This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

We’ve covered a wide range of supplements so far, from caffeine and creatine to omega-3s, iron, electrolytes, and nitrates, trying to give a picture of what the evidence shows and if/when a supplement may be useful for you. Some of these supplements have solid performance and/or health benefits under the right conditions, while others have a narrower role, or weaker evidence, than some might suggest. But there is another layer of this conversation we have not yet addressed, which is the quality and safety of the supplements themselves.

The supplement industry is enormous and largely self-regulated, and that combination creates real risks. You might not be getting what the label claims is in the bottle, and/or you might be getting things the label doesn’t mention at all, including substances that are banned by the World Anti-Doping Agency (WADA), harmful to your health, or both. Further, even well-intentioned supplement use can interact with medications in ways that are not anticipated. This article lays out some of the potential risks and steps you can take to reduce them.

1. The Regulatory Gap of the Supplement Industry

The core problem with supplement safety begins with how supplements are regulated, or more accurately, how lightly they are regulated compared with pharmaceutical drugs. In the United States, the Dietary Supplement Health and Education Act of 1994 established that dietary supplements are presumed safe and do not require Food and Drug Administration (FDA) approval or safety review before being sold. (1,2) Rather than requiring manufacturers to prove a product is safe before it reaches consumers, the burden largely falls on regulators to identify harm after the product is already on the market. This is quite different from the process used for pharmaceutical drugs, which undergo extensive premarket testing and review.

This means the supplement industry is essentially self-regulated before products reach consumers. Manufacturers are responsible for ensuring their products are safe and accurately labelled, but no independent authority routinely verifies this. As the sports nutrition market has expanded into a multi-billion-dollar sector, monitoring every product, ingredient source, and manufacturing process has become increasingly difficult for government agencies. (4)

One certification you will commonly see on supplement labels is GMP (Good Manufacturing Practice). GMP indicates that a facility meets certain manufacturing process standards: consistent procedures, cleanliness, proper documentation (e.g., batch records that log which ingredients were used and in what quantities, written standard operating procedures, and records of who performed each step). What it does not mean is that the product has been tested for WADA-prohibited substances, or screened for undeclared ingredients. GMP tells you something about how a product was made. It also tells you very little about what is actually in it. (2)

2. What’s on the Label Isn’t Always in the Bottle

One consequence of this regulatory environment is poor label accuracy. A 2023 study examined 57 sports supplements labelled as containing various botanical performance-enhancing ingredients. (5) Forty percent of products did not contain a detectable amount of the ingredient listed on their label. Of those that did contain the listed ingredient, the quantity ranged from 0.02% to 334% of the labelled amount, and only 11% of products were within 10% of the stated quantity.

In practical terms, you may be paying for a product that contains far less of an ingredient than advertised, or far more, which carries its own risks if that ingredient has dose-dependent effects or interacts with something else you’re taking.

3. What’s in the Bottle That Isn’t on the Label

The more serious concern for cyclists, particularly those who compete, is the presence of substances the label doesn’t mention at all. Multiple independent laboratory analyses have found WADA-prohibited substances in commercially available sports supplements at rates that are difficult to dismiss as manufacturing anomalies.

Researchers from the Doping Authority Netherlands purchased 66 sports nutrition supplements from Dutch web shops, selecting products based on performance claims related to hormone modulation, muscle mass, fat loss, or energy, and had them screened for doping substances. (6) Thirty-eight percent contained undeclared doping substances! What was found included stimulants such as oxilofrine, DMAA (1,3-dimethylamylamine), and beta-methylphenethylamine; the anabolic steroids boldione and 17α-AED; the beta-2 agonist higenamine; and the beta-blocker bisoprolol. For some products, the quantities detected were sufficient to pose a meaningful risk of a doping violation.

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In the previous KIW Research Note, we opened the series on physiological models explaining fatigue during endurance exercise, starting with the Cardiovascular/Anaerobic Model, In this KIW Research Note, we continue the series by focusing on the second key model: the Energy Stores Depletion Model.

As outlined in the previous note, understanding fatigue mechanisms during endurance exercise is essential for applying the Physiological Model of Endurance Performance (PMEP). This approach aims to optimize preparation strategies—training, nutrition, supplementation, technology, and recovery—by targeting the specific physiological mechanisms that limit performance in a given competition or effort.

Have a good read! :)

1. What Causes Fatigue in the Energy Stores Depletion Model?

When producing energy (i.e., power output in watts), the human body relies on two key components: fuels and—when available—oxygen. The cardiovascular/anaerobic model focuses on the latter, highlighting the role of oxygen delivery and utilization in limiting performance. The energy stores depletion model, instead, shifts the focus to the first component: fuels. Specifically, this model links fatigue to the depletion of key energy substrates that are essential to sustain performance. (1)

Let’s explore which energy stores are involved, and in which scenarios.

2. The Human Body Fuels

Here’s a overview of all the energy fuels the human body can use to produce energy (watts):

1. Muscle phosphocreatine (PCr)

2. Carbohydrates (muscle glycogen, liver glycogen, blood glucose)

3. Fats (intramuscular triglycerides and adipose tissue)

4. Proteins

5. Ketones

6. Lactate

Fuel selection depends on two key factors:

1. availability

2. the rate at which its metabolic pathway can generate energy (its power).

If a single fuel source were both unlimited and capable of producing energy at very high rates—without generating limiting by-products or disturbing homeostasis—we could theoretically sustain extremely high power outputs (e.g., 1000 W for an hour).

Clearly, this is not the case.

For this reason, it is essential to break down each fuel source to understand how and in which scenarios fatigue is linked to the depletion of specific energy stores.

3. Muscle Phosphocreatine

The ultimate goal of all metabolic pathways is to produce ATP (adenosine triphosphate), the molecule that represents the cell’s energy currency and directly supports muscle contraction as well as other physiological functions. At the onset of exercise, energy is initially supplied by the small pool of ATP already stored within the muscle. However, these reserves are extremely limited and are depleted within ~1–2 seconds. As ATP levels begin to fall, the first metabolic system to take over is the anaerobic (alactic) phosphagen system, which generates high power output by relying on phosphocreatine (PCr) stored in muscle fibers.

The key reaction is catalyzed by Creatine Kinase (CK), which transfers a phosphate group from PCr to adenosine diphosphate (ADP), rapidly resynthesizing ATP (2):

This metabolic pathway reaches its peak power output at ~3-5 seconds and is very powerful: it can produce a lot of ATP per second, more than any other metabolic pathways. (2) Why? Because creatine phosphate is stored in the cytosol in close proximity to the sites of energy utilisation and phosphocreatine breakdown does not depend on oxygen availability, or necessitate the completion of several metabolic reactions before energy is liberated to fuel ATP regeneration. (3)

While extremely powerful, the phosphocreatine (PCr) system is limited by its small capacity. PCr stores are rapidly depleted—within ~10–15 seconds of high-intensity work—after which ATP resynthesis progressively shifts toward glycolysis (carbohydrate/glucose-dependent, discussed in the next sections), which becomes the dominant energy pathway. (4)

So, which types of performance is limited by phosphocreatine (PCr) availability within the Energy Stores Depletion model?

Intuitively, short-duration, high-intensity, explosive efforts—typically lasting ~3–20 seconds—are those most directly limited by PCr stores. In addition, also repeated short sprints with uncomplete recovery are likely limited by PCr storage.

How to apply phosphocreatine depletion/availability within the PMEP Framework?

Here are two practical applications of the PMEP framework in the context of PCr depletion/availability, which means understanding phsyiology to implement successful prepration strategies:

• Creatine Supplementation
  Creatine is the substrate for PCr synthesis. Chronic creatine supplementation increases intramuscular PCr availability. Starting exercise with larger PCr stores can enhance peak sprint power, slightly prolong time to fatigue in short efforts, and improve the capacity to repeat high-intensity sprints. (5) (To learn more about creatine supplementation you can read our relative KIW Research Note by Dr Jeff Rothschild).

• Aerobic Training and PCr Resynthesis

  When high-intensity efforts are intermittent (repeated sprints), PCr can be partially restored during recovery phases through an oxygen-dependent process. This means that developing aerobic capacity—even through low-intensity volume—can meaningfully improve PCr resynthesis between efforts and so improving the ability to repeat short high intensity sprints with incomplete recovery. (6) In cycling, this has clear implications for disciplines such as road racing during stochastic phases, MTB XCO, cyclocross, and certain track events like the points race.

4. Carbohydrates and Fats

Read more

As anticipated in the last KIW Research Note, here we start the series about the 6 Physiological Model to to explain fatigue during cycling. These are crucial to understand which physiological systems should be targeted to choose proper preparation strategies (training, nutrition, supplements, etc.) to optimize specific race performance, following the Physiological Model of Endurance Performance.

We start with probably the most popular one: the Cardiovascular-Anaerobic Model.

