Dan Plews is a successful age group athlete and coach who has staked out his place in triathlon advocating for low carb fueling. But does his success with this strategy mean others should try it? What does the evidence say?

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Table of Contents

• Low carb fueling for triathlon-it’s really time to …

  • References used for the MMB

Low carb fueling for triathlon-it’s really time to move on from this idea

Dan Plews, the Kiwi who has had otherworldly success as an age group triathlete continues to advocate to anyone who will listen for a low-carbohydrate model of nutrition in training and racing. In his mind, if he can do it and have success, so can everyone else. And with the recent publication of a very biased review paper, he feels vindicated. On the Medical Mailbag, we put his claims to the test.

As we have found when we have looked at this before, the reality is, and this is based upon decades of science, just the opposite. The simple truth is that low-carbohydrate fueling is not considered an optimal primary strategy for high-intensity triathlon training or racing when judged against the current body of sports science. While low-carbohydrate or ketogenic approaches can increase fat oxidation, the demands of high-intensity triathlon performance rely heavily on carbohydrate metabolism.

At race intensities near threshold, during repeated surges, climbs, accelerations, and strong finishing efforts, carbohydrate is the preferred fuel because it can generate ATP more rapidly and with greater oxygen efficiency than fat. This matters in triathlon because swim starts, tactical bike segments, hilly terrain, and the final stages of the run often require sustained work above moderate aerobic intensity. When glycogen availability is low, athletes commonly experience reduced power output, impaired ability to change pace, and higher perceived exertion.

Research consistently shows that low-carbohydrate adaptation increases rates of fat burning, sometimes substantially. However, studies in trained endurance athletes have also found that this shift often comes with reduced exercise economy at race pace and diminished performance in high-intensity efforts. Work led by Louise Burke and colleagues has been particularly influential: athletes adapted to low-carbohydrate, high-fat diets improved fat oxidation but did not outperform carbohydrate-supported athletes in race-performance outcomes, and in some cases showed worse economy at higher intensities.

That does not mean low-carbohydrate strategies have no place in triathlon. Some athletes may use selected “train low” sessions—such as occasional easy aerobic workouts with reduced carbohydrate availability—to stimulate metabolic adaptations. Others racing very long events at conservative intensities may benefit from improved fat utilization and reduced dependence on frequent carbohydrate intake. But these are targeted uses, not evidence that full-time low-carbohydrate fueling is superior for hard training or competitive racing.

For most triathletes, the strongest evidence supports periodized carbohydrate availability: using ample carbohydrate before and during key interval sessions, race-specific workouts, and races, while strategically using lower-carbohydrate sessions when appropriate. This approach preserves the ability to train and race at high quality while still developing metabolic flexibility.

In practical terms, if the goal is to maximize performance in Olympic-distance, 70.3, or Ironman racing with meaningful intensity, carbohydrate remains the most evidence-based fuel. Low-carbohydrate fueling can be a tool in specific contexts, but it is not the best default strategy for high-intensity triathlon performance.

References used for the MMB

Low-carb fueling

1. Wilson, P. B. (2026). A Narrative Review of the High-Carbohydrate Fueling Revolution (≥ 100 g/h) in the Professional Peloton. Sports Medicine (Auckland, N.z.), 56(2), 295–313. https://doi.org/10.1007/s40279-025-02372-6 
   
   Narrative review that discusses current carb intake recommendations, current literature, and history of fueling: (Wilson, 2026) - this is the most recent, most scoping 

   1. History of fueling recommendations: 

      1. Bergström and other Swedish researchers circa 1960s measured muscle glycogen levels in athletes and observed that exhaustion occurred when glycogen dropped to very low levels.

      2. This developed into the recommendation circa 1990 of fueling at a rate of 30-60 g/hr. This was formally stated by the American College of Sports Medicine (ACSM) in 2009.

      3. In 2016, given the publication of new literature, the ACSM updated their position: “up to 90 g/h recommended for athletes partaking in prolonged exercise”

   2. Research Comparing High-Carbohydrate Fueling (≥ 100 g/h) with Traditional Carbohydrate Guidelines (30–90 g/h): this specific research is scarce with low sample sizes and offers limited support toward either fueling methodology. Studies have not established a linear relationship between carbohydrate dose and performance - likely, there is a curvilinear relationship with some optimal carbohydrate ingestion dosage, which likely has much variation given 1) individual variation, 2) tendency of an individual towards GI distress, 3) the demands of a particularly activity (swimming vs. running vs. cycling), and 4) the duration of activity (short vs. long vs. multi-day). However, doses seem to hover around the recommended amounts, with one paper that specifically studied a curvilinear relationship suggesting 78 g/h.
      
      

2. Sundberg, C. W., & Fitts, R. H. (2019). Bioenergetic basis of skeletal muscle fatigue. Current Opinion in Physiology, 10, 118–127. https://doi.org/10.1016/j.cophys.2019.05.004
   
   
   
   General notes on TAT vs. central regulation: 

4. Noakes, T. D., Prins, P. J., Buga, A., D’Agostino, D. P., Volek, J. S., & Koutnik, A. P. (2026). Carbohydrate Ingestion on Exercise Metabolism and Physical Performance. Endocrine Reviews, 47(2), 191–243. https://doi.org/10.1210/endrev/bnaf038 

The DP Endocrine Reviews paper: (Noakes et al., 2026). This is a beast of a paper.

