What is the role of the autonomic nervous system during exercise?
Exercise is a major challenge to homeostasis due to the increased metabolism of
contracting skeletal muscles. Since physical activity was once essential for survival,
humans have evolved to cope with exercise by physiological adaptations that are
needed to meet the increased demand for oxygen and substrates in active skeletal
muscles, as well as the increased removal of metabolites and carbon dioxide. The
adaptive responses during dynamic exercise require both feedforward and feedback
signalling involving the autonomic nervous system (ANS), which will be discussed in
this essay.
To begin with, the major physiological adaptations to exercise include cardiovascular
and ventilatory responses because they can potentially limit the maximal oxygen
consumption hence exercise intensity, but humoral and metabolic changes also occur.
During exercise, oxygen transport to skeletal muscles must increase to meet their
raised metabolic demands, for instance, oxygen consumption during maximal aerobic
exercise can increase by 12 times from the resting level of 250ml/min to about
3000ml/min. Oxygen delivery to muscles (V O2) can be represented by the following
equation: VO2 =CO x (Cao2 - Cvo2) where CO=cardiac output; Cao2/ Cvo2= arterial/ venous
oxygen content. To accommodate the large increase in oxygen demand during
exercise, oxygen delivery has to increase via changes in both CO and Cvo2, Cao2 is already
at maximum since arterial blood is already almost fully saturated with oxygen so it
does not further increase in exercise. Physiological adaptations during exercise are
driven by two types of signals (1) the feedforward signal, or “central command”, is sent
in parallel with motor output and it activates selected brain regions to stimulate
increase in CO and ventilation; (2) feedback from elevated muscle pressure and
metabolic disturbance fine-tune the central command, they involve the pressor reflex
via receptors on type III and IV afferents in contracting muscles, carotid
chemoreceptors and metaboreceptors. The role of these signalling mechanisms in
physiological changes during exercise will be illustrated in the following paragraphs.
Ventilation (VE) increases markedly with exercise intensity, the change is attributable to
the increase in both tidal volume and respiratory rate and is necessary to match the
increase in oxygen uptake and carbon dioxide output. Due to changes in blood flow, as
described later, blood spends only 0.2 seconds in lung capillaries so gas exchange
becomes diffusion-limited, rapid ventilation is therefore required to maximize the
diffusion gradient. With ventilatory adaptation, arterial partial pressures of oxygen
(Pao2) and carbon dioxide (Paco2) remain almost constant despite exercise. V E is
controlled by the medullary respiratory centre which receives input from other brain
regions and from feedback systems during exercise, the changes can be broken down
into 3 phases – an abrupt rise followed by a gradual increase then a steady V E. There
have been a number of hypotheses regarding what influences V E during exercise but
Exercise is a major challenge to homeostasis due to the increased metabolism of
contracting skeletal muscles. Since physical activity was once essential for survival,
humans have evolved to cope with exercise by physiological adaptations that are
needed to meet the increased demand for oxygen and substrates in active skeletal
muscles, as well as the increased removal of metabolites and carbon dioxide. The
adaptive responses during dynamic exercise require both feedforward and feedback
signalling involving the autonomic nervous system (ANS), which will be discussed in
this essay.
To begin with, the major physiological adaptations to exercise include cardiovascular
and ventilatory responses because they can potentially limit the maximal oxygen
consumption hence exercise intensity, but humoral and metabolic changes also occur.
During exercise, oxygen transport to skeletal muscles must increase to meet their
raised metabolic demands, for instance, oxygen consumption during maximal aerobic
exercise can increase by 12 times from the resting level of 250ml/min to about
3000ml/min. Oxygen delivery to muscles (V O2) can be represented by the following
equation: VO2 =CO x (Cao2 - Cvo2) where CO=cardiac output; Cao2/ Cvo2= arterial/ venous
oxygen content. To accommodate the large increase in oxygen demand during
exercise, oxygen delivery has to increase via changes in both CO and Cvo2, Cao2 is already
at maximum since arterial blood is already almost fully saturated with oxygen so it
does not further increase in exercise. Physiological adaptations during exercise are
driven by two types of signals (1) the feedforward signal, or “central command”, is sent
in parallel with motor output and it activates selected brain regions to stimulate
increase in CO and ventilation; (2) feedback from elevated muscle pressure and
metabolic disturbance fine-tune the central command, they involve the pressor reflex
via receptors on type III and IV afferents in contracting muscles, carotid
chemoreceptors and metaboreceptors. The role of these signalling mechanisms in
physiological changes during exercise will be illustrated in the following paragraphs.
Ventilation (VE) increases markedly with exercise intensity, the change is attributable to
the increase in both tidal volume and respiratory rate and is necessary to match the
increase in oxygen uptake and carbon dioxide output. Due to changes in blood flow, as
described later, blood spends only 0.2 seconds in lung capillaries so gas exchange
becomes diffusion-limited, rapid ventilation is therefore required to maximize the
diffusion gradient. With ventilatory adaptation, arterial partial pressures of oxygen
(Pao2) and carbon dioxide (Paco2) remain almost constant despite exercise. V E is
controlled by the medullary respiratory centre which receives input from other brain
regions and from feedback systems during exercise, the changes can be broken down
into 3 phases – an abrupt rise followed by a gradual increase then a steady V E. There
have been a number of hypotheses regarding what influences V E during exercise but
