Describe how the nervous and endocrine systems sense change and coordinate the body, explain intrinsic and extrinsic control of heart rate, and evaluate how key hormones, including the reproductive hormones, affect health and performance.
Each is in the SEHS glossary, with every other term in the subject.
A pair of endocrine glands on top of the kidneys; the adrenal medulla releases epinephrine and norepinephrine, and the adrenal cortex releases hormones such as cortisol and aldosterone.
The part of the peripheral nervous system that carries nerve impulses from receptors towards the central nervous system; also called the sensory division.
The increase in heart rate and other sympathetic responses before exercise begins, caused by sympathetic stimulation and the release of epinephrine in response to the expectation of exercise.
A hormone made by the hypothalamus and released by the posterior pituitary when the blood is too concentrated, which increases water reabsorption by the kidneys; also called vasopressin.
A group of specialised cells between the atria and ventricles that receives the impulse from the atria and delays it by about 0.1 s before passing it to the bundle of His.
The branch of the efferent division that controls involuntary functions through cardiac muscle, smooth muscle and glands; it has sympathetic and parasympathetic divisions.
Outline the organisation of the nervous system, from the central and peripheral nervous systems to the sympathetic and parasympathetic divisions.
Describe the roles of neurons, synapses and neurotransmitters in passing information through the nervous system.
Distinguish between the effects of the sympathetic and parasympathetic nervous systems on cardiac function, breathing and temperature control.
Explain how intrinsic control (the conduction system) and extrinsic factors work together to control heart rate.
Describe what proprioceptors, baroreceptors and chemoreceptors detect, and outline one exercise response started by each.
Compare nervous and endocrine communication in terms of signal, pathway, speed and duration.
Describe the sources and effects of epinephrine, norepinephrine, insulin, glucagon and antidiuretic hormone.
Explain how progesterone, oestrogen and testosterone affect health and performance, and place the phases of the menstrual cycle on a hormone graph.
Evaluate the evidence that menstrual cycle phase affects athletic performance.
The body’s systems work together only because they constantly exchange information. Two systems carry that information: the nervous system, which sends fast electrical signals along nerve cells, and the endocrine system, which releases chemical messengers into the blood. During a 400 m race, nerves raise heart rate within a second of the gun, while hormones keep blood glucose available and heart rate high until the finish.
Inter-system communication matters through both lenses of the course. For performance, it explains how heart rate and breathing rise to meet the demands of exercise and how hormones such as testosterone shape strength and endurance. For health, it underpins the control of blood glucose (which fails in diabetes), water balance, and the effects of the menstrual cycle on sleep and bone health.
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A stretch receptor in the walls of the aortic arch and carotid arteries that detects changes in blood pressure and informs the cardiovascular control centre.
A bundle of specialised conducting fibres that carries the impulse from the AV node down the septum of the heart, dividing into left and right bundle branches.
A region of the medulla oblongata that receives information from receptors and higher brain centres and regulates heart rate, force of contraction and blood vessel diameter through the autonomic nervous system.
The brain and spinal cord, which receive sensory information from the whole body, integrate it and send out instructions to muscles and glands.
A receptor that detects changes in the chemical composition of the blood, mainly carbon dioxide, hydrogen ions (pH) and oxygen; found in the medulla and in the carotid and aortic bodies.
The part of the peripheral nervous system that carries nerve impulses from the central nervous system to effectors (muscles and glands); also called the motor division.
A ductless gland that secretes hormones directly into the bloodstream, such as the pituitary, thyroid, adrenal glands, pancreas, ovaries and testes.
The body's endocrine glands and the hormones they release into the blood, which together regulate processes such as metabolism, growth, water balance and reproduction.
A hormone released by the adrenal medulla in response to sympathetic stimulation, which raises heart rate, stroke volume, blood pressure and blood glucose; also called adrenaline.
A hormone produced mainly by the kidneys, in response to low blood oxygen and stimulated by testosterone, which increases red blood cell production in the bone marrow.
Control of the heart from outside it, by sympathetic and parasympathetic nerves and by hormones such as epinephrine, which change the rate of SA node firing and the force of contraction.
The first phase of the menstrual cycle, from the start of menstruation to ovulation, in which oestrogen rises as ovarian follicles develop while progesterone stays low.
A hormone released by the alpha cells of the pancreas when blood glucose is low, which raises it by stimulating glycogenolysis and gluconeogenesis in the liver.
The production of new glucose in the liver from non-carbohydrate sources such as lactate, glycerol and amino acids, stimulated by glucagon.
The breakdown of glycogen stored in the liver or muscle into glucose, stimulated by glucagon and epinephrine.
A proprioceptor at the junction of a muscle and its tendon that detects tension in the muscle; very high tension causes the muscle to relax, protecting it.
A chemical messenger released by an endocrine gland into the blood, which carries it to target cells elsewhere in the body, where it changes their activity.
A region at the base of the brain that links the nervous and endocrine systems; it controls body temperature, thirst and water balance, makes ADH and controls the pituitary gland.
A hormone released by the beta cells of the pancreas when blood glucose is high, which lowers it by increasing glucose uptake into muscle, liver and fat cells and its storage as glycogen.
A neuron within the central nervous system that links sensory neurons to motor neurons and allows information to be integrated.
Control of the heartbeat from within the heart by its conduction system (SA node, AV node, bundle of His and Purkinje fibres), without input from nerves or hormones.
A proprioceptor in the capsule and ligaments of a joint that detects the joint's angle, its movement and the pressure on it.
The phase of the menstrual cycle after ovulation, lasting about 14 days, in which the corpus luteum secretes progesterone and oestrogen, so both hormones are relatively high.
The lowest part of the brainstem, which contains the cardiovascular and respiratory control centres that regulate heart rate and breathing without conscious thought.
The recurring cycle of hormone-controlled changes in the ovaries and uterus that prepares the body for a possible pregnancy, counted from the first day of menstruation and lasting about 21–35 days.
A neuron that carries impulses from the central nervous system to an effector, such as a skeletal muscle or gland.
A proprioceptor lying between skeletal muscle fibres that detects the length of the muscle and how quickly it is stretched, and can trigger the stretch reflex.
