Triglycerides are the main form in which the body stores and transports fat. In the lipidogram, they are often given less attention than cholesterol, although this indicator says a lot about metabolism, nutrition and cardiovascular risk. For an athlete, triglycerides are also a mirror of how the body uses energy. The editors explain what the analysis measures and how to interpret it correctly.
What are triglycerides
A triglyceride molecule consists of glycerol and three fatty acids. This is the most compact way to store energy: a gram of fat contains approximately 9 kcal, which is more than twice the energy value of carbohydrates and proteins. The main depot of triglycerides is adipose tissue, and smaller reserves are in the muscles and liver.
Intramuscular triglycerides play an important role in sports: they serve as a source of fuel during prolonged aerobic exercise. Endurance-trained athletes have more such reserves, and the muscles use them more efficiently.
In the blood, triglycerides, like cholesterol, are transported as part of lipoproteins. After eating, fats from the intestines enter the blood in the form of chylomicrons, the largest lipoprotein particles. The liver, in turn, synthesizes triglycerides from excess carbohydrates and fatty acids and releases them into the blood as part of very low-density lipoproteins (VLDL).
The key enzyme that "unloads" these particles is lipoprotein lipase on the walls of the capillaries of muscles and adipose tissue. It breaks down triglycerides into fatty acids, which cells use as fuel or store.
What the analysis shows
The analysis for triglycerides measures their total concentration in the serum, regardless of the composition of which particles they are. On an empty stomach, the main share is provided by VLDL, and after a meal, also chylomicrons and their remnants. In Ukraine, the result is usually given in mmol/l.
Triglycerides are the most "mobile" indicator of the lipidogram. They depend on the last meal, alcohol consumption, recent training, and even from day to day in one person can fluctuate by tens of percent. Therefore, the unit value should be evaluated cautiously.
Previously, the lipidogram was necessarily taken on an empty stomach. The EAS/EFLM consensus (Nordestgaard et al., 2016) concluded that for most people, testing after a typical meal is acceptable: triglycerides rise modestly after a typical meal. A separate threshold of 2.0 mmol/L has been proposed for evaluating the analysis without fasting, while the desired level for fasting is less than 1.7 mmol/L.
| Fasting triglyceride level | Interpretation according to ESC/EAS 2019 |
|---|---|
| Less than 1.7 mmol/l | Desired level, lower risk |
| 1.7–10 mmol/l | Hypertriglyceridemia; value as a marker of cardiovascular risk |
| More than 10 mmol/l | Severe hypertriglyceridaemia, high risk of acute pancreatitis |
The laboratory level of triglycerides also affects the calculation of LDL cholesterol: the Friedwald formula becomes unreliable at high triglycerides, so in such cases other methods of calculation or direct measurement are required.

Triglycerides and cardiovascular risk
The relationship between triglycerides and atherosclerosis has long remained a subject of debate. A scientific statement from the American Heart Association (Miller et al., 2011) recognized triglycerides as an important risk marker reflecting metabolic abnormalities, but not a primary target of therapy.
Later it became clear that the damage is not caused by triglycerides themselves, but by the particles that carry them — VLDL and remnants of chylomicrons. These particles contain apolipoprotein B and cholesterol, capable of penetrating the artery wall. Cholesterol in such particles is called "residual" (remnant).
A large Danish study by Nordestgaard et al (2007) found that triglycerides measured in non-fasting conditions were associated with the risk of myocardial infarction and death even more strongly than expected. This reflects the fact that most of the day a person is in a post-meal state.
Moderately elevated triglycerides most often accompany insulin resistance, abdominal obesity, fatty liver disease, and prediabetes. Therefore, this test is a useful indicator of overall metabolic health.
Features of athletes
Fasting triglycerides are usually lower in physically active people than in sedentary people. Regular training increases the activity of lipoprotein lipase in muscles and sensitivity to insulin, thanks to which fats from the blood are disposed of faster.
An interesting feature is the acute load effect. One long aerobic workout can lower triglycerides the next day, as well as reduce their rise after a fatty meal. The effect is short-lived and disappears in a few days without training, so it is important to take it into account when comparing tests.
At the same time, there are situations in sports nutrition that increase triglycerides: carbohydrate loading, an excess of simple sugars and fructose in drinks and gels without an appropriate load, caloric surplus during weight gain, drinking alcohol after competition.
- Lowers triglycerides: regular aerobic training, reduction of fat mass, restriction of sugar and alcohol, omega-3 fatty acids from fish.
- Increase triglycerides: excess calories and fast carbohydrates, alcohol, insulin resistance, certain medications.
- Influence on the analysis result: food intake, training the day before, acute illness.
How to pass the analysis correctly
For comparison in dynamics, the editors advise to submit a lipidogram under the same conditions. Optimal — in the morning, after 10–12 hours without food, in the absence of alcohol for 1–2 days before the analysis.
It is desirable that the training regime the day before be habitual. If there was a rest break before one test and a long cardio workout before the other, the difference in triglycerides will reflect that, not metabolic changes.
If triglycerides after a meal exceed approximately 5 mmol/l or the result is inconsistent, the analysis should be repeated on an empty stomach. During an acute illness, the indicator may change, so it is better to postpone the examination.
For a more complete picture, along with triglycerides, it is useful to evaluate fasting glucose, glycated haemoglobin, liver enzymes, and, on the doctor's recommendation, apolipoprotein B, which takes into account all atherogenic particles.
Editorial conclusions
Triglycerides are the main form of fat storage and a sensitive indicator of metabolism. Their level depends on nutrition, alcohol, training and metabolic health in general.
Elevated triglycerides reflect the accumulation of atherogenic particles and often indicate insulin resistance, and very high triglycerides threaten pancreatitis. In athletes, the indicator is usually lower, but eating habits can change the picture.
The editors also recommend reading "Triglycerides above or below normal: causes in athletes and what to do", "HDL and LDL: what the analysis shows and why it is important for the athlete" and "Apolipoprotein B: what the analysis shows and why it is important for the athlete".
List of used literature
- Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111â188.
- Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011;123(20):2292â2333.
- Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298(3):299â308.
- Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile. Eur Heart J. 2016;37(25):1944â1958.
- Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18(6):499â502.
- Kraus WE, Houmard JA, Duscha BD, et al. Effects of the amount and intensity of exercise on plasma lipoproteins. N Engl J Med. 2002;347(19):1483â1492.




