Cardiovascular Exercise Physiology – Lecture Review

Acute Cardiac Responses to Exercise

• Whole-body oxygen consumption ((\dot V O2)) rises proportionally with exercise intensity. • Determined by simultaneous increases in cardiac output ((Q)) and peripheral oxygen extraction. • Fick ("A-V O\textsubscript{2}") Equation: \dot{V}O2 = Q \times (a - v)O_2\, \text{difference}
• Cardiac output itself is the product of heart rate (HR) and stroke volume (SV):
Q = HR \times SV

• During dynamic exercise, sympathetic stimulation (EPI/NE) binds to (\beta_1) receptors to raise HR and increase myocardial contractility (thereby raising SV). Parasympathetic withdrawal produces the initial rapid rise in HR.

• Typical resting values vs. heavy exercise (untrained):
• Resting (Q \approx 5\,L\,\text{min}^{-1})
• Heavy exercise (Q \approx 25\,L\,\text{min}^{-1}) or higher in endurance-trained athletes.

Cardiac Output, Heart Rate & Stroke Volume Across Intensities

• HR rises almost linearly with workload (e.g., graded Bruce protocol). Cardiac output mirrors this rise until very high intensities where SV plateaus.

• Stroke Volume behaviour:
• Increases rapidly from rest but reaches a plateau at ~50\% (range 40!–!60\%) of (\dot V O_2\text{max}) in average adults.
• Above that intensity, further gains in (Q) are driven almost exclusively by HR.

• Major determinants of SV during exercise

1. Pre-load (end-diastolic volume): augmented by the muscle pump & venous return.

2. After-load (arterial resistance): moderated by vasodilation of active muscle.

3. Contractility: boosted by sympathetic (\beta_1) activity and catecholamines.
   • Low-intensity work: Frank-Starling (stretch-induced force) predominates.
   • Moderate-to-high intensity: direct sympathetic inotropy predominates.

• HRmax estimation – largely age-dependent, minimally influenced by training:
HR_{max} \approx 208 - 0.7 \times age (Tanaka et al.)
(Classic "220 − age" is a cruder approximation.)

Submaximal (Steady-State) Exercise

• Once a constant workload is maintained (e.g., jogging 5 mph on 0 % grade), (Q), HR, and SV rise quickly then level off (plateau) within ~3 min.

• “Steady state” merely means no change in intensity—independent of an individual’s fitness level. An elite runner may hold an 8-min mile whereas a sedentary person may hold 2 mph; both can still achieve a steady state for their respective intensity.

Neural & Reflex Modulation of HR

• Mechanoreceptors (in muscle spindles/Golgi tendons) sense length/tension changes → afferent signalling ↑ sympathetic outflow.

• Chemoreceptors sense metabolic by-products (↑H\^+, ↑CO\textsubscript{2}, lactate) → further sympathetic drive to sustain HR & contractility.

Cardiovascular Drift (Prolonged Steady-State ≥40 min)

Traditional (Thermoregulatory) Theory
• ↑Core temperature → sweating (fluid loss) + cutaneous vasodilation → ↓central blood volume & ↓venous return → ↓SV.
• To maintain (Q), HR gradually “drifts” upward.

Alternative (HR-Driven) Theory
• Sustained sympathetic firing and shortened diastolic filling time elevate HR first → reduced filling reduces SV.

Consensus: both mechanisms act concurrently.
• Observable ~45 min into moderate exercise (earlier in hot/humid conditions).
• Practical implication: HR at a fixed workload will be higher late in the bout; prescribing intensity via HR alone must account for drift.

Vascular Responses & Redistribution of Flow

• During exercise, a larger proportion of (Q) is directed to:
• Active skeletal muscle
• Skin (thermoregulation)
• Coronary circulation (absolute flow ↑ even though % of (Q) is constant)

• Flow is diverted away from GI tract, kidneys, liver via sympathetic α-mediated vasoconstriction.

