Today’s Dietitian
Vol. 28 No. 4 P. 26
Athletes are often viewed as metabolically protected. Compared with the general population, they typically demonstrate greater mitochondrial density, lower visceral fat, higher insulin sensitivity, and lower rates of cardiometabolic disease. Yet sports dietitians and clinicians occasionally encounter findings that appear contradictory, including elevated fasting glucose, impaired glucose tolerance, or temporary reductions in insulin sensitivity in otherwise highly trained endurance athletes.
This phenomenon is commonly referred to as the “athlete paradox.” The term originally described the observation that endurance-trained athletes store large amounts of intramyocellular triglycerides (IMTG), like individuals with obesity or type 2 diabetes, while remaining highly insulin sensitive.1 Rather than reflecting metabolic dysfunction, these lipid stores appear to function as an efficient fuel reservoir to support endurance exercise.
Importantly, endurance-trained athletes store and utilize IMTG differently than sedentary insulin-resistant populations. Trained muscle stores lipids in smaller droplets located near mitochondria and enriched in proteins involved in fatty acid oxidation, thereby allowing rapid mobilization during exercise. In contrast, lipid accumulation in obesity and type 2 diabetes is more strongly associated with impaired mitochondrial function and reduced metabolic flexibility.1
More recent research has expanded the athlete paradox beyond lipid storage alone. In studies, endurance-trained athletes experienced significantly reduced glucose tolerance the morning after prolonged cycling despite otherwise exceptional metabolic health. These athletes demonstrated elevated free fatty acids, increased ketone levels, and greater reliance on fat oxidation during recovery while preserving mitochondrial function.2
This distinction is clinically important because temporary reductions in glucose tolerance after prolonged exercise do not necessarily indicate chronic metabolic disease. Instead, these findings may reflect short-term substrate prioritization during periods of glycogen depletion and recovery. At the same time, exercise physiology does not always fit neatly into traditional clinical interpretation. Training load, carbohydrate availability, sleep, recovery status, and chronic low energy availability can all influence glucose regulation in athletes.
For sports dietitians and clinicians, the challenge is determining when these findings reflect adaptive exercise physiology and when they may signal inadequate recovery or emerging metabolic strain.
Understanding the athlete paradox has implications not only for cardiometabolic health but also for recovery, adaptation, training quality, and long-term performance sustainability.
Physiological Mechanisms Behind Reduced Insulin Sensitivity in Athletes
Glucose regulation is highly dynamic in endurance athletes, particularly during periods of heavy training, glycogen depletion, and repeated recovery demands. In many cases, temporary reductions in glucose tolerance appear to reflect adaptive physiology rather than chronic metabolic dysfunction.
Increased Glucose Uptake During Exercise
During prolonged endurance exercise, skeletal muscle dramatically increases glucose uptake to support ATP production and maintain exercise intensity. Muscle contraction stimulates translocation of glucose transporter type 4 (GLUT4) to the muscle cell membrane, allowing glucose uptake independent of insulin signaling.3 Endurance-trained athletes also demonstrate greater mitochondrial density and oxidative capacity, improving their ability to utilize both carbohydrate and fat as fuel.
Glycogen Depletion and Fat Oxidation
As exercise duration increases, glycogen stores progressively decline and the body increasingly shifts toward fatty acid oxidation to preserve glucose availability. Research revealed endurance-trained athletes experienced impaired glucose tolerance the morning after three hours of continuous cycling despite preserved mitochondrial function. They also experienced elevated free fatty acids, increased ketones, decreased glucose oxidation, and greater reliance on fat oxidation during recovery.2
These findings suggest that temporary reductions in insulin sensitivity after prolonged exercise may reflect short-term substrate prioritization rather than impaired metabolic health. Endurance-trained athletes store IMTG in smaller lipid droplets positioned near mitochondria, facilitating rapid fatty acid mobilization and metabolic flexibility during exercise.1
The Role of Recovery and Carbohydrate Availability
Although these responses may be adaptive, recovery support still matters. Inadequate carbohydrate intake, chronic low energy availability, or repeated high-volume training without sufficient replenishment may prolong glycogen depletion and impair subsequent training quality. The International Society of Sports Nutrition (ISSN) recommends carbohydrate intake relative to training demands, typically ranging from 8 to 12 g/kg/day, depending on exercise intensity and duration.4
Stress Hormones and Inflammatory Signaling
Heavy training also activates several acute physiological stress responses that temporarily influence glucose regulation. During prolonged exercise, catecholamines and cortisol rise substantially to stimulate hepatic glucose production and maintain circulating fuel availability. While these responses help sustain exercise capacity, they may transiently impair insulin signaling during the immediate recovery period.