A nerve cell, specialised to carry electrical impulses, with a cell body, dendrites that receive signals and an axon that carries impulses away.
A chemical released from the end of a neuron that crosses a synapse and passes the signal to the next neuron or to an effector cell, such as acetylcholine or norepinephrine.
A hormone of the adrenal medulla and the neurotransmitter of most sympathetic nerve endings, which raises heart rate and constricts blood vessels in non-active tissues; also called noradrenaline.
A group of reproductive hormones released mainly by the ovaries, which control the follicular phase of the menstrual cycle, promote fat use and glycogen sparing and help maintain bone density.
The release of an egg from an ovary, triggered by a surge of luteinising hormone (LH) around the middle of the menstrual cycle.
The division of the autonomic nervous system that dominates at rest and conserves energy (rest and digest), for example by slowing heart rate through the vagus nerve.
All the nerves and receptors outside the brain and spinal cord, which carry information between the central nervous system and the rest of the body.
A small endocrine gland below the hypothalamus that releases hormones such as ADH, FSH, LH and growth hormone, many of which control other endocrine glands.
A reproductive hormone released mainly by the corpus luteum after ovulation, which prepares the uterus for pregnancy and raises core body temperature by about 0.3–0.5 °C in the luteal phase.
A receptor in a muscle, tendon or joint that detects body position, movement, muscle length or tension and sends this information to the central nervous system.
Specialised conducting fibres in the ventricle walls that spread the impulse rapidly through the ventricular muscle, so that the ventricles contract together from the apex upward.
A region of the medulla oblongata, working with the pons, that sets the rate and depth of breathing by sending impulses to the diaphragm and intercostal muscles.
A neuron that carries impulses from a receptor to the central nervous system; sensory neurons make up the afferent division.
The heart's pacemaker: a group of specialised cells in the wall of the right atrium that generates the electrical impulse starting each heartbeat.
The branch of the efferent division that controls skeletal muscle, mostly under voluntary (conscious) control.
The division of the autonomic nervous system that prepares the body for activity and stress (fight or flight), for example by increasing heart rate, force of contraction and blood glucose.
The junction between a neuron and another neuron or an effector cell, across which a signal is passed by a chemical neurotransmitter.
A cell that has specific receptors for a particular hormone, so that the hormone changes its activity; cells without the receptor do not respond.
A reproductive (androgen) hormone released mainly by the testes, which stimulates muscle protein synthesis, bone formation and erythropoietin production.
The cranial nerve that carries parasympathetic impulses from the medulla to the heart and other organs; its stimulation slows the SA node and lowers heart rate.
The nervous system has three linked jobs: it detects changes inside and outside the body (sensory input), processes the information and decides on a response (integration), and sends instructions to muscles and glands (motor output). Every exercise response, from a goalkeeper’s dive to a rise in sweating, follows this sequence.
The pathway starts with a stimulus, a change that a receptor can detect, such as a stretch of a muscle, a rise in blood carbon dioxide or the sound of a starting gun. The receptor converts the stimulus into nerve impulses. These travel to the control centre in the brain or spinal cord, which compares the information with the body’s current state and sends impulses out to an effector, the muscle or gland that produces the response.
The central nervous system (CNS) is the brain and the spinal cord. It receives information from the whole body, integrates it and initiates responses. The brain holds the higher centres for voluntary movement, memory and emotion, and the brainstem, including the medulla oblongata, holds the centres that control heart rate and breathing without conscious thought.
The peripheral nervous system (PNS) is everything outside the brain and spinal cord: the cranial and spinal nerves and the receptors linked to them. It is the communication link between the CNS and the rest of the body.
The PNS is divided by the direction in which information travels. The afferent division (sensory division) carries impulses towards the CNS from receptors in the skin, muscles, joints, blood vessels and organs.
The efferent division (motor division) carries impulses away from the CNS to effectors: skeletal muscle, cardiac muscle, smooth muscle and glands. Every response the body makes, voluntary or automatic, travels along efferent neurons.
The efferent division has two branches that control different types of effector. The somatic nervous system controls skeletal muscle. Its actions are usually voluntary, such as kicking a ball, although some reflexes also use somatic motor neurons.
The autonomic nervous system (ANS) controls the body’s internal environment without conscious effort. Its effectors are cardiac muscle in the heart, smooth muscle in the walls of blood vessels, airways and the gut, and glands such as the sweat glands and the adrenal glands. Heart rate, sweating and the diameter of blood vessels adjust automatically to exercise, heat and stress.
The ANS has two divisions that usually supply the same organs and have opposite effects. The sympathetic nervous system prepares the body for action, stress and emergencies: it is often summarised as “fight or flight”. It raises heart rate, widens the airways, redirects blood to the working muscles and releases glucose into the blood.
The parasympathetic nervous system dominates at rest and is summarised as “rest and digest”. It slows the heart, narrows the airways slightly, and promotes digestion and the storage of energy. Most of its fibres to the heart, lungs and gut travel in a single pair of cranial nerves, the vagus nerve.
Most organs receive both divisions, so their activity depends on the balance between the two, like a car with an accelerator and a brake. At rest the heart is under a steady parasympathetic “brake”; at the start of exercise the brake is released and the accelerator is pressed.
YouTubeA neuron (nerve cell) is the basic unit of the nervous system. It has a cell body, short branches called dendrites that receive signals, and one long fibre, the axon, that carries the impulse away. Many axons are insulated by a fatty myelin sheath, which speeds up the impulse. A nerve is a bundle of many axons.
Neurons are classified by the direction they carry information:
Sensory neurons carry impulses from receptors to the CNS (they form the afferent division).
Motor neurons carry impulses from the CNS to effectors (they form the efferent division). A motor neuron and the muscle fibres it controls make up a motor unit.
Interneurons (relay neurons) lie within the CNS and link sensory and motor neurons.
A nerve impulse is a brief electrical change that travels along a neuron. Neurons do not touch each other: the junction between two neurons, or between a neuron and an effector cell, is a synapse, a tiny gap across which the signal is passed chemically.
