A note upfront: this is a private work. I do not follow every formal standard of academic publishing, nor are the texts polished to the last stylistic detail. I do this in my spare time, and I don’t have an institute with a diligent team of assistants to handle the tedious, time-consuming legwork for me ;)

Table of Contents

01 Preface and Introduction
02 Lactate and “Muscle Burn” 03 Energy Systems and Thresholds
04 LIT/MICT/HIT and the “Aerobic Base”
05 Fat Metabolism and the Crossover Point
06 Surrogate Markers and Target Performance
07 High Intensity, Low Volume – Efficiency as a Principle
08 False Expectations and Misconceptions 09 Side Chapter: Anthropology and Evolution
09 Side Chapter: Anthropology and Evolution

06 – Surrogate Markers and Target Performance

After lactate, energy systems, Zone 2, and fat metabolism, the focus now shifts to the metrics that are most highly valued in endurance sports: VO₂max, lactate and ventilatory thresholds, Critical Power/FTP, heart rate variability (HRV), and related parameters. These metrics have their uses – as measurement and orientation tools – but in practice they are often elevated to standalone training goals, even though by their very nature they are surrogate markers: proxies for what actually matters, such as concrete race performance, real-world functional capacity, or a stable state of health. These actual outcomes are in principle directly observable, but they cannot be captured in a single number like VO₂max or a threshold value.

This chapter initially focuses on competitive sport, where the critical stance toward isolated marker optimization applies most sharply. For people who train without competitive ambitions, the situation is different – this will be specifically addressed at the end of the chapter.

What Surrogate Markers Can Do – and What They Cannot

Surrogate markers are measurable quantities that correlate with relevant outcomes and are therefore used as indirect targets – in the hope that optimizing them is the path to the actual goal. In endurance sports, these include above all VO₂max or cardiorespiratory fitness (CRF) as a measure of maximal oxygen transport and utilization capacity, lactate, ventilatory, and performance-based thresholds (e.g., LT1/LT2, VT1/VT2, MLSS, Critical Power) that mark specific points on exertion curves, as well as heart rate-based metrics and, increasingly, HRV-derived thresholds and steering parameters.

The practical value of surrogate markers lies first and foremost in enabling standardized testing, longitudinal comparisons, and the classification of training status and adaptations – for instance, before and after training blocks. They condense complex system states (cardiovascular capacity, metabolic shifting, autonomic balance) into manageable numbers that can be communicated and tracked. In this way, they provide a shared language among athlete, coach, and diagnostician.

At the same time, each marker captures only a slice of reality: VO₂max, for example, primarily describes maximal oxygen uptake – not technique, tactics, neuromuscular explosiveness, or mental toughness in competition. Moreover, their predictive power is context-dependent. In heterogeneous populations, CRF is a strong health and fitness marker; in elite samples that are already homogeneous on these criteria, VO₂max loses considerable discriminatory power – a phenomenon that runs through all endurance disciplines.

Particularly relevant is a practical insight from training research and coaching: surrogate markers can be misleading when they are made the primary training objective. A parameter may correlate with performance, but optimizing it does not automatically lead to better race results – because, as noted, other factors (economy, technique, tactics, mental toughness, pacing ability) determine actual success at least as much. An athlete can raise their VO₂max without getting meaningfully faster. Another can deliver a markedly better performance without any notable VO₂max improvement, because they run more economically or race more tactically.

For this analysis, therefore, the central point is that surrogate markers are tools, not goals. They are suited to structuring and monitoring the path – but they should not define where the path leads.

Lactate, Thresholds, VO₂max, HRV, and Their Role in Training

Lactate and ventilatory thresholds were already critiqued in chapters 2 and 3: they treat arbitrary points on smooth, step-free curves as though they were natural boundaries between distinct operating modes. In reality, the lactate and ventilation curves are continuous – there is no hard edge or step where metabolism “switches over.” At most there are subtle changes in slope, but no true discontinuities. The various definition methods (4 mmol, Dmax, individual turnpoints, ventilatory markers) merely select different points on this smooth curve, which explains why threshold values differ considerably depending on the method used. On top of this come methodological problems with lactate measurement itself (sampling timepoints, sample collection, analytics), which introduce additional scatter. Both together – the artificial threshold concept and measurement uncertainty – substantially limit reproducibility and predictive power.

VO₂max: “Gold Standard” With Limits – and Epistemological Problems

VO₂max – maximal oxygen uptake – is often regarded as the gold standard in sports and clinical research. This claim typically rests on epidemiological data showing a robust association between measured CRF and mortality. However, considerable caution is warranted here: epidemiology can, at best, provide hints – and even that under problematic conditions. The method is highly susceptible to bias, methodological manipulation (p-hacking, selective data mining/cherry picking), and misinterpretation. Often enough, epidemiology itself generates the patterns it subsequently claims to describe. Moreover, very few people possess sufficient statistical competence to detect such distortions.

An instructive example is a recent Mendelian randomization study (MR study on VO₂max and longevity, Kjaergaard et al. 2024; see references): while VO₂max is consistently associated with longevity in observational studies, this genetic analysis – which is better suited to establishing causality than mere observation – showed that genetically predicted VO₂max had no significant association with lifespan. (Note: Mendelian randomization methods are themselves methodologically contested and should not be taken uncritically, but they at least point toward possible confounding.)

This suggests that the epidemiological association may not be causal but rather driven by other factors (better general health, higher income, lifestyle, overall activity level).

Added to this is a methodological problem specific to sports research: a systematic review of VO₂max intervention studies confirmed this picture – across 27 included studies, bias risks were predominantly high or unclear, and only about 7% reported adequately randomized sequence generation (see references: “Risk of bias and reporting practices in studies comparing VO₂max outcomes,” 2021). Complementary current reviews on CRF diagnostics show that at the individual level, VO₂max is limited by considerable measurement variability and random fluctuation – there too, VO₂max is discussed as a population-level marker of reasonable utility but only conditionally stable at the individual level (see references: “Assessing cardiorespiratory fitness in clinical and research settings,” 2024).