Exercise-induced inflammatory signaling likely contributes, as well. Importantly, this acute inflammatory response differs substantially from the chronic low-grade inflammation observed in obesity and cardiometabolic disease. In endurance athletes, these changes are typically temporary and occur alongside preserved mitochondrial function and high oxidative capacity.2
Exercise may activate a coordinated network of hormonal, vascular, metabolic, and immune signaling pathways involved in tissue repair and adaptation.5 Exercise-induced cytokines and myokines, including IL-6, brain-derived neurotrophic factor, fibroblast growth factor-21, and others, appear to help regulate substrate mobilization, inflammation, mitochondrial adaptation, and recovery responses following exercise.6 Marathon running significantly increases many of these signaling molecules during recovery and adaptation.
Energy Availability and Underfueling in Endurance Athletes
Not all metabolic changes observed in endurance athletes are purely adaptive. In some cases, altered glucose regulation may overlap with inadequate recovery, chronic under-fueling, or low carbohydrate availability.
Low Energy Availability and RED-S
Many endurance athletes are not intentionally under-fueling. Instead, inadequate intake may gradually develop due to high training volumes, appetite suppression after exercise, travel, busy schedules, gastrointestinal discomfort, or body composition pressures. Female endurance athletes may be particularly vulnerable because high training loads often coexist with messaging promoting leanness or carbohydrate restriction as performance strategies. Importantly, inadequate carbohydrate intake remains remarkably common. It has been demonstrated in studies that 45% to 98% of female athletes across multiple sport types fail to meet current carbohydrate recommendations.7
Low energy availability (LEA) occurs when insufficient energy remains to support normal physiological function after accounting for exercise energy expenditure. Relative energy deficiency in sport (RED-S) expands upon the Female Athlete Triad model by recognizing the broader consequences of chronic underfueling, including disruptions in endocrine function, bone health, immune function, metabolism, recovery, and performance.7 Recent evidence further suggests these conditions are highly prevalent in athletes and associated with impaired performance, reduced training response, increased fatigue, and greater risk of bone stress injuries.8
Emerging evidence suggests carbohydrate availability itself may independently influence health and performance outcomes. Some experts propose that low carbohydrate availability (LCA) may contribute to many of the physiological disruptions associated with RED-S even beyond the effects of LEA alone. Low carbohydrate availability has been associated with reduced glucose utilization, muscular fatigue, impaired recovery, hormonal disruption, and suppressed metabolic rate.7
Masters Athletes and Aging Considerations
As endurance athletes age, interpreting glucose patterns and metabolic health status becomes increasingly complex. Many adaptations that support endurance performance, including high mitochondrial density, enhanced fat oxidation, and strong cardiorespiratory fitness, remain beneficial across the lifespan. However, aging also introduces physiological changes that may influence recovery, inflammation, endothelial function, and insulin sensitivity independent of training status.
Masters athletes are often healthier than sedentary age-matched populations, and lifelong exercise remains strongly protective against cardiometabolic disease. Still, high fitness does not eliminate the effects of aging. Recovery capacity, hormonal regulation, anabolic responsiveness, and glucose metabolism continue to change over time, even in highly trained individuals.