When an impulse reaches the end of an axon, it causes the release of a neurotransmitter, a chemical that diffuses across the synapse and binds to receptors on the next cell, starting an impulse there or changing that cell’s activity. Acetylcholine is the neurotransmitter at the junction between motor neurons and skeletal muscle and at parasympathetic endings on the heart. Norepinephrine is released at most sympathetic endings, which is why the effects of sympathetic nerves and of the hormone epinephrine are so similar.
A reflex is a rapid, automatic response that bypasses conscious decision. When a runner steps on a sharp stone, sensory neurons carry impulses to the spinal cord, interneurons pass them straight to motor neurons, and the leg lifts before the brain registers pain. A sprinter reacting to the gun uses a longer, voluntary pathway through the brain, so their reaction time is longer than the time taken by a reflex.
The sympathetic and parasympathetic divisions act on almost every internal organ, and in most cases one reverses what the other does. The sympathetic effects are exactly what an athlete needs during exercise: more blood pumped, wider airways, more blood to the muscles, more fuel in the blood and more heat lost through sweat.
Organ or function | Sympathetic effect (exercise, stress) | Parasympathetic effect (rest) |
|---|---|---|
Heart rate (SA node) | Increases | Decreases |
Force of contraction of the ventricles | Increases, so stroke volume rises | Little direct effect |
Airways (bronchioles) | Smooth muscle relaxes: bronchodilation | Smooth muscle contracts: bronchoconstriction |
Arterioles to skeletal muscle | Dilate (with local factors), so more blood reaches working muscle | No significant effect |
Arterioles to the gut and kidneys | Constrict, so less blood goes to them | Dilate after a meal (more blood to the gut) |
Digestion | Slowed | Stimulated (gut movement and secretions) |
Sweat glands | Stimulated to secrete sweat | No effect |
Liver | Glycogen broken down, glucose released into the blood | Glycogen storage promoted |
Adrenal medulla | Stimulated to release epinephrine and norepinephrine | No effect |
The parasympathetic system does not switch off during exercise, but its influence falls; its return after exercise brings heart rate back down in recovery.
During intense exercise, heart rate can more than double within a minute. Two levels of control make this possible. The heart sets its own rhythm (intrinsic control), and nerves and hormones speed it up or slow it down (extrinsic control).
Cardiac muscle is myogenic: it generates its own electrical impulses without a signal from a nerve, which is why a transplanted heart beats even though its nerves have been cut. The impulses come from specialised cardiac muscle cells, the conduction system, which starts each heartbeat and spreads it through the heart in a fixed order.
The sinoatrial node (SA node) is a small patch of cells in the wall of the right atrium, near where the vena cava enters. Its cells fire impulses spontaneously and, because they fire faster than any other part of the heart, they set the pace for the whole heart: the SA node is the pacemaker. Without nervous or hormonal input it would fire about 100 times a minute.
The impulse spreads across the walls of both atria, which contract together and push blood into the ventricles. The atria and ventricles are separated by a layer of non-conducting tissue, so the impulse can only pass to the ventricles through the atrioventricular node (AV node), at the bottom of the right atrium near the septum.
The AV node delays the impulse by about 0.1 s. The delay is essential: it gives the atria time to finish contracting and the ventricles time to fill with blood before they contract. After the delay, the impulse passes into the bundle of His, a bundle of conducting fibres that runs down the septum between the two ventricles and divides into left and right bundle branches.
The bundle branches lead into the Purkinje fibres, which spread rapidly through the walls of both ventricles. They carry the impulse to the apex (bottom) of the heart first, so the ventricles contract from the apex upward. This squeezes blood up and out through the aorta and pulmonary artery, like squeezing toothpaste from the bottom of the tube.
The sequence can be learned as a chain of six steps, each of which explains part of the cardiac cycle: the atria contract before the ventricles, the ventricles fill during the AV delay, and the ventricles contract together from the bottom up.
Extrinsic control of heart rate means control from outside the heart: by the autonomic nervous system and by hormones in the blood. It does not replace the intrinsic rhythm. It changes the rate at which the SA node fires and the force with which the ventricles contract, so that cardiac output matches the body’s needs.
The nervous part of extrinsic control is coordinated by the cardiovascular control centre (CVCC) in the medulla oblongata. The CVCC receives information from receptors around the body and from higher brain centres, and sends impulses to the heart along two routes.
Sympathetic route. Cardiac accelerator nerves release norepinephrine at the SA node, the AV node and the ventricles, so the SA node fires faster (higher heart rate) and the ventricles contract more forcefully (higher stroke volume).
Parasympathetic route. The vagus nerve releases acetylcholine at the SA and AV nodes, which slows the SA node and lowers heart rate.
Hormonal route. Sympathetic nerves also stimulate the adrenal medulla to release epinephrine (and some norepinephrine) into the blood. These reach the heart through the blood and have the same effects as the sympathetic nerves, but they last longer.
At rest, the vagus nerve fires continuously. This “vagal tone” is why resting heart rate in most adults is about 60–80 beats min⁻¹ rather than the SA node’s own rate of about 100 beats min⁻¹. Endurance training increases vagal tone, which is one reason why trained endurance athletes often have a resting heart rate below 60 beats min⁻¹, a condition called bradycardia.
At the start of exercise, heart rate rises in two stages. In the first few seconds, the CVCC reduces the impulses sent along the vagus nerve. Removing the parasympathetic brake lets the SA node fire closer to its own rate, so heart rate rises quickly to about 100 beats min⁻¹. Above this, further increases need sympathetic stimulation: impulses along the cardiac accelerator nerves, followed by circulating epinephrine and norepinephrine, raise heart rate further and increase stroke volume through more forceful contraction.
Information from receptors keeps the response matched to the exercise. Proprioceptors signal movement almost immediately; as exercise continues, chemoreceptors detect rising carbon dioxide and hydrogen ions and the CVCC increases sympathetic output; baroreceptors help keep blood pressure within a safe range. A warmer SA node also fires faster, which adds to the rise in heart rate during long exercise in the heat.
