Chronic Exercise and the Structural Evolution of Coronary Atheroma: A Critical Appraisal of Regression, Remodeling, and the Athlete’s Paradox

The quest to determine whether physical exertion can fundamentally reverse the progression of malattia coronarica has transitioned from early epidemiological observations to a highly technical discourse centered on the micro-architecture of the vessel wall. In the modern era of cardiology, characterized by rapid advancements in artificial intelligence–enabled quantitative coronary computed tomography angiography (AI-QCTA) and high-resolution intravascular imaging, the traditional metric of luminal stenosi is increasingly viewed as an insufficient silhouette of a far more complex biological process [1]. The fundamental tension in preventive cardiology today lies in whether the undisputed cardiovascular benefits of exercise are realized through the actual reduction of placca mass — true regression — or whether exercise serves as a master regulator of vascular remodeling and plaque stabilization, effectively mitigating the risk of clinical events without necessarily eliminating the underlying disease burden [2].

This report critically evaluates the evidence surrounding this tension, prioritizing high-fidelity imaging data from intravascular ultrasound (IVUS), optical coherence tomography (OCT), and coronary computed tomography angiography (CCTA). By synthesizing data from matched cohorts, longitudinal athlete registries, and mechanistic models of shear stress, this analysis tests the hypothesis that exercise primarily functions as a stabilizer and remodeler of the coronary tree rather than a primary agent of regressione della placca.

Plaque Volume versus Lumen Size: The Glagovian Context

The accurate assessment of exercise-induced changes in the arterie coronarie requires a nuanced understanding of the relationship between the vessel’s external boundaries and its internal lumen. For decades, the gold standard for diagnosing coronary arteria disease was invasive coronary angiography, which provides a two-dimensional map of the lumen — a “lumenogram.” However, this approach is fundamentally limited by the fenomeno di Glagov, oppure positive remodeling, wherein the coronary artery undergoes a progressive enlargement of its external elastic membrane (EEM) in response to the accumulation of plaque [3].

This compensatory expansion allows the vessel to maintain its luminal cross-sectional area even as a significant atheroma develops. In Glagov’s seminal histologic study of 136 autopsied left main coronary arteries, lumen area did not decrease as a function of percent stenosis between 0 and 40 percent, but diminished markedly above that threshold (r = −0.73, P < 0.001) [3]. This implies that an angiographically normal vessel may harbor a substantial, and potentially vulnerable, carico di placca. The PROSPECT IVUS sub-analysis confirmed in vivo that EEM cross-sectional areas increase in proportion to plaque-and-media area in 552 left main coronary arteries (r = 0.61, P < 0.0001 overall, rising to r = 0.88 when plaque burden was at or below 20 percent) [4].

Exercise is a potent stimulus for vascular remodeling. Chronic aerobic training induces sustained increases in blood flow and shear stress, which activate endothelial pathways that increase nitric-oxide bioavailability and the structural caliber of conduit arteries [5]. Consequently, any study claiming that exercise reduces aterosclerosi based solely on luminal diameter is likely measuring a combination of actual plaque loss and compensatory vessel expansion. To distinguish between these effects, researchers rely on percent atheroma volume (PAV), which normalizes plaque mass to the total volume of the vessel. PAV is calculated as the sum of (EEM area − lumen area) divided by the sum of EEM area, expressed as a percentage. This metric ensures that if a vessel grows larger (increased EEM) but the plaque area remains constant, PAV decreases, reflecting a relative reduction in the occluded proportion of the artery, even when absolute total atheroma volume (TAV) remains stable [6].

