EP - Cardiovascular Correlates of Exercise

Question 1

Describe Sympathetic loading and parasympathetic unloading as methods for increasing cardiac output:

Answer 1

Sympathetic loading:

• exercise increases sympathetic outflow from the medulla (via the rostral ventrolateral medulla).
• Enhances heart rate, myocardial contractility, and vasoconstriction in non-essential tissues
• Triggers splenic contraction (in some species) and venoconstriction, increasing central venous pressure

Parasympathetic unloading:

• withdrawal of parasympathetic (vagal) tone which normally acts to decrease heart rate, thus allowing for an exercise induced increase in heart rate
• Vagal withdrawal from the SA node allows for rapid initial rise in HR (within seconds of exercise onset)
• Important for immediate HR increase before sympathetic activation fully develops
• Parasympathetic tone remains low throughout sustained exercise

Question 2

Describe the Frank Starling mechanism as a method for increasing cardiac output:

Answer 2

Is a physiological principle stating that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (end-diastolic volume), due to myocardial fibre stretch leading to a more forceful contraction

• increased venous return during exercise increases end diastolic volume
• enhanced myocardial stretch results in a more forceful contraction
• this increases stroke volume and CO

Question 3

Describe hormonal influences as a method for increasing cardiac output:

Answer 3

β-Adrenergic Effects

Catecholamines - epinephrine and norepinephrine bind to β1-adrenergic receptors on cardiac myocytes, enhancing heart rate and contractility

Renin-Angiotensin-Aldosterone System:

• exercise induced SNS activation stimulates renin release
• increases angiotensin II production
• angiotensin II has vasoconstrictive properties and stimulates aldosterone release
• this aids in blood pressure maintenance and fluid balance

Question 4

Describe the role of sympathetic activation during exercise:

Answer 4

The SNS is a branch of the autonomic nervous system responsible for the ‘fight or flight’ response, increasing heart rate and contractility

Exercise stimulates the SNS, leading to the release of catecholamines (epinephrine and norepinephrine) from the adrenal medulla

These catecholamines bind to β1-adrenergic receptors on cardiac myocytes, enhancing heart rate (chronotropy) and myocardial contractility (inotropy), thereby elevating CO

Question 5

Describe Starling forces and sympathetic stimulation as a mechanism for increasing cardiac output:

Answer 5

Starling forces:

• Increased venous return → increased end-diastolic volume (EDV) → greater myocardial fibre stretch
• This enhances cross-bridge formation in sarcomeres, increasing stroke volume (SV).
• Thus, preload directly determines contractile force — important during early and moderate exercise

Sympathetic stiumulation:

• Noradrenaline (from sympathetic nerves) and adrenaline (from adrenal medulla) bind to β₁-adrenergic receptors on the myocardium
• Increases chronotropy (HR) and inotropy (contractility) → increasing both HR and SV → ↑ cardiac output (CO = HR × SV)
• Also reduces systolic duration, allowing time for diastolic filling at higher HRs

Question 6

Describe the integrated cardiovascular response to exercise:

Answer 6

Central command:
- Brain anticipates movement → ↑ sympathetic & ↓ parasympathetic tone
- Early ↑ in heart rate (HR) and cardiac output (CO)

HR and Stroke Volume:
- HR increases with intensity, CO= HR x SV
- Stroke Volume (SV) ↑ due to ↑ venous return + ↑ contractility

Blood Pressure:
- Systolic BP ↑, Diastolic BP ↔ or ↓, MAP ↑ slightly

Blood Flow Redistribution:
- ↑ flow to working muscles
- Vasoconstriction in gut, kidneys, skin (early)

Venous return aids - skeletal muscle pump, respiratory pump

Oxygen delivery:
- ↑ pulmonary flow and ventilation
- Bohr effect → better O₂ unloading
- ↑ arteriovenous O₂ difference (a-vO₂ diff)

Hormonal role:
- Adrenaline/noradrenaline → ↑ HR, SV, vasoconstriction
- RAAS & ADH conserve fluid in prolonged exercise

Sensory feedback:
- Mechanoreceptors & metaboreceptors enhance CV response
- Baroreceptors reset to allow ↑ BP

Question 7

Describe vasodilation as a mechanism for increasing muscle perfusion:

Answer 7

The widening of blood vessels, leading to decreased vascular resistance and increased blood flow

Local factors such as increased CO₂, H⁺ ions, adenosine, and nitric oxide (NO) promote vasodilation in active muscles
These metabolites cause arteriolar smooth muscle relaxation → vasodilation → ↑ blood flow

Must be against a background of increased cardiac out put to maintain muscular perfusion in the face of the opening of these vessels

Despite systemic sympathetic vasoconstriction, local vasodilators in active muscle override α-adrenergic constriction

Ensures that oxygen delivery meets demand where it’s needed most.

Question 8

Describe the role of the endothelium in muscle perfusion:

Answer 8

Endothelium is the thin layer of cells lining blood vessels, crucial in regulating vascular tone and blood flow

Endothelial cells release vasodilators like NO in response to increased shear stress during exercise, facilitating enhanced blood flow to active muscles

Endothelial cells also release vasoconstrictors (e.g., endothelin-1) for balance.

Question 9

Describe Endothelium-Derived Relaxing Factor and its role in increasing muscle perfusion:

Answer 9

Originally identified as a factor causing vasodilation, now known to be nitric oxide (NO)

NO diffuses into vascular smooth muscle cells, activating guanylate cyclase, leading to vasodilation and increased blood flow to exercising muscles

Synthesised by endothelial nitric oxide synthase (eNOS) in response to: shear stress and
acetylcholine, bradykinin, histamine, ATP

Vasodilation occurs when NO penetrates smooth muscle cells

Crucial for matching blood flow to metabolic activity and preventing excessive vasoconstriction

Question 10

Describe decrease in total peripheral resistance and increased BP as a mechanism of increasing muscle perfusion:

Answer 10

TPR is the overall resistance to blood flow in the systemic circulation

Widespread vasodilation in active muscles reduces TPR, facilitating increased CO and muscle perfusion

Despite reduced TPR, CO increases substantially during exercise, leading to a rise in mean arterial pressure (MAP) to ensure adequate perfusion of active tissues

Increased Mean Arterial Pressure (MAP) = CO × TPR

This pressure gradient drives blood into vasodilated muscle beds, enhancing perfusion pressure and oxygen delivery

Question 11

Describe Muscle Blood Flow During Rhythmic Exercise:

Answer 11

Rhythmic contractions (e.g. walking, running) cause alternating compression and relaxation of skeletal muscle

Compression phase temporarily reduces blood flow (due to vascular compression)

Relaxation phase allows hyperaemic rebound — high flow due to vasodilation and muscle pump action

Adaptations:

• enhanced rhythmic contractions promote a muscle pump effect, aiding venous return and sustaining CO
• continuous vasodilation maintains elevated blood flow to meet metabolic demands

Coordinated by:
Mechanical factors (muscle pump)
Neural signals (sympathetic adjustments)
Metabolic vasodilators