are needed to test whether the gene drives the phenotype.

Bioinformatics uses databases and computational tools to compare DNA, RNA or protein sequences, predict relationships and identify patterns. The output depends on the input sequence, reference database and comparison method.

Check alignment quality, sequence length, conserved regions and the scoring or statistical assumptions before interpreting a match.

A high sequence similarity can support common ancestry or a shared function, while a low-quality or partial sequence may produce a misleading result.

Genetic modification can add a useful characteristic, such as producing a medicine or resisting a pest. Its value depends on effectiveness, containment, ecological effects, ownership, welfare and who receives the benefit.

Benefits may include reliable therapeutic protein production or reduced losses; risks include unintended gene flow, resistance, ecological disruption and ethical objections to animal or food applications.

A GM microorganism making insulin is contained and purified, whereas a GM crop releasing a trait into wild relatives raises a different monitoring problem.