When exercise stops, vagal stimulation returns within seconds, so heart rate falls rapidly at first, then more slowly as circulating hormones are removed. A slow fall in the first minute (poor heart rate recovery) is associated with poorer cardiovascular health.
Heart rate often rises before exercise begins. This anticipatory rise is caused by the higher brain centres: the thought of the coming effort, or the stress of a competition, stimulates the sympathetic nervous system and the release of epinephrine from the adrenal medulla. Heart rate, stroke volume and blood pressure rise, and the body is prepared for exercise before the first step.
The anticipatory rise is usually larger before an important competition than before training, and before short, intense events than before a long run. It links physiology with the study of arousal in sport psychology, where the same sympathetic response is felt as nerves, a pounding heart and sweaty hands.
A heart transplant cuts the nerves between the donor heart and the recipient’s brain. The new heart is denervated: neither the vagus nerve nor the sympathetic cardiac nerves reach it. Its SA node still works, so it beats on its intrinsic rhythm. Without vagal tone, the resting heart rate of a heart transplant recipient is higher than normal, often around 90–110 beats min⁻¹, close to the SA node’s own rate.
During exercise, the denervated heart cannot respond to nerve impulses, so heart rate rises only when epinephrine and norepinephrine from the adrenal medulla reach the SA node through the blood. It keeps rising for several minutes, peaks lower than in a healthy heart and stays raised for longer in recovery. Early in exercise, cardiac output rises mainly through a larger stroke volume, because more blood returning to the heart stretches the ventricles and they contract more forcefully.
Transplant recipients therefore benefit from longer warm-ups and cool-downs, and their exercise intensity is often set by perceived exertion rather than heart rate. The transplanted heart shows the three levels of control separately. Intrinsic control keeps the heart beating, nerves make the normal response fast, and hormones give a slower, longer-lasting increase.
Breathing is controlled by the respiratory control centre in the medulla oblongata, with help from centres in the pons above it. The respiratory control centre sets the basic rhythm of breathing. It sends impulses along the phrenic nerves to the diaphragm and along the intercostal nerves to the external intercostal muscles, which contract to draw air into the lungs. At rest, breathing out happens passively as these muscles relax.
Breathing is controlled both automatically and voluntarily: the breathing muscles are skeletal muscles supplied by somatic motor neurons, so a swimmer can time breaths with the stroke. Normally, though, the respiratory control centre adjusts the rate and depth of breathing automatically, using information from receptors:
Chemoreceptors detect the rise in carbon dioxide and hydrogen ions (fall in pH) in the blood during exercise; the respiratory control centre increases the rate and depth of breathing to remove the extra carbon dioxide.
Proprioceptors in the working muscles and joints signal movement at the very start of exercise, so ventilation rises within the first few breaths, before blood chemistry has changed.
Higher brain centres cause an anticipatory rise in breathing rate before exercise, in the same way as they raise heart rate.
The autonomic nervous system also controls the diameter of the airways. Sympathetic stimulation and circulating epinephrine relax the smooth muscle in the walls of the bronchioles, causing bronchodilation: the airways widen and air flows in and out with less resistance. Parasympathetic stimulation through the vagus nerve has the opposite effect, bronchoconstriction. Many reliever inhalers used to treat asthma contain drugs that copy the sympathetic effect on the airways, which is a direct health application of autonomic control.
The mechanics of breathing and the calculation of minute ventilation are part of the study of the transport system.
About 75–80% of the energy used by muscles is released as heat rather than movement. Body temperature is controlled by the hypothalamus, which receives information from thermoreceptors in the skin and detects the temperature of the blood flowing through it.
When core temperature rises, the hypothalamus increases sympathetic stimulation of the sweat glands, which secrete sweat onto the skin; its evaporation removes heat. At the same time, it reduces sympathetic constriction of the arterioles supplying the skin, so they widen and more warm blood flows near the surface, where heat is lost to the air. When the body is cold, the opposite happens: sympathetic nerves constrict skin arterioles to keep heat in the core, and the hypothalamus triggers shivering through somatic motor neurons to skeletal muscle.
How these responses form a negative feedback loop, and how the body copes with heat, humidity and cold, are part of thermoregulation and homeostasis. Hormones also play a part: progesterone, for example, raises the temperature around which the hypothalamus regulates the body during the second half of the menstrual cycle.
A nervous response can only begin when a change is detected. Receptors are specialised cells that respond to a particular kind of stimulus by starting impulses in sensory neurons. Three groups matter most in exercise: proprioceptors (the body’s own movement), baroreceptors (blood pressure) and chemoreceptors (the chemistry of the blood).
Proprioceptors are receptors in the muscles, tendons and joints that tell the CNS about the position of body parts, the movement of joints and the tension in muscles. They give the sense of where the limbs are without looking, which is called proprioception (sometimes the “sixth sense”). There are three main types.
Muscle spindles lie between the fibres of a skeletal muscle and detect how far and how fast the muscle is being stretched.
Golgi tendon organs lie where a muscle joins its tendon and detect the tension (force) in the muscle and tendon.
Joint receptors lie in the joint capsule and ligaments and detect the angle of the joint, its movement and the pressure on it.
Each type starts a different exercise response. When a muscle is stretched quickly, impulses from its muscle spindles cause a reflex contraction of the same muscle, the stretch reflex. It helps a countermovement jump, with a quick dip before take-off, go higher than a squat jump. Golgi tendon organs do the opposite: when tension becomes very high, they cause the muscle to relax, which protects the muscle and tendon from damage. This relaxation is used in some stretching methods, such as PNF stretching.
Joint receptors contribute to balance and coordination. After an ankle sprain, damage to the ligaments and their joint receptors reduces the sense of the joint’s position, and the ankle is more likely to “give way” again. Rehabilitation therefore includes balance exercises on unstable surfaces to retrain proprioception. Proprioceptors also start the rapid rise in heart rate and breathing at the onset of exercise.
Baroreceptors are stretch receptors in the walls of the aortic arch and the carotid arteries (the carotid sinuses in the neck). When blood pressure rises, the artery walls stretch more and the baroreceptors send more impulses to the cardiovascular control centre; when it falls, they send fewer.
