Vitamin B1 in Athletes: Thiamine, the Overlooked Coenzyme Behind Every Training Session
Table of Contents
Key Takeaways: Vitamin B1 in Athletes
- Vitamin B1 in athletes matters because thiamine is involved in carbohydrate metabolism and mitochondrial energy production.
- Intensive training may lower blood thiamine concentrations, but the practical performance impact in otherwise healthy, well-nourished athletes is still uncertain.
- Classic thiamine deficiency, such as beriberi, is unlikely in athletes eating a normal, varied diet.
- I do not routinely recommend vitamin B1 testing or supplementation simply because someone trains hard.
- Testing or supplementation may be more relevant in athletes with clear risk factors, such as severe dietary restriction, malnutrition, malabsorption, alcohol-related disease, or unusually narrow eating patterns.
- For most athletes, the best vitamin B1 strategy is simple: eat enough, eat broadly, and avoid unnecessary micronutrient over-optimization.
Introduction: Vitamin B1 in Athletes
Vitamin B1 in athletes is not a topic that usually gets much attention. Most athletes think about protein timing, carbohydrate periodization, iron status, vitamin D, or magnesium long before they think about thiamine. In everyday clinical practice, the same pattern is visible. Thiamine is usually grouped under the broad label of “B vitamins,” even though the B-vitamin family includes several different compounds with distinct physiological roles.
In my own clinical work, thiamine rarely comes up in routine occupational health checks or standard follow-up blood panels. It is not something we commonly test in otherwise healthy people. My most regular contact with thiamine has been in alcohol-related care, where it is given to reduce the risk of Wernicke encephalopathy, particularly before glucose administration in at-risk patients. Outside that setting, classic thiamine deficiency syndromes such as beriberi are something most doctors in modern Western practice mainly read about during medical school rather than encounter regularly in clinic.
But athletes are not always “ordinary healthy people” metabolically. Without adequate thiamine, key metabolic pathways linking carbohydrate catabolism to mitochondrial energy production may be impaired — with potential consequences that accumulate quietly across a training block. Classic beriberi is unlikely in an otherwise healthy athlete eating a reasonable diet, but subtle or nonspecific symptoms may still occur in marginal states. What is more relevant in the athletic context is not dramatic deficiency, but a gradual erosion of status during intensive training without overt clinical signs.
This article reviews what vitamin B1 does in athletes, how training may affect thiamine status, how to assess it, and what the evidence says about when supplementation may be warranted.
What Vitamin B1 in Athletes Actually Does — and Why Demand May Increase With Training
Thiamine (vitamin B1) is a water-soluble vitamin that functions as a cofactor for pyruvate dehydrogenase (PDH), one of three enzymes composing the pyruvate dehydrogenase complex (PDC), which is a rate-limiting enzyme in carbohydrate metabolism by catalyzing acetyl-CoA production from pyruvate acid [1]. In practical terms: when thiamine is insufficient, impaired PDH activity can limit pyruvate entry into the Krebs cycle and favor lactate accumulation in a deficiency state [8].
Thiamine diphosphate (ThDP, also called thiamine pyrophosphate or TPP) — the biologically active form of vitamin B1 — is an essential cofactor for a number of metabolic enzymes, particularly those associated with oxidative and nonoxidative carbohydrate metabolism [2]. These include pyruvate dehydrogenase (responsible for the conversion of pyruvate to acetyl-coenzyme A), α-ketoglutarate dehydrogenase in the Krebs cycle, and the branched chain α-keto acid dehydrogenase complex [2]. The latter is involved in the catabolism of branched-chain amino acids (BCAAs), thereby connecting vitamin B1 to amino acid metabolism as well.
Because exercise stresses metabolic pathways that depend on thiamine, riboflavin, and vitamin B-6, the requirements for these vitamins may be increased in athletes and active individuals [3]. This is mechanistically plausible: higher training volumes mean more glycolytic flux and more demand on ThDP-dependent enzymes. However, the evidence base for thiamine-specific requirement increases in athletes is less direct than for riboflavin and vitamin B-6, for which more targeted data exist [4].
In practical terms, this is also reflected in how I advise patients in clinic. Even if athletes may theoretically have a higher thiamine turnover, I do not routinely recommend specific thiamine supplementation or encourage people to aggressively optimize vitamin B1 intake simply because they train a lot. In an athlete eating a normal, varied diet without major dietary restrictions, clinically meaningful thiamine deficiency is still something I would consider relatively unlikely.
How Training May Deplete Vitamin B1 Status
Active individuals with poor or marginal nutritional status for a B-vitamin may have decreased ability to perform exercise at high intensities [4]. The word “marginal” is important here. While you do not need a classic clinical deficiency for thiamine status to potentially become relevant, the more important practical question is whether this marginal decline actually impairs performance in well-nourished athletes. The available evidence suggests this risk is primarily relevant for athletes with preexisting poor dietary intake or significant energy restriction.
The most direct human evidence comes from college swimmers. Blood thiamin concentration decreased significantly during the intensive-training period compared with the preparation period — from 41 ± 6 ng/ml to 36 ± 3 ng/ml for male subjects (p = .048), and from 38 ± 10 ng/ml to 31 ± 5 ng/ml for female subjects (p = .004) — without any significant changes in dietary thiamine intake [5]. The decline occurred during intensive training despite no significant change in reported thiamin intake; the study does not establish the causal mechanism.
Exercise appears to decrease nutrient status even further in active individuals with preexisting marginal vitamin intakes or marginal body stores, and active individuals who restrict their energy intake or make poor dietary choices are at greatest risk for poor thiamine, riboflavin, and vitamin B-6 status [3]. These are plausible high-risk groups in clinical practice: combat sport competitors cutting weight, endurance athletes in caloric deficit, and aesthetic athletes restricting food groups.