Evidence for True Plaque Regression: Benchmarking against Pharmacotherapy

When evaluating the capacity of exercise to induce regression, it is necessary to establish a benchmark using lipid-lowering therapies (LLTs), which have the most robust data for reducing PAV and TAV. A comprehensive meta-analisi of 51 studies involving 9,113 adults demonstrated that LLTs as a class reduce PAV by a mean of −1.10 percent (95% CI −1.63 to −0.56, P < 0.01) and reduce TAV by −5.84 mm³ (95% CI −8.64 to −3.04, P < 0.01); high-intensity statins drove the largest TAV effect (−7.60 mm³; 95% CI −11.89 to −3.31, P < 0.01) [6]. Direct head-to-head plaque-imaging evidence from the GLAGOV randomized trial further demonstrates that PCSK9 inhibition added to statina therapy produces incremental PAV regression in patients with established coronary artery disease [2].

In comparison, the direct evidence for exercise-induced regression is emerging but remains modest. The studio CENIT (Coronary Disease and the Effect of High-Intensity Interval Training) provided critical longitudinal data by randomizing 60 patients with stable coronary artery disease, all of whom underwent percutaneous coronary intervention, to either six months of supervised high-intensity interval training (HIIT) at 85–95 percent of peak frequenza cardiaca or to contemporary preventive guidelines [7]. The study used IVUS to measure changes in PAV and TAV in residual coronary segments.

Parameter	HIIT Group (n=30)	Control Group (n=30)	Between-Group Difference
Change in PAV (%)	−1.2 (95% CI: −2.1 to −0.2; P=0.017)	+0.2 (95% CI: −0.7 to 1.1; P=0.616)	−1.4 (95% CI: −2.7 to −0.1; P=0.036) [7]
Change in TAVnorm (mm³)	−9.0 (95% CI: −14.7 to −3.4; P=0.002)	—	−12.0 (95% CI: −19.9 to −4.2; P=0.003) [7]

The CENIT results are notable because they demonstrate that exercise can achieve PAV reductions of a magnitude comparable to lipid-lowering therapy (−1.2% vs. −1.10%) [6], [7]. Importantly, this regression was observed in a population already receiving guideline-directed medical therapy, making it difficult to isolate the independent contribution of exercise from a synergistic interaction with statins.

The Endurance Athlete Paradox

While interventional trials in patients with established coronary artery disease suggest the potential for regression, observational data from healthy veteran athletes present a challenging paradox. Large registries, including MARC (Measuring Athlete’s Risk of Cardiovascular Events) and Master@Heart, consistently report that lifelong endurance athletes have a higher prevalence of coronary atherosclerotic plaque and higher Coronary Artery Calcium (CAC) scores than less active individuals with comparable cardiovascular risk profiles [8], [9].

Il Studio Master@Heart, a prospective observational cohort analysis of 191 lifelong master endurance athletes, 191 late-onset athletes (initiating endurance sports after age 30), and 176 healthy non-athletic controls (all male, low cardiovascular risk profile, median age 55 years), reported the following adjusted associations for lifelong endurance sports relative to a healthy non-athletic lifestyle [9]:

• ≥1 coronary plaque: OR 1.86 (95% CI 1.17–2.94)
• ≥1 proximal plaque: OR 1.96 (95% CI 1.24–3.11)
• ≥1 calcified plaque: OR 1.58 (95% CI 1.01–2.49)
• ≥1 calcified proximal plaque: OR 2.07 (95% CI 1.28–3.35)
• ≥1 placca non calcificata: OR 1.95 (95% CI 1.12–3.40)
• ≥1 non-calcified proximal plaque: OR 2.80 (95% CI 1.39–5.65)
• ≥1 mixed plaque: OR 1.78 (95% CI 1.06–2.99)

The finding of higher odds of non-calcified (lipid-rich) plaques in proximal segments is particularly notable, as such plaques are typically associated with higher near-term risk than purely calcified lesioni [9].