1. Evidence 1: TAT is Biologically Implausible and Disproven; 

   1. Identifies a supposed issue with TAT literature: critical, exercise-induced reductions in ATP ought to cause muscle rigor. However, this assumes that ATP levels much reach 0 during exercise for fatigue to occur - however, ATP levels even in fatigued states do not fall to 0 (Sundberg & Fitts, 2019: This paper reports that muscle fatigue is caused not 0 ATP, but by the inability to sustain ATP turnover, which leads to metabolite accumulation that impairs muscle contraction.)

   2. Attempts to propose that TAT is false by presenting a lack of evidence as proof of fallacy: “Fifty-six years after the foundational study (4), the mechanism linking glycogen depletion to contractile failure remains unknown—if real, it should be well established by now.”

2. Evidence 2: The Original Scandinavian Study Linking Muscle Glycogen and Exercise Duration Ignored Key Findings of EIH and High-fat Oxidation in CHO-restricted Individuals

   1. Points out that the landmark Bergström paper’s results focused on glycogen, despite also having marked evidence towards low blood glucose impairing performance. Authors say that this was “overlooked for 56 years” - it was just not the study Bergström conducted, which was one of the first muscle biopsy studies and exceptionally well-positioned to look at muscle glycogen. 

3. Evidence 3: 1930s Scandinavian Studies Showed CHO Ingestion at Exhaustion Reverses EIH and Fatigue, Without Immediately Reversing Muscle Glycogen Depletion or RQ (CHO Oxidation Rates)

   1. Looks at three papers (Boje, 1936; Christensen and Hansen, 1937; Pruett 1970) to support the conclusion that low blood glucose causes exercise termination. Only the Pruett paper additionally examined liver glycogen, which was depleted over exercise and the authors conclude causes low blood glucose that causes exercise termination. 

4. Paper is rife with cherry-picking - this is a narrative review, but these are examples seemingly specifically chosen to set up an argument for central regulation without specifically tackling literature that looks at TAT vs. central regulation. 

5. Rothschild, J. A., Dudley-Rode, H., Carpenter, H., Smith, A. S. M., Plews, D. J., & Maunder, E. (2026). Carbohydrate ingestion during prolonged exercise and net skeletal muscle glycogen utilization: A meta-analysis. Journal of Applied Physiology, 140(1), 76–87. https://doi.org/10.1152/japplphysiol.00861.2025 
   
   Another deep dive into a recent DP paper: (Rothschild et al., 2026)

   1. Methods: this meta-analysis looked at studies (n=31, 48 comparisons) that had a crossover design where muscle glycogen in the vastus lateralis/quadriceps femoris or gastrocnemius was measured via muscle biopsy or MRS in subjects who performed exercise (running or cycling for >20 min) with and without carbohydrate ingestion. 

   2. Results: 

      1. The authors report “a small but statistically significant muscle glycogen-sparing effect of carbohydrate ingestion” with a standardized mean difference of -0.16. Specifically, this means that there was lower glycogen depletion in the muscles of athletes who consumed carbohydrates compared with the control.

         

      2. Subgroup analysis: in running trials, the glycogen sparing effect is significant (SMD: -0.38); however, in cycling trials, the glycogen sparing effect is not significant (SMD: -0.12). The authors note this lack of statistical significance does not necessarily mean that there is no glycogen sparing effect. “These findings suggest that the glycogen-sparing effect of carbohydrate ingestion may be more detectable in running protocols; however, these null findings likely reflect limited statistical power within subgroups, increasing the risk of type II errors, rather than confirming a true absence of moderation.”

   3. Discussion: 

      1. The authors begin: “The primary finding from this meta-analysis is that carbohydrate ingestion during exercise induces a small but statistically significant reduction in net skeletal muscle glycogen utilization.”

      2. They go on, however, to hypothesize about the role of fat oxidation on why their effect size is small, saying that some of the energy from ingested carbs replaces fat use instead of glycogen use, limiting how much glycogen is actually saved. Their reasoning goes something like:

         1. Carbohydrate ingestion shifts fuel use toward blood glucose, reducing reliance on stored fuels (“some of the additional plasma glucose oxidation… reduces the reliance on intramuscular glycogen”)

         2. However, this shift is partly offset by a decrease in fat burning (“the small size of the muscle glycogen-sparing effect… reflects the simultaneous suppression of fatty acid oxidation”)

         3. Because fat oxidation is suppressed, carbs don’t fully replace glycogen use (“the reduction in net muscle glycogen utilization must be smaller than the net increase in plasma glucose oxidation”)

What the low carb folks continue to believe is that utilizing a low carb strategy will spare glycogen by shifting metabolism to ketones and fats thereby preventing the sensation of fatigue. However this comes at significant costs:

The main limitation comes down to energy yield and efficiency:

• Carbohydrate oxidation produces more ATP per unit of oxygen than fat.

• At higher intensities (tempo, threshold, racing efforts), performance depends on this efficiency.

This ties into the concept of exercise intensity vs fuel use:

• Low intensity → fat can meet energy demands

• High intensity → requires carbohydrate