These models are built on the seminal 2006 review published by Chris Abbiss and Paul B. Laursen on Sports Medicine, updated with key insights from the past two decades of research. (1)

Enjoy the Read! :)

1. What Causes Fatigue in the Cardiovascular-Anaerobic Model?

In this model, fatigue is caused by the inability of oxygen-dependent (aerobic) metabolism to fully meet the energy demand required for a given power output, forcing a greater reliance on anaerobic pathways. (1) As this shift occurs, there is an increased production of hydrogen ions and lactate:

• hydrogen ions are directly involved in the development of fatigue through their negative effects on muscle function and blood oxygen transport. (2)

• lactate should not be viewed as a cause of fatigue, but rather as a valuable alternative fuel for adjacent muscle fibres, as well as for the liver, brain, and heart, and as a marker of underlying metabolic stress. (3)

2. The Physiological Factors Determining the Cardiovascular-Anaerobic Model

How much an athlete is strong in this cardiovascular-anaerobic domain is described by the aerobic performance indicators — VO₂max, power at thresholds, critical power, and FTP — which all represent, from different angles and using different metrics, the ability to sustain high rates of aerobic energy production. These performance indicators depend on the efficiency (how fast) of oxygen transport and utilization across the entire physiological cascade, from ambient air to the muscle mitochondria, where it is utilized to produce energy (power output). (4)

This process is governed by two 2 macroprocess and 5 crucial physiological characteristics:

• MACROPROCESS 1: The ability of the cardiovascular system to deliver oxygen to the working muscles,

  It is determined by

  1. Pulmonary Diffusion

  2. Cardiac Output

  3. Haemoglobin Mass

• MACROPROCESS 2: The skeletal muscle’s capacity to extract that oxygen from the blood and utilize it to produce energy (watts).

  It is determined by:

  4. Muscle Capillarization

  5. Muscle Mitochondrial Density/Mass

Let’s break down each of these 5 crucial physiological characteristics.

3. Cardiac Output (Stroke Volume)

Cardiac output is the volume of blood pumped per minute and is defined as the product of heart rate (HR - the number of heart beat per minute) and stroke volume (SV - the volume of blood pumped by each beat):

A higher cardiac output permit more oxygen to arrive at the working muscle and more wasting product to be removed. Of the two components of cardiac output, the one that truly distinguishes performance level is stroke volume, not heart rate. (5) In fact. compared to an average person, in elite endurance athlete:

• Maximal Stroke Volume ≈ 1.5-2× higher

• Maximum Heart Rate is similar

Why?

Maximum heart rate is largely determined by the interaction between intrinsic sinoatrial node pacemaker activity and autonomic neurohumoral input, both of which are determined by age and genetics but are not meaningfully trainable; with training, maximum heart rate tends to remain relatively stable or even slightly decrease. For this reason, it does not differentiate performance level: a sedentary individual can present a maximal heart rate similar to that of a world-class endurance athlete. (6)

Maximum stroke volume, on the other hand, is highly trainable, differ dramatically between elite athletes and average sedentary Joe, and so it represents a key determinant of endurance performance. In sedentary individuals, maximal stroke volume is typically in the range of ~90–110 mL per beat, whereas in elite cyclists it can reach ~150–220 mL per beat (1.5-2x higher). (5) These differences are driven by structural and functional adaptations of the cardiovascular system (7):

• a larger left ventricular cavity (eccentric myocardial hypertrophy) which allows more blood to fill the heart during diastole (relaxation between beats) and therefore more to be ejected with each contraction.

• an increased myocardial wall thickness (concentric myocardial hypertrophy) which favour more powerful contraction and so the blood ejected at each beat

• improved diastolic (relaxation) filling

• a greater total blood volume an expansion in plasma volume increases venous return, leading to greater ventricular filling and stretch before contraction, which in turn enhances stroke volume

This “athlete’s heart” could be in part genetic. In this regard, it is interesting to note that some exceptional endurance athletes, such as Fausto Coppi and Jonas Vingegaard, display particularly pronounced thoracic morphology, which may reflect, at least in part, a favourable genetic predisposition for larger cardiac dimensions. However, as stated above, stroke volume is not only genetic but can continue to develop even in already professional endurance athletes; for example, in a cohort of professional cyclists followed between 1995 and 1998, left ventricular end-diastolic diameter—an index of cardiac size—increased by approximately 3.4% over that period. (8)

So, resuming elite athletes has higher cardiac output due to different cardiac adaptations which lead to a higher stroke volume, but not higher heart rate. Here below a typical example considering two individuals between 20 and 30 years old.

4. Haemoglobin Mass

Haemoglobin (Hb) is the protein that carries oxygen in the blood. It also contributes to carbon dioxide (CO₂) transport and helps buffer hydrogen ions (H⁺), supporting acid–base balance during exercise. Haemoglobin is contained within red blood cells. (9)

When it comes to performance, what really matters is not haemoglobin concentration—it’s haemoglobin mass (Hb mass). Hb mass represents the total amount of haemoglobin in the body, and therefore the true oxygen-carrying capacity. Elite endurance athletes typically present ~30–40% higher Hb mass compared to untrained individuals. (10) This trait is partly genetic, but also trainable, and can be further enhanced through special environmental stressors such as hypoxia (altitude) and heat (active or passive) exposure. Values reported in the literature show ~14.6 g/kg in trained male endurance athletes versus ~9–11 g/kg in untrained individuals (10). Instead of just grams, expressing Hb mass relative to body mass (grams/kg) allows for meaningful comparisons across individuals with different body size.

Importantly, Hb mass is not measured in routine blood tests. It requires specific assessment techniques, such as the carbon monoxide rebreathing method, typically used in research or elite sport settings. Standard blood panels report variables like:

• Haemoglobin concentration (Hb, g/dL)

• Haematocrit (Hct, %) represents the percentage of blood volume occupied by the cellular components, primarily red blood cells.

These are concentration-based measures, not total quantities. Both are heavily influenced by plasma volume (the liquid part of the blood), which fluctuates with hydration and training status. For example:

• Dehydration → ↓ plasma volume → ↑ Hb (g/dL) and Hct (%)

• Chronic endurance training → ↑ both plasma volume and Hbmass (g) → Unchanged Hb (g/dL) and Hct (%)

So what? Changes in Hb concentration and Haematocrit are not necessarily linked to any real change in oxygen-carrying capacity. For example, due to chronic high-load endurance training, elite cyclists typically have both higher Hb mass and larger plasma volume. The net effect? Hb concentration and haematocrit that often look completely normal—or even slightly low. Regarding this, while Hb mass clearly distinguishes athletes from sedentary individuals—and even correlates with performance within well-trained cyclists (VO₂max ~70–80 ml·kg⁻¹·min⁻¹; (11))—Hb concentration and haematocrit are often similar between elite athletes and sedentary. (12)

Hb mass is tightly linked to erythropoietin (EPO), the hormone regulating red blood cell production erythropoiesis and ultimately raising Hb mass.

5. Muscle Capillarization

At the local level, the exchange between muscle and blood happens through capillaries — the final branches of the vascular network. Muscle capillarization can be expressed as number of capillaries per fibre or capillary density (capillaries per mm² of muscle). Muscle capillarization is a key determinant of endurance performance, strongly linked to VO₂max, exercise thresholds, and performance in efforts lasting from ~30 seconds to 30 minutes. (13) More capillaries = better exchange between blood and muscles. Oxygen gets in faster, metabolites (such as hydrogen ions) get out more efficiently. It is not by chance that elite athletes have ~3× more capillaries per muscle fibre than untrained individuals. (14) Think of capillaries as entry and exit ramps. The more access points you have, the easier it is to move things in and out. Fewer bottlenecks, less “metabolic congestion,” less fatigue.

6. Muscle Oxidative Capacity

Once oxygen arrives at the muscle, what really matters is the ability to use it to produce energy. That happens in the mitochondria — the main site of aerobic energy production.

If oxygen delivery through the cardiovascular system is high but mitochondrial/muscle oxidative capacity is limited, pyruvate produced by glycolysis won’t be fully oxidised. Instead, it’s converted to lactate, with an associated accumulation of hydrogen ions (H⁺), which contribute to fatigue through multiple mechanisms. In this scenario:

Mitochondrial volume (more precisely, mitochondrial volume density) refers to the percentage of muscle fibre volume occupied by mitochondria. This is typically ~4–5% in sedentary young adults and ~7.5–9% in elite endurance athletes. (5)

7. Pulmonary Diffusion

The first step in the oxygen cascade—from ambient air to muscle utilisation—is the transfer of oxygen from the lungs to the blood (Pulmonary Diffusion). Despite being the initial step, it is discussed last here because, under normal conditions, it is not a limiting factor in the cardiovascular–anaerobic model of fatigue (4). In fact, even during maximal exercise, arterial oxygen saturation (SaO₂) typically remains above ~95%, indicating that pulmonary oxygen loading is generally well maintained.

However, two important exceptions should be considered, in which pulmonary diffusion can become a limiting step:

1. Elite endurance athletes
   Highly trained athletes can achieve exceptionally high cardiac outputs during exercise. This shortens pulmonary capillary transit time, reducing the window for oxygen diffusion from the alveoli to the blood. As a result, arterial oxygen saturation may decline during intense exercise—a phenomenon known as exercise-induced arterial hypoxemia (15).

2. High altitude
   At elevations above ~2500 m, the reduced partial pressure of oxygen lowers alveolar PO₂ and the driving gradient for diffusion. Under these conditions, the lungs’ ability to fully oxygenate the blood is compromised, making pulmonary limitations more relevant within the oxygen transport chain.

8. Which Type of Performance is Limited by the Cardiovascular-Anaerobic Model?

To understand which types of performance or race are most influenced by the Cardiovascular–Anaerobic Model, it is essential to consider the relative contributions of the aerobic and anaerobic energy systems across exercise durations performed at maximal intensity.