Il MARC-2 study added longitudinal granularity by distinguishing exercise volume from intensity in 289 middle-aged and older male athletes (median age 54 years) followed for a mean of 6.3 years [8]. Total exercise volume (MET-hours/week) showed no association with progression of CAC or plaque. By contrast, exercise intensity stratified by metabolic equivalents — vigorous (6–9 METs) versus very vigorous (≥9 METs) — was significantly associated with imaging outcomes:

Exercise Intensity	Effect on CAC Score (β per 10% increase)	Plaque Progression
Vigorous (6–9 METs)	−0.05 (95% CI −0.09 to −0.01; P=0.02) [8]	Less progression
Very Vigorous (≥9 METs)	+0.05 (95% CI 0.01 to 0.09; P=0.01) [8]	aOR 1.09 (95% CI 1.01–1.18) per 10% increase [8]
Total Volume	No significant association [8]	No significant association [8]

That intensity rather than volume drives plaque and CAC progression in athletes suggests a physiological threshold beyond which exercise may exert pro-atherogenic effects. Proposed mechanisms include exercise systolic blood pressures that can exceed 200 mmHg in well-trained athletes during near-maximal effort [25], repetitive mechanical stress on the coronary wall, and inflammatory signaling pathways implicated in athlete-related vascular calcificazione [10].

The defining feature of the athlete’s paradox, however, is that despite higher plaque burden, endurance athletes have lower rates of major adverse cardiovascular events (MACE) than the general population. Although the rank order of plaque morphology (calcified > mixed > non-calcified) is broadly similar across active and sedentary populations, lifelong endurance athletes who harbor plaque are more likely than sedentary controls to harbor exclusively calcified lesions, which are considered more stable [12]. This phenotypic enrichment for dense, calcified (stable) lesions — rather than for mixed or non-calcified vulnerable lesions — suggests that high-volume exercise may accelerate the natural healing or densification process of atherosclerosis [10], [11].

Matched Cohort Evidence and Socioeconomic Confounders

A critical requirement for validating the impact of exercise is the control of social and economic confounders. Higher socioeconomic status (SES) is independently associated with both greater capacità di esercizio and improved cardiovascular outcomes [13]. In the Heart and Soul Study, an analysis of 943 men and women with stable malattia coronarica, exercise capacity decreased in a graded fashion across categories of income, education, housing, and occupation. After multivariable adjustment, the difference in exercise capacity between the highest and lowest categories was 2.4 METs for household income, 1.8 METs for education, 2.3 METs for housing, and 1.3 METs for occupation (P < 0.001 for all trends) [13].

Spousal Concordance and Partner Studies

Cohabiting partners share a micro-environment encompassing diet, socioeconomic stress, and access to healthcare. In a US nationwide cohort of 5,364 married or domestic-partner couples, within-couple concordance exceeded 50 percent for every component of the American Heart Association’s Life’s Simple 7 framework, ranging from 53 percent for colesterolo totale to 95 percent for healthy diet score; concordance for metabolic syndrome reached 73 percent [14]. Despite this strong concordance for behaviors and fattori di rischio, marital status itself, when adjusted for cardiovascular risk factors, was not independently associated with subclinical coronary atherosclerosis on CCTA in a study of 9,288 asymptomatic individuals [15]. Together, these findings suggest that the shared environment of a partnership produces a background risk level, but the trajectory of plaque burden is more heavily influenced by individual health behaviors — including the choice to exercise regularly — than by partnership status itself.

Occupational Activity as a Controlled Environment

The London Transport Workers Study remains the canonical example of an occupational analog [16]. By comparing conductors and drivers within the same transport system — men of similar age and social class — Jeremy Morris was able to isolate occupational physical activity from most confounders. Morris and colleagues studied tens of thousands of London bus and postal workers and reported that physically active conductors, who climbed and descended hundreds of stairs per shift, experienced approximately half the rate of acute and sudden coronary deaths observed among the sedentary drivers [16], [17]. This natural experiment provides some of the earliest robust evidence that occupational physical activity independently modifies the clinical expression of coronary disease, even when the macro-environment is held constant.

