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REVIEW 5 major objections 6 minor 47 references

Analysis of Biomedical Data to Assess the Risk of Heart Rate Variability in Athletes Participating in Long-Term Excessive Endurance Exercise

T0 review · 5 major / 6 minor · reviewed 2026-08-06 · deepseek-v4-flash

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Pith's one-line read This paper argues that long-term high-intensity marathon training improves several cardiovascular risk factors but leaves atherosclerosis unchanged, because artery thickening tracks age and conventional risk rather than exercise.

desk verdict The abstract's central finding about non-runner wives is not present anywhere in the paper; the manuscript is a disjointed literature review with no original analysis. read the letter →

arxiv 2507.10556 v1 pith:4A7SWWRX submitted 2025-06-29 q-bio.OT

Saeid Aghasoleymani Najafabadi , Hadi Jabbari Saray This is my paper · ORCID
classification q-bio.OT
keywords marathonrunnersenduranceexerciseatherosclerosiscarotidintima-mediathicknesscardiovascularriskfactorsheartratevariabilitycardiacbiomarkersmasterathletes
verification ladder T0 review T1 audit T2 compute T3 formal

The pith

A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.

The reading

The paper sets out to separate what endurance exercise does and does not do to the cardiovascular system. It claims that master marathon runners show better blood pressure, body weight, lipids, and inflammation markers than non-runner controls, yet their carotid artery wall thickness—a direct measure of subclinical atherosclerosis—is the same. The paper interprets this as evidence that atherosclerosis is driven by age and conventional risk factors, and that regular high-intensity running neither slows nor accelerates it. The practical point is that an athlete can be metabolically healthy and still carry significant atherosclerotic burden, so fitness should not be mistaken for vascular immunity.

What carries the argument

The central object is the carotid intima-media thickness (cIMT), an ultrasound-based measure of the artery wall's inner layers that serves as a marker of subclinical atherosclerosis, together with carotid augmentation pressure, a measure of wave reflection and arterial stiffness. The paper uses age, the Framingham risk score, and these carotid measures to compare master marathon runners with controls, relying on Pearson correlation and linear regression to relate the measures to age and risk score. The absence of a runner–control difference in cIMT is the load-bearing result: it is what turns 'exercise improves risk factors' into 'exercise does not alter atherosclerosis.'

What would settle it

Reproduce the comparison with a documented measurement protocol: recruit the same master-marathon-runner and control groups, measure left and right carotid intima-media thickness and carotid augmentation pressure under blinded conditions with pre-registered statistical tests, and check whether the runner–control difference is truly zero; the claim fails if a reliable group difference appears or if the reported p-values cannot be regenerated from the data.

Watch

Extended reading notes

Core claim

On the paper's own terms, the core finding is that the beneficial cardiovascular profile of long-term marathon runners—lower BMI, higher HDL, lower non-HDL cholesterol, triglycerides, and CRP—does not translate into a thinner carotid intima-media thickness or lower carotid augmentation pressure than in controls. The paper therefore concludes that atherosclerosis is little affected by exercise itself and is governed by age and the same traditional risk factors that apply to non-athletes. It also argues that post-race cardiac biomarker elevations are often physiological 'false positives' that complicate diagnosis without reversing the overall risk-benefit picture of habitual endurance exercise.

Load-bearing premise

The argument's load-bearing premise is that Table 1 and Figures 1–4 report real measurements from the described cohort and that the reported p-values came from statistical tests that were actually run.

Editorial extensions

If this is right

  • Clinicians evaluating master endurance athletes should not infer low atherosclerosis from a good risk-factor profile, since the paper argues the two can diverge.
  • Post-marathon elevations in cardiac biomarkers should be interpreted with caution; the paper treats many as physiological false positives that do not by themselves prove cardiac damage.
  • Risk assessment for older marathon runners should keep age and conventional risk scores central, because exercise-induced improvements may mask the true plaque burden.
  • If the claimed null effect on cIMT holds, then exercise prescription can be promoted for metabolic and vascular function without the expectation that it will reverse age-driven arterial thickening.

Reading between the lines

Editorial extensions of the paper, not claims the author makes directly.

  • The runner–wife comparison mentioned in the abstract, if reported in full, would be a natural experiment because spouses share household environment and lifestyle while differing in exercise exposure; the present paper gestures at this design but does not present the wife data separately.
  • If plaque composition rather than thickness were measured, the paper's own speculation that shear stress changes calcified versus non-calcified plaque could be tested, which would decide whether exercise alters the character of atherosclerosis even if total thickness is unchanged.
  • The same logic could be extended to younger runners aged 20 to 29, where sudden cardiac death risk is concentrated; the paper notes this gap and its design could be adapted to that age range.
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Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, and a circularity audit.

