Cardiometabolic Health in Athletes: What the Evidence Says

Why "Athlete" Does Not Mean "Cardiometabolically Protected"

Sustained physical training improves insulin sensitivity, lowers resting blood pressure, and reduces visceral adiposity, yet it does not fully protect against cardiometabolic disease. The 2023 ACC/AHA guideline on cardiovascular risk assessment explicitly notes that high cardiorespiratory fitness lowers but does not eliminate 10-year ASCVD risk, particularly when genetic lipid disorders, chronic inflammation, or hormonal disruption are present [1]. Elite endurance athletes, for example, can develop coronary artery calcification (CAC) scores that exceed age-matched sedentary controls, a finding replicated in the MASTER@Heart trial (N=191), which found that lifelong endurance athletes had a higher prevalence of non-obstructive coronary artery disease compared with sedentary controls (P<0.001) [2].

Cardiometabolic risk in athletes clusters into four clinical phenotypes that require distinct management approaches. First: athletes with diagnosed or subclinical diabetes. Second: older or masters athletes whose hormonal and metabolic milieu has shifted with age. Third: female athletes, where the interplay of sex hormones, energy availability, and cardiovascular remodeling creates a distinct risk profile. Fourth: pregnant athletes managing gestational glucose dysregulation while trying to maintain fitness. Each group is addressed below.

The "athlete halo" can delay diagnosis. Clinicians sometimes dismiss a fasting glucose of 105 mg/dL in a marathon runner as a stress artifact rather than pre-diabetes. This delay has real consequences.

Diabetes in Athletes: Type 1, Type 2, and the Gray Zone

Blood Glucose Management During Training

Glycemic control during exercise differs fundamentally between Type 1 diabetes (T1D) and Type 2 diabetes (T2D). In T1D, aerobic activity causes glucose to fall rapidly because muscle glucose uptake is amplified while hepatic glucose output lags; anaerobic or high-intensity intervals can paradoxically spike glucose by 30 to 50 mg/dL due to catecholamine-driven glycogenolysis. The 2022 American Diabetes Association (ADA) Standards of Care recommend a pre-exercise glucose target of 126 to 180 mg/dL for most adults with T1D performing moderate aerobic work, with a carbohydrate supplement of 15 to 30 g if glucose is <126 mg/dL at exercise onset [3].

Hypoglycemia affects up to 40% of aerobic training sessions in adults with T1D who do not pre-emptively reduce basal insulin or consume carbohydrate [4]. Continuous glucose monitoring (CGM) has changed practice substantially. The ALERTT1 trial demonstrated that CGM use reduced nocturnal hypoglycemia by 43% in physically active T1D adults compared with standard finger-stick monitoring [5].

For athletes with T2D, exercise itself acts as a glucose-lowering therapy. A 2019 Cochrane review (k=23 trials, N=1,253) found that structured aerobic training reduced HbA1c by 0.67% (95% CI 0.43 to 0.91%) compared with no exercise, independent of weight change [6].

GLP-1 Receptor Agonists in Athletes with Diabetes or Obesity

GLP-1 receptor agonists such as semaglutide and tirzepatide are increasingly prescribed to masters and recreational athletes managing T2D or obesity-related insulin resistance. In STEP-1 (N=1,961), semaglutide 2.4 mg once weekly produced 14.9% mean body weight reduction at 68 weeks versus 2.4% placebo, with favorable changes in waist circumference, blood pressure, and triglycerides [7]. No dedicated trial has enrolled competitive athletes, so extrapolation requires clinical judgment.

One practical concern: GLP-1-associated nausea and delayed gastric emptying can impair carbohydrate absorption during prolonged events. Athletes on semaglutide or liraglutide should pre-race nutrition time their dosing to avoid peak drug effect within 24 hours of a long-duration event. The FDA label for Ozempic (semaglutide injection) does not list exercise restrictions but does flag dehydration risk [8].

A staged protocol for initiating GLP-1 therapy in athletes with T2D or prediabetes includes: confirming that resting HbA1c warrants therapy (>6.5% for T2D or >5.7% with additional risk factors), titrating slowly (semaglutide 0.25 mg for 4 weeks before advancing), scheduling the weekly injection on a rest day or low-intensity training day, and scheduling a CGM-monitored training session at week 6 to assess glycemic response.

Cardiometabolic Health in Older and Masters Athletes

The masters athlete category typically encompasses adults over age 35 in competitive sport, though many guidelines use 50 or 65 as thresholds for cardiometabolic re-screening. Regular training preserves insulin sensitivity significantly longer than sedentary aging does. A cross-sectional analysis published in the Journal of the American College of Cardiology (2020) found that masters cyclists aged 55, 79 had VO2 max values 38% higher than age-matched non-athletes and HOMA-IR scores consistent with insulin sensitivity seen in adults 15 to 20 years younger [9].