Oxidative Stress and Recovery Demands
Older adults may demonstrate elevated oxidative stress, inflammation, endothelial dysfunction, impaired mitochondrial fatty acid oxidation, and reduced insulin sensitivity compared with younger adults.9 These findings do not suggest endurance exercise causes metabolic dysfunction. Rather, they highlight how aging physiology, recovery demands, and metabolic regulation interact over time.
This may become especially relevant in masters athletes balancing high training volumes with inadequate recovery, chronic under-fueling, poor sleep, or significant life stress outside of sport. Recovery timelines may lengthen with age, and repeated glycogen depletion or insufficient energy intake may carry greater physiological consequences over time.
Recognizing Underrecovery
Importantly, many masters athletes normalize chronic under-recovery. Persistent fatigue, soreness, declining performance, or disrupted sleep are often viewed as inevitable aspects of aging rather than potential indicators of inadequate recovery support.
For clinicians and sports dietitians, this creates an important distinction. Temporary reductions in glucose tolerance after prolonged exercise may still represent adaptive physiology in masters athletes, but distinguishing adaptive responses from accumulating cardiometabolic strain may become more difficult as age-related changes in insulin sensitivity, inflammation, and endothelial function occur simultaneously.
Supporting Long-Term Performance
Ultimately, supporting long-term sport participation in masters athletes may require greater emphasis on recovery quality, adequate energy availability, sleep, protein intake, carbohydrate periodization, stress management, and individualized monitoring rather than focusing exclusively on training volume or performance output alone.
Interpreting Cardiometabolic Health in Athletes
One of the most important clinical questions surrounding the athlete paradox is whether transient reductions in glucose tolerance or insulin sensitivity represent meaningful cardiometabolic risk. Based on current evidence, the answer appears far more nuanced than a simple yes or no.
Highly trained athletes generally demonstrate high mitochondrial density, preserved mitochondrial function, superior cardiorespiratory fitness, lower visceral adiposity, enhanced endothelial function, and greater metabolic flexibility. In endurance athletes, transient reductions in glucose tolerance often occur alongside exceptionally high rates of fat oxidation and preserved mitochondrial respiration rather than progressive metabolic dysfunction.2
During periods of prolonged exercise, glycogen depletion, or incomplete recovery, the body may temporarily prioritize fat oxidation and conserve glucose availability as part of a coordinated adaptive response. Temporary physiological insulin resistance is therefore not automatically pathological.
At the same time, high fitness levels do not eliminate the influence of genetics, aging, chronic sleep disruption, psychosocial stress, hormonal dysfunction, poor dietary quality, chronic low energy availability, or prolonged underrecovery. In some athletes, particularly those in weight-sensitive sports, repeated restrictive eating and chronic physiological stress may accumulate over time.
Cardiometabolic risk exists on a continuum rather than appearing only once clinical thresholds are crossed.10 The CALERIE trial demonstrated that insulin sensitivity, inflammation, blood pressure, and lipid metabolism remain highly responsive to long-term lifestyle behaviors, even in relatively healthy adults. These findings reinforce that metabolic health should not be viewed through glucose regulation alone. Inflammation, vascular function, oxidative stress, recovery quality, and nutrition status all interact.
Practical Applications
These metabolic changes should not be viewed as evidence of “broken metabolism.” In most cases, the goal is to support recovery, maintain training quality, and preserve long-term health rather than aggressively “correct” isolated laboratory values.
For endurance athletes, carbohydrate availability remains one of the most important considerations. Heavy training blocks often involve repeated glycogen depletion with incomplete restoration between sessions. Matching carbohydrate intake to training demands helps support glycogen restoration, immune function, recovery, and subsequent training quality.
At the same time, carbohydrate strategies do not need to be universally rigid. Relatively small carbohydrate doses during prolonged exercise may improve endurance performance primarily by maintaining blood glucose availability and preventing exercise-induced hypoglycemia.11 Similarly, Researchers have demonstrated that trained triathletes maintained endurance performance after adapting to either high-carbohydrate or very-low-carbohydrate diets, although small carbohydrate doses during exercise improved performance in both groups.12
Importantly, these findings should not be interpreted as evidence that carbohydrate is unnecessary. High-intensity training, repeated sprint exercise, and multiple daily sessions still rely heavily on carbohydrate availability. Fueling strategies should therefore remain individualized according to sport demands, training intensity, recovery windows, gastrointestinal tolerance, and overall energy intake.
