Neurone Structure and Resting Potential — AQA A-level Biology

SPEC 3.6.1.3 - CONTROL OF HEART RATE

Control of Heart Rate

Myogenic stimulation, SAN, AVN, Purkyne tissue, chemoreceptors, pressure receptors & the autonomic nervous system

The Heart Is Myogenic

Myogenic

Self-exciting. The heart muscle can initiate its own contraction without nervous stimulation. The rhythmic contraction of the heart originates within the cardiac muscle itself — not from the nervous system.

This is the most important foundational principle of this topic. The nervous system modulates an already self-beating heart — it does not start it.

Evidence for Myogenic Control

A heart removed from the body and placed in oxygenated saline will continue to beat spontaneously. If the heart required nervous input to beat, it would stop immediately on removal. It does not — confirming that the beat originates within the cardiac muscle.

Examiner Alert

"The nervous system controls the heartbeat" — this statement is dangerously incomplete. The nervous system modifies the rate of an already beating heart. The heartbeat originates from the sinoatrial node (SAN) within the heart muscle itself.

SAN — The Pacemaker

Sinoatrial Node (SAN)

A group of specialised cells in the wall of the right atrium that spontaneously generates a wave of electrical excitation, setting the intrinsic rhythm of the heart. The SAN is the pacemaker.

The wave of electrical excitation spreads across both atria, causing atrial systole (atrial contraction). However, it cannot pass directly from atria to ventricles — a band of non-conducting tissue at the atrioventricular junction prevents this.

Why Must the Impulse Be Delayed?

The impulse must be delayed before reaching the ventricles. This allows the atria to complete their contraction and finish emptying blood into the ventricles before the ventricles contract. Without this delay, atria and ventricles would contract simultaneously — an inefficient pumping action.

Key Point

The SAN has an intrinsic rate of approximately 100 beats per minute — but at rest, the parasympathetic nervous system dominates, slowing this to the typical resting rate of ~70 bpm. The autonomic nervous system can accelerate or slow the SAN above or below its intrinsic rate, but the rhythm itself always originates in the SAN.

AVN, Bundle of His & Purkyne Tissue

Atrioventricular Node (AVN)

A group of specialised cells located between the atria and ventricles. It receives the impulse from the atria and introduces a delay of approximately 0.1 seconds before transmitting to the ventricles. This delay ensures atrial contraction completes before ventricular contraction begins.

Bundle of His & Purkyne Tissue

The Bundle of His is a group of conducting fibres in the interventricular septum that carries the impulse from the AVN downward. The impulse then spreads through Purkyne tissue in the walls of both ventricles, causing the ventricles to contract from the apex upward.

Why Apex-Upward Contraction?

Ventricular contraction from the apex upward pushes blood upward into the aorta and pulmonary artery. This direction is mechanically optimal for ejecting the maximum volume of blood with each beat.

Intrinsic Conduction Pathway

Extrinsic Control — Overview

The intrinsic rate set by the SAN can be modified by the autonomic nervous system. The cardiovascular centre in the medulla oblongata coordinates this control, receiving input from two types of receptor:

Chemoreceptors

Detect changes in the chemical composition of blood — specifically rising CO₂ concentration and the resulting fall in blood pH. Located in the aortic arch and carotid bodies (adjacent to carotid arteries in the neck).

Rising CO₂ → blood pH falls → chemoreceptors stimulated → medulla → sympathetic output → ↑ heart rate.

Pressure Receptors (Baroreceptors)

Detect changes in blood pressure. Located in the walls of the aortic arch and carotid sinus.

Rising blood pressure → baroreceptors stimulated → medulla → parasympathetic output → ↓ heart rate (baroreceptor reflex).

The Medulla Oblongata

The cardiovascular centre in the medulla oblongata integrates all signals from chemoreceptors and baroreceptors and sends the appropriate motor output via the autonomic nervous system to the SAN.

Autonomic Nervous System — Heart Rate Control

FeatureSympathetic NSParasympathetic NS (Vagus Nerve)

Neurotransmitter at SANNoradrenalineAcetylcholine

Effect on SANIncreases firing rateDecreases firing rate

Effect on heart rateIncreases (↑HR)Decreases (↓HR)

When activatedExercise, stress, low pH/high CO₂Rest, high blood pressure

Examiner Alert — Adrenaline vs Noradrenaline

The autonomic nervous system releases noradrenaline at the SAN (via sympathetic neurones). Do not confuse this with adrenaline, which is a hormone released by the adrenal gland into the bloodstream. Adrenaline can also increase heart rate, but it is not part of Spec 3.6.1.3 — the spec asks about the autonomic nervous system, not hormones.

