Studies of L-carnitine in healthy athletic populations have yielded equivocal results. Further scientific-based knowledge is needed to clarify the ability of L-carnitine to improve exercise capacity and expedite the recovery process by reducing oxidative stress. This study aimed to examine the 9-week effects of L-carnitine supplementation on exercise performance, anaerobic capacity, and exercise-induced oxidative stress markers in resistance-trained males.
In a double-blind, randomized, and placebo-controlled treatment, 23 men (age, 25±2y; weight, 81.2±8.31 kg; body fat, 17.1±5.9%) ingested either a placebo (2 g/d, n=11) or L-carnitine (2 g/d, n=12) for 9 weeks in conjunction with resistance training. Primary outcome measurements were analyzed at baseline and at weeks 3, 6, and 9. Participants underwent a similar resistance training (4 d/w, upper/lower body split) for a 9-week period. Two-way ANOVA with repeated measures was used for statistical analysis.
There were significant increases in bench press lifting volume at wk-6 (146 kg, 95% CI 21.1, 272) and wk-9 (245 kg, 95% CI 127, 362) with L-carnitine. A similar trend was observed for leg press. In the L-carnitine group, at wk-9, there were significant increases in mean power (63.4 W, 95% CI 32.0, 94.8) and peak power (239 W, 95% CI 86.6, 392), reduction in post-exercise blood lactate levels (-1.60 mmol/L, 95% CI -2.44, -0.75) and beneficial changes in total antioxidant capacity (0.18 mmol/L, 95% CI 0.07, 0.28).
L-carnitine supplementation enhances exercise performance while attenuating blood lactate and oxidative stress responses to resistance training.
L-carnitine (LCR) is an endogenous compound synthesized in mammals from the essential amino acids lysine and methionine
As a potent anti-inflammatory compound, LCR has been shown to significantly reduce the levels of inflammatory markers such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF- α)
LCR can also act as an antioxidant during recovery from exercise, thereby mitigating oxidative stress, which may then decrease exercise-induced muscle damage. Guzel et al.
A diagram of the study enrollment is illustrated as a CONSORT (
A placebo-controlled, double-blind design was used to conduct this study. All the testing was conducted in the exercise physiology laboratory at Tarbiat Modares University. Participants were matched into either the PLA or LCR group based on body mass, age, and resistance training experience. During the familiarization session and following informed consent, a research nutritionist and a professional strength and conditioning specialist met with each participant and explained in detail the strength training regimen as well as the nutritional and supplement requirements for the study period.
The timeline of the testing protocol is presented in
In the familiarization session, upper and lower body muscular strength was assessed using an isotonic bench press and leg press (Pullum Power Sports, Luton, United Kingdom) to determine the 1-repetition maximum (1RM). The 1RM was determined following a standard warm-up including 10 repetitions using 50% of participants’ estimated 1RM, 5 repetitions using 70% of their estimated 1RM, and 1 repetition using 90% of their estimated 1RM. Weight was added until the 1RMs were determined. Verbal encouragement was provided during the test to ensure maximal effort. In the testing sessions, participants initially performed a general warm-up of ~5 min of light activity involving all muscles to be tested. Next, using the 1RM that was determined in the familiarization session, participants performed 3 sets of bench and leg press tests. For the first and second sets, participants performed 10 repetitions at 70% of 1RM on the bench press and leg press interspersed by 2 min of rest between sets and 5 min of recovery between each exercise. During the third set, participants were asked to complete as many repetitions as possible. Total lifting volume was calculated by multiplying the lifted weight times the number of completed repetitions. Test-retest reliability of performing upper and lower body strength assessments in our laboratory on resistance-trained participants showed low day-to-day mean coefficients of variation (CVs) and high reliability for the bench press (5.2%, intraclass,
Participants underwent a Wingate test on a computerized Lode Sport Cycle Ergometer (Lode BV, Groningen, The Netherlands) equipped with toe clips at a standardized torque factor of 0.7. The torque factor was set based on the manufacturer’s guidelines relative to the population being tested. The seat position, seat height, handlebar position, and handlebar height were determined during familiarization sessions and repeated for all testing sessions. Participants were instructed to begin pedaling 10 s prior to application of the workload and continue at an all-out maximal capacity for the 30-s Wingate test. Test-retest reliability of performing Wingate test on participants in our laboratory yielded low day-to-day mean CVs and high reliability for absolute peak power (9.3%, intraclass,
Body composition was determined by dual energy X-ray absorptiometry (DXA) (
BL levels were analyzed from finger prick capillary blood samples (
Resting heart rate (RHR) was measured after 10 min of rest in the supine position using standard procedures
Venous blood samples of approximately 10 mL were drawn after fasting for 12 h at the beginning of each testing session. Samples were collected from the antecubital vein in two 7.5-mL collection tubes utilizing a standard vacutainer apparatus. Blood samples were kept at room temperature for 15 min and then centrifuged at 3500 rpm for 10 min. The serum supernatant was removed and stored at -80℃ in polypropylene microcentrifuge tubes for later analysis.