The media routinely generate headlines with relative risks – “20% improvement!” – while the absolute numbers may be vanishingly small. A typical schematic example: a study shows that a particular form of training reduces mortality risk from 2% to 1.6%. In absolute terms, that is a reduction of 0.4 percentage points – but in relative terms it becomes a “20% risk reduction,” which turns into a headline sensation. The practical relevance for the individual remains questionable. A robust statement about general or individual risk was likewise never made.

Even the prominent Mandsager study (2018, >122,000 subjects; see references), often cited as proof that ever-higher CRF/VO₂max extends life expectancy, explicitly states in its limitations: “The association between CRF and mortality does not prove causation.” (Study authors are expected to describe the weaknesses of their work.) Unmeasured confounders – socioeconomic status, ethnic factors, overall activity level – could fully explain the observed association. The epidemiological rhetoric around VO₂max thus often suggests a certainty that is methodologically simply not there.

What matters here is less the caveat – almost formulaic in observational studies – that association does not prove causation, but rather the structural limitation of the design itself: even with >122,000 subjects and high statistical power, residual confounders and selection mechanisms remain in principle uncontrollable. Other methodological approaches, such as Mendelian randomization analyses or bias reviews, are likewise not free of problems, but they at least demonstrate how easily strong VO₂max gradients can be explained without any genuine causal “VO₂max lever.” Put simply: even when two things are closely linked in a massive study, that still does not mean one causes the other.

The Whole Package Matters

This does not mean that VO₂max is worthless. But its value lies not in epidemiological long-term studies or longevity theories, but in something more direct and more honest: CRF is a measurable marker indicating that the cardiovascular system is trained and adapted. A trained cardiovascular system works more economically, recovers faster, is more resilient in daily life, and reduces orthopedic and metabolic vulnerability – this can be directly observed and experienced in practice, not merely suspected epidemiologically or modeled on the grand mixing console of data. Whoever raises their VO₂max is investing in a more stably functioning organ and muscle system. That is a sufficient and honest justification, without resorting to methodologically questionable longevity rhetoric.

However, what was already emphasized in earlier chapters remains decisive: VO₂max alone is not an adequate marker for health or performance. Muscular strength, body composition, and functional capacity are at least equally important. An athlete with excellent VO₂max but weak musculature and poor mobility is no more robust or healthy than someone with moderate VO₂max but good strength and flexibility. For genuine functional health in daily life – let alone in competition – the whole package matters: sufficient endurance fitness, preserved muscle mass and strength, mobility, and everyday resilience.

A digression that cannot be fully explored here could, however, highlight that a practical “workload capacity” in everyday life is generally more important than long-distance endurance on a piece of sports equipment. Examples like carrying crates of drinks or moving apartments may illustrate the point: what matters from this perspective is which everyday demands can be met in what time. In most cases, it is not maximal strength or long-distance endurance that counts, but a strength-endurance and athletic profile of the kind that functional forms of Metcon and resistance training promote.

HRV and Other Steering Parameters

Similar considerations apply to HRV-based markers. HRV-guided training models have shown in several studies that they can improve VO₂max and performance at least as well as rigid fixed plans, and often lead to better recovery management. At the same time, HRV itself is susceptible to day-to-day variability, measurement conditions, and interpretive ambiguity; HRV-derived thresholds only approximately match classical threshold methods. HRV-based thresholds do show a generally high correlation with classical lactate and ventilatory thresholds, but agreement in detail is heterogeneous: depending on the reference method, HRV approach, and measured variable (heart rate, power, speed), the deviations can be practically relevant. HRV is thus a helpful monitoring tool, but not a magic steering parameter that could reduce the complex reality of training to a single number.

What the Markers Actually Deliver – in Competitive Sport

These findings yield a clear synthesis for competitive sport: VO₂max/CRF is a strong health and fitness marker, but a weak predictor of concrete race performance at the high end. Thresholds and HRV provide additional information, but are methodologically and conceptually limited. What should be decisive for training is what the competition actually demands – not which surrogate marker rises most impressively.

Designing Training From the Target Demand – for Different Groups

This raises the question: for whom does it make sense to put VO₂max and other markers at the center – and for whom does it not? A differentiated answer depends on context.

Competitive Athletes With Clear Performance Goals

For athletes training toward specific competitions – from 5K races through marathons to the widely varying race profiles in road cycling (sprinter stages, mountain stages, classics, time trials, puncheur profiles) – VO₂max is a useful framing marker but not a suitable primary goal. What matters in each case is the specific demand profile: a sprinter optimizes explosive peak outputs and positioning battles on short lead-ins. A puncheur focuses on repeated, relatively short maximal efforts with extreme muscular and systemic intensity on ramps and in race-deciding moments. A climber trains long high-performance segments in the mountains. A time trialist aims for aerodynamically stable, steady power over defined distances. No sprinter would seriously assume they could win a mountain stage with their specific profile – and vice versa.

Training is then designed along these demands: intensive, race-specific stimuli at the center, flanked by sufficient recovery and targeted easy sessions with a clear function. VO₂max, thresholds, and HRV serve as feedback loops – they help make adaptations visible and detect overload – but the evaluation of a training phase hinges primarily on whether target performance in the relevant profile has improved, not on whether VO₂max has risen by x ml/min/kg. In this group, the VO₂max critique applies most sharply: training that tries to push a number as high as possible without optimizing the race profile can misallocate resources and even cause harm – for instance, by neglecting technique, tactics, or neuromuscular resilience.

Recreational Athletes Without Competitive Goals – VO₂max as a Legitimate Training Target

For people who do not race but want to remain capable, robust, and healthy, different standards apply. Here, VO₂max/CRF is in fact a worthwhile and pragmatic training target – not for theoretical or epidemiological-statistical reasons, but for a combination of practical and functional arguments.

First: CRF is a measurable expression of a trained cardiovascular system and correlates in practical experience with stable health and everyday resilience. Anyone who measures their own endurance capacity (e.g., via a treadmill or field test) and then deliberately trains to improve it is investing in a functionally superior organ and muscle system. This is motivationally valuable and practically tangible. That said, a faster time would be the more intuitive and obvious target, even without competitive ambitions.

