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Department of Nutrition and Agricultural Experiment Station, The University of Tennessee, Knoxville, TN 37996-1900
2To whom correspondence should be addressed. E-mail: dsachan{at}utk.edu
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • carnitine • choline • fat • exercise • humans • leptin
Carnitine is essential for fatty acid translocation (1
) and muscle function (2
), and some studies have shown that carnitine supplementation improves exercise performance (3
–5
). Choline is a lipotropic agent (6
,7
) that prevents deposition of fat in the liver. It is an essential nutrient for humans (8
,9
), providing structure to cell membranes and facilitating transmembrane signaling as well as synthesis and release of acetylcholine (10
,11
). The potential use of choline supplementation for improving physical performance has been reported (12
); however, no direct experimental data are available to support a requirement of choline supplementation for increased physical performance (13
).
Recently, we reported interactive effects of choline and carnitine in normal healthy humans and animals. Choline supplementation resulted in significant conservation of carnitine in humans and guinea pigs (14
,15
); however, this effect of choline did not occur in the adult rats given a choline dosage similar to that of humans and guinea pigs (14
,16
). When rats were given relatively higher doses of choline in combination with caffeine plus carnitine for 4 wk, there was significant conservation of carnitine (17
,18
). The functional consequences of choline-mediated carnitine accretion in tissues have been studied in animal models. Choline supplementation, alone, significantly increased carnitine concentration in the skeletal muscle (14
) and loss of the carcass fat in guinea pigs (19
). In rats, a combination of choline, carnitine and caffeine supplementation significantly reduced fat pad mass and serum leptin concentration (20
) and altered biochemical markers that were indicative of enhanced fatty acid oxidation to acetate (17
). Although exercise endurance was increased in both guinea pigs and rats by the supplements, the respiratory quotient (RQ)3 was not significantly altered to support the argument that fat was being used as the energy substrate in these animals. This contradiction was explained by the fatty acid dumping hypothesis that states that fatty acids are oxidized to acetate, which is excreted in urine as acetylcarnitine (AC) (17
). In light of these observations, we hypothesized that choline and carnitine supplementation with or without exercise would alter carnitine status, body fat and biochemical markers of fat oxidation in free-living humans.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The 19 participants were healthy women who met the inclusion criteria of the study protocol approved by the Institutional Review Board for the Protection of Human Subjects in Research. Most of the participants were from the faculty and student population of the University of Tennessee, Knoxville. They varied in age, 18–54 y; body weight, 47.5–92.7 kg; body mass index (BMI), 18.9–35.9 kg/m2; body fat, 17.9–37.8%; and waist-to-hip ratio (WHR), 0.71–0.89 (Table 1
). They met the following inclusion criteria: 1) no clinical diagnosis of cancer, cardiovascular, gastrointestinal, hepatic or renal disease, hypertension or diabetes; 2) no current use of antibiotics or other prescription medication; 3) no use of vitamin or mineral supplements within 2 wk of the start of the experimental periods; 4) no specific dietary practice for weight loss, such as low fat diet or reduced energy intakes within the past 1 y. Further, women who were pregnant, lactating or using exogenous hormones were excluded from the study. Subjects who met eligibility requirements participated in an orientation meeting where they were specifically asked about their willingness to undertake extra physical activity during the exercise intervention period. Each subject was informed about the nature and the purpose of the study and was required to provide written informed consent to participate in the study.
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The randomized, placebo-control study with three groups lasted 35 d, during which interventions were carried out as shown in Figure 1
. At baseline, habitual dietary intake was assessed and anthropometric measures were taken. Fasting venous blood and 24-h urine samples were collected from each subject on 2 consecutive days before any of the treatments and the mean of the 2-d values was established as the baseline or zero time value. All participants were instructed to maintain their usual dietary pattern and lifestyle including exercise, work and recreation but not to indulge in sexual intercourse a day before or during the 24-h urine collection. They were also asked not to introduce any new foods to their diets or take any nutritional supplements for the duration of the experiment.