Conveniently, Professor Gastin has recently (2026) published an updated review on this topic, reporting the percentage contributions of aerobic and anaerobic metabolism during all-out efforts of varying durations.

Here below the results.

Read more

In 2026, data is everywhere in modern cycling—and increasingly central to performance. What was once a niche discussion has gone mainstream, accelerated even further by the rise of Artificial Intelligence in sport. One of the key objective is clear: accurately quantifying race demands.

• total duration

• average power

• kilojoules expended

• time spent in specific power zones

• duration and intensity of key winning efforts.

• …and dozens more (easily 100+, depending on how deep you go).

Within this scenario, a common approach is to translate these demands into training—replicating race requirements, either partially or in full, to prepare the body for competition-specific stress. This approach can be called ‘chasing race demands’.

At Knowledge is Watt, we believe that measuring race demands is important—but basing the MAIN PART of the preparation on copy-pasting them into training is not the best-solution Instead, these data should be used to decode the physiology underpinning race performance.

That means, starting from race data and asking:

• Which physiological systems are being stressed?

• What physiological mechanism are driving fatigue?

• Where are the true performance limiters?

• How can they be improved?

In this context, one of the core ideas behind Knowledge is Watt is simple:

It’s no coincidence that much of the cycling performance research we translate in KIW Research Notes comes from the International Journal of Sports Physiology and Performance. And it’s no coincidence that at Auckland University of Technology—ranked among the world’s top 25 institutions for sport science, where I spent the final year of my PhD—the laboratory responsible for much of the research on endurance performance is simply named ‘Sports Physiology Lab’.

Because ultimately, performance isn’t just about metrics—it’s about the physiology driving them.

This is exactly why to plan your preparation strategies you should use the PHYSIOLOGICAL MODEL OF ENDURANCE PERFORMANCE (PMEP) which provides a framework (a map) to translate race demands into actionable physiological targets and, ultimately, into preparation (training, nutrition, supplementation, recovery, equipment choice) strategies. It works in this way:

1. Start by analyzing race demands

2. Identify which physiological systems and metabolic pathways are involved and to what extent

3. Define the mechanisms of fatigue at the physiological level

4. Understand which systems need to be upregulated to delay fatigue and improve performance

5. Build the optimal preparation strategy by integrating training, nutrition, recovery, environmental exposure, and supplementation to maximally stimulate the key physiological adaptations within the time available.

If you’re not using the PMEP, how are you making decisions about your preparation strategy?

Without a solid grounding in exercise physiology, it’s easy to fall into replicating race demands, copying what others are doing, repeating what’s always been done, or chasing the latest wearable, software “performance decoder,” or supplement in an ever-changing web of trends and marketing claims. These approaches shift constantly. Physiology doesn’t. It’s rooted in human biology—timeless, robust, and only incrementally refined by new research. That foundation allows you to critically evaluate emerging trends, form your own evidence-based opinions, and —combined with your intuition and personal experience — make informed decisions with confidence.

A compelling example of the PMEP’s practical relevance comes from world-class track pursuiters. A recent study (1) by Stadnyk and colleagues (2024, University of Technology Sydney) examined the training strategies of the five male cyclists from the Australian team who set the world record (3:49.804) in the 4,000-metre team pursuit at the 2018 Commonwealth Games. Despite competing in an event lasting ~4 minutes and in moderate environmental conditions (<25°C), two key features of their preparation stood out:

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Torque training — cycling at an imposed low cadence with higher force production — is a widespread training method among cyclists, from amateurs to professionals.

Although the term torque training is generally used to describe any exercise performed at a low cadence, it can actually refer to very different combinations of exercise intensity (power output) and pedalling cadence (rpm). These combinations result in different levels of force production and, potentially, different physiological adaptations. (1) This variability may partly explain the conflicting findings reported in the literature regarding the effects of torque training on cycling performance. (2) For example, at the same cadence, increasing exercise intensity from the first lactate threshold to VO₂max almost doubles the percentage of maximal dynamic force applied to the pedals. (1)

Regarding this, recent studies have shown that:

• An 8-week intervention consisting of low-cadence, long intervals (4–6 min) performed in Zone 3 (5/7 zone model) was not more effective than the same training performed at freely chosen cadence for improving VO₂max, power at 4 mmol·L⁻¹, efficiency, and 30-min maximal mean power output in middle-aged amateur cyclists. (3) Learn more here.

• In contrast, a very recent study reported that 8 weeks of high-intensity torque training — including 30 s sprints and VO₂max intervals performed at 50–70 rpm, twice per week — improved aerobic physiological parameters more than the same training performed at freely chosen cadence (>80 rpm) in young female cyclists. (4)

  Learn more here.

On the other hand, heavy gym strength training has repeatedly been shown to improve cycling performance (5). One possible hypothesis is that torque training may enhance cycling performance only when exercise intensity is high enough to stimulate specific adaptations that are not elicited by lower-intensity force production.

A study directly comparing high-intensity versus medium-intensity torque training has just been published (May 2026) in the Scandinavian Journal of Medicine & Science in Sports by de Pablos and Colleagues (Universidad Europea de Madrid, Spain). (5)

This study may help further clarify whether exercise intensity is a key factor regulating the adaptations induced by torque training.

Have a good read! 🙂

WHAT DID THEY DO?

For 10 weeks, 46 well-trained male cyclists (mean VO₂max: 63 mL·kg⁻¹·min⁻¹; range: 56–78) were divided into three groups. All groups completed a similar overall training load in terms of volume and time spent in training zones. The only difference between groups was the type of torque training performed.

HIGH-INTENSITY TORQUE GROUP (HTRQ)

Participants performed two weekly high-intensity torque training sessions consisting of:

• 5 × 7 stationary start maximal voluntary pedal cycles (all-out efforts)

• uphill on a 6% gradient, using a large gear

• cyclists remained seated throughout the effort

• 4 min recovery between sprints

• Average cadence was ~40 rpm, resulting in sprint durations of approximately 10 s. This protocol corresponded to ~70% of maximal dynamic force production during each pedal cycle.

MEDIUM-INTENSITY TORQUE GROUP (MTRQ)

Participants performed two weekly medium-intensity torque training sessions consisting of:

• 5 × 4 min intervals

• Cadence fixed at 50 rpm

• Intensity at ~85–90% FTP

• 2 min passive recovery between intervals

• This protocol elicited force production corresponding to ~35% of maximal dynamic force.

CONTROL GROUP (CON)

The control group followed the same overall endurance training program but did not perform any torque training.

WHAT DID THEY FIND?

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This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

You ride outdoors, spending many hours in the sun. It is natural to assume your vitamin D is fine, but for many cyclists it may not be. The combination of early-morning rides, sunscreen, and the physics of UV radiation means that many riders who consider themselves “outdoor athletes” might be producing far less vitamin D from sun exposure than they think.

1. What is Vitamin D?

Unlike true vitamins, which must be obtained through food because the body cannot make them, vitamin D is synthesised in the skin when exposed to ultraviolet B (UVB) radiation in sunlight. Its molecular structure and downstream effects make it more accurately a hormone than a vitamin, acting through a receptor (the vitamin D receptor, or VDR) found in virtually every tissue in the body, including skeletal muscle, bone, the immune system, the cardiovascular system, and the kidneys.

Vitamin D exists in two dietary forms: D3 (cholecalciferol, from animal sources and produced in the skin) and D2 (ergocalciferol, from plant and fungal sources). Both are biologically inactive until converted. The first step occurs in the liver, producing 25-hydroxyvitamin D — 25(OH)D — the main circulating storage form and standard blood-test marker. A second activation step in the kidney yields the biologically active hormone 1,25-dihydroxyvitamin D (calcitriol), which binds to VDR and drives downstream effects. Because 25(OH)D has a half-life of about 2–3 weeks and reflects both sun exposure and dietary intake, it is the accepted measure of vitamin D status.

But D3 and D2 are not equivalent. D3 raises 25(OH)D concentrations roughly 10x more than D2,³ and sun exposure produces only D3. This distinction matters when choosing a supplement.

2. Why Does Vitamin D Matter For Cyclists?

1. The VDR is expressed throughout skeletal muscle, which is why vitamin D status has a direct impact on muscle physiology relevant to cycling. Active vitamin D promotes protein synthesis, supports muscle remodeling, and has particular effects on type II muscle fibres, which are the fast-twitch fibres responsible for sprint power and explosive efforts. Deficiency leads to atrophy of these fibres, reduced contraction velocity, and decreases in strength and power.⁹

2. Beyond muscle, vitamin D maintains bone mineral density through calcium and phosphate regulation. When vitamin D levels are low, there is an increase in bone destruction to meet the body’s calcium requirements. ¹⁰ This can increase the risk of bone injuries such as stress fractures. In a study of adolescent athletes, bone injuries were significantly more common in those with lower vitamin D levels, and injured athletes had meaningfully lower 25(OH)D concentrations than their uninjured counterparts (26 vs 30 ng/mL).¹⁰

3. Immune function is another major area of importance. VDRs are expressed throughout the immune system, and vitamin D has both antimicrobial and anti-inflammatory effects. Athletes with lower vitamin D levels show higher rates of upper respiratory infections, particularly during heavy training blocks, which can be a real concern during base-training winters when volume is high and sun exposure is minimal.⁹

3. Sunshine

Sun exposure is the primary source of vitamin D for most people, accounting for 80–90% of the body’s 25(OH)D under normal conditions.³ But “sun exposure” is nuanced. The UVB radiation responsible for vitamin D synthesis varies dramatically with latitude, season, time of day, skin coverage, and skin pigmentation, and many of these factors work against cyclists in ways that are easy to miss (Figure 1).