Laboratory measures were conducted at baseline, and weeks 3, 6, and 9. The tests included total and free carnitine, total antioxidant capacity (TAC), MDA, glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), IL-6, and TNF-α. All blood samples were analyzed in a biochemistry laboratory located at Tarbiat Modares University in Tehran, Iran. Day-to-day variability of the oxidative stress markers in our lab yielded a CV range of 0.06-0.23 and an intraclass correlation coefficient range of 0.67-0.90.
Using a randomization code in a double-blind, placebo-controlled manner, participants in both the LCR and PLA groups were orally administered either 2 g/d-1 of LCR (Sina Nutrition, Inc., Tehran, Iran) or PLA (maltodextrin) for a 9-wk period. Both the LCR and PLA supplements were in the form of identical-looking ingestible capsules. Participants were instructed to consume 1 capsule with breakfast and 1 capsule with lunch (1 g per serving). The use of this dose has been shown to be safe and efficacious in previous studies
Participants were instructed to maintain their current dietary intake throughout the study. In addition, they were given instructions during the familiarization session on how to record portion sizes and quantities. Participants completed a 3-day food recall (i.e., 2 weekdays and 1 weekend day) 1 week before all testing sessions. Dietary records were analyzed for total kilocalories, carbohydrate, protein, and fat using the NutraBase IV Clinical Edition (
Participants in both the PLA and LCR groups completed a 4-day/week resistance training program previously described in detail
Further, participants maintained their training intensity between 70-85% of 1RM throughout the study. Rest periods between exercises were 1-2 min. Two certified strength and conditioning specialists supervised all lifts and showed participants how to record training data (i.e., lifts performed, reps, amount of weight lifted, etc.). Training was performed at 3 different training facilities, recorded in training logs, and signed off by selected fitness instructors to verify compliance. All 3 sports clubs used identical training equipment. Furthermore, at each testing session, participants were required to complete a physical activity questionnaire, describing their physical activity during the previous month.
LCR fraction in all samples was analyzed by SRL Inc. (Tokyo, Japan). Total and free LCR levels were measured using an enzyme cycling method with an autoanalyzer (JCA-BM8000 series; JEOL, Tokyo, Japan)
Study-related side effects were assessed using a questionnaire completed at each study visit. Participants reported how well they tolerated the supplement, how well participants followed the supplementation protocol, and whether participants encountered any medical issues and/or adverse symptoms throughout the study. The questionnaire consisted of the following 13 supplement-related symptoms: abdominal or stomach cramps, diarrhea, headache, nausea or vomiting, abdominal discomfort, body odor, depression, dizziness, impaired vision, loss of appetite or weight, swelling in hands or lower legs and feet, tingling sensation, and weakness. The options for each symptom were not at all, somewhat, moderately, very much, or extremely. Participants were asked to rank the frequency and severity of their symptoms during the supplementation period.
Data were analyzed using two-way ANOVA with repeated measures, evaluating for between-group differences as well as changes from baseline in body composition, HR and blood pressure, exercise performance, and blood markers. Data were considered statistically significant when the probability of error was 0.05. Data are presented as mean ± SD or mean change ± 95% CI as appropriate.
The demographic characteristics of the groups are presented in
Group | Mean | |
---|---|---|
Age (y) | PLA | 24.5 ± 1.5 |
LCR | 25.5 ± 1.5 | |
Height (cm) | PLA | 170.4 ± 5.8 |
LCR | 171.3 ± 3.1 | |
Weight (kg) | PLA | 77.9 ± 6.8 |
LCR | 84.1 ± 8.7 | |
Body mass index | PLA | 26.6 ± 3.4 |
LCR | 28.7 ± 3.5 | |
Body fat (%) | PLA | 16.1 ± 5.7 |
LCR | 18.0 ± 6.0 | |
Resting HR (b/min) | PLA | 57.0 ± 5.5 |
LCR | 60.5 ± 7.8 | |
Resting SBP (mmHg) | PLA | 116.1 ± 5.9 |
LCR | 114.5 ± 5.3 | |
Resting DBP (mmHg) | PLA | 77.2 ± 3.9 |
LCR | 74.0 ± 5.3 |
Values are means ± standard deviations. Data for the PLA (n= 11) and LCR (n=12) groups were analyzed by one-way ANOVA.