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) so as to minimize development of "fishy" breath and thus ensure compliance. The supplements were U.S. Pharmacopeia (USP) grade with purity >98.6%. Each supplement was dissolved in distilled water and a week’s supply dispensed in amber-colored bottles with a coded label and dosing instruction. The placebo bottle provided citric acid at the dosages of 1 g or 0.2 mmol/d. All participants were asked to take supplements with daily meals and keep a record on a daily-supplement sheet that was brought back with the empty bottle on the day of the visit. After taking choline (S1) or carnitine (S2) from 1 to 7 d, both groups consumed choline as well as carnitine from d 8 to d 21. The 1- to 7-d period was established as the choline or carnitine preloading period. Physical activity intervention.
The physical activity intervention period consisted of light to moderate exercise as recommended by the American College of Sports Medicine for cardiorespiratory fitness in healthy adults (21
). All participants were asked to undertake >20 min of aerobic activity, such as walking, jogging and stair climbing, 3–5 d/wk over and above their normal physical activity. In wk 2 of this study all subjects were introduced to an electronic pedometer, the Yamax Digi-Walker SW-701 (Yamax Inc., Tokyo, Japan), and its use for recording their physical activity. They recorded daily walking steps and walking distance (estimated from their strides) as well as nonexercise-related physical activities, such as occupational and household activities. All participants were asked to wear a pedometer all the time during wk 3. There was no attempt to monitor exercise intensity.
Assessment of body composition.
The assessments of body composition were made after an overnight fast on d 0, d 21 and d 35. Body weight was measured at each visit with a Physician Mechanical scale. Barefoot standing height was measured to the nearest 0.1 cm with a vertical height scale. BMI was calculated by dividing weight (in kg) by height (in m2). Skinfold thicknesses were measured three times to the nearest 0.1 mm with a Lange skinfold caliper (Cambridge Scientific Industries, Cambridge, MD) on the one side of the body at the triceps, subscapular, suprailiac, thigh and abdomen. Percentage body fat was estimated using the mean of three readings of triceps, abdomen and suprailiac measurements, as described by Jackson and Pollock (22
). Percentage body fat was also estimated by bioelectrical impedance analysis (BIA). Waist circumference was measured, with a measuring tape, midway between the inferior angle of the ribs and the suprailiac crest, whereas hip circumference was measured at the outermost points of the greater trochanters (23
). The WHR was then calculated.
Dietary assessment.
Dietary intake was assessed at baseline and weekly during the intervention period from the 3-d dietary records. Each of the five 3-d periods consisted of 1 weekend day and 2 weekdays to control for day-of-the-week effects. The participant were instructed by a registered dietitian about recording dietary intake on the food record sheets. Subjects were asked to record the exact description of all food and drink consumed during the 3-d period of 1 wk. Food portion sizes were estimated by using standard household measures. All completed dietary records were reviewed by the dietitian, and were discussed with the subject, if necessary, to resolve any ambiguities regarding accuracy or completeness. Food records were coded, entered and analyzed using the Nutritionist IV program (version 4.1, 1997, First Data Bank,San Bruno,CA).
Blood collection and analysis.
Venous blood samples (13 mL) were collected after overnight fasting (8–12 h) at the beginning or baseline (0 d) and at each visit (Fig. 1)
. Whole blood was collected in vacutainer tubes without anticoagulants and kept on ice. After clotting, serum was separated by centrifugation at 1500 x g for 10 min at 4°C and stored at -80°C until used for determination of ß-hydroxybutyrate, leptin and carnitine concentrations. Serum leptin concentration was determined using a commercial radioimmunoassay kit (Linco Research, St. Louis, MO). The assay used 125I-labeled human leptin and a human leptin antiserum to determine the concentration of leptin in serum. Serum ß-hydroxybutyrate was determined spectrophotometrically at 340 nm by NAD+-linked enzymatic reactions (Sigma kit no.310; Sigma, St. Louis, MO). The serum samples used for ß-hydroxybutyrate determination went through one freeze/thaw cycle for 1.5 y of storage at -80°C before the determination. Serum carnitine was determined by the radioisotopic-enzymatic procedure originally described by Cederblad and Lindstedt (24
) as modified by Sachan et al. (25
). Acetylcarnitine was determined separately according to the method of Pande and Caramancion (26
).
Urine collection and analysis.