Referee Report

5 major / 6 minor

Summary. The paper claims that a comparison of amateur marathon runners with their non-runner wives shows that long-term high-intensity endurance training improves many components of the cardiovascular profile but does not reduce atherosclerosis. It offers a literature review, a short section on split-half reliability formulas, a brief description of a cohort of approximately 100 master marathon runners, a descriptive table, and four figures labeled Runner and Control, followed by a conclusion reiterating the abstract's assertion. The manuscript does not present any analysis of a wife comparison, does not describe a control-group measurement protocol, and provides no statistical test details for the p-values reported in Section 4.

Significance. If the central claim were supported by original data, the paper would address a real controversy: whether long-term endurance exercise improves cardiovascular risk factors while leaving atherosclerosis progression unchanged. The framing of the runners-versus-wives comparison is potentially a useful design for controlling lifestyle factors. However, as submitted, the claim is unsupported by any presented data or analysis, and the methods and results are so incomplete that the reported findings cannot be verified. The paper therefore does not currently make a substantive scientific contribution beyond its literature review, and even that review contains many unrelated or misnumbered references.

major comments (5)
  1. [Abstract and Section 5 (Conclusion)] The central claim—that comparing runners with their non-runner wives shows that training does not reduce atherosclerosis—is never supported by any data in the manuscript. The Abstract states this comparison as a finding, the Conclusion repeats it, but no wives are mentioned in Section 3 (Methods), Table 1, or Figures 1-4. Section 3.2 describes only approximately 100 master marathon runners, and the text labels the comparison groups in Figures 1-4 as 'Runner' and 'Control,' not 'Wives.' The conclusion therefore rests on an unsupported assertion rather than on the presented evidence.
  2. [Section 3.1, Eqs. (1)-(3)] The split-half reliability formulas in Section 3.1 (Equations 1-3) are never connected to the stated aim of assessing heart rate variability or atherosclerosis risk. No reliability analysis is applied to any of the reported variables, and the section does not explain how Pearson correlation, Spearman-Brown prophecy, or the Rulon/Flanagan formulas relate to the data in Table 1 or Figures 1-4. This portion of the Methods is irrelevant to the central claim and does not provide any methodological basis for the subsequent results.
  3. [Section 4.1, Results and Discussion] The paper reports numerous p-values and correlation coefficients without specifying the statistical tests, sample sizes, adjustment procedures, or comparison groups. For example, the statement 'there were no group differences in aortic SBP (p value=0.67)' and 'left cIMT and aortic SBP (Pearson coefficient=0.32; p value 0.31)' are presented with no description of the underlying model or test. The claim that 'runners had body mass index that was 11% lower, CRP that was 63% lower...' is not accompanied by any data table, confidence interval, or test statistic for the runner-versus-control comparison. These results cannot be evaluated or reproduced.
  4. [Figures 1-4] Figures 1-4 lack axis labels, legends, units, error bars, and any description of how the plotted data were generated. Figure 1 and Figure 2 show 'Runner' and 'Control' groups with linear trend lines, but the control group is never defined in the Methods and no group sizes are given. Figure 3 and Figure 4 plot 'carotid augmentation pressure' without units or a description of the measurement protocol. Without this information, the figures do not support the paper's claims about group differences or correlations.
  5. [Author contribution statement] The author contribution statement names 'Bahmani and Valizadeh,' 'Adelfahmideh and Asadi,' and 'Akbari,' none of whom is listed as an author of this manuscript. This indicates that the contribution statement was not written for this submission. It also raises concerns about the provenance of the abstract's 'runners versus their non-runner wives' comparison, which is otherwise absent from the manuscript body. The manuscript should not be considered publishable in its current form while this discrepancy exists.
minor comments (6)
  1. [Title and Abstract] The title promises an analysis of heart rate variability (HRV), but the manuscript contains no HRV measurements or HRV analysis; HRV is only mentioned in cited references. The Abstract should be revised to match the content actually presented.
  2. [Section 3.1, paragraph 1] The text states that Pearson correlation 'provides a value between 0 and 1,' but Pearson correlation ranges from -1 to 1. This is a factual error in a methods section.
  3. [Table 1] Table 1 is poorly annotated: the 'Smoke' row reports a mean of 4.6 with no standard deviation, the 'Diabetes' row reports 0 with no standard deviation, and there is no description of what 'N' refers to for each row. The table also contains only runner data, despite the text claiming comparisons with controls.
  4. [Section 3.2, Data collection] The inclusion criteria sentence is garbled: 'Among those ages C50, at least five have completed a full-distance marathon (42.195 kilometers) within the past three years' contains an undefined symbol 'C50' and does not clearly specify the inclusion rule. The exclusion criteria are also presented in a fragmentary way.
  5. [Section 5, Conclusion] The acronym 'HNRS' appears without definition, and the sentence 'Atherosclerosis is caused by age and cardiovascular risks; however, is little affected by it' is grammatically unclear. The conclusion also discusses limitations such as selection bias, but these limitations are not connected to the specific data presented.
  6. [References] Several references are unrelated to the topic of the paper, including items on deep learning for breast tumor detection, neuromorphic vision sensors, bone-conducted hearing, and codec quality-rate convex hulls. These citations appear to be text-reuse artifacts and should be removed or properly integrated if they are meant to support any argument.