Food logs were used to measure the average daily caloric and macronutrient intake (
Group | Time (wk) | p-level | |||||
---|---|---|---|---|---|---|---|
Week 0 | Week 3 | Week 6 | Week 9 | ||||
Mean ± SD | Mean ± SD | Mean ± SD | Mean ± SD | ||||
Energy Intake (kcals/day) | PLA | 2,116 ± 718 | 2,147 ± 723 | 2,250 ± 546 | 2,000 ± 311 | G x T | 0.48 |
LCR | 2,449 ± 529 | 2,414 ± 490 | 2,457 ± 549 | 2,444 ± 439 | |||
Protein (g) | PLA | 145.9 ± 38.5 | 151.9 ± 44.2 | 153.6 ± 44.0 | 156.4 ± 59.3 | G x T | 0.57 |
LCR | 147.7 ± 37.4 | 156.3 ± 39.1 | 157.1 ± 38.2 | 162.9 ± 46.1 | |||
Fat (g) | PLA | 74.4 ± 36.7 | 72.2 ± 35.3 | 73.5 ± 33.1 | 74.2 ± 26.0 | G x T | 0.73 |
LCR | 93.4 ± 32.1 | 98.8 ± 28.3 | 96.2 ± 22.8 | 95.0 ± 25.7 | |||
Carbohydrate (g) | PLA | 198.9 ± 68.1 | 202.0 ± 50.3 | 218.2 ± 70.2 | 185.1 ± 32.1 | G x T | 0.46 |
LCR | 258.5 ± 106.0 | 231.2 ± 81.2 | 240.7 ± 91.0 | 218.9 ± 61.0 | |||
Body Weight (kg) | PLA | 77.9 ± 7.09 | 78.1 ± 7.12 | 77.6 ± 7.26 | 78.1 ± 7.36 | G x T | 0.10 |
LCR | 84.3 ± 8.98 | 84.5 ± 8.78 | 84.3 ± 8.85 | 83.7 ± 8.92 | |||
Fat Mass (kg) | PLA | 12.1 ± 5.05 | 12.2 ± 5.29 | 12.0 ± 5.34 | 12.2 ± 5.14 | G x T | 0.15 |
LCR | 14.8 ± 5.26 | 15.1 ± 4.94 | 14.5 ± 4.73 | 14.2 ± 4.74 | |||
Fat-Free Mass (kg) | PLA | 54.1 ± 2.70 | 54.2 ± 2.70 | 54.0 ± 2.67 | 54.2 ± 2.63 | G x T | 0.06 |
LCR | 56.2 ± 2.78 | 56.3 ± 2.67 | 56.1 ± 2.56 | 56.8 ± 2.70 |
Values are means ± standard deviations. Dietary intake data were analyzed by two-way ANOVA with repeated measures. Greenhouse-Geisser group (G), time (T), and group x time (G x T) interaction p-levels are reported with univariate treatment p-levels. The analysis revealed the overall Wilks’ Lambda group (p=0.17), time (p=0.07), and group x time (p=0.44) effects.