Memory Aid

Sympathetic = Speedy (accelerator — noradrenaline). Para-sympathetic = Pause (brake — acetylcholine via vagus nerve).

Full Pathway — Heart Rate During Exercise

This is the mechanism AQA mark schemes require in full for exercise questions. "You need more oxygen" is not sufficient — every step must be stated.

1

Muscles respire faster during exercise → more CO₂ produced

2

CO₂ dissolves in blood plasma → carbonic acid forms → blood pH falls

3

Chemoreceptors in the aortic arch and carotid bodies detect the fall in pH (rise in CO₂)

4

Chemoreceptors send impulses to the cardiovascular centre in the medulla oblongata

5

Medulla sends impulses via the sympathetic nervous system to the SAN

6

Noradrenaline is released at the SAN → SAN increases its firing rate

7

Heart rate increases → more blood delivered to muscles per minute

Examiner Alert — Mark Scheme Precision

Marks are lost for: saying "chemoreceptors detect O₂" (spec focuses on CO₂/pH), omitting the medulla oblongata step, omitting noradrenaline, or saying "adrenaline" instead of "noradrenaline" from the sympathetic nervous system.

Baroreceptor Reflex — Reducing Heart Rate

When blood pressure rises above normal (e.g. during vigorous exercise when cardiac output is high, or following intense vasoconstriction), baroreceptors initiate a reflex that reduces heart rate:

1

Blood pressure rises in the aortic arch and carotid sinus

2

Baroreceptors (pressure receptors) in the walls of the aortic arch and carotid sinus are stimulated

3

Baroreceptors send impulses to the cardiovascular centre in the medulla oblongata

4

Medulla sends impulses via the parasympathetic nervous system (vagus nerve) to the SAN

5

Acetylcholine is released at the SAN → SAN decreases its firing rate

6

Heart rate decreases → blood pressure falls back toward normal

Negative Feedback

The baroreceptor reflex is a classic example of negative feedback: a rise in blood pressure triggers a response (decreased heart rate) that acts to reduce blood pressure back toward the set point.

Cardiac Output Calculation

The AQA spec (MS 2.2) requires students to calculate cardiac output using heart rate and stroke volume.

Cardiac Output (CO) = Heart Rate (R) × Stroke Volume (V) Units: dm³ min⁻¹ = beats min⁻¹ × dm³ beat⁻¹

Stroke Volume

The volume of blood ejected by one ventricle per beat. Typical resting value: ~0.07 dm³ (70 cm³ or 70 ml).

Worked Example

Q: A person has a resting heart rate of 70 beats per minute and a stroke volume of 0.07 dm³. Calculate their cardiac output.

A: CO = R × V = 70 × 0.07 = 4.9 dm³ min⁻¹

During exercise: HR = 160 bpm, SV = 0.12 dm³ → CO = 160 × 0.12 = 19.2 dm³ min⁻¹

Unit Check

Always check your units: if heart rate is in beats min⁻¹ and stroke volume is in dm³ beat⁻¹, then cardiac output is in dm³ min⁻¹. If stroke volume is given in cm³, divide by 1000 to convert to dm³ first.

Common Exam Errors — 2024 Examiner Report

Error 1 — Confusing SAN and AVN

The SAN generates the impulse (pacemaker, in right atrium wall). The AVN receives the impulse and delays it (between atria and ventricles). Many students reverse these roles or name the wrong node as the pacemaker. The SAN is always the pacemaker.

Error 2 — Omitting the AVN delay

The 0.1-second delay at the AVN must be stated and explained — it allows atria to complete contraction before ventricles contract. Simply stating "the impulse passes to the ventricles" without mentioning the delay loses marks.

Error 3 — Confusing Bundle of His and Purkyne tissue

The Bundle of His conducts the impulse down the interventricular septum. Purkyne tissue (in ventricular walls) conducts the impulse into the ventricle muscle. Get the sequence right: AVN → Bundle of His → Purkyne tissue → ventricles contract apex-upward.

Error 4 — "The nervous system starts the heart"

The heart is myogenic. The nervous system modulates the rate — it does not initiate the beat. Never say the nervous system "starts" or "causes" the heartbeat.

DEEP Framework — Extended Answer

Model answer for: "Explain the mechanism by which an increase in carbon dioxide concentration in the blood leads to an increase in heart rate." [5 marks]

DEEP Chain

D

Define: The heart is myogenic — its rate is set intrinsically by the SAN. However, the autonomic nervous system can modify this rate in response to changes in blood chemistry detected by chemoreceptors.