The CVCC responds within one or two heartbeats. A rise in blood pressure increases vagal and decreases sympathetic stimulation, so heart rate falls and arterioles widen; a fall in pressure does the reverse.
If a runner stops suddenly at the end of a hard race, the leg muscles stop squeezing the veins (the skeletal muscle pump), blood pools in the legs, less blood returns to the heart and blood pressure falls. The baroreceptors detect the fall, and the CVCC keeps heart rate high and constricts blood vessels to restore pressure. A large drop can make the athlete dizzy or faint; an active cool-down, such as jogging slowly, keeps the muscle pump working and reduces this effect.
Chemoreceptors detect the chemical composition of the blood. Central chemoreceptors lie in the medulla oblongata and respond mainly to rises in carbon dioxide, which lower the pH of the fluid around the brain. Peripheral chemoreceptors lie in the carotid bodies (in the neck) and the aortic bodies (in the aortic arch). They respond to a rise in carbon dioxide, a rise in hydrogen ion concentration (fall in pH) and, especially, a large fall in oxygen.
During exercise, working muscles produce more carbon dioxide and hydrogen ions. Chemoreceptors detect the change and signal the respiratory control centre, which increases the rate and depth of breathing, and the CVCC, which increases heart rate. At altitude, where the air holds less oxygen, the peripheral chemoreceptors detect the low oxygen in the blood and cause an increase in breathing at rest, one of the first responses to altitude training.
Receptor | Location | What it detects | Example of an exercise response |
|---|---|---|---|
Muscle spindle (proprioceptor) | Between fibres of skeletal muscle | Muscle length and speed of stretch | Stretch reflex adds force in a countermovement jump |
Golgi tendon organ (proprioceptor) | Muscle–tendon junction | Tension in the muscle and tendon | Muscle relaxes under very high tension, protecting the tendon |
Joint receptor (proprioceptor) | Joint capsule and ligaments | Joint angle, movement, pressure | Balance and coordination; immediate rise in heart rate and breathing at the onset of exercise |
Baroreceptor | Aortic arch and carotid sinuses | Blood pressure (stretch of artery walls) | Heart rate kept high when blood pressure falls after a sudden stop |
Chemoreceptor (central) | Medulla oblongata | CO₂ (via pH of fluid around the brain) | Deeper, faster breathing as CO₂ rises |
Chemoreceptor (peripheral) | Carotid and aortic bodies | O₂, CO₂ and H⁺ (pH) in arterial blood | Higher heart rate and ventilation during intense exercise; more breathing at altitude |
The endocrine system is the second communication system of the body. It is made up of endocrine glands, which release hormones directly into the blood. The blood carries the hormones to every part of the body, but each hormone acts only on its target cells, which have specific receptors for that hormone on their surface or inside them. A hormone that meets a cell without the matching receptor has no effect on it.
A hormone may be released in the neck, the abdomen or the brain and still change the activity of cells in muscle, liver or kidney a few seconds or minutes later.
An endocrine gland has no duct: it secretes its hormones straight into the blood that flows through it. This distinguishes it from exocrine glands, such as sweat glands and the salivary glands, which release their secretions through ducts onto a surface. The pancreas is both: it releases digestive enzymes through a duct into the gut and hormones into the blood.
Whether a cell responds to a hormone depends on its receptors, not on how close it is to the gland. Insulin, for example, acts on muscle, liver and fat cells throughout the body because they carry insulin receptors.
The pituitary gland is often called the “master gland” because many of its hormones control other glands. It is itself controlled by the hypothalamus, which sits directly above it and is part of the brain. This link makes the hypothalamus the main connection between the nervous and endocrine systems: it receives nervous information and responds by releasing hormones or by controlling the pituitary.
Gland | Main hormones | Main effects |
|---|---|---|
Hypothalamus | Makes ADH; releasing hormones that control the pituitary | Links the nervous and endocrine systems; controls temperature and water balance |
Pituitary gland | Releases ADH (posterior pituitary); FSH and LH, growth hormone (anterior pituitary) | Controls other glands; water reabsorption; menstrual cycle |
Thyroid gland | Thyroxine | Sets the metabolic rate |
Adrenal glands | Epinephrine and norepinephrine (adrenal medulla); cortisol and aldosterone (adrenal cortex) | Fight or flight; fuel release; salt and water balance |
Pancreas | Insulin and glucagon (islets of Langerhans) | Regulate blood glucose concentration |
Ovaries | Oestrogen and progesterone | Menstrual cycle; bone; fuel use; thermoregulation |
Testes | Testosterone | Muscle protein synthesis; bone; red blood cell production |
The adrenal glands have two distinct parts. The inner medulla is really part of the sympathetic nervous system: it is stimulated by sympathetic nerves and releases epinephrine and norepinephrine within seconds. The outer cortex releases slower-acting hormones such as cortisol and aldosterone.
YouTubeBoth systems carry information, but they suit different jobs. Nerve impulses reach precise targets in milliseconds and their effects stop when the impulses stop, which suits movement and rapid adjustment. Hormones spread through the whole circulation and their effects last until the hormone is broken down, which suits slower, widespread changes such as fuel release, water balance and the menstrual cycle.
Feature | Nervous system | Endocrine system |
|---|---|---|
Signal | Electrical impulses along neurons; neurotransmitters across synapses | Chemical (hormones) |
Pathway | Neurons, directly to specific effector cells | The bloodstream, to target cells anywhere in the body |
Speed of response | Very fast (milliseconds) | Slower (seconds to hours) |
Duration of effect | Short; stops when impulses stop | Longer; lasts until the hormone is removed |
Area affected | Localised and precise | Widespread (all cells with the receptor) |
Examples in exercise | Contraction of skeletal muscle; fast rise in heart rate | Release of glucose by the liver; water reabsorption by the kidneys |
The two systems are closely linked: sympathetic nerves trigger the adrenal medulla to release epinephrine, and the hypothalamus is part of the brain but also makes ADH. Most exercise responses involve both, with nerves starting the response quickly and hormones sustaining and spreading it.
Epinephrine and norepinephrine are also called adrenaline and noradrenaline. Both are released into the blood by the adrenal medulla when it is stimulated by sympathetic nerves; most of what the adrenal medulla releases is epinephrine.
