Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans.

Journal Title (Medline/Pubmed accepted abbreviation): J. Physiol.
Year: 2011
Volume: 589
Page numbers: 963-973
doi (if applicable): 10.1113/jphysiol.2010.201343

Summary of Background and Research Design

Background:Carnitine is present in skeletal muscle and plays important roles in both low- and high intensity exercise. During low intensity, endurance exercise, carnitine is responsible for shuttling fatty acids into the mitochondria for oxidation. Oral ingestion of carnitine is hypothesized to increase the carnitine concentration in skeletal muscle, thereby increasing fatty acid oxidation, sparing muscle glycogen, and delaying fatigue. During high intensity exercise, a high ratio of free coenzyme A (CoASH):acetyl-coenzyme A (acetyl-CoA) is ideal to achieve optimum rates of carbohydrate oxidation via the TCA cycle. Carnitine is able to receive acetyl groups (to form acetylcarnitine), thereby helping to maintain an optimum CoA ratio. Flux through the TCA cycle will reduce the need for lactate production (necessary to maintain NAD+ for glycolysis). Therefore, increased carnitine could potentially increase performance in anaerobic exercise as well by reducing lactate formation and delaying fatigue.

Hypotheses: 1) Oral carnitine ingestion will increase carnitine concentrations in skeletal muscle. 2) Increased carnitine concentrations in skeletal muscle will increase fat oxidation and spare glycogen during low intensity exercise. 3) Increased carnitine concentrations in skeletal muscle will reduce lactic acid formation during high intensity exercise. 4) Increased carnitine concentrations in muscle will increase performance.

Research design: randomized, double-blind, repeated measures

Subjects:14 healthy, recreational athletes, age 25.9 ± 2.1 yrs old

Treatment: 700 mL of a solution containing 80 g of a carbohydrate polymer twice per day for 24 wks (Control). The Carnitine group (7 subjects) consumed the Control beverage with 2.0 g L-carnitine tartrate added (4 g carnitine per day).

Experimental protocol: Subjects cycled on an ergometer at 50% of their previously determined VO2max for 30 min (low intensity exercise) and then, immediately after, at 80% VO2max for 30 min (high intensity exercise). Immediately after that, subjects cycled as far/fast as they could for 30 min where work output was dependent on volitional cycling cadence. Blood samples were acquired before exercise and muscle biopsies from the vastus lateralis (quadraceps) muscle were collected before and immediately after exercise

After the first exercise session, subjects began supplementation and continued for 24 wks. They reported back to laboratory at 12 wks and again at 24 wks.

Summary of research findings:
  • Fasting serum carnitine concentrations increased from 44 ± 4.2 µM to 52 ± 4.0 µM in 12 wks and 54 ± 3.3 µM in 24 wks (p < 0.05) in="" the="" Carnitine="" group.="" Carnitine="" concentrations="" were="" not="" altered="" in="" the="" Control="" group.=""
  • Total carnitine content within muscle increased 30% in the Carnitine group in 24 wks (P < 0.05), while there were no changes in the placebo group. It was interesting that the increase in muscle carnitine in the Carnitine group was not significant at 12 weeks of supplementation.
  • Muscle glycogen content was 35% higher in the Carnitine group after low intensity exercise than the Control group after 24 wks of supplementation. This means that 55% less glycogen was utilized during exercise.
  • Because high intensity exercise was performed immediately after low intensity exercise, it was difficult to compare glycogen usage rates during the high intensity exercise stints. However, lactate accumulation during the high intensity exercise was 44% lower in the Carnitine group compared to the Control group after 24 wks of supplementation.
  • Activation status of pyruvate dehydrogenase (PDAa, indicative of TCA cycle activity) was 31% lower than baseline after low intensity exercise after 24 wks of carnitine supplementation. However, activity of citrate synthase, an enzyme in the TCA cycle, was not significantly different in either group after 24 wks of carnitine supplementation.
  • During the all-out cycling session, the Carnitine group’s work output was 35% greater than the Control group after 24 wks of supplementation. This is an 11% increase from before their pre-supplementation value.

Interpretation of findings/Key practice applications:

This article provides very clear scientific evidence that 4.0 g carnitine/day for 24 weeks can significantly increase carnitine content in skeletal muscle. The resultant increase in carnitine is beneficial in both low- and high intensity exercise; in low intensity exercise carnitine is able to spare glycogen stores. In high intensity exercise carnitine is able to reduce lactic acid accumulation. Carnitine supplementation was able to provide a direct benefit in sports performance; those who were supplemented demonstrated 11% greater voluntary work output in a timed, 30 min, all-out cycling session. There were no adverse effects reported from carnitine supplementation.


Resting muscle glycogen levels before the 24-week performance test were somewhat higher (21%, non-significant). Whether this alteration in muscle glycogen was due to an effect of the carnosine supplementation or some other dietary/exercise variable is not clear. Other than having the subjects obstain from strenuous exercise and alcohol for at least 48 h before the trial, and caffeine for at least24 hours before the trial, there were no other mentions of controls of either diet or activity before the performance trials.
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