Second: targeted VO₂max training can be reliably and variably structured through high-intensity intervals (HIT/HIIT) – practically speaking, one to two sessions per week with more or less short, intense stimuli (e.g., 4 × 4 minutes at 90% VO₂max or 15/15 formats). This structure is efficient, time-saving, and produces lasting adaptations. Research consistently shows that even a single HIT session per week can yield measurable VO₂max improvements, while two sessions per week are widely regarded in the literature as sufficient to capture the bulk of the effect at moderate time investment.

What Matters Is That You Train

It is worth noting, however, that there is no consensus on optimal protocols. Research shows different formats (30/30 intervals, 4×4 models, 15/15 formats) – all of which work under certain conditions. There is no need to adhere to a race-like protocol – the structure remains flexible. Anyone who trains at high intensity once or twice a week will see adaptations – regardless of the protocol. The practical efficiency lies in the training stimulus itself, not in loyalty to a specific formula. At the same time, this removes the mental burden of a “competition mindset” in everyday training: one or two focused intense sessions per week, with genuine recovery or light functional movement in between, is a formula that works.

What remains important, however, is that even in this group a pure VO₂max focus is not sensible. Strength, mobility, functional capacity, and everyday movement remain necessary components of a comprehensive fitness framework. Improving VO₂max/CRF is a legitimate intermediate goal within a broad program – ideally implemented through a mix of intense stimuli, strength work, and everyday movement, not as an isolated end in itself.

People With High Health Risk or Clear Need for Action

For individuals with overweight, metabolic syndrome, prediabetes, or manifest cardiovascular disease, CRF as well as muscular strength, body composition, and functional capacity are all important intervention targets. Here, surrogate markers play multiple roles: CRF/VO₂max-related measures serve as established clinical markers for prognosis and treatment success. Strength and functional markers (e.g., gait speed, sit-to-stand tests) help capture frailty and fall risk. Yet here too: the goal is not to maximize a VO₂max number at all costs, but to build a more robust, more resilient organism – with better endurance, more muscle mass and strength, better balance, and metabolic stability. The needs of this group often differ fundamentally from recreational and competitive sport; a medical-functional perspective takes priority.

Implications for Training Logic

Across all three groups, a consistent message emerges: surrogate markers like VO₂max, thresholds, and HRV are useful tools and health indicators, but not standalone training goals – with one important exception in the non-competitive fitness space, where VO₂max/CRF as a proxy for “general endurance health” is pragmatically and motivationally valuable. For competitive athletes, training should be designed primarily from the target performance backward; markers serve as feedback, not as trophies. For non-competitive exercisers, a deliberate increase in CRF – through simple, regular high-intensity intervals (once or twice per week) – can be a sensible and efficient training goal, without requiring a theoretical optimization chase.

This is how chapter 6 fits seamlessly into the argumentative arc so far: after the deconstruction of hard thresholds, base zones, fat-burning zones, and a “too slow” fat metabolism, the favorite numbers of diagnostics are now also evaluated within a framework where performance and functional health form the primary goals – and surrogate markers retain their place as helpful but limited landmarks. For competitive athletes this means: do not train from markers. For fitness enthusiasts it means: improving VO₂max is fine – but without theoretical overcomplexity of training programs.

References for Chapter 6

Ioannidis JPA (2005): “Why Most Published Research Findings Are False” – PLoS Med.

Foundational critique of publication bias, p-hacking, and the reproducibility of research findings. Shows that under realistic conditions, more than 50% of published effects may be false positives. https://pubmed.ncbi.nlm.nih.gov/16060722/

Royal Society Publishing (2023): “Big little lies: a compendium and simulation of p-hacking strategies.”

Explicit demonstration of p-hacking techniques and their impact on research findings. Shows how easy it is to manipulate statistical significance. https://royalsocietypublishing.org/rsos/article/10/2/220346/92017/Big-little-lies-a-compendium-and-simulation-of-p

Bonafiglia JT et al. (2021). “Risk of bias and reporting practices in studies comparing VO₂max outcomes.” J Sport Health Sci.

Systematic review of 27 SIT-vs-MICT studies shows consistently unclear bias and poor reporting quality; only 7% report adequate randomization, no study reports adequate allocation concealment. https://pmc.ncbi.nlm.nih.gov/articles/PMC9532877/

Ross R et al. (2024). “Assessing cardiorespiratory fitness in clinical and community settings.” Prog Cardiovasc Dis.

Review of measurement methods, estimation procedures, and test protocols for CRF/VO₂max; emphasizes clinical relevance but also considerable measurement variability and limited individual-level reliability of many approaches. https://www.sciencedirect.com/science/article/abs/pii/S0033062024000306

Mandsager K et al. (2018). “Association of cardiorespiratory fitness with long-term mortality among adults undergoing exercise treadmill testing.“JAMA Netw Open.

Retrospective cohort study with 122,007 treadmill tests, often cited as “proof” that ever-higher CRF/VO₂max extends life expectancy, whose authors explicitly state that CRF here is only an associated surrogate marker and no causal effect can be demonstrated (confounding, selection). https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

Spiering BA et al. (2021). “Maintaining physical performance: the minimal dose of exercise needed to preserve endurance and strength over time.” J Strength Cond Res.

Narrative review showing that endurance performance can be maintained for weeks with drastically reduced training volume (down to a few short, intense sessions per week), provided the stimulus intensity of the original training is preserved – volume and frequency are far less decisive than classical surrogate marker logic would suggest. https://pubmed.ncbi.nlm.nih.gov/33629972/

Lenk M et al. (2025). “Impact of weekly frequency of high-intensity interval training on cardiorespiratory, metabolic, and performance measures in recreational runners: an exploratory study.” Physiol Rep.

Six weeks of 4×4 HIIT at 1, 2, or 3 sessions per week show: 2–3 sessions markedly improve VO₂max and time to exhaustion, 1 session has only a weak effect; a clear additional benefit of 3 over 2 sessions is not discernible – supporting an efficiency window of roughly 2–3 intense sessions per week. https://pubmed.ncbi.nlm.nih.gov/40976973/

Bacon AP et al. (2013). “VO₂max trainability and high intensity interval training in humans: a meta-analysis.” PLoS One.