Dose-Response Relationships and the Mortality Curve

The relationship between exercise dose and mortality is widely regarded as curvilinear, with the most substantial risk reductions occurring as individuals move from sedentary to moderately active. The revisione sistematica and meta-analysis by Blond and colleagues, encompassing 48 prospective cohort studies, used random-effects restricted cubic spline dose-risposta modeling to estimate hazard ratios across the full exposure range. Compared with the recommended physical activity dose (750 MET-min/week), risk continued to decrease beyond recommendations: at 5,000 MET-min/week, hazard ratios were approximately 0.86 for all-cause mortality and 0.73 for cardiovascular mortality. No excess risk was observed at the highest exposure levels examined [18].

The Lee et al. Circulation analysis of 116,221 adults pooled from the Nurses’ Health Study and the Health Professionals Follow-up Study, with up to 30 years of follow-up and approximately 47,000 deaths, examined long-term physical activity intensity in detail [19]. Compared with no leisure-time vigorous physical activity (VPA), participants meeting the guideline (75–149 min/week of VPA) had hazard ratios of 0.81 (95% CI 0.76–0.87) for all-cause mortality, 0.69 (95% CI 0.60–0.78) for CVD mortality, and 0.85 (95% CI 0.79–0.92) for non-CVD/non-cancer mortality. Participants performing two to four times the recommended minimum had a 21–23 percent lower all-cause mortality for VPA (150–299 min/week) and a 26–31 percent lower all-cause mortality for moderate physical activity (300–599 min/week) [19]. Higher long-term doses (≥300 min/week VPA or ≥600 min/week moderate activity) did not provide further mortality reduction, but no excess risk was observed [19].

This mortality benefit persists despite the athlete’s paradox of increased CAC, supporting the conclusion that the plaques found in highly active individuals are compositionally more benign in their clinical manifestation [10], [11].

Mechanistic Model: How Exercise Modifies Plaque

The biological mechanisms by which exercise potentially reduces plaque burden or facilitates stabilization act both systemically and locally.

Fluid Mechanics and Wall Shear Stress

Plaque development is governed by patterns of blood flow. Laminar flow produces high wall shear stress (WSS), which maintains endothelial homeostasis through the mechanosensitive transcription-factor axis (KLF2 and KLF4) and downstream activation of endothelial ossido nitrico synthase. Disturbed or oscillatory flow, common at coronary bifurcations, produces low WSS that promotes an atherogenic endothelial phenotype, including upregulation of NF-κB-driven adhesion molecules, monocyte recruitment, and increased endothelial transcitosi of LDL [20]. Exercise-induced increases in flow rate directly enhance the protective frictional force at the vessel wall. Direct molecular evidence in human coronary arteries has shown that regular physical activity in patients with coronary artery disease increases phosphorylation of endothelial nitric oxide synthase at Ser1177, the key regulatory site governing nitric oxide production [5].

Reverse Cholesterol Transport and HDL Functionality

Exercise facilitates the removal of lipids from plaque via the trasporto inverso del colesterolo pathway, beginning with colesterolo efflux from cellule schiumose to HDL particles, which transport lipids to the liver for hepatobiliary excretion. A randomized exercise-dosing trial measuring multiple HDL functional metrics has shown that increasing both exercise intensity and dose produces dose-responsive improvements in HDL cholesterol efflux capacity, anti-oxidant capacity, and anti-inflammatory function — effects that are largely independent of changes in HDL cholesterol concentration alone [22].

Plaque Stabilization, Matrix Metalloproteinases, and the Fibrous Cap

Beyond regression, exercise promotes structural stabilization through fibrous-cap thickening, mediated in part by reduced intra-plaque matrix metalloproteinase activity. Animal studies in apolipoproteina E knockout mice show that aerobic exercise training reduces intra-plaque MMP-8 and MMP-9 activity, increases tissue inhibitor of metalloproteinases (TIMP-1, TIMP-2), increases fibrous-cap thickness, and reduces the relative size of the necrotic lipid core [23]. Human systematic-review evidence links chronic physical activity to favorable changes in circulating MMP-9, oxidized LDL, and inflammatory mediators relevant to plaque vulnerability [21]. Concurrent reductions in systemic infiammazione, including C-reactive protein, may further contribute to plaque stabilization [11], [21]. The net effect in chronically active individuals is a transition from compositionally vulnerable to compositionally stable plaque morphology, even when total volume della placca increases [10], [12].