All subjects collected two 24-h urine samples during the baseline period and one 24-h urine sample every wk thereafter and recorded the date and time of collection. They were instructed to exclude the first morning void of the starting day but to include the first morning void of the ending day. Polyethylene collection bottles containing thymol as a preservative were provided. The volume of urine was measured then thoroughly mixed, and portions of urine were centrifuged at 1500 x g for 10 min at 4°C, placed in 13 mL of plastic tubes and stored immediately at -80°C until analyzed.
Carnitine in urine was determined by the same method as used for the serum (24
,25
). Samples of urine (20–30 µL) were added to the tubes containing 200 µL of 0.6 mol/L perchloric acid. To form pellets, 100 µL of bovine serum albumin (80 g/L) and enough double-distilled water to make the total volume of 400 µL were added. The tubes were centrifuged at 1500 x g for 10 min at 4°C. An aliquot of supernatant and pellets were used for carnitine assay. For the assay of the urinary AC the urine samples of carnitine-supplemented subjects were diluted 2 to 10 times, depending on the concentration of AC in the urine.
Statistical analysis.
The data are expressed as means ± SEM. All data were statistically evaluated for differences among the means using the Personal Computer Statistical Analysis System for Windows (Version 8e, 2000; SAS Institute,Cary,NC). Two-way ANOVA with repeated measures was performed and, if there was a significant main effect (group, time, interaction of group and time), Duncan’s multiple range test was performed. Simple regression analysis was performed to calculate correlations between the dependent variables. Differences were considered significant at P < 0.05. The superscript letters indicate significant differences among the treatment group means on a given day and the asterisk indicates significant difference from the baseline.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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. There was a reduction of 0.6 to 1.2 kg in the body weight of all groups between 21 and 35 d (wash out period). Body fat (by skinfold thickness) reductions were 0.7 and 1.3% in the S1 and S2 groups, respectively, but that of the placebo group did not change (Table 1)
. Percentage body fat determined by BIA was significantly correlated (r = 0.89) with that determined by the skinfold thickness measurements. Before exercise intervention (7–14 d) the subjects in the S2 group recorded <5000 steps (i.e., <3.7 km/d), which was 51–53% fewer than those taken by the placebo and S1 groups (P < 0.05). The increases in the steps taken due to exercise intervention were significant for the S1 and S2 groups (Table 1)
.
The concentration of serum ß-hydroxybutyrate was higher in the S2 group than in the other groups after 1 wk of carnitine supplementation, and after 2 wk it was lower than the 1 wk peak but still greater than that in the placebo group (Table 2
). The placebo and S1 groups showed peak ß-hydroxybutyrate concentrations on d 21, at which time all values were higher than those at the baseline. Serum leptin concentration was reduced (P < 0.05) after the exercise period (21 d), but there were no significant differences among the groups (Table 2)
. Serum leptin concentration was positively correlated (P < 0.05) with all the anthropometric measurement except the WHR (data not shown).
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). However, on d 7 and d 21, serum TC and NEC were significantly higher in the S2 group than in the placebo group and higher than in the S1 group on d 7. The serum acid-soluble acylcarnitine (ASAC) and AC concentrations were significantly higher in the S2 group than in the other groups after 7 d. On the other hand, the serum acid-insoluble acylcarnitine (AIAC) concentration was higher in the S2 group than in the placebo group after d 21. The serum TC concentration in the placebo group was very stable (within 
2 µmol/L) throughout experimental period. In the S1 group, the serum AC concentration was significantly higher than the baseline concentration after 1 wk of choline plus carnitine (d 14) and it was maintained even after wk 2 of the washout period on d 35. Serum AC concentration was significantly higher in the S2 group after 1 wk of carnitine supplementation and tended to be elevated for the rest of the experiment (P < 0.05). Urinary excretion of various carnitine fractions was significantly higher after 7 d in the S2 group, but after 21 d in S1 group, and it remained elevated until d 35 (Table 4
). The excretion of AC in urine was threefold higher in the S2 group after 7 d compared to the baseline amount. The excretion of carnitine was lower after d 7 in the S1 group compared to the baseline amount but it was elevated from d 14 to d 35 (P < 0.05).
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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) and animals (14
). This conservation would be expected to increase the plasma concentrations of carnitine, but it did not in this study or in our earlier studies (14
,15
). The reason for this is a significant shift of carnitine into the tissues of animals supplemented with choline (14
,17
–19
). It is reasonable, therefore, to expect that choline also promotes preferential portioning of carnitine into human tissues. This explains the relative stability of carnitine concentrations in the plasma compartment of humans and animals in spite of dramatic decreases in urinary carnitine excretion that has been, for most part, accounted for by the tissue pool of carnitine (19
).