Meta-analysis of 37 studies showing that widely varying HIIT protocols (short, medium, long intervals, some combined with continuous training) all improve VO₂max as long as enough hard minutes per week and sufficient program duration are accumulated – the differences lie more in total volume than in any “magic” interval formula. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0073182

Podlogar T, Leo P, Spragg J (2022). „Using V̇O₂max as a marker of training status in athletes – can we do better?” J Appl Physiol.

Viewpoint emphasizing the limited predictive power of VO₂max in well-trained athletes and arguing for classifying training status and performance capacity through critical intensity (CP/CS), economy, and performance-based metrics rather than a single marker. https://pubmed.ncbi.nlm.nih.gov/35175104/

Commentaries on “Using V̇O₂max as a marker of training status in athletes – can we do better?” (2022).

Collection of commentaries highlighting the limitations of VO₂max as a standalone marker and the advantages of alternative or complementary metrics. https://pmc.ncbi.nlm.nih.gov/articles/PMC9306772/

Follador L et al. (2022): “Relationship of critical speed derived from a 10-min submaximal treadmill test to 5-km and 10-km running performances.” Appl Physiol Nutr Metab 47(2):159–164.

Submaximal 10-min treadmill test for determining critical speed; CS explains a large proportion of the variance in 5K and 10K personal bests and thus proves to be a more performance-proximal and practically convenient marker than classical VO₂max tests. https://pubmed.ncbi.nlm.nih.gov/34610270/

World Health Organization (2020): “WHO Guidelines on Physical Activity and Sedentary Behaviour.” Geneva: WHO.

Current guidelines that explicitly recommend muscle- and bone-strengthening exercises as well as balance and functional training alongside endurance activity – and that also drop the old 10-minute rule, explicitly stating that even very short, and indeed intense, activity bouts fully count. In other words: the concept of short, intense, and functional training advocated here has by now arrived even at the official WHO level. https://www.ncbi.nlm.nih.gov/books/NBK566040/

Bahls M et al. (2025): “Physical activity and mortality: towards healthspan-oriented metrics and outcomes. A Scientific Statement from the European Association of Preventive Cardiology (EAPC) of the ESC.” Eur J Prev Cardiol, zwaf578.

Scientific statement from the EAPC arguing for moving away from one-dimensional, purely mortality-focused surrogate markers and instead adopting healthspan-oriented metrics that jointly consider physical function, cardiorespiratory fitness, strength, mental and cognitive health, chronic disease, and quality of life – precisely the perspective advocated here has thus arrived in the cardiological mainstream. https://academic.oup.com/eurjpc/advance-article/doi/10.1093/eurjpc/zwaf578/8248968

Kjaergaard AD et al. (2024): “Cardiorespiratory Fitness, Body Composition, Diabetes, and Longevity.” J Clin Endocrinol Metab 110(1):dgae393.

Bidirectional Mendelian randomization of large GWAS datasets in which genetically predicted cardiorespiratory fitness (VO₂max) shows no clear causal relationship with type 2 diabetes or longevity, while body composition, physical activity, and diabetes itself appear causally relevant – suggesting that VO₂max here functions primarily as a surrogate marker and not as the actual “longevity lever.” https://pmc.ncbi.nlm.nih.gov/articles/PMC12012764/

Is fruit healthy? I don’t think so.

This is a draft of a narrative opinion piece and not a paper by scientific standards. Even though the argument is scientifically grounded on all the decisive points. As for the presence of the constituents in apples, no one is likely to seriously dispute that.

I largely avoid plant-based food. And when it does occasionally make it in, it’s things I know reasonably well won’t cause me any particular problems in occasional consumption. Thanks to my highly restricted diet (mainly meat, eggs, fish, some dairy), I can by now identify disruptive factors quite well — and eliminate them right away.

I’ve never particularly enjoyed most fruit, and with apples in particular I could feel right away that they didn’t sit well with me. Now I can guess why my digestive system was always against apples and why I had this instinctive aversion. For decades, however, even I failed to put two and two together and think clearly. I too had simply parroted what passed for common sense. If you aren’t even capable of hearing and understanding what your own body is telling you … well, then you’re clearly in some kind of dysfunctional relationship with everything.

In the end, this analysis applies more or less across the board to any plant food. The apple is a symbolically charged fruit (even myths about poisoned apples aren’t all that far from biological reality, as we’ll see below). The simplistic saying “An apple a day keeps the doctor away” is practically screaming for a thorough debunking. The apple is a typical, almost ubiquitous fruit in our latitudes and is anchored in cultural traditions (though strictly speaking a neophyte). So I simply picked the apple. Even though, as I’ll return to in the final section, it isn’t even the best example of how plant food rather quickly loses its mystique under critical scrutiny.

Another point I’ll largely set aside here is that the apple, while not native to Germany, has somehow become naturalized. That is to say, devastating monocultures and ecological disasters, as well as the global transport logistics of other fruit and vegetable varieties, don’t even apply to it. But that’s for another day…

To get concrete and put the decisive points up front: I see no reason ever to eat an apple. Nutrition is, at its root, a biochemical matter. Not an ethical, religious, or political one. So what needs clarifying, above all, are the physiological aspects. What we need as food, meaning what we must consume, are — besides water — three main groups: fats and proteins as macronutrients (in relatively large amounts), and, among other things, various vitamins and minerals as micronutrients (in relatively small amounts). Carbohydrates in any form, or sugar (carbohydrates consist of nothing else), are not required. On the contrary, once consumed beyond the amount the body itself generates precisely on demand via gluconeogenesis, they tend to be harmful (unless the organism has individual peculiarities that shift these signs a little).

This is established biochemistry — there’s no serious biochemical dispute to be had about it, even though nutrition guidelines stubbornly ignore this point and it is politically inconvenient within nutrition policy. The Food and Nutrition Board of the National Academies of Sciences — the U.S. body that has scientifically grounded the official American dietary recommendations since 1940 and sets the Recommended Daily Allowances — formulated this unequivocally as early as 2005:

“The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed.” (National Academies Press, 2005, p. 275)

I’ll leave it at that for now. But I want to make my position clear: anyone who, for example, presents themselves as a nutrition expert and doesn’t know and/or ignores this fact is not qualified for this job.