Norepinephrine has a double role. It is a hormone of the adrenal medulla, but it is also the neurotransmitter released at most sympathetic nerve endings, and some of it spills over into the blood from these nerves during exercise.
Their concentrations in the blood change little in light exercise but rise steeply as intensity approaches maximum, and also before and during competition. Their effects combine to make more oxygen and fuel available to working muscles:
Heart rate and stroke volume increase (acting on the SA node and ventricles), so cardiac output rises.
Blood pressure rises, as cardiac output increases and arterioles in the gut and kidneys constrict.
Blood is redistributed to the working muscles.
Airways dilate (bronchodilation), so air flows more easily.
Blood glucose rises, because epinephrine stimulates glycogenolysis, the breakdown of glycogen to glucose, in the liver and in muscle. It also stimulates the release of fatty acids from fat stores.
Drugs that block their receptors, beta blockers, lower heart rate and reduce trembling of the hands, so they are banned in precision sports. At the 2008 Beijing Olympics, the shooter Kim Jong-su of North Korea won silver in the 50 m pistol and bronze in the 10 m air pistol, but was stripped of both medals after testing positive for propranolol, a beta blocker.
Sources: International Olympic Committee announcement, 15 August 2008, reported on Wikipedia (Kim Jong-su).
The brain and working muscles depend on glucose from the blood, so blood glucose is kept within a narrow range, about 3.9–5.6 mmol L⁻¹ in a healthy fasting adult. Two hormones regulate it, both made in the islets of Langerhans in the pancreas: beta (β) cells make insulin and alpha (α) cells make glucagon.
Insulin is released when blood glucose rises, for example after a meal containing carbohydrate. It lowers blood glucose by stimulating muscle and fat cells to take up glucose from the blood, stimulating the liver and muscles to convert glucose into glycogen for storage, and reducing the release of glucose by the liver.
Glucagon is released when blood glucose falls, for example during fasting or prolonged exercise. It raises blood glucose by stimulating the liver to break down its glycogen into glucose (glycogenolysis), which is released into the blood.
Glucagon also stimulates the liver to make new glucose from non-carbohydrate sources such as lactate, glycerol and amino acids, a process called gluconeogenesis. This becomes more important as the liver’s glycogen stores run low during very long exercise or fasting.
During exercise, insulin release falls while glucagon and epinephrine rise, so the liver releases more glucose. At the same time, contracting muscle takes up glucose from the blood even without much insulin, because muscle contraction itself moves glucose transporters to the muscle cell membrane. This is one reason regular exercise helps people with type 2 diabetes or insulin resistance to control their blood glucose.
How insulin and glucagon act together in a negative feedback loop to keep blood glucose stable is part of blood glucose regulation. In type 1 diabetes, the beta cells are destroyed and the body makes no insulin, so it must be injected. Injected insulin cannot be switched off when blood glucose falls, so exercise needs careful planning; Team Novo Nordisk, a professional cycling team whose riders all have type 1 diabetes, shows that it can be done at professional level.
Sources: Team Novo Nordisk, Wikipedia (accessed 2026).
Antidiuretic hormone (ADH), also called vasopressin, regulates the amount of water the kidneys keep in the body. It is made in the hypothalamus and stored in and released from the posterior part of the pituitary gland. The hypothalamus contains osmoreceptors that detect the concentration of the blood.
During long exercise in the heat, sweating removes water and the blood becomes more concentrated. The osmoreceptors detect this, the posterior pituitary releases more ADH, and ADH makes the collecting ducts of the kidneys more permeable to water. More water is reabsorbed into the blood, so a smaller volume of more concentrated, darker urine is produced and water is conserved. When the body has too much water, ADH release falls and a large volume of dilute urine is produced.
ADH reduces water loss but cannot replace the water lost in sweat, so athletes still need to drink. The wider control of water and salt balance involves the hormone aldosterone and the risks of dehydration.
The reproductive hormones are made mainly by the ovaries (oestrogen and progesterone) and the testes (testosterone), under the control of the hypothalamus and pituitary gland. Besides reproduction, they act on muscle, bone, blood, fuel use and temperature control, which makes them important for both health and performance.
The menstrual cycle is the monthly cycle of hormone changes that prepares the body for a possible pregnancy. It is counted from the first day of menstruation (bleeding) and lasts about 28 days on average, but cycles of about 21–35 days are normal and length varies between individuals and from month to month.
The cycle has two main phases, separated by ovulation. Hormone concentrations change in a regular pattern, controlled by two pituitary hormones, follicle-stimulating hormone (FSH) and luteinising hormone (LH), and by the ovarian hormones oestrogen and progesterone.
Follicular phase (from day 1 to ovulation). It begins with menstruation, when oestrogen and progesterone are both low (the early follicular phase). FSH stimulates follicles in the ovary to develop, and the growing follicles release more and more oestrogen, which peaks just before ovulation (the late follicular phase).
Ovulation (around day 14 of a 28-day cycle). The high oestrogen concentration triggers a sharp surge of LH from the pituitary gland, which causes the ovary to release an egg.
Luteal phase (from ovulation to the next menstruation, usually about 14 days). The empty follicle becomes the corpus luteum, which secretes large amounts of progesterone and some oestrogen; both are high in the mid-luteal phase. If no pregnancy occurs, the corpus luteum breaks down, both hormones fall in the late luteal phase, and menstruation begins.
The luteal phase is fairly constant in length, at about 14 days, so most of the variation in cycle length comes from the follicular phase. This matters when estimating the phase on a given day: in a 32-day cycle, ovulation is likely to occur around day 18, not day 14.
Hormonal contraceptives, such as the combined pill, supply synthetic hormones that stop ovulation and replace the natural rise and fall of oestrogen and progesterone with a steadier pattern. Studies of the cycle therefore analyse users and non-users separately.
Progesterone has a thermogenic effect: it acts on the hypothalamus to raise the temperature around which the body is regulated. In the luteal phase, resting core temperature is therefore about 0.3–0.5 °C higher than in the follicular phase, and sweating and skin blood flow begin at a higher core temperature.