Figure 1. Sun exposure required for vitamin D synthesis varies substantially with UV index, skin tone, latitude, and season. (Left) Estimated minutes of sun exposure needed to synthesize ~1000 IU of vitamin D3, shown for three broad skin tone groups and a range of UV index values. Estimates assume ~25% body surface area exposed (arms and legs) under clear-sky conditions. (Right) Estimated clear-sky UV index across the day for four latitude bands in summer (June) and winter (December) in the Northern Hemisphere. In both panels, the shaded region under UV index 2 indicates the approximate threshold below which UV-B intensity is typically insufficient for meaningful synthesis. All values are approximate and will vary with cloud cover, altitude, surface reflection, and individual factors including age and sunscreen use.

3.1 UV index and the threshold for synthesis

Vitamin D synthesis requires UVB radiation in the 290–315 nm range. This is only available in sufficient quantity when the UV index (UVI) is at least 2, roughly corresponding to the sun being more than 30–45° above the horizon. Below that angle, the atmosphere absorbs most of the relevant UVB before it reaches the skin, and vitamin D synthesis is negligible regardless of how long you are outside.⁴

The exact window for meaningful UVB depends on latitude and season, but for riders in northern cities in summer it is generally limited to roughly 10 AM to 2 PM, but under typical cloud cover conditions this window could be shorter. Before 9 AM or after 3 PM, the UVI is typically too low for meaningful synthesis. In winter at higher latitudes, the window closes entirely.

3.2 Latitude and the Vitamin D Winter

At latitudes greater than approximately 40 degrees north or south, which includes most of the northern United States, Canada, the United Kingdom, northern Europe, New Zealand, and southern Australia, there is a period each year when the UVI does not rise above 2 even at midday.⁴ This has been called the “vitamin D winter,” and for riders in these regions it typically spans several months: roughly November through February in the UK (53°N), and a shorter but still real window in cities like Chicago (42°N) or Auckland (37°S).

Research on professional athletes in the UK found that 62% showed inadequate vitamin D concentrations (below 50 nmol/L) during the winter months (athletes who were training outdoors regularly were included in this cohort).² The global picture is similar: a 2025 meta-analysis of data from over 2.3 million people across 102 countries found that 47% of healthy adults worldwide had 25(OH)D below 50 nmol/L.¹

3.3 Early Morning Rides

Many riders train before work, typically between 5 and 8 AM. At that time of day, even in midsummer at relatively low latitudes, the UV index is near zero. The sun is too low in the sky for significant UVB to penetrate the atmosphere. A cyclist who rides three hours before 8 AM does not produce meaningful vitamin D from that exposure.

The result can be paradoxical: a cyclist riding outside15 hours per week, all of it before 8 AM, may be generating less vitamin D than a person who walks their dog briefly at noon. The sense of being “outside a lot” does not translate into vitamin D if the UV timing is wrong. Cycling kit introduces additional complications, as jerseys, arm warmers, bibs, and gloves reduce skin surface area significantly compared to someone outdoors in just shorts and a T-shirt, further limiting synthesis even on rides where UV conditions would otherwise be adequate.

4. What The Research Shows

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Traditionally, endurance performance has been explained by three key physiological factors:

1. VO2max: the maximal rate of oxygen consumption, reflecting the power of the aerobic engine

2. Thresholds: the percentage of VO2max at which a metabolic steady state is delayed (1st threshold) or can’t be attained (2nd threshold)

3. Gross Efficiency: how effectively metabolic energy is converted into mechanical power (watts)

More recently, however, a fourth dimension has been proposed: Durability.

Durability refers to the ability to minimize the decline in physiological parameters and performance during prolonged exercise. It has also been described as fatigue resistance or fatigue resilience.

How often have we heard commentators, coaches, and sports directors say something like this? That’s exactly what durability captures.

Across the web—and even in scientific conferences—it is often suggested that durability is closely tied to aerobic fitness. The idea is simple: if an athlete produces higher power over 20 or 60 minutes, or has a higher FTP, CP, or threshold, then they must also be more durable.

But is that really the case?

Is durability truly linked to aerobic characteristics? In other words, does having a higher VO2max, FTP, CP, or thresholds necessarily mean imply superior durability?

In this KIW Research Note, we’ll examine all (!) laboratory-based studies—where measurements are highly standardized and accurate—published on this topic to explore the relationship between these variables and answer this question.

Enjoy the read! :)

Durability and Aerobic Characteristics: 8 Studies in Total

Below is a complete overview of the studies that have investigated whether durability and aerobic characteristics are related.

In total, 8 studies have been performed. This alone highlights how recent durability is as a topic in sport science: 7 out of 8 studies have been published in the last four years, and 5 out of 8 in just the last two years!

Below is an overview of the studies, including participants and how aerobic characteristics and durability were measured. If you’d prefer to skip the methodological details and jump straight to the big picture, you can move to the results section

Studies Overview

1. Passfield et al. (1), 2000
   Investigated 10 trained amateur cyclists:

   • Durability: decline in 5-min maximal power after a fatiguing protocol

   • Aerobic characteristics: VO2max and 2nd lactate threshold (measured in a rested state)

2. Spragg et al. (2), 2022
   Investigated 10 professional road cyclists:

   • Durability: decline in Critical Power after a fatiguing protocol

   • Aerobic characteristics: VO2max, 1st and 2nd threshold, gross efficiency (measured in a rested state)

3. Stevenson et al. (3), 2022
   Investigated 14 trained amateur cyclists:

   • Durability: decline in power at 1st threshold after a fatiguing protocol

   • Aerobic characteristics: VO2max (measured in a rested state)

4. Valenzuela et al. (4), 2024
   Investigated 12 professional road cyclists:

   • Durability: decline in 20-min maximal power after a fatiguing protocol

   • Aerobic characteristics: VO2max, 2nd ventilatory threshold, and FTP (measured in a rested state)

5. Hamilton et al. (5), 2024
   Investigated 13 trained amateur cyclists:

   • Durability: decline in 5-min power and power at 1st threshold after a fatiguing protocol

   • Aerobic characteristics: enzymatic aerobic profile of the vastus lateralis

6. Ørtenblad et al. (6), 2024
   Investigated 12 continental-level cyclists:

   • Durability: decline in 6-min power after a fatiguing protocol

   • Aerobic characteristics: VO2max and efficiency (measured in a rested state)

7. Gallo et al. (7), 2024
   Investigated 12 trained amateur cyclists:

   • Durability: time to a 5% reduction in power at 1st threshold during a fatiguing protocol

   • Aerobic characteristics: VO2max, 1st and 2nd thresholds, efficiency (measured in a rested state).

8. Barsumyan et al. (8), 2025
   Investigated 20 trained amateur cyclists:

   • Durability: decline in 5- and 20-min power after a fatiguing protocol

   • Aerobic characteristics: VO2max (measured in a rested state)

The Results

Read more

One of the most compelling questions in sport performance science is how to identify the physiological principles that truly drive training adaptations—and, crucially, how to translate them into effective training workouts/plans.

In this context, in a previous KIW Research Note we highlighted a key concept: to maximize aerobic adaptations from high-intensity training (HIT, i.e., above the 2nd threshold), athletes should aim to accumulate as much time as possible at a high fraction of VO₂max (maximal oxygen consumption). Building on this principle, some interval HIT formats have been identified to better target this goal:

• Fast-start long intervals (Learn more here)

• Short intermittent intervals (Learn more here)

• Pre-loaded short intermittent intervals (Learn more here)

• Decreasing-length intervals (Learn more here)

However, this raises an important question:

Is accumulating more time at a high fraction of VO₂max a universal principle for optimizing aerobic adaptations, or is it specific to high-intensity training?

More specifically, could the same principle apply also to medium-intensity training (MIT), performed between the first and second thresholds? In other words, does spending more time at a relatively high fraction of VO₂max optimize aerobic adaptations when exercising at zone 3 in a 5/7 zones model)?

An exploratory analysis conducted by Professor Bent Rønnestad and Colleagues (University of Inland Norway) published in the European Journal of Sport Science in November 2025, tried to address this question. (1)

If we can clearly identify the physiological principles/factors that drive adaptations at each different training intensities, we could design workouts more effectively for each zone.

WHAT DID THEY DO?

• A total of 22 well-trained cyclists—ranging from high-level amateurs to professionals—were recruited for the study (VO₂max ≈ 70 mL·kg⁻¹·min⁻¹; age ≈ 19 years).

• All participants completed both a Medium-Intensity Training (MIT) block and a High-Intensity Training (HIT) block, separated by a two-month washout period.

