The Clinical Question
When an echocardiogram technician reports an ejection fraction of 45–50%, most clinicians pause. Normal EF is ≥55%. The gray zone below that — now classified as Heart Failure with Mildly Reduced Ejection Fraction (HFmrEF) — typically carries implications of structural heart disease, dyssynchrony, or early cardiomyopathy.
But what if that same patient is completing a 1,000-meter swim in 25 minutes at a heart rate of 72 bpm? What if they are rowing competitively? How can the heart be "failing" and yet sustaining elite endurance performance?
Ejection fraction is a fraction. It tells you the percentage of blood ejected per beat — not the absolute volume. In a significantly enlarged heart, EF 45% may represent a larger stroke volume than EF 60% in a normal-sized heart.
This is not a contradiction. It is fundamental cardiac physiology — and understanding it is essential for any clinician managing athletes with implantable devices, borderline EF findings, or suspected pacing-induced cardiomyopathy.
What Ejection Fraction Actually Measures
Ejection fraction is defined by a simple ratio:
What EF does not tell you is how much blood is ejected in absolute terms. That is stroke volume (SV), and stroke volume is the true currency of cardiac output.
Consider two patients:
The athlete's heart — with an EF of 45% — is delivering 25% more cardiac output than the sedentary patient with a "normal" EF of 60%. The fraction is lower; the performance is superior.
Athlete's Heart: Eccentric Remodeling
Decades of endurance training produce a well-characterized structural adaptation known as athlete's heart or athletic cardiac remodeling. The dominant change is eccentric left ventricular hypertrophy — the cavity enlarges proportionally more than the wall thickens.
The Frank-Starling Mechanism at Work
With a chronically enlarged EDV, the Frank-Starling law predicts enhanced stroke volume — the stretched myocardium contracts with greater force. Simultaneously, peripheral adaptations reinforce this advantage:
| Parameter | Sedentary Adult | Elite Endurance Athlete |
|---|---|---|
| Resting HR (bpm) | 70–80 | 40–60 |
| EDV (mL) | 100–130 | 170–220 |
| ESV (mL) | 40–60 | 80–120 |
| Stroke Volume (mL) | 60–80 | 100–140 |
| EF (%) | 55–65% | 45–58% |
| Max Cardiac Output (L/min) | 15–20 | 25–40 |
| a-vO₂ Difference | Standard | Enhanced (+20–30%) |
Notice that the EF range for elite athletes overlaps with what, in a sedentary patient, would prompt a cardiomyopathy workup. This is the paradox — and the diagnostic trap.
The Swimming Performance Context
A 1,000-meter swim in 25 minutes corresponds to a 2:30 per 100-meter pace. For context, competitive Masters swimmers typically achieve 1:20–1:50 per 100 meters. This pace is a moderate aerobic effort — likely 60–75% of VO₂max for a recreational swimmer, and closer to 40–50% for a well-trained one.
A heart rate of 72 bpm during or after this effort is the key clinical signal. There are two possible interpretations:
HR 72 reflects resting or early recovery measurement. During the swim, HR rose appropriately and recovered quickly. This is consistent with high parasympathetic tone, large stroke volume, and efficient oxygen delivery — classic athletic remodeling.
HR 72 during the swim itself indicates extraordinarily high stroke volume compensating for chronotropic limitation. This might be seen in a paced patient with a programmed lower rate limit, or an athlete with marked vagal tone maintaining output via volume rather than rate.
In either case, the cardiovascular demand is being met. The heart is performing. EF alone is not the arbiter of functional capacity.
The Critical Distinction: Athlete's Heart vs. Pathology
The clinical challenge is not explaining how an athlete with EF 45% can swim. The challenge is determining whether that EF 45% is benign physiological adaptation or the early signal of a progressive cardiomyopathy — particularly pacing-induced cardiomyopathy (PICM) in patients with implantable devices.
| Feature | Athlete's Heart | Pathological (PICM / DCM) |
|---|---|---|
| EF range | 45–55% | <45%, progressive decline |
| EDV | Enlarged, symmetric | Enlarged, may be asymmetric |
| Wall motion | Normal, uniform contraction | Regional or global hypokinesis |
| Diastolic function | Normal to supranormal | Often impaired (elevated E/e') |
| LA dimension | Mildly enlarged (<4.5 cm) | Significantly enlarged (>4.5 cm) |
| BNP / NT-proBNP | Normal | Often elevated |
| Response to detraining | EF normalizes in 3–6 months | Persists or worsens |
| Pacing burden (if device) | N/A | >20–40% RV pacing → high risk |
| Septal dyssynchrony | Absent | Septal flash, LBBB-pattern |
| Symptoms at peak exertion | None | Dyspnea, fatigue, reduced ceiling |
A significantly dilated left atrium (>4.5–5.0 cm) in combination with declining EF is not consistent with pure athletic remodeling. LA dilation at this degree reflects chronically elevated LV filling pressures — a pathological signal demanding further workup regardless of exercise capacity.
The Pacing-Induced Cardiomyopathy Consideration
In patients with implantable pacemakers — particularly those with right ventricular pacing (as with leadless pacemaker systems such as the Aveir VR) — a declining EF warrants specific interrogation of pacing burden.
RV pacing creates an iatrogenic LBBB-like activation pattern, inducing ventricular dyssynchrony. Studies consistently demonstrate that pacing burden above 20–40% is associated with measurable EF decline, and the risk increases linearly with higher burden and longer duration.
Critically, in athletic patients, symptoms emerge late. The athlete's physiological reserve — large stroke volume, enhanced peripheral oxygen extraction, high-efficiency skeletal muscle — compensates for early contractile dysfunction. The patient may continue swimming, rowing, and performing at high levels while EF silently declines from 56% toward 45%, toward 40%.
A fit heart with EF 45% can outperform a deconditioned heart with EF 60% on any given day — but that athletic reserve is not protection against progressive remodeling. It is camouflage.
— ABC Farma · Cardiac Electrophysiology EducationThe threshold for intervention — upgrade to Left Bundle Branch Area Pacing (LBBAP) or biventricular CRT — should be driven by EF trajectory and pacing burden, not by symptoms alone. Waiting for dyspnea in a trained athlete means waiting too long.
Clinical Bottom Line
EF 45% in an endurance athlete is not automatically pathological. The heart's eccentric remodeling, augmented stroke volume, and Frank-Starling advantages can sustain — and even exceed — the cardiac output of a normal-EF sedentary heart.
However, the following constellation should prompt urgent evaluation beyond a reassuring exercise tolerance:
1. EF declining serially (e.g., 56% → 50% → 45% over 5 years) · 2. Left atrial dimension >4.5 cm · 3. High RV pacing burden (>20%) in a device patient · 4. Septal dyssynchrony on echo · 5. Elevated BNP without alternative explanation.
In the presence of any of these, the question shifts from "How can they still perform?" to "How much time do we have before this becomes irreversible?" — and the answer, in pacing-induced cardiomyopathy, is measured in months, not years.
The upgrade to LBBAP, evaluated proactively, offers the best probability of complete reverse remodeling. The window is now.