Sex-Specific Differences in Plaque Risk

A crucial refinement in modern preventive cardiology is the recognition that plaque burden carries different prognostic implications in men and women. In a recent analysis of the Studio PROMISE CCTA arm (4,267 patients, approximately 51 percent women, median follow-up 26 months), women had lower coronary plaque prevalence than men (55 percent versus 75 percent; P < 0.001) and lower median total plaque volume, yet a similar incidence of major adverse cardiovascular events (2.3 percent versus 3.4 percent) [24]. Critically, when MACE risk was modeled against total plaque burden using sex-stratified spline Cox regression, the hazard ratio crossed unity at a substantially lower plaque-burden threshold in women than in men.

Funzionalità	Women	Men	Implication
Plaque prevalence	55%	75%	Lower prevalence in women [24]
Plaque volume	Lower (median)	Higher (median)	Smaller absolute burden in women [24]
Total plaque burden at HR=1.0	≈20%	≈28%	Risk emerges at a lower burden in women [24]
Total plaque burden at HR=1.5	≈32%	≈42%	Steeper risk trajectory in women [24]

These data indicate that uniform thresholds for high-risk plaque underestimate risk in women: because women have smaller coronary arteries, a smaller absolute plaque volume produces a larger relative plaque burden and a more rapid acceleration of MACE risk [24]. This implies that for female athletes, the ceiling for compositionally benign subclinical plaque may be considerably lower than for their male counterparts.

Testing the Hypothesis: Remodeling or Regression?

The hypothesis under examination is that exercise does not meaningfully reduce total coronary plaque burden but rather improves vessel caliber and plaque stability. The evidence supports a population-dependent answer:

In patients with established CAD on guideline-directed therapy: Exercise can meaningfully reduce total plaque burden. The CENIT trial demonstrated a between-group PAV difference of −1.4 percent and a TAVnorm reduction of −12 mm³ after six months of HIIT [7].

In healthy lifelong endurance athletes: Exercise does not reduce total plaque burden but is associated with higher prevalence and burden across all plaque types [9]. In this population, the hypothesis is largely supported: the cardiovascular benefit of exercise is realized through vascular remodeling and stabilization (calcification) rather than removal.

Apparent versus true benefits: Increased lumen size in trained individuals reflects a real physiological adaptation (positive remodeling) that confers significant clinical protection through enhanced coronary flow reserve [3], [4]. This remodeling benefit is distinct from the discrete benefit of true plaque regression, and the two effects operate on different timescales.

Final Verdict: Regression, Progression, or Stabilization?

The totality of the evidence indicates that chronic exercise is a multi-modal modifier of coronary atherosclerosis. True regression — measurable reductions in PAV and TAV — is achievable through high-intensity exercise interventions, particularly in populations with existing coronary artery disease, where the magnitude approaches that of intensive lipid-lowering therapy [2], [6], [7]. Among individuals without known disease, moderate exercise appears to slow the progression of soft, vulnerable, lipid-rich plaques through favorable lipid metabolism, enhanced HDL cholesterol efflux capacity, and reduced systemic inflammation [21], [22]. In high-volume endurance athletes, exercise functions primarily as a stabilizing agent, paradoxically accelerating calcification while expanding vessel caliber through positive remodeling — yielding a compositionally benign atherosclerotic burden that does not translate into elevated clinical risk [9], [10], [12].

Critically, the survival benefit of exercise is decoupled from absolute plaque volume: extreme athletes have more plaque yet exhibit substantially lower all-cause and CVD mortality than the general population [18], [19]. The clinical emphasis should therefore shift from quantifying how much plaque is present toward characterizing what kind of plaque is present and what functional reserve the individual’s coronary tree retains.

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