Circularity Check

0 steps flagged · score 0.0 of 10

No circular derivation chain exists; the central claim about runners' wives is asserted without supporting data, which is an evidentiary failure, not a circular reduction.

full rationale

This paper does not contain a derivation chain that could be circular. The abstract's central finding, 'By comparing runners with their non-runner wives, we find that regular, high intensity run training improves many components of the cardiovascular profile but does not reduce atherosclerosis,' is never supported by any data in the body: no wives are mentioned in Section 3, no measurement protocol for carotid intima-media thickness or augmentation pressure is given, and no statistical test comparing runners with wives is reported. The conclusion repeats the abstract's assertion ('Atherosclerosis is caused by age and cardiovascular risks; however, is little affected by it') without deriving it from equations, fitted parameters, or cited theorems. Section 4 reports p-values and Pearson coefficients, but the corresponding tests are not described in the Methods, so these claims are unverifiable rather than circular. The many citations to Ahmadi, Farhadi Nia, and colleagues are external literature-review entries; even if some authors were connected to this manuscript, they are not used as a load-bearing proof of the paper's own findings. The mismatched author-contribution statement raises a question of text reuse, but text reuse is not circularity. Because no prediction is constructed from an input and no fitted parameter is renamed as a result, the appropriate circularity score is 0.

Assumptions & free parameters 0 free parameters · 3 assumptions · 0 invented entities

The paper introduces no new entities, parameters, or derivations; its central claim is an unsupported assertion assembled from prior literature.

assumptions (3)
  • domain assumption The descriptive statistics in Table 1 are assumed to be real measurements from a cohort of 100 master marathon runners.
    Section 3.2 and Table 1 present sample characteristics without provenance or sampling method details.
  • domain assumption The p-values and correlations reported in Section 4 are assumed to result from valid statistical tests.
    Methods section does not describe the statistical procedures that would produce these values.
  • domain assumption The cited studies are assumed to be represented accurately and to be relevant to the topic.
    Several citations are unrelated (lumbar spine, dental AI, neuromorphic vision), undermining this assumption.

how reviews work

0 comments
Cite this review

Pith. "Pith review of Analysis of Biomedical Data to Assess the Risk of Heart Rate Variability in Athletes Participating in Long-Term Excessive Endurance Exercise." pith.science (2026). https://pith.science/paper/4A7SWWRX

@misc{pith2026250710556,
  author       = {Pith},
  title        = {Pith review of: Analysis of Biomedical Data to Assess the Risk of Heart Rate Variability in Athletes Participating in Long-Term Excessive Endurance Exercise},
  year         = {2026},
  howpublished = {\url{https://pith.science/paper/4A7SWWRX}},
  note         = {Machine review of arXiv:2507.10556}
}
read the original abstract

Amateur marathon runners who exercise excessively over time have pathological structural changes in their hearts and aortas. Amateur marathon runners' cardiovascular system adaptations and dangers are discussed in this article. After completing endurance races, amateur athletes experience a series of cardiac modifications, including temporary elevation and changes in biomarkers of cardiac damage associated with an increased risk of coronary atherosclerosis, arrhythmias, and sudden cardiac death. As a result of the high prevalence of "false positive" biomarkers in athletes, the health benefits of aerobic activity are questioned, and treatment is complicated. Reports on long-term aerobic exercise contradict atherosclerosis risk. Differences may influence the results in lifestyle characteristics among participants. By comparing runners with their non-runner wives, we find that regular, high intensity run training improves many components of the cardiovascular profile but does not reduce atherosclerosis. Although metabolomic approaches have been developed to evaluate the physiological response of marathon runners, there is still controversy concerning the biomarkers of cardiovascular system alterations caused by long-term high-intensity endurance training. The cardiovascular risk profile is improved by habitual endurance exercise. Atherosclerosis is caused by age and cardiovascular risks; however, is little affected by it.

Figures

Figures reproduced from arXiv: 2507.10556 by the authors.

Figure 1
Figure 1. The plot of age versus left carotid [PITH_FULL_IMAGE:figures/full_fig_p012_1.png] view at source ↗
Figure 2
Figure 2. The plot of age versus right carotid 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 20 30 40 50 60 70 80 90 LCI (mm) Age Runner Control Linear (Runner) Linear (Control) 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 20 30 40 50 60 70 80 90 RCIMT (mm) Age Runner Control Linear (Runner) Linear (Control) [PITH_FULL_IMAGE:figures/full_fig_p012_2.png] view at source ↗
Figure 3
Figure 3. Carotid augmentation pressure for both Runner and control samples [PITH_FULL_IMAGE:figures/full_fig_p014_3.png] view at source ↗

Discussion (0). Continue with ORCID to comment.

Reference graph

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Pith tools

Reviewed August 6, 2026 · model on record in the stance chip above.