• Exercise Hyperemia = the large ↑ in muscle blood flow caused by:
• Local metabolic vasodilators (NO, adenosine, prostaglandins, ↓O\textsubscript{2}, ↑CO\textsubscript{2}, ↑H\^+).
• Mechanical muscle pump & "flow-mediated dilation" (reactive expansion of vessels after transient occlusion).

Blood Pressure & Total Peripheral Resistance (TPR)

• Mean arterial pressure (MAP) relationship:
MAP = Q \times TPR
or clinically: MAP = \frac{SBP - DBP}{3} + DBP

• Systolic BP (SBP) climbs proportionally with (Q) and intensity; plateaus slightly below maximal effort when SV tops out.

• Diastolic BP (DBP) usually changes little (±10 mmHg) during rhythmic aerobic exercise because widespread vasodilation in working muscle offsets systemic vasoconstriction elsewhere, keeping overall TPR relatively unchanged.
• If most muscle mass is active (running, cycling) → DBP unchanged or slight ↓.
• If small muscle mass/high resistance (heavy lifts) → DBP may ↑.

• Result: MAP rises modestly with intensity due mainly to the SBP component.

Exercise Stroke Work & Pressure-Volume Considerations

• Stroke work (area inside pressure–volume loop) ↑ during exercise because both SV and systolic pressures are higher.

• Upper limitation of (Q): once SV plateaus, only HR can compensate; when HR cannot rise further, exercise capacity hits its ceiling.

Total Peripheral Resistance Trends

• Aerobic modalities → overall TPR ↓ owing to massive vasodilation (muscle + skin).
• Magnitude of drop depends on: number of active muscles & exercise intensity (↑metabolite accumulation → ↑local vasodilators).

Exercise Hyperemia – Detailed Elements

1. Metabolic vasodilators (NO, adenosine, K\^+, CO\textsubscript{2}, H\^+, Pi).

2. Mechanical factors: rhythmic contractions compress veins → augment venous return; pause between contractions allows arterial filling.

3. Flow-mediated dilation (FMD): Transient occlusion → vessel senses ↓shear → post-cuff release causes rapid ↑shear → endothelial NO → dilation.

Exercising in the Heat – Additional Cardiovascular Strain

• ↑Ambient temperature accelerates core heating → earlier & greater sweat rate.

• Consequences
• Progressive plasma volume loss (sweat + diffusion of intracellular water to extracellular space).
• Enhanced cutaneous blood flow (vasodilation) → further central volume depletion.
• ↓SV → compensatory ↑HR at any fixed workload (larger HR drift vs. thermoneutral).
• Potential modest ↓SBP or MAP if vasodilation outpaces (Q) rise.

• Practical Considerations
• Hydration slows but cannot fully prevent plasma decline.
• Performance often limited by cardiovascular capacity before true metabolic exhaustion (“hitting the wall” ~mile 20 of marathon).
• Extreme cases: excessive sympathetic drive + volume loss may precipitate syncope or arrhythmia at finish line (seen in ultra-events).

Integrative Summary – Key Variable Responses

Study Tip Checklist

For ANY exercise scenario, be able to state whether each of the following rises, falls, or stays unchanged and why:
• HR, SV, (Q)
• SBP, DBP, MAP
• TPR
• ((a - v)O_2) difference
• Local muscle blood flow vs. splanchnic/renal flow
• Sympathetic vs. parasympathetic tone
• Metabolic by-products prompting chemoreflex

Connections to Prior Material / Real-World Relevance

• Frank-Starling principle (stretch (\rightarrow) force) underlies preload-mediated SV changes.
• Beta-blockers ((\beta_1) antagonists) would blunt HR & contractility, limiting exercise (Q); to be revisited in “Diseases & Medications” unit.
• Cardiovascular drift concepts feed directly into the final lab project examining HR responses in thermoneutral vs. hot environments.
• Understanding DBP stability explains why clinicians use SBP rise as the main diagnostic marker in graded exercise testing (abnormal DBP rise may indicate vascular pathology).
• Marathon ‘wall’ illustrates combined glycogen depletion, cardiovascular drift, and thermoregulatory strain.