The Testosterone and Estrogen Drop

Despite high fitness, older male athletes experience age-related testosterone decline averaging 1 to 2% per year after age 40, which contributes to visceral fat accumulation, reduced insulin receptor expression, and dyslipidemia. Female masters athletes face a sharper hormonal transition at menopause: estrogen withdrawal accelerates LDL oxidation, promotes central fat redistribution, and raises 10-year ASCVD risk by an average of 3, 5 absolute percentage points in the first 5 years post-menopause, according to data from the Women's Health Initiative [10].

Testosterone replacement therapy (TRT) in male masters athletes requires careful cardiometabolic monitoring. The TRAVERSE trial (N=5,246, mean age 63.5 years) showed that testosterone gel did not increase major adverse cardiovascular events versus placebo in men with hypogonadism and pre-existing or high-risk cardiovascular disease, with a hazard ratio of 1.02 (96% CI 0.86, 1.20) [11]. This resolved a decade of uncertainty but does not imply cardiovascular neutrality in all athletic populations.

Lipid Screening Intervals for Masters Athletes

The U.S. Preventive Services Task Force recommends lipid screening for all adults over 35 (men) and 45 (women) with any cardiovascular risk factor [12]. High-volume endurance training alone does not justify extending screening intervals. A 40-year-old male triathlete with a family history of premature CAD should receive a fasting lipid panel, lipoprotein(a) measurement, and a CAC score discussion regardless of weekly training volume.

Cardiometabolic Health in Female Athletes

Sex-Specific Metabolic Differences

Women store a higher proportion of fat intramuscularly and oxidize fat at a greater rate than carbohydrate during moderate aerobic exercise compared with men matched for fitness. This metabolic pattern protects against short-term insulin resistance during training but does not prevent long-term dyslipidemia when energy availability is chronically low. Relative Energy Deficiency in Sport (RED-S), which was previously framed narrowly as the "Female Athlete Triad," now encompasses cardiometabolic consequences including reduced HDL cholesterol, elevated cortisol, and ventricular remodeling abnormalities [13].

A 2022 British Journal of Sports Medicine consensus statement defined RED-S cardiometabolic sequelae as including bradycardia below 45 bpm, QTc prolongation, and early atherosclerosis markers in women with chronic low energy availability, effects that may persist for years after energy balance is restored [14].

Oral Contraceptives and Cardiometabolic Risk in Active Women

Combined oral contraceptives (COCs) containing ethinyl estradiol raise triglycerides by 15 to 30% and can slightly reduce insulin sensitivity, effects that are clinically relevant in female athletes with borderline metabolic risk. The American College of Obstetricians and Gynecologists (ACOG) advises that women with a personal history of hypertriglyceridemia or insulin resistance discuss progestin-only alternatives with their clinician before starting COCs [15]. Progestin-only pills and hormonal IUDs carry a lower triglyceride burden and are often preferred in female athletes with cardiometabolic risk factors.

Gestational Diabetes and the Pregnant Athlete

Prevalence and Cardiometabolic Stakes

Gestational diabetes mellitus (GDM) affects approximately 7 to 10% of US pregnancies, with the CDC reporting 8.3% prevalence in 2021 [16]. Even physically active women who exercised before conception are not fully protected. GDM is driven primarily by placental hormones (human placental lactogen, cortisol, and progesterone) that antagonize insulin signaling regardless of maternal fitness level. Women who develop GDM face a 50% lifetime risk of progressing to T2D, and their children carry elevated cardiometabolic risk [17].

Exercise as First-Line Therapy for GDM

The ADA 2024 Standards of Care state: "Physical activity is recommended for all pregnant women without contraindications, including those with gestational diabetes mellitus" [3]. Supervised walking or water aerobics for 30 minutes per session, 5 days per week, reduces postprandial glucose excursions by 10 to 15 mg/dL on average and can halve the need for insulin therapy in mild GDM [18].

For pregnant athletes who wish to maintain higher-intensity training, the ACOG Practice Bulletin 804 (2020) permits continued vigorous activity in uncomplicated singleton pregnancies but recommends discontinuation if any of the following develop: vaginal bleeding, dyspnea before exertion, dizziness, chest pain, or reduced fetal movement [15]. Women with GDM who train at higher intensities need CGM or frequent fingerstick monitoring because exercise-induced hypoglycemia can occur, particularly in the second trimester when insulin sensitivity is briefly heightened after activity.