The increase in energy demand during physical exercise can alter the requirements for these vitamins [6]. For vitamin B1, this relationship is mechanistically plausible, but the quantitative relationship between training load and thiamine requirement has not been directly established [6].
In practice, I reassure most athletes about this. Even if training may increase the metabolic demand for B vitamins, clinically significant thiamine deficiency is still unlikely in someone eating a varied diet. I would not expect beriberi to develop in a healthy athlete simply because they train hard.
The kind of thiamine deficiency that leads to classic beriberi usually requires a much more extreme nutritional situation: a very restricted diet, severe food insecurity, malabsorption, alcohol-related disease, or another major risk factor. Historically, diets based almost entirely on polished white rice created that risk. In modern Western clinical practice, however, true vitamin B1 deficiency is not something I commonly expect to see in otherwise well-nourished athletes, even if intensive training may lower thiamine status to some degree.
The obvious clinical exception is alcohol-related disease. In patients with heavy alcohol use, thiamine deficiency can be very real because of poor intake, impaired absorption, altered metabolism, and increased requirements. This is why thiamine is commonly given parenterally in alcohol-related care, especially when there is concern about Wernicke encephalopathy. In my own clinical setting, this often means intramuscular thiamine, for example 250 mg, depending on the local protocol and clinical situation.
What Insufficient Vitamin B1 May Mean for Performance — and Why I Do Not Routinely Test or Supplement It
Vitamin B1’s role in the PDH complex is central to aerobic carbohydrate oxidation [1]. In a state of thiamine deficiency, reduced PDH activity shifts pyruvate metabolism away from the Krebs cycle and toward lactate production — this is the well-established biochemical basis of lactic acidosis in clinical thiamine deficiency. Whether subclinical insufficiency produces a measurable performance effect on this pathway in otherwise healthy athletes is less well established and remains an area of active interest [1][8].
Despite their fundamental roles in energy-producing pathways, only the intake of thiamine-derivative substances showed some positive effects on exercise performance and fatigue among the B vitamins directly involved in energy metabolism [6]. Riboflavin and niacin supplementation did not show consistent ergogenic effects; supplementation with high-dose niacin may even impair performance [6]. Vitamin B1’s position at the entry point of mitochondrial carbohydrate metabolism appears to give its derivatives a distinctive, if still modest, functional role.
The most direct human evidence comes from a double-blind, randomized, crossover study in which lactate levels, VO₂max, and heart rates in 27 male athletes were compared at rest and after exercise, following administration of placebo (sodium chloride 0.9%) or TPP (1 mg/kg) [7]. At rest, serum lactate levels after placebo or TPP were similar; however, after exercise, the levels were lower in the athletes after taking TPP than after placebo. During exercise, VO₂max in athletes on TPP was higher than on placebo. At rest, heart rate after taking placebo or TPP was similar but, after exercise, heart rate was lower after taking TPP than after placebo. It is concluded that TPP caused serum lactate levels and heart rate to be lower than placebo and VO₂max to be higher in athletes performing aerobic physical activity [7].
Important limitations apply: this was a small study, the athletes were all male, and the intervention was intravenous TPP rather than oral supplementation. These results should not be extrapolated directly to oral vitamin B1 supplementation in trained athletes.
From a practical clinical perspective, this is also where I become fairly conservative. Even if we can observe metabolic or biochemical changes related to thiamine status — for example changes in pathways linked to lactate metabolism or cellular energy production — we still have limited evidence that these changes translate into meaningful differences in real-world athletic performance in otherwise healthy, well-nourished athletes.
In my own practice, I would not routinely recommend vitamin B1 testing or thiamine supplementation simply because somebody trains hard. I would generally advise athletes to focus on maintaining a normal, varied, nutrient-dense diet rather than trying to optimize individual vitamins in isolation. For most people eating a reasonably balanced diet, I would consider clinically meaningful thiamine deficiency unlikely.
I also do not routinely test thiamine in athletes with no specific risk factors. In practice, I would be much more likely to think about thiamine assessment in situations involving alcohol-related disease, significant malnutrition, severe dietary restriction, malabsorption disorders, or unusually restrictive eating patterns. Outside those contexts, I would generally not expect vitamin B1 status to become a meaningful limiting factor for performance.
Conclusion: Vitamin B1 in Athletes
Vitamin B1 is essential for carbohydrate metabolism, but that does not mean every athlete needs to test it, supplement it, or worry about it. The biochemistry matters: thiamine is directly involved in the metabolic steps that help convert carbohydrate into usable energy, and intensive training may lower blood thiamine concentrations in some athletes. However, the practical interpretation needs to stay grounded. In otherwise healthy, well-nourished athletes, clinically meaningful thiamine deficiency is still unlikely.
From my clinical perspective, vitamin B1 is not something I routinely measure or supplement in athletes simply because they train hard. The priority should remain a normal, varied, nutrient-dense diet. Testing or supplementation becomes more relevant only when there are clear risk factors: severe dietary restriction, malnutrition, malabsorption, alcohol-related disease, or unusually narrow eating patterns.
So the practical message is simple: vitamin B1 deserves awareness, not obsession. For most athletes, the best “thiamine strategy” is not another supplement bottle — it is eating enough, eating broadly, and recognizing when dietary restriction or medical risk factors change the picture.
References
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC8838653/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC8451777/
[3] https://pubmed.ncbi.nlm.nih.gov/10919966/
[4] https://pubmed.ncbi.nlm.nih.gov/17240780/
[5] https://pubmed.ncbi.nlm.nih.gov/21719900/
[6] https://doi.org/10.1016/j.scispo.2020.11.007