A higher starting temperature leaves less room for heat to build up before core temperature becomes limiting, and some studies have found that prolonged exercise in hot conditions is harder in the mid-luteal phase, while performance in cool conditions changes little. This links progesterone to the regulation of core temperature and to how athletes prepare for competition in the heat.
Progesterone also affects sleep. It has a mild sedative effect, but the higher night-time body temperature in the luteal phase, and the premenstrual symptoms some people experience as both hormones fall at the end of the cycle, are associated with poorer sleep quality and more waking in the late luteal phase. Poor sleep matters because sleep is a major part of recovery from training.
Progesterone affects fuel availability too. It increases the breakdown of body protein, so protein needs may be slightly higher in the luteal phase, and it opposes some of oestrogen’s effects on fuel use. It also stimulates breathing, so ventilation is slightly higher in the luteal phase at the same intensity, which may help explain why some athletes find exercise harder then.
Oestrogen is released mainly by the developing follicles in the ovary. Beyond reproduction, it affects which fuels muscles use. Oestrogen increases the release and use of fatty acids for energy and reduces the use of muscle glycogen during submaximal exercise. This is called glycogen sparing: the limited glycogen stores last longer, which could benefit endurance performance when oestrogen is high.
Oestrogen also affects connective tissue. Ligaments and tendons have oestrogen receptors, and higher oestrogen concentrations are associated with greater laxity (looseness) of ligaments and lower stiffness of joints and muscle–tendon units, particularly around ovulation, when oestrogen peaks. Greater laxity of the knee may reduce its stability during landing and cutting, and this has been proposed as one reason why female footballers have a higher rate of anterior cruciate ligament injury than male players. The evidence linking cycle phase to ACL injury is mixed, and many other risk factors are involved.
Oestrogen also slows the breakdown of bone. In athletes with low energy availability, the body may stop ovulating and menstruating (amenorrhoea), oestrogen stays low, and bone mineral density falls. This is one of the health consequences of relative energy deficiency in sport (REDs) and increases the risk of stress fractures.
Testosterone is released mainly by the testes in males, and in much smaller amounts by the ovaries and adrenal glands in females. At male puberty, testosterone production rises 20- to 30-fold. This rise drives most of the physical differences between adult men and women that affect sport: larger and stronger muscles, larger and denser bones, a larger heart and lungs, and a higher concentration of haemoglobin in the blood.
Testosterone has three main effects relevant to performance and health:
Protein synthesis. It increases muscle protein synthesis, so training produces greater hypertrophy (growth of muscle fibres) and strength. This anabolic (tissue-building) effect is why synthetic forms of testosterone, the anabolic steroids, are banned in sport.
Bone formation. It stimulates bone formation and increases bone density and size, which helps protect against osteoporosis later in life.
Erythropoietin. It stimulates the kidneys to produce erythropoietin (EPO), a hormone that increases the production of red blood cells in the bone marrow. More red blood cells mean more haemoglobin, so the blood can carry more oxygen to the working muscles.
Because more red blood cells improve oxygen delivery, synthetic EPO has been used illegally to enhance endurance. In 2012 the US Anti-Doping Agency concluded that the cyclist Lance Armstrong had used EPO, along with blood transfusions and other banned substances. He was banned for life and lost all his results from August 1998 onwards, including seven Tour de France titles. Artificially raising red blood cell counts also makes the blood thicker, which increases the risk of blood clots, stroke and heart attack.
Sources: Handelsman and Tomkinson, Journal of the Endocrine Society, 2026; USADA reasoned decision, October 2012, reported on Wikipedia (Lance Armstrong doping case).
The table summarises how each reproductive hormone links to health and to performance.
Hormone | Health lens | Performance lens |
|---|---|---|
Progesterone | Sleep quality and well-being in the late luteal phase | Higher core temperature may reduce endurance in heat |
Oestrogen | Protects bone; low oestrogen in REDs raises fracture risk | Glycogen sparing; possible link with ligament laxity |
Testosterone and EPO | Bone and muscle mass with ageing; doping risks | Strength, hypertrophy, oxygen-carrying capacity |
Before and during the 2019 FIFA Women’s World Cup, the staff of the United States women’s national football team tracked each player’s menstrual cycle. Players logged their cycles and symptoms in the FitrWoman app, made by the sports science company Orreco, and the team’s high performance coach, Dawn Scott, received a profile for each player showing her estimated cycle phase and symptoms.
Staff used the information alongside other monitoring data to plan training loads, recovery and nutrition advice. The reasoning was that if progesterone raises core temperature and breathing in the luteal phase, and menstruation brings pain and fatigue for some players, knowing each player’s phase could help. The team won the tournament, and Scott described tracking as one of the strategies that helped.
In 2024, Scott and colleagues published an analysis of data from 20 outfield players over 45 days of the tournament. Loads were measured with GPS units and heart rate monitors, and each player gave a session rating of perceived exertion (sRPE) after every session and rated her fatigue, soreness, sleep quality and sleep duration each morning.
Cycle phase was not measured with hormone tests: it was estimated by an algorithm from a questionnaire before the tournament and the symptoms players reported in the app. The phase analysis included only the 16 players who did not use hormonal contraceptives.
Outcome | Finding (16 players not using hormonal contraceptives) |
|---|---|
sRPE after sessions of 5 km or more | Higher in the luteal phase than during menstruation, by 0.6–1.0 units (p ≤ 0.018) |
Fatigue rating 48 hours after a match | Worse in the luteal phase than the follicular phase, by 0.73 units (p = 0.028) |
Sleep quality, sleep duration, soreness | Not typically associated with cycle phase |
Other relationships between load and response | No other clear trends |
The same running distance felt harder in the luteal phase, and players felt more fatigued after matches. Both findings fit the physiology of progesterone (higher core temperature and ventilation at the same workload), but the authors described them as preliminary.
A single team cannot show whether cycle phase affects performance in general. In 2020, McNulty and colleagues combined the results of 78 studies, involving 1,193 women with natural cycles, in a systematic review and meta-analysis. Pooling the studies, performance in strength and endurance tests was on average slightly lower in the early follicular phase (menstruation) than in all other phases combined, but the effect was trivial (a median effect size of 0.06). The largest difference was between the early and late follicular phases (effect size 0.14), the only comparison whose credible interval did not include zero.