• The MIT block consisted of six sessions performed over seven days, structured as follows:

  • 5–7 intervals of 10–14 minutes, with 2–4 minutes of recovery between efforts

  • Rating of perceived exertion (RPE): 14–15 on the Borg 6–20 scale

  • Average heart rate: 86 ± 4% of maximum heart rate

  • Blood lactate at the end of intervals: 2.9 ± 0.8 mmol·L⁻¹

• The HIT block included five short intermittent sessions completed over six days, structured as follows:

  • 5 × 8.75-minute intervals alternating 30 seconds “on” at ~118% of 40-minute maximal sustainable power and 15 seconds “off” at ~60%, with 3 minutes of recovery between intervals

  • RPE: 16–18 on the Borg 6–20 scale

  • Average heart rate: 90 ± 3% of maximum heart rate

  • Blood lactate at the end of intervals: 7.5 ± 1.5 mmol·L⁻¹

• During the second and final training session of each block, oxygen uptake (V̇O₂) was continuously measured using a laboratory metabolic cart. The aim was to determine whether the VO₂ response during MIT and HIT sessions could explain inter-individual differences in aerobic adaptations.

• For both training blocks, physiological and performance assessments were conducted two days before the intervention and again after six days of active recovery following its completion.

WHAT DID THEY FIND?

Read more

This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

Caffeine is the most thoroughly researched ergogenic aid in sports nutrition, and its benefits for cycling performance are not in dispute. What is less clear — or at least underappreciated — is how to use it well. Dose matters more than most cyclists realise, timing depends on the form you choose, and individual response varies enough that a single generic protocol won’t work the same for everyone. Since the ergogenic effects of caffeine are extremely well established, this article will focus on context, and how to best make it work for you.

1. What Is Caffeine?

Caffeine is a methylxanthine compound found naturally in coffee beans, tea leaves, cocoa, guarana, and kola nuts. It is available in a wide range of supplemental forms — capsules, caffeinated gum, gels, and energy drinks — as well as in coffee and tea. After ingestion, caffeine is almost completely absorbed from the gastrointestinal tract, with peak blood concentrations reached within 40–80 minutes.⁶ Its half-life (the time for half the dose to be cleared from the body) averages around five hours, but this varies substantially between individuals: as little as 1.5 hours in fast metabolisers, and as long as 9.5 hours in slow ones.⁶ This very large range has practical consequences, which we will look at in more detail.

2. Why Does It Matter For Cyclists?

Caffeine improves cycling performance across a range of intensities and event durations: It reduces perceived effort during sustained aerobic work, improves neuromuscular power for sprint and high-intensity efforts, and helps maintain decision-making and reaction time during long races where you face both cognitive and physical fatigue. Recent research has also highlighted a potential role in durability, helping maintain power output late in a long event.⁵

The primary mechanism is adenosine antagonism. During prolonged exercise, adenosine (a byproduct of cellular energy turnover) accumulates in the brain and promotes fatigue and sleepiness by binding to adenosine receptors. Caffeine competes for those same receptors without activating them, blunting the fatigue signal. Adenosine doesn’t affect the muscles directly, but it essentially convinces the brain the effort is harder than it is. This reduces the brain’s willingness to keep sending the signal to push.

At doses below 3 mg/kg, this central nervous system (CNS) effect appears to account for the full ergogenic benefit, as there are no measurable changes in peripheral muscle physiology at low doses.¹ At higher doses, some peripheral effects on muscle contractility may also contribute, though the CNS mechanism remains primary.

Caffeine is metabolised primarily by the liver enzyme CYP1A2, which varies substantially in activity between individuals and is determined by genetics. This is one of the main reasons caffeine’s ergogenic effects are not uniform across athletes.

3. How Much?

The most consistently ergogenic dose range for time trial performance is 3–6 mg/kg body mass.³ For a 70 kg rider, that is 210–420 mg — roughly two to four standard espresso shots, or one to two caffeine capsules depending on product dose. Below 3 mg/kg, effects on time trial performance are less reliable, though low doses (~1–2 mg/kg) remain effective for reducing perceived exertion and maintaining alertness during long rides.¹ Above 6 mg/kg, no additional performance benefit has been demonstrated, and the likelihood of side effects (e.g., GI distress, jitteriness, anxiety, sleep disruption) increases substantially. For a criterium or hard group ride lasting under 90 minutes, 3 mg/kg is a reasonable starting point and often sufficient. You should also consider the time of day when determining your dose, as large doses late in the day can significantly impact your sleep.⁷

4. Timing

Read more

Hi there! 👋

We’ve just launched the KIW Web App, designed to help you compare a rider’s power outputs across different durations against normative data from professional male road cyclists.

Inside the app, you’ll find simple instructions to guide you through its features and get started quickly.

With this tool, you can identify the effort durations where a rider is most likely to be competitive in road racing. You can also save and organize data over time, build your own dataset with multiple riders, and easily compare their performance profiles.

Please find below the link and password required to access the web app!

Read more

In a previous KIW Research Note, we saw the “magic numbers” (W and W/kg) required to compete—and win—in professional men’s road cycling.

Those benchmarks were based on data from 2013-2021. But cycling is continuously evolving. The level is rising. Advances in sport science, combined with greater financial investment in the sport, are pushing performance to new heights.

At the same time, the post-COVID era has accelerated another clear trend: riders are getting good—very good—much earlier. Names like Isaac Del Toro, Giulio Pellizzari, Juan Ayuso, Albert Whiten Philipsen and Paul Seixas are not exceptions anymore. They are part of a new norm: U23 riders already capable of competing—and winning—at the highest level.

So it can be interesting to know:

What are the power numbers of world-class U23 riders in 2026?

New data published in April 2026 (collected during the 2025 season) by Manuel Mateo-March and colleagues (Miguel Hernández University, Elche, Spain) on Scandinavian Journal of Medicine & Science in Sports answered this question.

They will show you how fast the bar is moving—and what it really takes for a young rider to make the jump to the highest level of the WorldTour.

WHAT DID THEY DO?

Read more

Power/velocity and heart rate are the most used markers to monitor exercise intensity in endurance sports. You perform a test, you calculate power and/or heart rate at 1st and/or 2nd threshold, and then you calculate your intensity zones.

However, a caveat when using power or heart rate to prescribe training intensity or analysing race efforts is that it has been observed that these variables at thresholds are not stable during prolonged exercise. In other words, in addition to normal day-to-day variability, both power and heart rate at VT1 and LT1 can change over time during long sessions. Specifically, a recent study (2022) led by Ed Maunder (Auckland University of Technology) showed that, in trained amateur cyclists, after 2.5 hours of Zone 2 riding without carbohydrate intake. on average:

• power output at VT1 decreases by ~10%

• heart rate at VT1 increases by ~6/7%

Moreover, the magnitude of these drifts varied considerably between individuals. For example, reductions in power at VT1 ranged from ~5% to ~22% in different athletes (1). Even if a follow-up study showed that carbohydrate ingestion can attenuate these changes, they are not completely eliminated (2).

So what?

The practical consequence is that if you cap your zones using power or heart rate at first threshold values measured in a fresh state, you may drift out of zone as the session progresses.

In this context, Maunder’s research group revisited their 2022 dataset in 2024, expanding the analysis to include ventilatory parameters—tidal volume, breathing frequency, and ventilation rate—measured with a laboratory metabolic cart. The updated findings were published in the European Journal of Applied Physiology (3).

Are any ventilatory parameters at exercise thresholds stable during prolonged exercise, and so potentially more reliable than power output or heart rate for monitoring intensity over long sessions?

If so, wearable devices capable of accurately measuring or estimating these parameters could offer a valuable alternative for tracking exercise intensity.

WHAT DID THEY DO?

Read more

This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

New Zealand blackcurrant (NZBC) extract has been studied in the context of endurance performance for the past decade. The interest comes from its unusually high content of plant pigments called anthocyanins — the same class of compounds that give blueberries and cherries their colour, and that have well-established effects on blood vessel function and metabolism. What makes NZBC stand out among other anthocyanin sources is the particular type it contains, which is among the most potent for influencing how the body moves blood and burns fuel during exercise.

1. What is New Zealand Blackcurrant Extract?

Blackcurrant is a fruit with an extremely high anthocyanin content, around 590 mg per 100 g of the fresh berry. Anthocyanins are polyphenolic pigments responsible for the fruit’s deep colour, and NZBC extract has attracted attention because the New Zealand cultivar contains among the highest concentrations of a specific type of anthocyanins (delphinidin is the dominant anthocyanin in blackcurrant) of any commercially grown variety [1].

The supplement used in essentially all of the published cycling research is CurraNZ, although several other brands are available. A 300 mg capsule provides 105 mg of anthocyanins; the standard research protocol uses two capsules daily, delivering 600 mg of extract and 210 mg of anthocyanins.

The physiological effects are thought to be mediated primarily by metabolites of anthocyanins, which peak approximately 60–120 minutes after ingestion [2]. This has direct implications for timing, discussed in the practical application section below.

2. Why is NZBC Relevant for Cyclists?

The proposed mechanisms overlap well with the demands of cycling. NZBC anthocyanins increase nitric oxide availability by upregulating endothelial nitric oxide synthase, which vasodilates blood vessels and improves tissue perfusion [3]. Greater blood flow means more oxygen delivered to working muscle and faster metabolite clearance, which can be meaningful during all efforts longer than 30 sec where peripheral blood flow can become limiting [14]. Separately, NZBC consistently shifts substrate oxidation toward fat during low/moderate-intensity exercise (zone 2 in a 5/7 zones model), which in theory spares muscle glycogen and so improves durability. A third effect is a reduction in blood pressure in the hours after exercise. This is less directly performance-relevant but may support recovery between sessions or between stages in multi-day racing.