It should also be noted that the quality of fats and proteins, as well as the form of the micronutrients (e.g., heme iron), matters. Animal food sources provide, for many critical nutrients (complete proteins, heme iron, zinc, vitamin B12, fat-soluble vitamins), a markedly higher bioavailability and density than most plant-based alternatives. In my assessment, this advantage clearly outweighs the antinutritive factors and toxin profiles of many plants, which I discuss in more detail elsewhere.

In what follows, we’ll first look at what an apple consists of. And with that, we get straight to the heart of the whole matter here. 85% water: I don’t need an apple to take in water. 15% carbohydrates/sugar: I don’t want them, I don’t need them, they harm me. Fiber is considered indispensable — the opposite is well supported, and those who cut out the indigestible plant fibers often notice surprisingly quickly that they don’t miss them at all. For many people, they aren’t a gain at all anyway but a disruptive factor — that sounds provocative but is physiologically justifiable. More on that elsewhere.

Well, and up to this point we’re already at nearly 100% apple that I don’t need, don’t want, and that harms me. The rest, the micros, as we’ll see, isn’t particularly worth mentioning either. I don’t need an apple for that, and certainly no other plant food. And now further caveats: there are also plenty of antinutrients and toxins in there. Plus problems arising from industrial production and processing.

In my view, then, it becomes immediately clear that the “healthy apple” thesis is quite a stretch: nutrient density in the minimal range, the nutrients that are present are middling, and the risks are demonstrably on the table.

The rest of the article I’ve structured in part as a dialogue. The basis was originally an AI dialogue (essentially Perplexity and Claude), which I’ve heavily condensed. Only then did I decide to turn it into an article. I find the question-and-answer format didactically useful and it takes the reader along. I hope you see it that way too :)

Question: What does an apple actually consist of?

The chemical composition of a typical apple per 100 g fresh weight — average values, varying slightly by variety and storage:

Water: 84–86 g

Carbohydrates: 10–18 g total · glucose 1.5–2.5 g · fructose 5–7 g · sucrose 2–4 g · starch 0.1–0.5 g · fiber 2–3 g

Protein and fat: crude protein 0.2–0.4 g · fat 0.1–0.4 g

Minerals: 0.3–0.5 g total · potassium 100–130 mg · phosphorus 10–15 mg · magnesium 5–8 mg · calcium 5–10 mg · iron 0.1–0.2 mg

Vitamins: vitamin C 4–14 mg · vitamin E 0.2 mg · vitamin K 2–3 µg · B vitamins (B1, B2, B6) each <0.1 mg

Organic acids: 0.4–0.8 g total · malic acid 300–600 mg · quinic acid 50–100 mg · citric acid 20–50 mg

Polyphenols / flavonoids: chlorogenic acid 10–50 mg · quercetin glycosides 5–20 mg · epicatechin 5–10 mg · procyanidins 20–100 mg · phloretin glycosides 1–5 mg

Aroma compounds: (traces, µg range) esters 100–500 µg · aldehydes 10–50 µg · alcohols 5–20 µg

Antinutrients / residues: polyphenols/tannins (inhibit mineral absorption) · patulin (mycotoxin, limit in juice 50 µg/kg) · pesticides (conventional cultivation, typically 0.01–1 mg/kg)

On the micronutrient side, the apple is average: it mainly provides low to moderate amounts of vitamin C and potassium, but stands out neither as a particularly dense nor as an essential micronutrient carrier. Typical values are around 10–20 mg vitamin C and roughly 100–130 mg potassium per 100 g, while fat-soluble vitamins (A, D, E, K) and B vitamins occur only in trace amounts and clearly fall behind many vegetables, berries, or herbs.

Its actual “specialty” lies in the realm of polyphenols: quercetin glycosides, procyanidins, epicatechin, chlorogenic acid, and phloretin glycosides occur in the double-digit mg range per 100 g, with higher concentrations in the peel and in old or cider varieties. These very classes of substances are simultaneously described in the specialist literature as antinutritive, because they bind, in particular, non-heme iron and other minerals via complex formation and demonstrably inhibit their absorption in the gut; for quercetin at least, this effect is experimentally well established in animal and in vitro models. Compared to other plant foods, the apple thus stands as follows: rather average on classic vitamins and minerals, conspicuous on polyphenols — whose potential benefit, from my perspective, is significantly relativized by their antinutritive effect.

Question: What antinutrients and phytotoxins does it contain — and what else is of concern?

Apples contain natural antinutrients such as polyphenols, which belong to the secondary plant compounds. They have antioxidant effects but can also qualify as antinutrients because they inhibit the absorption of certain minerals. In fact, it is well documented in the specialist literature that antinutrients such as polyphenols and phytic acid, under typical experimental conditions, measurably inhibit the absorption of certain minerals (e.g., non-heme iron, zinc, calcium) and, in part, also of vitamins; this effect on bioavailability is considered an established phenomenon in nutrition science, even if the extent in individual cases depends on the overall meal context.

The LfL presentation on apple constituents lists in detail polyphenols such as chlorogenic acid, procyanidins, flavonols (e.g., quercetin glycosides), and dihydrochalcones (phloretin or phloridzin glycosides) as typical constituents of apple peel and flesh. These substances belong to the polyphenols known in nutrition science as antinutritive (complex formation with proteins and minerals). Review articles on polyphenols explicitly describe that polyphenols/tannins bind minerals (e.g., iron, zinc, calcium) and lower their bioavailability. Since precisely such polyphenols (chlorogenic acid, quercetin glycosides, procyanidins) are documented in apples, the antinutrient effect is not theoretical but biochemically well established.

Further substances of concern in connection with apples can be allergens, especially in people with birch pollen allergy, since certain apple proteins can trigger cross-reactions. The LfL Bayern states, in essence, that roughly one in twenty people in Germany has problems, to varying degrees, with apple consumption (apple allergy, cross-reactions, etc.). This shows: even in a mainstream-adjacent, agriculture-related context, it is acknowledged that apple consumption is not harmless for a relevant share of the population.