Body composition data is shown in
Bench press. Results for all exercise performance variables are presented in
Group | Time (wk) | p-level | |||||
---|---|---|---|---|---|---|---|
Week 0 | Week 3 | Week 6 | Week 9 | ||||
Mean ± SD | Mean ± SD | Mean ± SD | Mean ± SD | ||||
Bench Press Repetitions (n) | PLA | 12.0 ± 3.3 | 12.3 ± 2.9 | 12.9 ± 3.4 | 13.4 ± 3.2 | G x T | 0.08 |
LCR | 14.1 ± 4.0 | 14.2 ± 4.2 | 16.1 ± 3.8 | 17.5 ± 4.1 | |||
Bench Press third Set Lifting Volume (kg) | PLA | 1,042 ± 374 | 1,075 ± 335 | 1,107 ± 321 | 1,159 ± 333 | G x T | 0.17 |
LCR | 1,005 ± 315 | 1,012 ± 311 | 1,152 ± 296 | 1,250 ± 306 | |||
Leg Press Repetitions (n) | PLA | 22.7 ± 8.32 | 24.4 ± 9.16 | 24.3 ± 7.7 | 23.8 ± 9.0 | G x T | 0.01 |
LCR | 26.0 ± 6.92 | 28.4 ± 8.79 | 31.0 ± 7.4 | 34.6 ± 7.59 | |||
Leg Press third Set Lifting Volume (kg) | PLA | 9,032 ± 3,556 | 9,665 ± 3,784 | 9,788 ± 4,036 | 9,364 ± 3,733 | G x T | 0.01 |
LCR | 8,662 ± 3,553 | 9,440 ± 4,062 | 10,145 ± 3,210 | 10,836 ± 3,835 | |||
Wingate Mean Power (Watts) | PLA | 545 ± 85 | 524 ± 76 | 553 ± 75 | 540 ± 92 | G x T | 0.08 |
LCR | 545 ± 85 | 553 ± 133 | 586 ± 120 | 624 ± 120 | |||
Wingate Peak Power (Watts) | PLA | 1,639 ± 303 | 1,580 ± 345 | 1,633 ± 388 | 1,595 ± 441 | G x T | 0.03 |
LCR | 1,712 ± 363 | 1,751 ± 329 | 1,755 ± 302 | 1,952 ± 424 | |||
Wingate Absolute Peak Power (Watts) | PLA | 21.2 ± 4.97 | 20.4 ± 5.34 | 21.1 ± 5.28 | 20.6 ± 6.51 | G x T | 0.04 |
LCR | 20.5 ± 4.70 | 20.9 ± 4.48 | 20.8 ± 4.02 | 23.2 ± 5.20 | |||
Wingate Relative Peak Power (Watts/kg) | PLA | 7.00 ± 0.82 | 6.73 ± 1.03 | 7.13 ± 0.74 | 6.91 ± 0.92 | G x T | 0.10 |
LCR | 6.78 ± 1.92 | 7.67 ± 2.02 | 7.95 ± 1.87 | 8.49 ± 1.82 |
Values are means ± standard deviations. Bench press, leg press, and cycling performance data were analyzed by two-way ANOVA with repeated measures. Greenhouse-Geisser group (G), time (T), and group x time (G x T) interaction p-levels are reported with univariate treatment p-levels. The analysis revealed the overall Wilks’ Lambda group (p=0.03), time (p<0.0001), and group x time (p=0.02) effects.
Leg press. The number of leg press reps increased in the LCR group compared to the PLA group (
Comparisons at week 3 demonstrated a significant increase in leg press third set lifting volume in the LCR group (777 kg, 95% CI, 32.3, 1523) but not in the PLA group (633 kg, 95% CI -145, 1,411). There was a significant mean change from baseline to week 6 in the LCR group (1,483 kg, 95% CI 416, 2,549) but not in the PLA group (756 kg, 95% CI -357, 1,870). A significant improvement was observed at week 9 only in the LCR group (2,683 kg, 95% CI 1,591, 3,774) but not in the PLA group (331 kg, 95% CI -808, 1,471). The percent changes from baseline in LP reps and third set lifting volume in the LCR group were 38.1% and 30.2%, respectively.