3. Does NZBC Improve Performance?

Read more

You’ve probably come across the idea that high training volume is pivotal to optimize endurance performance —and rightly so. Both scientific evidence and collective field experience consistently show that accumulating a large volume of training is one of the key drivers of endurance performance over the medium to long term, regardless of the discipline—be it running, cycling, swimming, skiing, or rowing.

But this raises an important question:

What does “high volume” actually mean?

Is it the same across different endurance sports?

For example, does 15 hours per week of training carry the same physiological weight in running as it does in cycling?

At first glance, endurance sports may seem comparable: they all involve cyclic movements repeated over prolonged durations. However, each discipline has its own biomechanical and physiological characteristics—such as mechanical load, muscle recruitment patterns, and impact forces—that can lead to markedly different internal responses and so load/stress.

This means that “high volume” may not be a universal concept, but rather a sport-specific one. The same number of training hours could impose very different levels of stress depending on the endurance discipline considered.

In this context, comparing running and cycling could be particularly interesting—especially in terms of muscle damage and inflammatory response when the training volume (in hours) is matched.

This question is highly relevant for:

• triathletes

• athletes using one discipline as cross-training

So, what happens when we compare the same number of hours of running and cycling? Do they induce the same degree of muscle damage and inflammatory response?

A study published by Nieman and Colleagues (Appalachian State University, USA) in 2013 on Brain, behaviour and immunity tried to answer this question. (1)

WHAT DID THEY DO?

• 13 well-trained runners and 22 well-trained cyclists (age 35, VO2max 70) were recruited.

• For 3 days in a row, they ran on treadmills (the runners) or cycled on their own bicycles on an indoor trainer (the cyclists) for 2.5-h at 70% of VO2max, which corresponds to high zone 2 or low zone 3 in a 5/7 zones model.

• Using blood samples taken the morning after the third training day, muscle damage and systemic inflammatory response and was compared between running vs cycling.

WHAT DID THEY FIND?

Read more

This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

Few topics in cycling nutrition generate more confusion than electrolytes. You’ve probably been told that you’re constantly losing sodium, potassium, and magnesium through sweat and need to aggressively replace them — or risk cramps, bonking, and collapsed performance.

Electrolytes are genuinely important for exercise performance. But the question of when and how much to supplement is more nuanced than often suggested. For many cyclists, the default answer is simpler than expected: eat well and drink when thirsty. This article will provide context around electrolytes, so you can make choices that are right for you.

1.WHAT ARE ELECTROLYTES?

Electrolytes are minerals that carry an electrical charge when dissolved in body fluids. The three most relevant to cyclists are sodium, potassium, and magnesium.

• Sodium is the primary electrolyte in extracellular fluid — the plasma, interstitial fluid, and everything outside your cells. It’s the main driver of plasma (blood) volume, blood pressure regulation, and nerve impulse transmission. Plasma sodium concentration is tightly defended at approximately 135–145 mmol/L, and the body has powerful mechanisms — kidney conservation, thirst, hormonal signaling — to keep it there.

• Potassium is the mirror image: primarily intracellular, where it maintains cell membrane excitability and is essential for muscle contraction and cardiac rhythm.

• Magnesium is a cofactor in over 300 enzymatic reactions, including energy production, muscle relaxation, and protein synthesis.

2. SODIUM

Unlike potassium and magnesium, whose body stores are large enough that sweat losses rarely deplete them meaningfully during exercise, sodium balance is closely tied to fluid intake and loss. Endurance athletes can sweat at rates far exceeding the general population, and it is this link between sweating and sodium — rather than any absolute risk of sodium depletion — that makes hydration management particularly relevant for cyclists. The sections below explain how that link works and when it actually matters in practice.

2.1 What Happens When You Sweat

Most cyclists assume that sweating depletes sodium and that blood sodium drops during exercise. The opposite is true, because we care about the concentration of sodium (more than the absolute amount). Sweat is hypotonic — it has a lower sodium concentration than blood. Average sweat sodium concentration across athletes is approximately 36–42 mmol/L,^[2,3] while plasma sodium sits at ~140 mmol/L. You lose proportionally more water than sodium in every drop of sweat. The consequence of this is straightforward, albeit counterintuitive: when you sweat, blood sodium concentration actually rises, not falls. A body mass loss of ~2% in a 70 kg cyclist — about 1.4 kg of sweat — increases plasma osmolality by approximately 6 mmol/kg.^[6] This rise triggers thirst and renal water conservation, which are the body’s primary defences against dehydration. The system is designed to protect sodium concentration within a constant range

This doesn’t mean sodium ingestion is irrelevant during exercise. Sodium in fluids serves several functions: it improves intestinal water absorption, stimulates the thirst drive, and helps retain ingested fluid rather than losing it through urine and (most importantly) can prevent Exercise-Associated Hyponatremia (EAH) which is a dangerous drop in plasma sodium concentration caused by drinking more fluid than you lose.^[1] Sodium also facilitates carbohydrate absorption: the sodium-glucose cotransporter (SGLT1) in the intestinal wall co-transports sodium and glucose together, meaning the sodium in a sports drink doesn’t just aid water uptake — it actively accelerates absorption of the carbohydrates the drink contains. Together, this means the reason to include sodium in a sports drink is to help you absorb and retain water and absorb carbohydrates while maintaining sodium blood concentration, not because your absolute amount of blood sodium is dropping.

2.2 How Much Sodium and Water Do You Actually Lose with Sweating?

Read more

Hi there! 👋

As highlighted in our latest KIW Research Note, we’ve launched a new web app designed to calculate the First Lactate Threshold (LT1) from an incremental step test with blood sampling using a combination of scientific evidence and practical guidelines. The app integrates both the Baseline +0.5 mmol/L approach and the Log-Log Method.

As of 2026, these metric represent the most effective balance between accuracy and real-world applicability for identifying the First Exercise Threshold—which represents the upper boundary of Zone 2 (low-to-moderate intensity) Training. 🚴‍♂️📊

To dive deeper into these methods, refer to Section 4 at this link and the instructions provided within the web app.

Please find below the link and password required to access the web app!

Read more

1. ZONE 2 TRAINING: BELOW THE FIRST THRESHOLD

In recent years, “Zone 2 Training” has been received incredible attention across social media. podcasts, Youtube videos.

Before discussing the potential benefits of Zone 2 training, it is essential to first understand what Zone 2 actually is. Across the web, many different definitions of Zone 2 are used, which can make it difficult to clearly understand what people are referring to.

When using definitions, it is generally better to rely on scientific definitions, which are essentially agreements among experts designed to ensure that everyone is referring to the same concept.

In this scenario, recently (2025) a 14 ‘experts’ panel of applied sport scientists and professional coaches led by Sebastian Sitko (University of Zaragoza, Spain) and Aitor Viribay (University of León) published a viewpoint which aimed to define zone 2 training. Here below the consensus definition reached:

An important note: the expression “just below” can be somewhat tricky. In the experts’ consensus, the upper boundary of the range was defined (first threshold), but no clear lower boundary was specified. In other words, it has not been indicated how far below the upper limit the zone 2 can extend. From a practical perspective, my suggestion is to set the lower boundary at what you consider the first training intensity above active recovery, extending up to the first threshold.

Anyway, you can now understand that the term Zone 2 training refers to Zone 2 within a 5- (or 7-) zone model, as shown in the upper part of the image above.

Let’s take it a step further.

As mentioned above, the “experts” define Zone 2 training as exercise performed just below the first lactate or ventilatory threshold. They go on to explain that the purpose of this demarcation is to elicit a steady-state physiological response, with minimal metabolic disturbance compared to baseline exercise levels. (1) This corresponds exactly to the scientific low/moderate intensity domain—i.e., below the First Exercise Threshold.

So, we can say that:

• Zone 2 training falls within the scientific low-moderate intensity domain, characterised by a steady-state physiological response and minimal metabolic perturbation relative to baseline exercise levels.

• In practical terms, this corresponds to exercising below the First Exercise Threshold.

• The first ventilatory (VT1) and lactate threshold (LT1) are the markers commonly used to estimate this 1st threshold to target the low-to-moderate intensity domain during Zone 2 training.

In this KIW Research Note, we take a closer look at VT1 and LT1 and other markers to identify the 1st exercise threshold and whether they can reliably be used to guide proper Zone 2 training. We’ll follow a similar approach to a the previous KIW Research Note, where we defined Critical Power (CP) as the gold standard for defining the 2nd exercise threshold, ‘aka’ Maximum Metabolic Steady State.

What are the most reliable markers and methods to accurately estimate the 1st exercise threshold and effectively regulate intensity during Zone 2 training?

Enjoy the read! :)

2. METABOLIC RESPONSE AND FATIGUE BELOW THE FIRST THRESHOLD (ZONE 2 TRAINING)

As anticipated above, scientifically, the first threshold delineate the boundary between the low/moderate and the medium/heavy intensity domains, that correspond to two well-distinct physiological response (2,3):

SCIENTIFIC ZONE 1 - THE LOW/MODERATE INTENSITY DOMAIN (‘ZONE 2 TRAINING’)

• Intensity: Below the first threshold.

• Metabolic response: oxygen consumption (VO2) and blood lactate reach steady‐state values rapidly (within 2-3 minutes) and there is no relevant perturbation of metabolites (H+-hydrogen ions, Pi - inorganic phosphate) or ions (K+ - potassium ions) at muscular level.