But fair enough: the extent of the harm depends strongly on the overall setting, including individual iron and mineral stores and the total amount of other antinutrients in the meal. Whether the antinutrients from the apple carry practical weight depends heavily on the context of the rest of the meal: heme iron from meat uses different transport pathways and is significantly less sensitive to polyphenols than plant-based non-heme iron, and vitamin C can increase the absorption of non-heme iron in ways that partially offset the inhibitory effects of polyphenols. For patulin, there are binding limits for products (e.g., 50 µg/kg in juice), but not “per apple/day” for consumers; whether critical amounts are reached depends on the quality/storage of the fruit and on the share of processed products. So one can’t say from how many apples within what time frame it becomes how critical for whom.

Phytotoxins such as the mycotoxin patulin can occur in rotten apples infected by mold fungi, especially when the fungus Penicillium expansum is involved. Patulin is heat-stable and of health concern, which is why affected parts of the apple should be generously removed.

Question: But I don’t eat rotten apples. Does that make me safe?

Authorities and specialist bodies explicitly emphasize that partially rotten windfall apples are a main source of patulin when processed into juice, purée, or concentrate. The LGL Bayern writes that even small amounts of moldy apples are sufficient to contaminate large quantities of apple juice up to or above the EU limit of 50 µg/kg. A Lower Saxony investigation found, among 120 apple juices, 3 samples above the limit of 50 µg/kg, one of them extreme at 1,429 µg/kg. Specialist reports and reviews on patulin in apple products show that a relevant share of apple juices display measurable patulin contents and that limits have therefore been regulatorily set (typically 50 µg/kg for juice, 10 µg/kg for infant products).

Patulin arises primarily in rotten spots due to mold fungi and, in soft apples, spreads into the healthy flesh (up to 1–2 g/kg in rot spots). In firm apples it usually stays local; generously removing rotten parts minimizes the risk.

In short: regarding industrial processing, the argument doesn’t hold up, because even a few rotten fruits in the raw material pool are enough to measurably contaminate entire juice batches — despite sorting measures and limits. At least one scientific review expressly calls patulin contamination in apple products a global problem for which no satisfactory solution exists to date (Zhong et al., 2018).

Question: How intensive is pesticide use in apple cultivation?

Pesticide use in apple cultivation in Germany is very intensive. Frequently used active ingredients include fungicides such as captan and dithianon, as well as the herbicide glyphosate and insecticides such as chlorantraniliprole. These substances can leave residues in the apple, some of which are classified as possibly carcinogenic or environmentally harmful. The apple is among the fruits with the highest number of different pesticide residues in consumer tests (cf. Umweltinstitut München).

Pesticides sit mainly on the peel but partly penetrate into the flesh (up to 0.03 mm deep). Simple washing removes only superficial residues; a baking soda solution (15 min.) or peeling reduces them more effectively but doesn’t remove everything (4–20% remain in the flesh).

After harvest, apples are often surface-treated, which serves as “preservation” or protection against spoilage and drying out. Common procedures include wax coatings (e.g., beeswax, carnauba wax, paraffin, or synthetic waxes), which reduce moisture loss and impart gloss. This layer can trap pesticide residues or dirt and hinders thorough washing. Synthetic waxes are in part controversial because of residues and environmental aspects. In some countries, additional antifungal agents such as fungicidal sprays or treatments (captan, imazalil) are used to prevent mold growth.

This process is problematic because it can trap chemical residues through the waxes, is in part difficult to wash off, and can mislead consumers regarding the ‘purity’ of the fruit. The wax and antifungal agents increase the pesticide cocktail, which can pose a risk for sensitive individuals or at high intake.

Question: Does the micronutrient profile contain anything that is not present in animal foods and that I’d be missing on a carnivore diet?

Apples contain phloridzin (phloretin glycoside) and phloretin, flavonoids that occur exclusively in apples and are absent from animal foods. These substances are localized in the peel and flesh, with concentrations of 1–5 mg/100 g for phloretin glycosides. Further plant-specific compounds such as quercetin glycosides (5–20 mg/100 g) and chlorogenic acid (10–50 mg/100 g) are not naturally present in animal products.

Animal foods mainly provide vitamins (B12, D, A as retinol), minerals (iron as heme iron), and no plant polyphenols. Apples, on the other hand, offer a matrix of flavonoids, phenolic acids, and organic acids (e.g., malic acid) that animal products do not replicate. These secondary plant compounds are exclusively plant-based and vary by variety (higher in old varieties).

Phloridzin inhibits glucose reabsorption in the gut, an effect without animal equivalent. The combination of these substances with pectin and aroma volatiles creates a plant-based profile for smell, texture, and acid balance that animal foods do not offer. If sugar/fiber are to be avoided, distilled apple cider vinegar or extracts (e.g., ApplePhenon with >70% OPC) could be an option to isolate only the micro components.

Question: As a practically sugar-free carnivore, what do I gain from the glucose reabsorption inhibition by phloridzin?

As a practically sugar-free carnivore, I gain no relevant benefit from the glucose reabsorption inhibition by phloridzin (an SGLT1 inhibitor in the gut). My diet already provides no or minimal glucose from carbohydrate-free animal sources, so no sugar uptake needs to be blocked — blood sugar remains stable without intervention.

The effect is primarily relevant for carbohydrate-rich diets, e.g., in diabetes to reduce postprandial glucose peaks or cravings, which is irrelevant on carnivore. Studies show effects only in glucose-loaded models (e.g., STZ diabetes mice), not in low-carbohydrate states.

Phloridzin could even be counterproductive, since it promotes caloric reduction and increased renal glucose excretion, which with zero sugar input would be unnecessary or burdensome.

Question: Does the body actually need any of this?

No. None of the micronutrients contained in apples (such as flavonoids, phenolic acids, or phloridzin) is essential or strictly required, since they are absent from animal foods but don’t need to be substituted by other sources or at all. Fiber, sugar, pesticides, and potential antinutrients clearly outweigh in the risk-benefit assessment — which, in my view, justifies a contra-apple conclusion.

