An elite endurance athlete at rest has a heart rate of 45 bpm, well below the SA node's intrinsic rate of ~100 bpm. If a drug that blocks all muscarinic acetylcholine receptors is administered, what would happen to the athlete's heart rate?
AIt would fall further, because blocking acetylcholine removes a stimulatory signal to the SA node
BIt would rise toward ~100 bpm, because the vagal suppression actively holding the rate down would be removed
CIt would remain at 45 bpm, because resting heart rate is determined by sympathetic tone, not parasympathetic
DIt would immediately exceed 180 bpm due to unmasked maximal sympathetic activation
The SA node's intrinsic pacemaker rate is ~100 bpm. At rest, the vagus nerve continuously releases acetylcholine onto the SA node, slowing its depolarization rate and holding heart rate well below 100 bpm — in a trained athlete, as low as 40–50 bpm. Blocking muscarinic receptors removes this vagal brake, allowing the SA node to fire at its intrinsic rate (~100 bpm). This demonstrates that resting bradycardia reflects active parasympathetic suppression, not a slow intrinsic pacemaker.
Question 2 Multiple Choice
A patient with chronically elevated arterial blood pressure has reduced stroke volume despite normal heart muscle contractility. Which mechanism best explains this reduction?
AHigher afterload opposes ventricular ejection, reducing the volume of blood pushed out per beat
BHigh blood pressure increases preload, compressing the ventricle and reducing its filling capacity
CHypertension causes the SA node to fire more slowly, reducing the time available for ventricular filling
Afterload is the pressure the ventricle must overcome to eject blood — essentially arterial blood pressure. When afterload is chronically elevated (as in hypertension), the ventricle must work harder with each beat to push blood into the aorta against higher resistance. With the same contractile force, less blood is ejected per beat. Over time, the heart compensates by hypertrophying (thickening the wall), but this also reduces compliance. Reduced stroke volume despite normal contractility is a hallmark of pressure-overload cardiac dysfunction.
Question 3 True / False
At the onset of exercise, heart rate increases primarily because sympathetic nerves immediately release norepinephrine to accelerate the SA node.
TTrue
FFalse
Answer: False
The first response at exercise onset is parasympathetic withdrawal — vagal tone decreases rapidly (within one heartbeat), releasing the brake that had been slowing the SA node. Only after this initial withdrawal does sympathetic activation add norepinephrine to further accelerate the SA node and enhance contractility. The sequence is analogous to releasing a brake before pressing a gas pedal. This distinction matters clinically: the initial rapid heart rate increase during mild exercise is largely parasympathetic withdrawal; the higher rates during intense exercise reflect active sympathetic drive.
Question 4 True / False
Cardiac output can increase approximately fivefold during maximal exercise in a healthy adult, achieved by increases in both heart rate and stroke volume.
TTrue
FFalse
Answer: True
Resting cardiac output is ~5 L/min (HR ~70 × SV ~70 mL). During maximal exercise, cardiac output can reach 20–25 L/min in healthy adults — a fivefold increase. This is achieved by roughly doubling heart rate (to ~150–180 bpm) and significantly increasing stroke volume (to 120+ mL per beat) via sympathetic enhancement of contractility and increased venous return (preload). In elite endurance athletes, maximal cardiac output can exceed 40 L/min due to exceptional stroke volume capacity.
Question 5 Short Answer
Why does the resting heart rate fall well below the SA node's intrinsic firing rate, and what sequence of autonomic changes occurs at the start of exercise?
Think about your answer, then reveal below.
Model answer: The SA node has an intrinsic pacemaker rate of approximately 100 bpm when isolated from all autonomic input. At rest, the vagus nerve (parasympathetic) continuously releases acetylcholine onto the SA node, slowing its spontaneous depolarization and holding heart rate to ~60–70 bpm — well below the intrinsic rate. This is called resting vagal tone, and it means the heart is actively braked at rest. When exercise begins, parasympathetic withdrawal occurs first: vagal tone decreases rapidly (within one heartbeat), releasing the brake and allowing heart rate to rise toward the intrinsic rate. Sympathetic activation follows, releasing norepinephrine to further accelerate the SA node and enhance contractility beyond the intrinsic baseline. The analogy is releasing the brake before pressing the accelerator.
Understanding the distinction between intrinsic rate, resting rate, and the two phases of autonomic modulation is fundamental to interpreting both normal physiology and clinical findings. For example, a patient whose heart rate doesn't increase appropriately at exercise onset may have impaired parasympathetic withdrawal (chronotropic incompetence), which can be distinguished from blunted sympathetic drive by the timing and pattern of the heart rate response.