University of Cambridge
Human Physiology
Cardiovascular response to exercise
➢ Exercise is an everyday stress that the cardiovascular system must cope with. From an
evolutionary stand point the ability to run away from a predator or catch a prey is of utmost
importance.
➢ There are two cardiovascular responses to exercise: local and systemic
Local: At rest 4 ml/min/100g needed by skeletal muscle, increase 25 fold to
100ml/min/100g in exercise. Increase caused by feedforward mechanism and functional
hyperaemia (match local demand to flow)
• To increase blood flow to skeletal muscle, there must be local vasodilation caused by
chemical responses to decrease in O2 and pH as well as increase in CO2, K+,
adenosine, lactic acid
• Also, an increase in O2 extraction
• Muscle pumping to create bigger pressure gradient across capillaries
• Anticipatory response of circulating adrenaline causes vasodilation
Systemic: To increase blood flow to skeletal muscle. Main changes that occur due to
sympathetic stimulation:
1. Increase in cardiac output, up to 4 times in a normal person to satisfy the metabolic
needs of the contracting skeletal muscle
➢ increases heart rate
➢ increasing ventricular contractility
2. Increase in venous return, achieved by venoconstriction. This increases SV by
Starling mechanism
3. Vasoconstriction of arterioles of gut, kidneys and skin (initially)
4. Overall vasodilation of skeletal muscle arteries and arterioles decreasing total
peripheral resistance, vasoconstriction only slightly offsets this decreases.
Local responses in skeletal muscle to exercise
➢ Contractions in skeletal muscle changes the chemical make-up of the interstitial fluid.
➢ There is a decrease in pO2, pH as well as increase in pCO2, lactic acid, ADP, adenosine.
These different factors also effect each other e.g. increase in lactic acid also decreases pH
➢ However, blood flow to skeletal muscle increases within 2 seconds of the onset of exercise
whereas changes in partial pressure of oxygen and carbon dioxide as well as changes in
concentration of adenosine and lactic acid occurs after several seconds
, ➢ Therefore, the immediate functional hyperaemia is caused by another factor, which is the
change in interstitial K+ concentration. Initial contraction of muscle fibres leads to the
release of K+
➢ Increase in extracellular K+ concentration causes vascular smooth muscle dilation through
the action of inwardly rectifying potassium channels.
• Increase in extracellular K+ concentration means that membrane potential is closer
to the equilibrium potential of K+ where the inwardly rectifying channels have a
higher conductance so some K+ ions move in, which allows many to move out
allowing repolarisation, leading to hyperpolarisation
• Also increased extracellular K+ leads to increased activity of Na-K pump as it has
more substrate to act on. It pumps 3Na+ out for every 2K+ which also leads to
hyperpolarisation.
• Hyperpolarisation means voltage gated L-type Ca2+ channels are inactivated. This
decreases intracellular [Ca2+] so less myosin-actin cross-bridges are formed so
contractile force of smooth muscle in arteriole wall decreases.
➢ The delayed chemical response to the other metabolic factors sustains the initial
vasodilation causes by K+ions
➢ Furthermore, some circulating adrenaline binds to Beta 2 adrenergic receptor which is also
a GPCR. Alpha-s subunit activates adenylate cyclase which catalyses formation of cAMP
which activates protein kinase A. PKA phosphorylates and inactivates myosin light chain
kinase in smooth muscle of arteriolar walls. Therefore, less myosin-actin cross-bridges are
formed causing smooth muscle relaxation and arteriolar dilation. This effect is
superimposed on the vasodilatory effect of K+.
➢ Vasodilation of upstream arterioles is important because it increases the blood flow through
capillaries. At rest, some capillaries in skeletal muscle have little or no blood flowing through
them.
• Increased capillary recruitment, increases capillary surface area for exchange of
oxygen and glucose
• Decreases the diffusion distance for oxygen and glucose to reach contracting muscle
fibres
➢ Muscle pump of skeletal muscle: rhythmic contractions during exercise causes mechanical
forces similar to pumping action of the heart.
• Veins have valves to prevent backflow
• Blood enters the veins continuously when muscle is relaxed.
• When muscle contracts it compresses the vein, opens the upper valve while closing
the lower valve which forces blood back towards the heart.
• When relaxed the subsequent reduction in venous pressure creates a bigger
pressure gradient across the capillaries therefore faster flow occurs from arterioles
and more exchange occurs.