E

Explain mechanism: A rise in blood CO₂ causes CO₂ to dissolve in plasma, forming carbonic acid. Blood pH falls. Chemoreceptors in the aortic arch and carotid bodies detect this fall in pH. They send nerve impulses to the cardiovascular centre in the medulla oblongata.

E

Elaborate: The cardiovascular centre activates the sympathetic nervous system. Sympathetic neurones release noradrenaline at the SAN. Noradrenaline increases the rate of spontaneous depolarisation in SAN cells, increasing the frequency of electrical impulses generated. Each impulse travels via the AVN, Bundle of His, and Purkyne tissue to the ventricles.

P

Practical significance: Heart rate increases → more blood pumped to muscles per minute → greater delivery of oxygen and removal of CO₂. This is a negative feedback system — as CO₂ is removed by increased ventilation and circulation, pH rises, chemoreceptor stimulation decreases, and heart rate returns toward normal.

Practice Question

A student measures his heart rate before and during a 10-minute run. His resting heart rate is 65 beats per minute with a stroke volume of 0.075 dm³. At peak exercise his heart rate is 175 bpm with a stroke volume of 0.115 dm³.

(a) Calculate the cardiac output at rest and at peak exercise. Show your working. [2 marks]

(b) Explain, in terms of the autonomic nervous system, the mechanism by which heart rate increases during exercise. You must refer to chemoreceptors, the medulla oblongata, and a named neurotransmitter. [4 marks]

(c) After the run, the student's heart rate returns to resting. State which division of the autonomic nervous system is responsible and name the neurotransmitter released at the SAN. [2 marks]

a:

Resting CO = 65 × 0.075 = 4.875 dm³ min⁻¹. Peak CO = 175 × 0.115 = 20.125 dm³ min⁻¹.

b:

During exercise, muscles produce more CO₂ → CO₂ dissolves in plasma, blood pH falls → chemoreceptors in the aortic arch and carotid bodies detect the fall in pH → they send impulses to the cardiovascular centre in the medulla oblongata → the medulla activates the sympathetic nervous system → sympathetic neurones release noradrenaline at the SAN → the SAN increases its firing rate → heart rate increases.

c:

The parasympathetic nervous system (via the vagus nerve) is responsible. The neurotransmitter released at the SAN is acetylcholine, which decreases the SAN firing rate, reducing heart rate back toward the resting level.

Synoptic Links

Synoptic Link — Paper 3

CO₂ and blood pH → Spec 3.5.2 (Respiration): CO₂ produced in respiration is the primary driver of the chemoreceptor pathway. A synoptic question could ask you to trace a molecule of CO₂ from production in a muscle mitochondrion through the blood to its detection by chemoreceptors and the consequent effect on heart rate.

Synoptic Link — Paper 3

Noradrenaline and acetylcholine → Spec 3.6.3 (Synaptic Transmission): The neurotransmitters released at the SAN by the sympathetic (noradrenaline) and parasympathetic (acetylcholine) nervous systems are the same molecules studied in synaptic transmission. A synoptic question could ask you to explain why noradrenaline increases SAN firing rate in terms of receptor binding and ion channel opening.

Synoptic Link — Essay

Negative feedback: The baroreceptor reflex and the chemoreceptor pathway both exemplify negative feedback (Spec 3.6.4 — Homeostasis). Both involve a receptor, a control centre (medulla oblongata), and an effector (SAN/heart). Both return a variable (blood pressure or pH) toward a set point. Essays on homeostasis or control systems should include these pathways.

Summary

Key Concepts — Lesson 6.03

ConceptKey Point

MyogenicHeart initiates its own beat — does not require nervous stimulation; the nervous system modulates rate only

SANPacemaker; in right atrium wall; generates wave of excitation that spreads across both atria → atrial systole

AVNBetween atria and ventricles; introduces 0.1 s delay; allows atria to complete contraction before ventricles contract

Bundle of His / Purkyne tissueConducts impulse from AVN down septum and into ventricular walls → ventricles contract apex-upward

ChemoreceptorsIn aortic arch and carotid bodies; detect ↑CO₂/↓pH → medulla → sympathetic → noradrenaline → ↑HR

BaroreceptorsIn aortic arch and carotid sinus; detect ↑BP → medulla → parasympathetic (vagus) → acetylcholine → ↓HR

Cardiac outputCO = heart rate × stroke volume (dm³ min⁻¹)

Top Exam Tip

For any heart rate question: always name the receptor (chemoreceptor or baroreceptor), its location (aortic arch / carotid body or carotid sinus), the control centre (medulla oblongata), the nervous system branch (sympathetic or parasympathetic), the neurotransmitter at the SAN (noradrenaline or acetylcholine), and the effect on SAN firing rate. Six steps — all six must be present for full marks.