Describe the effects of exercise on the respiratory system

Introduction

During exercise, the demand for metabolic substrates by contracting muscles increases
and this is matched by increases in ventilation. Due to exercise, O2 consumption can rise
from a resting level of 300ml/min to a maximum of 4000ml/min and CO2 production
from 240ml/min to a maximum of 3000ml/min in a fit young subject. The respiratory
system responds to this by increasing tidal volume from 0.5L to 5L (vital capacity), and
ventilation frequency increases from 12/min to approximately 60/min. At low to
moderate exercise, ventilation is linearly correlated to both CO2 production and O2
consumption. In order to increase ventilation during exercise, respiratory muscles
contract more forcefully and accessory muscles are recruited as described later.
Cardiovascular responses to exercise and changes in the ventilation/perfusion ratio (V/Q)
further contribute to the responses of the respiratory system to exercise.

Respiratory system changes

At rest, the diaphragm and external intercostals muscles contract to cause inspiration by
lowering thoracic pressure, and expiration is passive. When exercising, inspiratory
muscles contract to a much greater extent to increase tidal volume and rate of inspiration,
e.g. diaphragm move 1cm during quiet breathing and as much as 10 cm during exercise.
Furthermore, accessory muscles contract forcefully to increase inspiration, e.g. scalene
muscles contract to elevate the sternocleidomastoid and alae nasi contract to cause nasal
flaring. Moreover, expiration is forced and involves the contraction of abdominal wall
muscles (rectus abdominis, transversus abdominis, internal and external oblique muscles)
and internal intercostals muscles to expel air quickly so that another breath can be taken.
An increase in adrenaline levels during exercise, due to activation of sympathetic nervous
system, also increases airflow by acting via β2 adrenoceptors on bronchial smooth
muscles to cause bronchodilation.

During exercise, the cardiovascular system responds by increasing cardiac output which
increases the flow of blood through lungs. This leads to recruitment of pulmonary
capillaries and these blood vessels distend easily thus lowering pulmonary vascular
resistance and keeping pulmonary blood pressure constant. The upper parts of lungs
receive a greater proportion of the increased blood flow producing a more uniform
distribution of perfusion in lungs. In normal subjects, this reduces V/Q inequality but this
may not occur during severe exercise due to interstitial pulmonary oedema. Not only does
O2 and CO2 exchange in lungs increase, O2 delivery and CO2 removal in peripheral
tissues also increase to meet the increased demand of exercising muscles. This is due to
an important mechanism called Bohr’s effect where an increase in PCO2, [H+] or
temperature, i.e. physiological effects of exercise, reduces affinity of haemoglobin for O2
and shifts the oxygen dissociation curve to the right.

Respiratory response mechanisms

Surprisingly, although the effects of exercise on the respiratory system have been well
characterized, the mechanisms by which these effects are brought about are unclear.
During low or moderate exercise, the arterial levels of PCO2, PO2 and pH remain the same
so neither hypoxia nor hypercarbia are responsible for increasing ventilation during
exercise. In fact, very intense exercise cause arterial levels PCO2 to drop and PO2 to rise.
One mechanism that is believed to be responsible for respiratory responses to exercise is
stretch reflexes, due to stretch receptors in joints or muscles, and this may explain how
ventilation suddenly increase at the onset of exercise. This hypothesis is supported by
experiments showing that passive movement of limbs stimulated ventilation in
anaesthetized animals.

Conclusion

The importance of respiratory system responses to exercise is clear in patients with

pulmonary diseases. In normal subjects undergoing exercise, cardiac output reaches a
maximum before VO2max is reached thus the cardiovascular system is the limiting factor
restricting muscle performance. However, asthmatic patients experience
bronchoconstriction which limits influx of air into lungs and cause V/Q mismatch to
worsen. Gaseous exchange in lungs is then limited and insufficient to meet the demands
of exercising muscles hence the respiratory system then becomes the limiting factor in
exercise.