Nutrient Timing and Recovery
The ISSN position on nutrient timing emphasizes that recovery nutrition should support the athlete’s overall training demands rather than rigidly applying universal rules.4 They recommend total daily carbohydrate intake ranging approximately 8 to 12 g/kg/day depending on exercise volume and intensity.
When rapid glycogen restoration is needed, such as between same-day training sessions or competitions, the ISSN recommends carbohydrate refeeding strategies of approximately 1.2 g/kg/hour during early recovery.4 Combining carbohydrate with protein may also help when adequate carbohydrate intake is difficult to achieve.
Carbohydrate intake substantially improves glycogen resynthesis during short-term recovery, although adding protein to adequate carbohydrate intake may not consistently accelerate glycogen restoration further.13 Protein still remains important for muscle protein synthesis, tissue repair, immune function, and preservation of lean body mass.
The ISSN also emphasizes that recovery extends beyond a narrow “anabolic window.” Consistent protein distribution across the day, approximately every three to four hours, appears to support muscle protein synthesis and recovery more effectively than inconsistent intake patterns.4
Laboratory Interpretation and Clinical Context
Energy availability, sleep, recovery behaviors, and training structure all influence how athletes tolerate physiological stress over time. Athletes cannot consistently adapt to high training loads if chronic energy deficits, inadequate sleep, poor recovery, or excessive training stress persist.
No single biomarker should be interpreted in isolation in athletes. A mildly elevated fasting glucose or reduced glucose tolerance test provides limited information without understanding training load, recovery status, carbohydrate availability, hormonal health, sleep quality, and overall physiological context.
The timing of laboratory testing also matters. An athlete tested shortly after prolonged exercise, glycogen depletion, or a demanding training block may present with metabolic markers that appear concerning when interpreted without context. Likewise, a well-fueled athlete recovering from heavy training may present very differently than an athlete demonstrating similar laboratory findings alongside chronic fatigue, recurrent illness, declining performance, menstrual dysfunction, or repeated bone stress injuries.
Ultimately, performance nutrition exists at the intersection of physiology, recovery, adaptation, and long-term health. The athlete paradox reinforces the idea that metabolic health cannot be reduced to a single laboratory value; rather, it requires individualized interpretation within the broader context of recovery, nutrition practices, training history, and long-term physiological resilience.
Conclusion
The athlete paradox reaffirms that metabolic health in athletes is far more complex than a single laboratory value. Temporary reductions in glucose tolerance or insulin sensitivity after prolonged endurance exercise are not necessarily contradictory to excellent fitness, nor are they automatically indicative of cardiometabolic disease. In many cases, these findings appear to reflect adaptive substrate prioritization, recovery physiology, and the metabolic flexibility that supports endurance performance.
At the same time, context remains critical. High fitness levels do not eliminate the effects of inadequate recovery, chronic low energy availability, poor sleep, psychosocial stress, aging, or restrictive fueling practices. The same glucose marker may represent very different physiological realities depending on the athlete’s training load, recovery status, fueling habits, symptoms, and long-term health patterns.
Recovery quality, carbohydrate availability, energy intake, sleep, and individualized monitoring all influence not only cardiometabolic health, but also adaptation capacity, training consistency, injury risk, and sport longevity.
When approached thoughtfully, these findings are less about fear and more about opportunity. They reinforce that performance nutrition is not simply about maximizing output today, but supporting the athlete’s ability to train, recover, and thrive for years to come.
— Krissy Ladner, DHSc, MS, RD, CSSD, CPT, is a sports dietitian and sports performance director with nearly 20 years of experience in nutrition and sports medicine. She is a media-trained dietitian, adjunct lecturer, and membership director for WISE San Diego. Based in San Diego, she supports athletes globally across performance, nutrition, and body image initiatives.
References
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