Question: Why are apples nevertheless promoted as unreservedly healthy?

Many sources and public narratives present apples as healthy, based on their content of vitamins, fiber, and secondary plant compounds. These narratives are widely communicated and part of recommendations for a balanced diet. But these narratives are hardly questioned.

The systematic analysis in this document focuses on the actual essential nutrient necessity, the ratio of undesirable substances (sugar, pesticides, antinutrients), and the real benefit of the micronutrients. This sober assessment pattern shows that the widespread health myth surrounding the apple is not automatically transferable to individual needs and contexts, especially not with dietary forms such as the carnivore diet. Moreover, the categorization “fruit = healthy” usually occurs without qualified definition; health-problematic aspects, although documented even in mainstream sources, are seldom systematically set against it. Yet such critical juxtapositions are precisely what’s needed to enable differentiated dietary decisions that go beyond blanket health recommendations.

Question: Is an apple, as it is marketed today, even still a real natural product? From what I know, for decades at least we’ve been dealing with selections and breeds that have little in common with the original forms. Cultivation is industrial, and the nutrient composition does not correspond to anything we ever encountered and consumed in nature over the course of our evolutionary history.

An apple as sold today is historically and genetically clearly not a “natural state,” but the result of millennia of domestication, modern breeding, and industrial cultivation.

Genetically, the cultivated apple traces back to wild apples such as Malus sieversii from Central Asia; today’s varieties, however, are hybrid products of several Malus species and have been deliberately selected over many generations for large fruit size, high sugar content, lower acidity, fewer bitter substances, and lower polyphenol content. Studies show that modern cultivated varieties on average have significantly less acid and up to roughly two-thirds fewer phenols than their wild ancestors — that is, precisely the profiles we never encountered in this form in free nature over the course of our evolutionary history. In parallel, cultivation is heavily industrialized: large-scale monocultures in a few main regions, high-performance rootstocks, intensive plant protection, and storage technology shape a product that, in yield, appearance, storability, and nutrient composition, massively deviates from historically “natural” wild apples and earlier landscape forms.

Compared to many other plant foods (e.g., nightshades, raw legumes, or highly oxalate-rich leafy greens), the content of classic, strongly toxic phytotoxins in the apple is rather moderate — which, within plant food, makes it almost a “more harmless” variant for me. That’s precisely why I deliberately use it as a model: if even with the comparatively mild apple what’s left on balance is mainly sugar, antinutritive polyphenols, possible mycotoxins, and a documented pesticide cocktail, I see no reason to fall back on “varied fruit consumption” — other fruits, or plant food as a whole, tend to exacerbate many of these problems rather than solve them.

References

Foundations / Biochemistry

National Academies of Sciences, Engineering, and Medicine (2005) – Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. National Academies Press, Washington DC.
Contains on p. 275 the statement that the lower limit of dietary carbohydrate intake compatible with life is zero, provided that adequate amounts of protein and fat are consumed. https://doi.org/10.17226/10490

Polyphenols / secondary plant compounds / composition

LfL Bayern – Inhaltsstoffe des Apfels
Documents water, sugar, acid, vitamin, and polyphenol contents (quercetin glycosides, procyanidins, phloretin glycosides, etc.), as well as the note that polyphenols are the most important secondary constituents of the apple. Also contains the statement that one in twenty people in Germany has problems with apple consumption (apple allergy). https://www.lfl.bayern.de/mam/cms07/iab/dateien/streuobsttagung_2018_vortrag_h%C3%B6hne.pdf

BUND Lemgo – Inhaltsstoffe des Apfels (Teil 1)
Detailed tabular listing of primary and secondary constituents (sugars, acids, polyphenols) in various varieties. https://www.bund-lemgo.de/download/FB_2012_05_Inhaltsstoffe_des_Apfels_-_717.pdf

Antinutrient properties (polyphenols, quercetin, etc.)

Vitalstofflexikon – Eisen / Interaktionen
Polyphenols/tannins as inhibitors of non-heme iron absorption via complex formation. https://www.vitalstoff-lexikon.de/Spurenelemente/Eisen/Interaktionen

Quercetin and iron absorption — human/in vitro data
Quercetin inhibits intestinal non-heme iron absorption and ferroportin expression. https://pmc.ncbi.nlm.nih.gov/articles/PMC6437293/ and https://www.springermedizin.de/quercetin-inhibits-intestinal-non-haem-iron-absorption-by-regula/15574648

Patulin (mycotoxin / mold toxin)

Verbraucherportal Bayern – Patulin
Basics on patulin in apples and apple products, toxicological assessment, EU limits (e.g., 50 µg/kg in juice, lower values for infant food). https://www.vis.bayern.de/essen_trinken/unerwuenschte_stoffe/patulin.htm

LGL Bayern – Patulin in Lebensmitteln
Spread of patulin in rotten apple sections, note that the toxin can also diffuse into the seemingly healthy flesh. https://www.lgl.bayern.de/lebensmittel/chemie/schimmelpilzgifte/patulin/index.htm

LAVES Niedersachsen – Patulin in Äpfeln und Apfelerzeugnissen
Analysis results on patulin in apples and processed products (apple juice), including samples exceeding the limit. https://www.laves.niedersachsen.de/startseite/lebensmittel/ruckstande_verunreingungen/patulin-in-apfeln-und-apfelerzeugnissen-151086.html

Zhong L, Carere J, Lu Z, Lu F, Zhou T (2018) – Patulin in Apples and Apple-Based Food Products: The Burdens and the Mitigation Strategies
Scientific review on occurrence, formation, stability, and levels of patulin in apples and apple products; describes patulin contamination as a global problem without satisfactory solution. https://pmc.ncbi.nlm.nih.gov/articles/PMC6267208/

Wikipedia – Patulin (overview only)
Brief overview of patulin as a mycotoxin in pome fruits, toxic properties. https://de.wikipedia.org/wiki/Patulin