➢ Also muscle must increase the percentage of oxygen extracted from the blood
Human Physiology
Cardiovascular response to exercise
➢ Exercise is an everyday stress that the cardiovascular system must cope with. From an
evolutionary stand point the ability to run away from a predator or catch a prey is of utmost
importance.
➢ There are two cardiovascular responses to exercise: local and systemic
Local: At rest 4 ml/min/100g needed by skeletal muscle, increase 25 fold to
100ml/min/100g in exercise. Increase caused by feedforward mechanism and functional
hyperaemia (match local demand to flow)
• To increase blood flow to skeletal muscle, there must be local vasodilation caused by
chemical responses to decrease in O2 and pH as well as increase in CO2, K+,
adenosine, lactic acid
• Also, an increase in O2 extraction
• Muscle pumping to create bigger pressure gradient across capillaries
• Anticipatory response of circulating adrenaline causes vasodilation
Systemic: To increase blood flow to skeletal muscle. Main changes that occur due to
sympathetic stimulation:
1. Increase in cardiac output, up to 4 times in a normal person to satisfy the metabolic
needs of the contracting skeletal muscle
➢ increases heart rate
➢ increasing ventricular contractility
2. Increase in venous return, achieved by venoconstriction. This increases SV by
Starling mechanism
3. Vasoconstriction of arterioles of gut, kidneys and skin (initially)
4. Overall vasodilation of skeletal muscle arteries and arterioles decreasing total
peripheral resistance, vasoconstriction only slightly offsets this decreases.
Local responses in skeletal muscle to exercise
➢ Contractions in skeletal muscle changes the chemical make-up of the interstitial fluid.
➢ There is a decrease in pO2, pH as well as increase in pCO2, lactic acid, ADP, adenosine.
These different factors also effect each other e.g. increase in lactic acid also decreases pH
➢ However, blood flow to skeletal muscle increases within 2 seconds of the onset of exercise
whereas changes in partial pressure of oxygen and carbon dioxide as well as changes in
concentration of adenosine and lactic acid occurs after several seconds
, ➢ Therefore, the immediate functional hyperaemia is caused by another factor, which is the
change in interstitial K+ concentration. Initial contraction of muscle fibres leads to the
release of K+
➢ Increase in extracellular K+ concentration causes vascular smooth muscle dilation through
the action of inwardly rectifying potassium channels.
• Increase in extracellular K+ concentration means that membrane potential is closer
to the equilibrium potential of K+ where the inwardly rectifying channels have a
higher conductance so some K+ ions move in, which allows many to move out
allowing repolarisation, leading to hyperpolarisation
• Also increased extracellular K+ leads to increased activity of Na-K pump as it has
more substrate to act on. It pumps 3Na+ out for every 2K+ which also leads to
hyperpolarisation.
• Hyperpolarisation means voltage gated L-type Ca2+ channels are inactivated. This
decreases intracellular [Ca2+] so less myosin-actin cross-bridges are formed so
contractile force of smooth muscle in arteriole wall decreases.
➢ The delayed chemical response to the other metabolic factors sustains the initial
vasodilation causes by K+ions
➢ Furthermore, some circulating adrenaline binds to Beta 2 adrenergic receptor which is also
a GPCR. Alpha-s subunit activates adenylate cyclase which catalyses formation of cAMP
which activates protein kinase A. PKA phosphorylates and inactivates myosin light chain
kinase in smooth muscle of arteriolar walls. Therefore, less myosin-actin cross-bridges are
formed causing smooth muscle relaxation and arteriolar dilation. This effect is
superimposed on the vasodilatory effect of K+.
➢ Vasodilation of upstream arterioles is important because it increases the blood flow through
capillaries. At rest, some capillaries in skeletal muscle have little or no blood flowing through
them.
• Increased capillary recruitment, increases capillary surface area for exchange of
oxygen and glucose
• Decreases the diffusion distance for oxygen and glucose to reach contracting muscle
fibres
➢ Muscle pump of skeletal muscle: rhythmic contractions during exercise causes mechanical
forces similar to pumping action of the heart.
• Veins have valves to prevent backflow
• Blood enters the veins continuously when muscle is relaxed.
• When muscle contracts it compresses the vein, opens the upper valve while closing
the lower valve which forces blood back towards the heart.
• When relaxed the subsequent reduction in venous pressure creates a bigger
pressure gradient across the capillaries therefore faster flow occurs from arterioles
and more exchange occurs.
➢ Also muscle must increase the percentage of oxygen extracted from the blood