The analysis revealed significant interaction effects for peak power (
We observed significant differences between groups in both the total (
Group | Time (wk) | p-level | |||||
---|---|---|---|---|---|---|---|
Week 0 | Week 3 | Week 6 | Week 9 | ||||
Mean ± SD | Mean ± SD | Mean ± SD | Mean ± SD | ||||
3-min post-Wingate test (mmol/L-1) | PLA | 10.7 ± 1.19 | 10.4 ± 1.47 | 10.2 ± 1.93 | 10.5 ± 2.04 | G x T | 0.04 |
LCR | 10.1 ± 0.99 | 9.80 ± 0.91 | 9.34 ± 1.46 | 8.29 ± 0.56 | |||
15-min post-Wingate test (mmol/L-1) | PLA | 10.7 ± 1.06 | 10.5 ± 1.64 | 10.3 ± 1.25 | 10.8 ± 1.24 | G x T | 0.01 |
LCR | 9.87 ± 1.49 | 9.70 ± 0.89 | 9.03 ± 0.92 | 8.27 ± 0.71 | |||
30-min post-Wingate test (mmol/L-1) | PLA | 5.73 ± 1.14 | 6.69 ± 0.98 | 5.75 ± 1.14 | 6.24 ± 1.25 | G x T | 0.04 |
LCR | 4.60 ± 0.97 | 4.51 ± 0.96 | 4.22 ± 1.27 | 3.96 ± 0.99 | |||
TAC (mmol/L) | PLA | 1.45 ± 0.22 | 1.41 ± 0.16 | 1.46 ± 0.19 | 1.43 ± 0.16 | G x T | 0.02 |
LCR | 1.49 ± 0.13 | 1.60 ± 0.10 | 1.66 ± 0.15 | 1.77 ± 0.14 | |||
MDA (μmol/L) | PLA | 0.64 ± 0.13 | 0.63 ± 0.18 | 0.62 ± 0.10 | 0.66 ± 0.14 | G x T | 0.02 |
LCR | 0.56 ± 0.15 | 0.47 ± 0.09 | 0.48 ± 0.16 | 0.31 ± 0.18 | |||
GPx (U/mL) | PLA | 11.9 ± 2.15 | 12.1 ± 2.21 | 11.9 ± 1.81 | 11.4 ± 2.05 | G x T | 0.03 |
LCR | 11.7 ± 2.23 | 12.1 ± 1.92 | 12.2 ± 1.50 | 13.5 ± 1.73 |
Values are means ± standard deviations. Oxidative stress data were analyzed by two-way ANOVA with repeated measures. Greenhouse-Geisser group (G), time (T), and group x time (G x T) interaction p-levels are reported with univariate treatment p-levels. The analysis revealed the overall Wilks’ Lambda group (p=0.056), time (p=0.003), and group x time (p=0.004) effects.
The analysis revealed a significant interaction effect between groups in serum TAC (
The main finding of our study was a significant increase in the BP and LP lifting volume at week 6 and week 9 in the LCR group. In addition, we observed a significant increase in mean power and peak power during the Wingate test. We further examined the effects of LCR on the metabolic response to exercise and found a significant attenuation in BL and markers of post-exercise inflammation. Interestingly, the observed changes in strength findings became manifest at week 6, while the Wingate and metabolic responses became significant at week 9.
There are limited data regarding the underlying mechanisms of LCR supplementation in relation to enhanced muscle mass and strength
We reported that there was a significant reduction in BL accumulation post-30-sec Wingate test. In agreement with this, Jacobs et al.
L-carnitine is involved in the transportation of activated long-chain fatty acids from the cytosol into the mitochondrion and the buffering of acetyl-CoA
The findings of our study also demonstrated that chronic LCR supplementation (2 g/d) increased TAC and GPx markers while it decreased MDA levels. Since no significant changes were observed in dietary intake during the study period, the changes in these markers may be attributed to the antioxidant capacity of LCR. Recent studies have indicated that LCR administration may prevent exercise-induced oxidative stress by decreasing lipid peroxidation, scavenging oxygen radicals, and upregulating the activities of antioxidant enzymes such as GPx, SOD, and CAT
A strength of our study was the duration of the intervention. Supplementing for this length of time helped to delineate the treatment effects; although strength performance improved by week 6, prolonged supplementation was necessary to observe the effects on anaerobic performance. Moreover, our findings were further strengthened by the fact that we recruited participants with 1 year of training experience, thus minimizing any neurological training effects and enhancing the generalizability of our study to individuals engaged in resistance training across various athletic disciplines. Hence, our results add to the known body of literature as LCR has been well studied in endurance athletes, but less is known regarding its effects on those involved in resistance training. A limitation of our study was the absence of muscle biopsy, which could have provided additional data regarding intramuscular LCR levels as well as molecular and cellular responses, including proteins involved in the mTOR pathway. Another limitation was the lack of measuring the stress factors related to the hypothalamus-pituitary-adrenal axis such as corticosterone, which may have helped explain the possible neurophysiological impact of LCR supplementation. From a practical point of view, our results suggested that 2 g/d of LCR supplementation improved muscle strength and anaerobic performance while decreasing post-exercise BL levels and attenuating exercise-induced oxidative stress markers in resistance-trained athletes. However, all of the abovementioned changes occurred independently of any change in body composition or hemodynamic parameters.
The authors acknowledge the subjects for their participation as well as our colleagues in the Kinesiology Department of Tarbiat Modares University who helped with data collection.
RBK has received externally funded grants from industry to research exercise and nutrition, serves as a scientific and legal consultant, and is a university approved scientific advisor for Nutrabolt. CP Earnest serves as a Director of Clinical Sciences for Nutrabolt and is a Research Associate in the ESNL. None of the remaining authors had financial or other interests in connection to the study.