Structure of the Respiratory System
Respiration covers four linked processes:
- Ventilation – air moving into and out of the lungs
- External respiration – gas exchange between the lungs and the blood
- Internal respiration – gas exchange between the blood and body cells
- Cellular respiration – using oxygen at the cell to release energy from fuels such as glucose
Air passes through the airways in a fixed order:
Nose/mouth → pharynx → larynx → trachea → bronchi (left and right) → bronchioles → respiratory bronchioles → alveoli
The alveoli are tiny air sacs where gas exchange with the blood actually happens. Three structural features make them very efficient at this:
- A huge surface area, from millions of alveoli in each lung, allowing a large volume of gas exchange at once
- Walls that are only one cell thick, giving oxygen and carbon dioxide a very short diffusion pathway between air and blood
- An extensive capillary network surrounding each alveolus, giving an excellent blood supply
Each lung is enclosed within a double-layered membrane called the pleura, with fluid between the two layers that reduces friction as the lungs expand and contract during breathing.
Mechanics of Breathing
Air always moves from an area of high pressure to low pressure – the bigger the pressure difference, the faster the airflow. Breathing works by changing the volume (and therefore pressure) of the thoracic cavity using muscle contraction.
Inspiration (breathing in) – increasing the volume of the thoracic cavity lowers the pressure inside the lungs below atmospheric pressure, so air flows in.
- At rest: the diaphragm contracts and flattens, and the external intercostal muscles contract, lifting the ribcage up and out
- During exercise, extra muscles are recruited to increase the volume further: the sternocleidomastoid, scalenes and pectoralis minor
Expiration (breathing out) – decreasing the volume of the thoracic cavity raises the pressure inside the lungs above atmospheric pressure, forcing air out.
- At rest, expiration is passive: the diaphragm and external intercostals simply relax and the elastic recoil of the lungs pushes air out
- During exercise, expiration becomes active, using the internal intercostal muscles and the abdominal muscles to force air out faster
Lung Volumes and Capacities
Several defined volumes make up total lung capacity:
- Tidal volume – the volume of air breathed in or out in one normal breath (around 0.5 litres at rest)
- Inspiratory reserve volume (IRV) – the extra volume of air that can be forcibly inspired after a normal breath in
- Expiratory reserve volume (ERV) – the extra volume of air that can be forcibly expired after a normal breath out
- Residual volume – the volume of air that always remains in the lungs even after maximal expiration, because the alveoli, bronchi and trachea are held open by rings of cartilage and can never fully empty
These volumes can be measured and displayed using a spirometer, a device that records breathing movements onto a trace as a person breathes in and out of a sealed chamber through a mouthpiece.
Minute ventilation is the total volume of air breathed in or out in one minute:
Minute ventilation = breathing rate (breaths per minute) × tidal volume
At rest, roughly 12 breaths/min × 0.5 litres ≈ 6 litres/min
Effects of Exercise on Lung Volumes and Minute Ventilation
During exercise, breathing becomes both deeper and faster, which changes each lung volume differently:
- Tidal volume increases substantially, since more of the available reserve volumes are used with each breath
- Inspiratory reserve volume decreases, because more of it is being used as part of the now-larger tidal volume
- Expiratory reserve volume decreases slightly, for the same reason
- Residual volume stays roughly the same, since it is fixed by the airways always remaining slightly open
- Minute ventilation increases greatly, driven by the rise in both tidal volume and breathing rate together
On a spirometer trace, this shows up as breathing lines that are taller (bigger tidal volume) and closer together (higher breathing rate). Minute ventilation also tends to rise sharply just before exercise begins, anticipating the coming demand – a response driven by the hormone adrenaline – before climbing further once exercise starts, and rising more the harder the exercise is.
Gaseous Exchange at the Alveoli and Muscles
Gases move by diffusion: from an area of high partial pressure to an area of low partial pressure. The larger this diffusion (concentration) gradient, the faster the gas moves. Partial pressure is the pressure exerted by one individual gas within a mixture of gases, measured in mmHg.
At the alveoli:
- Oxygen partial pressure is higher in the alveoli (~100mmHg) than in the arriving capillary blood (~40mmHg), so oxygen diffuses into the blood
- Carbon dioxide partial pressure is higher in the arriving blood (~45mmHg) than in the alveoli (~40mmHg), so carbon dioxide diffuses into the alveoli to be breathed out
At the muscles:
- Oxygen partial pressure is higher in the arriving blood (~100mmHg) than in the muscle tissue (~40mmHg), so oxygen diffuses into the muscle
- Carbon dioxide, produced by the working muscle, has a higher partial pressure in the tissue (~46mmHg) than in the blood (~40mmHg), so it diffuses into the blood to be transported away
Diffusion pathway summary: oxygen travels alveoli → blood → muscle; carbon dioxide travels the reverse route, muscle → blood → alveoli.
Neural and Chemical Regulation of Pulmonary Ventilation
Breathing rate and depth are controlled by the respiratory centre, located in the medulla oblongata of the brain, which has two parts: an inspiratory centre and an expiratory centre.
The sympathetic nervous system increases breathing rate to prepare the body for exercise, while the parasympathetic nervous system decreases breathing rate back towards resting levels – the same nervous pathways involved in heart rate control.
Chemical control: exercise raises the acidity of the blood, caused by rising levels of carbon dioxide and lactic acid. Chemoreceptors, located in the carotid arteries and the aortic arch, detect this rise in blood acidity and send impulses to the inspiratory centre to increase ventilation until acidity returns to normal.
Neural control pathway for inspiration: the inspiratory centre sends impulses via the phrenic nerve to stimulate the diaphragm and external intercostals (and, during exercise, the sternocleidomastoid, scalenes and pectoralis minor) to contract, causing inspiration. This stimulation lasts about two seconds before it stops and passive expiration occurs through elastic recoil of the lungs.
Neural control pathway for expiration (active, during exercise): the expiratory centre sends impulses via the intercostal nerve to the internal intercostals and abdominal muscles, increasing expiration.
Other Receptors Involved in Ventilation Control
- Proprioceptors, located in the muscles and joints, detect increased movement at the start of exercise and send impulses to the respiratory centre to increase breathing rate immediately, even before blood chemistry has changed
- Baroreceptors, located in the aorta and carotid arteries, detect a decrease in (diastolic) blood pressure and respond by increasing breathing rate
- Stretch receptors in the lungs detect when the lungs become over-inflated during deep breathing and send impulses to the expiratory centre, and on via the intercostal nerve, to trigger expiration and prevent the lungs over-stretching
Impact of Lifestyle Choices on the Respiratory System
Smoking has several damaging effects on the respiratory system:
- It irritates and narrows the airways (trachea and bronchi), reducing lung function and increasing breathlessness
- It damages the cilia – microscopic hair-like structures lining the airways that normally sweep mucus out of the lungs – causing mucus to build up and triggering a smoker's cough
- It breaks down and merges alveoli walls into larger, less efficient air spaces, reducing the surface area available for gaseous exchange and increasing the risk of COPD (chronic obstructive pulmonary disease), a long-term progressive lung condition that causes shortness of breath
- Carbon monoxide from cigarette smoke binds to haemoglobin more readily than oxygen does, reducing the blood's oxygen-carrying capacity and increasing breathlessness during exercise