• Determinants of Fatigue: when exercising (for hours) at this intensity, fatigue is due to depletion of muscle glycogen, central nervous system fatigue, and muscle damage.

  From these features, you can easily understand that the defining characteristics of zone 2 training (below the 1st threshold) is the ability to sustain exercise for prolonged durations (from 2 to 6+ hours) without reaching exhaustion. As discussed later in this KIW Research Note, this property makes Zone 2 particularly effective for accumulating large training volumes, which is its key distinguishing characteristics.

  *Note that Zone 2 training is in the 1st scientific zone/domain.

• SCIENTIFIC ZONE 2 - THE MEDIUM/HEAVY INTENSITY DOMAIN (ZONE 3-LOW ZONE 4)

  • Intensity: between the first threshold and the second threshold (Maximum Metabolic Steady State, MMSS, the maximum exercise intensity at which a steady state in oxygen consumption and muscle metabolites is still achievable).

  • Metabolic response: Steady-state values for V̇O₂, blood lactate, and other metabolites are delayed but still achieved, typically within 10–20 minutes. This delay is due to the V̇O₂ slow component—a gradual increase in oxygen consumption at the onset of exercise required to meet the higher metabolic demand compared to the low/moderate intensity domain.

  • Determinants of fatigue: A combination of metabolic and ionic disturbances within the muscle (H⁺, K⁺, Pi accumulation) and muscle glycogen depletion. As a result, the sustainable exercise duration is reduced compared to the low/moderate intensity domain.

    *Note that Scientific Zone 2 does not correspond to the commonly referenced “Zone 2 training”; rather, it aligns with Zone 3 in a 5–7 zone model.

So,

• the First Exercise Threshold marks the highest metabolic rate not associated with disruption to physiological homeostasis compared to baseline exercise levels, and separate the low/moderate and medium/heavy intensity domains.

• On the other hand. the Second Exercise Threshold represents the maximum metabolic steady state, which is the boundary between the medium/heavy and high/severe intensity domain. For completeness, a description of the high/severe intensity domain is provided below.

• SCIENTIFIC ZONE 3 - THE HIGH/SEVERE INTENSITY DOMAIN

  • Intensity: Above the Maximum Metabolic Steady State.

  • Metabolic response: at this exercise intensity, even when performing a constant power bout, a steady state physiological can’t be reached with oxygen consumption and blood lactate continuing to rise until VO2max and the limit of tolerance are then shortly reached, and power output can’t be maintained anymore. This occurs upon reaching a critical intramuscular metabolic and ionic environment: reduced phosphocreatine availability, decreased potassium concentration, and increased hydrogen ions.

  • Determinants of fatigue: the critical intramuscular metabolic and ionic environment described above (linked to phosphocreatine, potassium and hydrogen ions).

In 2026, the gold standard to determine the 2nd threshold is the Critical Power (learn more here).

2. FIRST THRESHOLD: HOW IT SHOULD BE MEASURED

Let’s go back to the main focus of this KIW Research Note:

How can we determine the First Exercise Threshold to define Zone 2 (low/moderate intensity Training?

Unlike the 2nd exercise threshold—where scientific field-based methods such as Critical Power exist—there is currently (as of 2026) no validated method to accurately determine the first threshold using only power or heart rate in a purely field-based test without physiological measurements.

The main methods used to determine the 1st threshold are:

• VT1: the First Ventilatory Threshold

• LT1: the First Lactate Threshold (defined using different methodologies)

• Relative anchors: percentages of Maximum Heart Rate or of the Second Threshold

In the following sections, we will evaluate these metrics to determine which methods provide the most accurate estimates of the first threshold—and, so, the most reliable markers for prescribing Zone 2 training.

3. THE FIRST VENTILATORY THRESHOLD (VT1): ACCURATE BUT IMPRACTICAL

AN IMPORTANT NOTE:

To properly understand the first lactate and the first ventilatory threshold, you should first know they are closely linked. They represent two different methods of detecting the same phenomenon: the first intensity-dependent metabolic perturbation due to the inability of the aerobic metabolism to meet the energy demand. In essence, they capture the same underlying process, but through different measurements and locations—ventilatory thresholds via expired gases, and lactate thresholds via blood markers.

3.1 VT1 Definition

The First Ventilatory Threshold (VT1) is the first rise in Ventilation Rate (V̇E) relative to oxygen consumption recorded during an incremental step test. Please not that ventilation rate is not breathing frequency, but the product between tidal volume (the air exhaled with each breath) and breathing frequency. So, Ventilation Rate represents how much air you expire each minute.

3.2 VT1 Testing

• The Instrument: A metabolic cart is required. This device collects and analyzes expired gases through a mask, allowing measurement of ventilation rate, oxygen consumption and carbon dioxide produced. Laboratory-grade metabolic carts provide the highest level of accuracy, but they are expensive (typically €20,000–30,000) and require a controlled lab setting, including regular calibration and power supply. In contrast, several companies now offer portable gas analysers that are more affordable and can be used in the field. However, both the scientific literature and my experience suggest that - as of 2026- these devices often lack the accuracy and precision needed for a reliable assessment of the first ventilatory threshold. (4)

• The Testing Protocol: An incremental step test. The test should begin at a very low intensity—approximately 70% of the estimated power at 1st exercise threshold—in order to build a gas-exchange profile range wide enough to facilitate then the identification through visual inspection of the data of the V̇E/V̇O₂ breakpoint (which represents VT1, see more below).

  

  After an initial warm-up, workload should be increased in steps of 15–50 W, depending on the athlete’s level, with each stage lasting 3–5 minutes. This duration is important to ensure that a steady state is achieved, meaning that physiological responses at the muscular and blood level are fully reflected in the expired gases.

  The test can be terminated once the respiratory exchange ratio (V̇CO₂/V̇O₂) reaches ~1.0, or when blood lactate (if measured) exceeds ~4.0 mmol/L . This ensures that the second threshold has been surpassed, providing confidence that also VT1 has been recorded. From the data of the test, oxygen consumption at VT1 is identified as the V̇E/V̇O₂ breakpoint, and the corresponding power output at VT1 can be determined by performing a regression analysis between power output and oxygen consumption. (5)
  

3.3 VT1 Physiology

From a muscle cell point of view, with the increasing metabolic demand above the first threshold, the oxidative (aerobic) pathways are unable to fully meet the energy demands of the working muscle and pyruvate is increasingly converted into lactate rather than entering aerobic metabolism in the mitochondria (Krebs Cycle). This shift is accompanied by metabolic disturbances, including a progressive increase of lactate (La-) and hydrogen ions (H⁺) both at muscle and blood level.

In other words, at the first threshold, the process in green here below starts.

From a gas exchange perspective, this phenomenon manifests as follows: up to the first threshold, increases in watt are accompanied by a proportional, linear rise in oxygen consumption (V̇O₂), carbon dioxide production (V̇CO₂), and ventilation (V̇E). Beyond the first threshold, the excess hydrogen ions (H⁺) produced alongside lactate are buffered in the blood by the bicarbonate (HCO₃⁻) system. This buffering process generates an additional source of CO₂ in the bloodstream. As a result, the equilibrium of the following reaction shifts to the right, promoting CO₂ production:

So after the first threshold point CO2 increase disproportionally to VO2 and Watts. Ventilation (V̇E) is regulated by CO2 concentration in the lungs and increase when CO2 goes up in order to minimize excessive CO2 accumulation, So, after the first threshold, V̇E also begins to increase disproportionately to V̇O2 or Watt. This breakpoint in VE/VO2 or VE/Watt relationships is defined as the first ventilatory threshold (VT1) and is typically identified through visual inspection of the data recorded by a metabolic cart by an experienced evaluator during metabolic testing. (6)

Alternatively, the same physiological transition can be detected using the V-slope method, which examines the relationship between V̇CO₂ and V̇O₂. The breakpoint identified with this method is referred to as the gas exchange threshold (GET).

In most cases, VT1 and GET occur at very similar intensities. However, for greater accuracy, it is advisable to consider both methods. When discrepancies arise, VT1 should be preferred to GET, as an isolated increase in V̇CO₂ may also reflect abnormalities in breathing patterns rather than a true metabolic threshold.

Below is an example of VT1 identification from a real-world test. Each circle represents a single breath.

3.4 Is VT1 an Accurate Estimate of the First Threshold? Yes but Impractical

• VT1 as the Gold Standard for the 1st Exercise Threshold

  While it has not been rigorously validated in all contexts (such validation would require assessing metabolic responses just above and below the breakpoint (±5%) and confirming distinct physiological differences consistent with the low/moderate and medium/heavy intensity domains) VT1 is currently considered the gold standard for identifying the 1st exercise threshold. Why? Because expired gas analysis provides a relatively direct reflection of metabolic processes. When an appropriate protocol is used—particularly step durations of 4–5 minutes—there is strong confidence that the measured ventilatory responses accurately represent what is occurring at the muscular and blood level.

• The limited practicality of VT1 measurement

  As of 2026, the main limit of using VT1 for zone 2 training is that it can be accurately measured only using a lab-graded metabolic cart. The use of a metabolic cart is limited by both cost and practicality. Laboratory-grade systems are expensive (typically €20,000–30,000), and individual tests can cost around €150–300. In addition, testing on an indoor trainer or stationary ergometer may underestimate the power output at VT1. Indeed, outdoor power output has been reported to be ~2–9% higher than indoor values, likely due to biomechanical differences such as reduced kinetic energy, limited side-to-side movement, and increased bike stiffness during indoor pedalling.