Pesticides in apple cultivation / residues

Umweltinstitut München – Pestizide im Apfelanbau
Description of intensive pesticide use in apple cultivation (multiple sprayings per season), examples of active ingredients, the problem of cocktail effects. https://umweltinstitut.org/landwirtschaft/pestizide-im-apfelanbau/

Umweltinstitut München – Bericht Apfelmessungen (PDF)
Measurement data on pesticide residues in apples (number of active ingredients per sample, concentrations, organic vs. conventional). https://umweltinstitut.org/wp-content/uploads/2024/11/Bericht_Apfelmessungen_11-2024-Umweltinstitut-Muenchen.pdf

LAVES Niedersachsen – Rückstände von Pflanzenschutzmitteln in Äpfeln
Official state investigation: share of samples with residues, frequently detected active ingredients (e.g., captan), number of active ingredients per sample. https://www.laves.niedersachsen.de/startseite/lebensmittel/ruckstande_verunreinigungen/ruckstande_von_pflanzenschutzmitteln/apfel-knackig-rund-und-frei-von-pflanzenschutzmittelruckstanden-239545.html

Greenpeace / WiWo – 90% der deutschen Äpfel mit Pestiziden belastet
Test evaluation: high share of samples with multiple pesticide residues, including active ingredients partly classified as particularly problematic. https://www.wiwo.de/technologie/umwelt/greenpeace-test-90-prozent-der-deutschen-aepfel-mit-pestiziden-belastet/12477848.html

Additional sources on the natural-product / breeding aspect

New Insight into the History of Domesticated Apple
Genetic and historical analysis: the cultivated apple is a domestication product of wild species (mainly Malus sieversii) with a long breeding history, not a “natural state.” https://pmc.ncbi.nlm.nih.gov/articles/PMC3349737/

The domestication and evolutionary ecology of apples
Review on domestication, selection, and ecological adaptation of the apple; shows, among other things, the transition from wild forms to today’s cultivated varieties and their altered trait profiles (size, taste, etc.). https://edepot.wur.nl/287886

Phenotypic divergence between the cultivated apple (Malus domestica) and its primary wild progenitor (Malus sieversii)
Comparative study: documents clear differences between wild and cultivated varieties (size, sugar, acid, polyphenols, among others) and thus the strong breeding-driven shift relative to the original forms. https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0250751

Traditional, Indigenous Apple Varieties, a Fruit with a Future
Shows that traditional/indigenous varieties mostly have higher polyphenol contents and different nutrient profiles than modern standard varieties — an indication of strong breeding-driven changes in today’s commercial apple. https://pmc.ncbi.nlm.nih.gov/articles/PMC7022233/

The roadmap of apple taste improvement
Specialist article on the targeted sensory “improvement” of apples (sugars, acids, aroma compounds) through modern breeding; documents the deliberate intervention in composition and sensory profile. https://www.nature.com/articles/s43016-021-00311-y

Advances in apple breeding for enhanced fruit quality and storability

Overview of modern apple breeding with a focus on fruit quality, yield, storability, and disease resistance; underscores the industrially optimized character of today’s cultivated varieties. https://www.inhort.pl/files/journal_pdf/journal_2004spec2/full2004-1Aspec.pdf

Efficiency and Technology Gap in European Apple Production
Analysis of European apple production showing how strongly production and the value chain are industrialized, technologized, and shaped by high-performance systems. https://literatur.thuenen.de/digbib_extern/dn069688.pdf

Other technical references

R-Biopharm – Patulin (Analytik)
Specialist information on the analytics of patulin, toxicological classification (genotoxic, possible carcinogen). https://food.r-biopharm.com/de/analyten/mykotoxine/patulin/

Spring cleaning for the kettlebell? Not exactly, though it looks like I’ll need to do it again soon. This post is from last autumn. All winter long, the climate in my home gym was such that I could probably have gotten through full 10-minute competition sets without chalk. But recently, when ramping up intensity, I realized that times are coming again when chalk will be necessary – at least for the snatch. So I always practiced the grip with chalk, even if sparingly, to train right away with maximum friction. Since hand sweat, along with air humidity, causes flash rust – which is why I’m mentioning it here. I had also once made the mistake of wiping it down with a damp cloth after a workout. Now I do wipe it after every session, but always only with a dry towel.

Now for the actual report:

I’ve mentioned it before – even with a premium Pro-Kettlebell, a little surface rust is unavoidable. I looked around to see how others handle this. Most tips were purely mechanical – sanding – and there was also something about Sidol rust remover.

So off to the hardware store I went, picking up the items pictured, including Ballistol oil, which promises exactly what you’d hope for here. The sandpaper didn’t work out – it tears too quickly and doesn’t wrap well around the handle. The scouring sponge (no-name brand), on the other hand, was excellent. The handle was back to bare metal in no time – slightly less so in the recesses, but fine enough. It seems to be sufficient. Most importantly, you can hold it as shown and fold and pull it around the handle.

The process produces a rather unpleasant dust, by the way. For subsequent rounds I dug out an old Covid mask (unused, naturally).

Now for the big Ballistol question. The manufacturer’s promise (translated from the German web page):

Ballistol on metal: Ballistol is used extensively in machine and tool manufacturing, in the production of precision instruments and scales. Ballistol forms an alkaline protective film on metals, neutralizes hand sweat and other acidic rust-promoting residues, and thus protects against corrosion. Due to its low surface tension and enormous creeping ability, Ballistol reaches even the tightest corners and finest cracks in metal. Ballistol is ideal for the care of precision and measuring instruments, scales and fine components.

I was naturally skeptical about whether the oil film would make the handle too slippery. I took the plunge and rubbed down the handle, as well as the entire bell including the inside. Not sure whether the corrosion protection actually holds there. At minimum it polishes away the rust dust. Inside, the oil film might actually hold.

Yesterday’s workout was with the kettlebell treated this way – no problem at all. By the time I applied the first layer of chalk, the oil was gone. Combined with the rust dust though, a memorable smell arose during the process. But I kind of like that – there’s something old-school and hands-on about it.

Conclusion: Now I know how it’s done and that it’s a quick job. Just make sure to take a few precautions and use a surface that catches the dust.