GLP-1 Therapy Is Contraindicated in Pregnancy

Semaglutide, liraglutide, tirzepatide, and all GLP-1 receptor agonists are contraindicated during pregnancy. Animal studies showed dose-dependent fetal growth restriction and skeletal abnormalities [8]. The FDA labels for both Ozempic and Wegovy carry explicit pregnancy warnings, and the ADA recommends discontinuing GLP-1 agents at least 2 months before planned conception [3]. Athletes who become pregnant while on GLP-1 therapy should contact their prescriber immediately.

Metformin remains an option for GDM when lifestyle measures are insufficient and insulin is not yet indicated, though ACOG notes that metformin crosses the placenta and long-term neonatal data beyond age 2 are limited [15]. Insulin (typically NPH plus rapid-acting lispro or aspart) remains the preferred pharmacologic agent for GDM that does not respond to diet and exercise alone.

Postpartum Cardiometabolic Reset

GDM resolves in most women within 6 weeks of delivery, but the cardiometabolic window does not fully close. A 2020 meta-analysis in Diabetologia (k=17, N=9,232 women) found that GDM history raised T2D risk 10-fold at 10 years postpartum compared with normoglycemic pregnancies [19]. The ADA recommends a 75-g oral glucose tolerance test at 4 to 12 weeks postpartum, then repeat metabolic screening every 1 to 3 years [3]. Breastfeeding for 6 or more months reduces T2D conversion risk by approximately 25% in women with prior GDM [20].

For athletic women returning to training postpartum, resuming structured aerobic exercise at 6 to 12 weeks (depending on delivery type and pelvic floor recovery) restores insulin sensitivity and lowers 10-year ASCVD risk trajectory. Pelvic floor physiotherapy should precede high-impact running for most postpartum athletes.

Lipids, Blood Pressure, and Structural Cardiac Adaptations

Athlete's Heart vs. Pathological Remodeling

Endurance training produces left ventricular eccentric hypertrophy: the chamber enlarges with a proportionally thickened wall. This physiological remodeling is benign. Pathological hypertrophy from hypertensive cardiomyopathy or hypertrophic obstructive cardiomyopathy (HOCM) requires different management. Distinguishing the two relies on tissue Doppler echocardiography and, when ambiguous, cardiac MRI. HOCM is the leading cause of sudden cardiac death in athletes under 35 in the United States, accounting for approximately 36% of cases in the Maron registry [21].

Blood pressure targets for athletes with hypertension follow standard JNC/AHA thresholds: <130/80 mmHg for adults with established cardiovascular risk [1]. Beta-blockers are generally avoided in competitive athletes due to performance impairment and are prohibited in certain sports (archery, shooting) by World Anti-Doping Agency rules. ACE inhibitors or ARBs are preferred first-line agents for hypertensive athletes.

LDL, Statins, and Athletic Performance

Statins reduce LDL by 30 to 55% depending on agent and dose and are the cornerstone of pharmacologic lipid management. A persistent concern among athletic patients is statin-associated muscle symptoms (SAMS), which occur in 5 to 10% of users in observational data and were reported in 1.5 to 3% of participants in the JUPITER trial (N=17,802) [22]. Creatine kinase (CK) elevation is common in athletes even without statins; athletes on statins should have a baseline CK drawn before initiating therapy and re-measured if myalgia develops. Rosuvastatin 5 to 10 mg daily is often preferred in athletes because it has lower muscle penetrance than lipophilic statins like atorvastatin or simvastatin.

Aerobic training alone reduces LDL cholesterol by approximately 5 mg/dL and raises HDL by 3 to 5 mg/dL, per a 2019 Cochrane review of 65 trials [23]. These are meaningful but insufficient changes for athletes with familial hypercholesterolemia or LDL >190 mg/dL.

Putting the Evidence Together: A Practical Framework

Every athlete should receive cardiometabolic screening calibrated not just to age and sex but to sport type, training load, hormonal status, and family history. A recreational 45-year-old female runner with a mother who had a myocardial infarction at 58 warrants a full fasting lipid panel, HbA1c, blood pressure assessment, and a conversation about hormonal contraceptive choice, none of which are usually prompted by a "good" resting heart rate or a recent 5K personal best.

The ADA 2024 Standards of Care state directly: "Providers should consider the unique physiology of athletes with diabetes, including the role of exercise intensity, duration, and type on glucose management" [3]. That guidance extends to the broader cardiometabolic picture. Athletes are not exempt from metabolic disease. They just need protocols that account for their physiology.

For any athlete with a fasting glucose of 100 to 125 mg/dL, a 2-hour 75-g OGTT is more informative than HbA1c alone, because high erythrocyte turnover from training can lower HbA1c by 0.2 to 0.4% below its true glycemic equivalent, potentially masking impaired glucose tolerance [3].