The quality of the evidence was a major limitation: only 8% of the studies were rated high quality and 24% moderate, while the rest were low or very low. Many studies were small (a mean of 14 participants per study in the main analysis) and estimated cycle phase from calendar counting rather than confirming it with hormone measurements. The authors concluded that general guidelines could not be given and recommended a personalised approach based on each athlete’s own responses.
Athletes’ own experience points in the same direction. When 15 international women’s rugby players were interviewed in depth, 93% reported cycle-related symptoms, 67% felt that these symptoms had impaired their performance, and about two-thirds had taken medication to relieve them. The size of the perceived effect contrasts with the trivial average effect measured in laboratory studies. Symptoms such as pain, heavy bleeding and poor sleep vary greatly between individuals, and short laboratory tests may not capture their effects on training and confidence.
Tracking gives staff a record of each player’s cycle and symptoms, encourages open conversation about a topic athletes often find difficult to raise, and identifies individuals whose symptoms consistently affect training, so their load or medical support can be adjusted. With large individual differences and small average effects, this individual approach fits the evidence better than a team-wide rule such as “reduce intensity in the luteal phase”.
The limitations are equally important. Phase was estimated rather than measured, so some players may have been assigned to the wrong phase. Sixteen players is a very small sample, there was no control group, and the outcomes were self-reported, so expectations about the cycle could have influenced the ratings. One author worked for the company that made the app, a possible conflict of interest. The World Cup win cannot be attributed to tracking, because many other factors were involved.
On balance, the evidence supports tracking as a tool for individual monitoring and athlete welfare, combined with other measures of load and recovery, rather than as a way to schedule a whole team’s training around hormone phases. Its value depends on accurate phase identification, honest reporting and the athlete’s trust.
Which hormone changes could explain why sRPE was higher in the luteal phase for the same running distance?
Why might the meta-analysis find a trivial average effect while most of the rugby players interviewed felt their performance was affected?
How could a future study confirm cycle phase more accurately, and why would this improve the validity of its conclusions?
How can it be established whether hormones are an “active ingredient” affecting performance, rather than athletes’ expectations about them?
Sources: Scott, Bruinvels, Norris and Lovell, International Journal of Sports Physiology and Performance, 2024; Good Morning America, 8 August 2019; McNulty et al., Sports Medicine, 2020; Findlay et al., British Journal of Sports Medicine, 2020; Ose et al., American Journal of Sports Medicine, 2025.
Multiple-choice questions on inter-system communication test names and sequences (the nervous system hierarchy, the conduction system, glands and hormones). Data-based questions often show heart rate, hormone or temperature data. Structured and extended questions ask you to label the conduction system, distinguish nervous from endocrine control, or explain how heart rate is controlled.
Labelling and interpreting the standard diagrams is the other skill that appears in almost every paper.
Some questions test the direction of a hormone’s effect rather than its name, so it helps to learn each hormone with an arrow (↑ or ↓) for its main effect.
Read the method of a data-based question carefully before the table: the variables, the sample and how measurements were made all carry marks.
Paper 1B: A group of 12 trained male and female sprinters took part in a study of the anticipatory rise (hypothetical data). Heart rate was measured with a chest-strap monitor while each athlete lay still in the morning (rest), and while standing still 60 s before the start of a 100 m sprint in a training session and in a regional championship final. The results are shown in the table.
Condition | Mean heart rate (beats min⁻¹) | Standard deviation (beats min⁻¹) |
|---|---|---|
Rest | 64 | 6 |
60 s before a training sprint | 78 | 8 |
60 s before a championship final | 101 | 10 |
Questions that use “distinguish” need a clear contrast on each point, ideally in a two-column format.
An extended response needs a short plan before writing. For an “evaluate” question, the plan should cover the mechanism, the evidence on both sides, the factors the conclusion depends on and a justified judgment.
The nervous system has central (brain and spinal cord) and peripheral parts; the PNS has afferent (sensory) and efferent (motor) divisions.
The efferent division has somatic (voluntary, skeletal muscle) and autonomic (involuntary) branches; the autonomic has sympathetic (“fight or flight”) and parasympathetic (“rest and digest”) divisions.
The SA node generates each heartbeat; the impulse passes through the AV node (with a delay), the bundle of His and the Purkinje fibres (intrinsic control).
The cardiovascular control centre adjusts heart rate through the cardiac accelerator nerve, the vagus nerve and epinephrine (extrinsic control), using information from proprioceptors, chemoreceptors and baroreceptors.
The autonomic nervous system also controls breathing (with the respiratory control centre) and temperature (with the hypothalamus).
Hormones are chemical messengers carried in the blood to target cells; nervous communication is faster, shorter-lived and more localised.
Epinephrine and norepinephrine raise heart rate, blood pressure and blood glucose; insulin lowers and glucagon raises blood glucose; ADH increases water reabsorption in the kidneys.
Progesterone raises core temperature and affects sleep and fuel use; oestrogen spares glycogen and is linked with joint laxity; testosterone increases protein synthesis, bone formation and EPO production.
Average effects of cycle phase on performance are trivial and the evidence is weak, so an individual approach is recommended.
I can draw and label the hierarchy of the nervous system from memory.
I can describe the roles of sensory neurons, motor neurons, interneurons, synapses and neurotransmitters.
I can distinguish the effects of the sympathetic and parasympathetic nervous systems on the heart, breathing and temperature control.
I can explain intrinsic and extrinsic control of heart rate, including the conduction system and the cardiovascular control centre.
I can describe what proprioceptors, baroreceptors and chemoreceptors detect and give an exercise response for each.
I can compare nervous and endocrine communication.
I can describe the sources and effects of epinephrine, norepinephrine, insulin, glucagon and ADH.
I can explain the effects of progesterone, oestrogen and testosterone and place the phases of the menstrual cycle on a hormone graph.
I can evaluate the evidence that menstrual cycle phase affects performance.