  Portable gas analyzers allow testing in sport-specific, real-world conditions, which is a clear advantage. However, their accuracy is generally lower than that of laboratory systems. (4) Moreover, even if accuracy would be acceptable, the testing setup itself may influence the results. Wearing a mask and carrying the analyzer unit (typically in a pocket) can alter natural movement patterns and physiological responses. As a result, the measurements obtained in the field may not fully reflect true conditions during normal riding.

4. THE FIRST LACTATE THRESHOLD (LT1): OK ACCURACY AND PRACTICAL

4.1 LT1 Definition and Physiology

The First Lactate Threshold (LT1) represents the lowest exercise intensity at which blood lactate begins to rise above baseline levels. It is the other way to look at the first intensity dependent metabolic perturbation induced by the inability of the muscle aerobic metabolism to fully meet the energy demand. (5) While VT1 capture this at the level of expired gases, LT1 detects it with blood lactate concentration. This inability of oxidative pathways to fully oxidize pyruvate within the mitochondria leads to the production of lactic acid (green pathway in the figure above).

Lactic acid rapidly dissociates into lactate and hydrogen ions (H⁺), which exit the muscle cell and enter the bloodstream. It is important to note that lactate itself does not cause fatigue. Instead, the accumulation of hydrogen ions impair the muscle contraction. So, lactate should be considered a marker of metabolic stress rather than the direct biochemical cause of fatigue. In fact, lactate can be reutilized as an energy substrate by adjacent muscle fibres or other tissues (e.g., heart, liver). In contrast, hydrogen ions interfere with cellular processes involved in energy production. So, you should see lactate as a valuable physiological indicator of metabolic perturbation, rather than the direct cause of fatigue. (7)

4.2 LT1 Testing

To directly identify LT1 , blood lactate concentration ([La⁻]) is measured during a step incremental exercise test, in which work rate is increased at regular intervals (typically 2–10 minutes) until exhaustion. Blood samples are collected at the end of each stage and plotted against the corresponding power output (watts). This results in a curvilinear relationship between blood lactate and work rate, which is then analysed to determine the intensity at which blood lactate begins to rise above baseline levels.

But here is the most important question:

How do we define ‘an increase in blood lactate above baseline levels’?

In other words,

How is LT1 actually determined?

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Chronic ketone supplementation (daily intake over several weeks) has become increasingly widespread in professional road cycling in recent years.

Why?

• Not because a single dose of ketones taken before or during exercise enhances performance—neither in time trials nor in prolonged races (1).

• On the other hand, an interesting study by Poffé and Colleagues (2023) reported that, during a 3-week overload period, daily post-exercise and pre-sleep ketone supplementation help to sustain a higher training load and enhance muscle capillarization (angiogenesis) (2). Muscle capillarization is a key physiological marker for endurance performance, as it has been shown to be strongly positively related to VO2max, exercise thresholds and all-out efforts lasting from 30s to 30 min. (3) A superior muscle capillarization permits faster muscles-blood exchanges such as oxygen delivery and waste products removal (hydrogen ions). It is not by chance that elite athletes have ~3 times more capillaries per muscle fibre compared to untrained individuals. (4)

So, it seems that the benefit of ketone supplementation lies in its chronic use to enhance training adaptations. In other words, if you daily ingest ketones during a certain training cycle, your body will get stronger than just do the same training without supplementing ketones. In fact, ketones seems to act as signalling molecules, triggering pathways that enhance aerobic physiological adaptations to training. (such as muscle angiogenesis)

However, an important limitation of the Poffé study should be highlighted. The study did not directly assess performance outcomes. While increased muscle capillarization is generally associated with improved endurance performance, this remains an assumption. Direct confirmation is needed through studies that measure the actual performance adaptations related to ketone supplementation, not just physiological changes such as capillarization.

In 2024 I attended the Cycling and Science Conference in Firenze, and the presentation hat struck me the most was by Ruben Robberechts (KU Leuven, Belgium). It focused precisely on this topic, showing that chronic ketone supplementation (daily intake over several weeks, post-exercise) can enhance not only physiological adaptations but also endurance performance!

That work has just been published (February 2026) in the The Journal of Physiology.

Does chronic ketone supplementation (daily intake over several weeks) enhance endurance performance?

WHAT DID THEY DO?

• 28 trained amateur cyclist (age ~25 years, VO2max ~55/60) were divided into two different groups: KETONES vs CONTROL.

• Both groups followed the same training program for 8 weeks.

  The authors didn’t report the exact training sessions in detail, but stated that training was matched between groups and consisted of a combination of low-intensity work, high-intensity intervals, and sprint training.

  Participants trained five days per week, without any excessive overload.

  This aspect is particularly interesting, as the Poffé’s study showing enhanced capillarization was conducted during an overload period, rather than under more typical training conditions. So, this study helps determine if ketones can enhance aerobic training adaptations even during normal training cycles.

• The only difference between the two groups was the following:

  • KETONES GROUP: consumed 25 g of a ketone monoester drink immediately post-training sessions and 30 min before bedtime on all training days

  • CONTROL GROUP: at the same time points (post-exercise and pre-sleep), participants consumed a control drink with the same total energy content of ketone drink, consisting of pure medium-chain triglycerides, supplemented with 1 mM bitter sucrose octa-acetate to match also the taste of the ketone drink.

Five minutes after each training session, both groups also consumed a 300 mL recovery shake delivering 64 g of carbohydrates and 30 g of proteins.

WHAT DID THEY FIND?

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In the latest KIW Research Notes we saw that, as of 2026, Critical Power (CP) represent the gold standard for the maximum metabolic stead state (MMSS) and so the 2nd exercise threshold. In other words, it is the metric that best approximates the highest intensity at which a steady state in oxygen consumption and muscle metabolites can still be maintained. So, CP should be preferred over other proxies of the 2nd threshold—such as the second lactate threshold (LT2) or FTP—when defining training intensity zones and planning race pacing strategies. If you would like to learn more about this topic, we suggest this reading.

But is Critical Power on a Road Bike equivalent to that measured on a Time Trial (TT) bike?

A study published by Kordi and Colleagues (English Institute of Sport and British Cycling) in 2018 on European Journal of Sport Science tried to answer this question. (1)

Addressing this question has important practical implications, as it helps determine if CP values obtained on a road bike can also be applied to a TT bike—and vice versa—for training planning and pacing strategies.

WHAT DID THEY DO?

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This KIW Research Note has been written by Dr Jeff Rothschild

Dr Jeff Rothschild is a Registered Dietitian (RD) with a PhD in Exercise Physiology and a Master’s degree in Nutritional Science. His work focuses on endurance performance, carbohydrate metabolism, and the practical application of sports nutrition science to real-world training. His doctoral research examined the periodization of carbohydrate availability for endurance athletes, with a particular focus on pre-training nutrition strategies.

Jeff works with a wide range of athletes, from Olympians and world champions to age-group competitors preparing for their first endurance events, helping them optimize fueling, performance, and long-term health. He is a Research Associate at the Sports Performance Research Institute New Zealand (SPRINZ) and regularly translates current research into practical guidance for athletes and coaches.

You can find Jeff at Jeff@eatsleep.fit

Enjoy the Read! :)

Omega-3 fatty acids have an established reputation in general health, with research linking cardiovascular benefits, reduced inflammation, and improved brain function, but if or how this translates into something meaningful for cyclists is a different question.

Overall, it appears omega-3s are genuinely useful for cyclists, with the strongest evidence around endurance capacity, cardiovascular function, and recovery. But the picture is complicated by the fact that most athletes are not starting from a great place, and the effects of supplementation depend heavily on your baseline levels.

1. WHAT ARE OMEGA-3 FATTY ACIDS?

Omega-3s are a class of polyunsaturated fatty acids. The three most relevant to health and performance are:

• alpha-linolenic acid (ALA)

• eicosapentaenoic acid (EPA),

• docosahexaenoic acid (DHA).

ALA comes primarily from plant sources — flaxseeds, chia seeds, walnuts. EPA and DHA come from marine sources: fatty fish, seafood, and algae (fish accumulate EPA and DHA by eating algae). The distinction matters because the body can convert ALA to EPA and DHA, but the conversion is poor. Only about 5–10% of ALA reaches EPA, and 2–5% reaches DHA.^[1] Plant sources alone are not a reliable pathway to adequate EPA and DHA. EPA and DHA are the biologically active forms that get incorporated into cell membranes throughout the body — including muscle cells, mitochondria, and red blood cells. ALA largely does not.

The table below shows how common food sources compare.

A common question is how much fish you’d need to eat to avoid supplementing altogether. To supply the ~1.4 g EPA+DHA per day needed to move a typical athlete from 4.4% to above 8% Omega 3 index (a way to measure your levels, discussed below), you’d need approximately 4–5 servings of fatty fish per week — roughly double the standard dietary recommendation of two servings per week. Two servings per week of salmon or sardines supplies around 3–4.5 g EPA+DHA total for the week, which narrows the gap but is unlikely to fully close it from a depleted baseline. For most athletes, a combination of regular fish intake and targeted supplementation is probably more practical than relying on either alone.

2. How Omega-3s Work

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