Biology (9610) | Control of heart rate

Control of Heart Rate: The Body's Internal Accelerator Pedal

Welcome to this exciting section on control mechanisms! Our heart is constantly beating—about 100,000 times a day—but its rate isn't fixed. Imagine driving a car: sometimes you need to speed up (like when exercising), and sometimes you need to slow down (like when resting). The body uses sophisticated control systems to ensure the heart rate matches the body's demand for oxygen and nutrients.

In these notes, we will break down exactly how the heart sets its own rhythm (myogenic control) and how the nervous system and receptors step in to finely tune this rate (extrinsic control) based on what the rest of your body needs. Don't worry if this seems tricky at first; we will use clear steps and analogies!

Quick Review: Why does the heart rate need to be controlled?

Heart rate dictates how much blood (and therefore oxygen and glucose) is delivered to the tissues per minute. Control is essential for homeostasis and adapting to changes:

• During exercise, tissues need more O₂ and must remove CO₂ quickly; heart rate increases.
• During rest, energy demand is low; heart rate decreases to conserve energy.

1. Intrinsic Control: The Heart's Built-in Rhythm (Myogenic Stimulation)

The heart muscle is special because it is myogenic, meaning it can initiate its own contraction without needing an external nerve impulse. It has its own internal pacemaker system.

The Sequence of Electrical Excitation (The Cardiac Cycle)

Think of this as the electrical wiring of the heart:

1. Sinoatrial Node (SAN): The Pacemaker
   The SAN is a small patch of specialised muscle tissue located in the wall of the right atrium. It spontaneously generates electrical impulses (depolarisation) at regular intervals. This impulse spreads immediately across the walls of both atria, causing them to contract (atrial systole).
2. Atrioventricular Node (AVN): The Gatekeeper
   The impulse reaches the AVN, located in the wall between the atria and ventricles. The AVN introduces a brief time delay (about 0.1 seconds).
3. The Importance of the AVN Delay
   Analogy: A traffic light turning yellow. This delay is crucial because it allows the atria to finish contracting and ensures that all the blood has moved into the ventricles before the ventricles contract.
4. Bundle of His and Purkinje Tissue
   The impulse leaves the AVN and travels down the Bundle of His (specialised fibres in the septum). These fibres branch out into the ventricular walls, forming the Purkinje tissue.
5. Ventricular Contraction
   The Purkinje tissue carries the impulse rapidly up the outer walls of the ventricles, causing the ventricles to contract from the base upwards (ventricular systole), effectively pushing blood into the arteries (aorta and pulmonary artery).

Key Takeaway: The SAN sets the basic rhythm. The AVN ensures coordination by delaying the impulse, allowing complete ventricular filling.

2. Extrinsic Control: Fine-Tuning via the Medulla Oblongata

While the SAN sets a baseline rhythm, the heart rate must constantly be adjusted to meet metabolic needs. This adjustment is controlled by the central nervous system (CNS) via the Autonomic Nervous System (ANS).

The Control Centre: The Medulla Oblongata

The control centre for heart rate regulation is located in the Medulla Oblongata in the brainstem. This area monitors information gathered by sensory receptors in the blood vessels and sends signals to the SAN to speed up or slow down the pace.

The Role of the Autonomic Nervous System (ANS)

The ANS has two branches that act antagonistically (oppositely) on the heart:

1. Sympathetic Nervous System (The Accelerator):
   Mnemonic: Sympathetic = Stress/Speed up.
   Nerves release neurotransmitters (like noradrenaline) that increase the frequency of impulses produced by the SAN, making the heart beat faster and more strongly.
2. Parasympathetic Nervous System (The Brake):
   Nerves release neurotransmitters (like acetylcholine) that decrease the frequency of impulses produced by the SAN, making the heart beat slower.

The Effectors

The structures that carry out the change in heart rate are called effectors. In this system, the primary effector that changes the rhythm is the Sinoatrial Node (SAN) itself. The autonomic nerves (sympathetic and parasympathetic) synapse directly onto the cells of the SAN.

3. Monitoring the Internal Environment (Receptors)

To know whether to use the accelerator or the brake, the medulla needs information from two main types of sensory receptors:

3.1. Chemoreceptors (Monitoring Chemical State)

These receptors are located primarily in the aorta and the carotid arteries (vessels leading to the brain).

• Function: They detect changes in the chemical composition of the blood, specifically the concentration of carbon dioxide (CO₂) and the resulting pH.
• The Link: During exercise, respiration increases, producing more CO₂. CO₂ dissolves in the blood to form carbonic acid, which lowers the blood pH.
• Action: If CO₂ levels are high (or pH is low), chemoreceptors send more frequent impulses to the medulla oblongata's cardiac centre.

3.2. Pressure Receptors (Baroreceptors) (Monitoring Physical State)

These receptors are also located in the walls of the aorta and the carotid arteries.

• Function: They monitor blood pressure (the stretch in the artery walls).
• Action:
  • If blood pressure rises (high stretch), baroreceptors send impulses to the medulla to decrease heart rate.
  • If blood pressure falls (low stretch), they signal the medulla to increase heart rate.

4. The Heart Rate Control Mechanism (Negative Feedback)

Control of the heart rate is a classic example of a negative feedback loop, which works to reverse any change and return the system to its optimum set point.

Case Study: Dealing with Exercise (Increased Demand)

Here is the step-by-step process of how heart rate increases when you start vigorous exercise:

1. Stimulus: Vigorous exercise increases the rate of cellular respiration, leading to increased CO₂ production and lower blood pH.
2. Receptor Action: Chemoreceptors in the aorta and carotid arteries detect the lowered pH (high CO₂). They fire impulses at a higher frequency.
3. Coordination: These impulses travel to the Medulla Oblongata (the cardiac control centre).
4. CNS Response: The Medulla oblongata activates the Sympathetic Nervous System pathway and simultaneously inhibits the Parasympathetic pathway.
5. Effector Action: The Sympathetic nerves release neurotransmitters onto the SAN.
6. Result: The SAN increases the frequency of its electrical impulses, leading to a faster and stronger heart beat, increasing blood flow to carry away CO₂ and supply O₂.

Case Study: Dealing with Rest (Decreased Demand)

When exercise stops, the reverse happens:

1. Stimulus: CO₂ production decreases, and blood pH rises back towards normal. Blood pressure may temporarily be high.
2. Receptor Action: Chemoreceptors decrease firing; Baroreceptors detect high pressure and increase firing.
3. CNS Response: The Medulla oblongata activates the Parasympathetic Nervous System pathway and inhibits the Sympathetic pathway.
4. Effector Action: The Parasympathetic nerves release neurotransmitters onto the SAN.
5. Result: The SAN decreases the frequency of its electrical impulses, causing the heart rate to slow down, returning the body to resting conditions.

Did you know? Adrenaline (a hormone) also increases heart rate, especially in "fight or flight" situations. It acts by attaching to receptors on the heart muscle and SAN, mimicking the effects of the sympathetic nervous system!