Restoration of normal urinary carnitine excretion by additional carnitine supplementation has not been adequately addressed until now. Addition of carnitine (4.2 mmol/d) for 1 wk normalized carnitine concentrations in the choline preloaded (S1) group. This was an important outcome of this study because in our earlier human study serum carnitine concentrations could be restored to only 40% of the control values after supplementation with 6.2 mmol carnitine/d for 3 d (15
). Thus, the choline-mediated deficit of serum and urinary carnitine is fully restored by addition of carnitine in smaller doses (4.2 mmol carnitine/d) for a longer time (7 d), indicating that the tissue compartment is replete. The effect of choline on partitioning of carnitine is consistent and strong, as can be seen in the S2 group where serum and urinary carnitine concentrations fell after 7 d of choline supplementation in spite of 7-d carnitine preloading and continuous carnitine supplementation (14-d values in Tables 3
and 4
). As for the mechanism of this phenomenon, we hypothesize that choline upregulates the sodium-dependent carnitine transporter (OCTN 2) present in most tissues (27
,28
). The possibility of cotransport of carnitine with choline and loss of carnitine in gut has been ruled out (29
).
Choline-mediated tissue carnitine accretion resulted in enhanced fatty acid oxidation, as indicated by the increase in serum ß-hydroxybutyric acid (Table 2)
, serum AC, and urinary acylcarnitines as well as AC (Tables 3
and 4)
. This is similar to the effects of these supplements in guinea pigs (14
) and in rats (17
,18
). Unlike in rats, caffeine was not a part of the supplement mixture in humans; however, the subjects in all groups consumed, on average, 240 mg of caffeine daily from a variety of self-selected foods and beverages as indicated by the nutrient intake data (not shown). This amount of caffeine was lower than that given to rats (360 mg/d) in earlier studies (17
,18
,20
). An inherent limitation of this study, compared to the rat studies, was consumption of about equal amounts of caffeine by the placebo as well as treatment groups. Thus, the independent variables in this human study were carnitine and/or choline and the impact of caffeine remains obscured. Body fat (Table 1)
was unchanged in this short intervention trial in women and thus the practical importance of the biochemical perturbations produced by the supplements remains to be established by a longer-term study.
Exercise intervention in all women decreased body weight and serum leptin concentration but not the body fat (Tables 1
and 2)
. The supplemented groups showed significant (55–120%) increases in walking steps (Table 1)
, and increases in ß-hydroxybutyric acid (Table 2)
as well as urinary acylcarnitine fractions (Table 4)
. The effect of combination of supplements and exercise on biochemical markers of fatty acid oxidation and disposal of acyl groups in urine is sustained 15 d beyond the intervention period (Tables 2
3
4)
. The postexercise decrease in serum leptin concentration was 53, 52 and 59% in placebo, S1 and S2 groups, respectively (Table 2)
. There were complementary decreases in the serum triglycerides and free fatty acids of the S2 group (data not shown). The dramatic effect of exercise on serum leptin in women of this study is unlike that reported in literature and remains a topic of future research.
The mild exercise routine enhanced fat utilization as energy substrate in both supplemented groups, but not in the placebo group, as indicated by the increase in the concentrations of serum ß-hydroxybutyrate beyond that raised by the supplements alone (d 21 vs. d 14 in Table 2
). The effect of exercise on AC was very small, but consistent with the idea of enhanced fatty acid oxidation. Whereas exercise caused a decrease in the urinary acylcarnitine excretion in the placebo group, there was a 21–27% increase in the S1 and S2 groups (d 21 vs. d 14 in Table 4
). Such a loss of acylcarnitines in urine has not been found in the individuals subjected to low or high intensity exercise without supplement (2
,30
). The urinary loss of fatty acid carbons in the form of ASAC and AC in the S2 group continued beyond the 21-d intervention period. It may thus be argued that increased demand for energy by exercise in choline/carnitine-preloaded individuals increases rates of fatty acid oxidation, albeit incomplete, resulting in sustained loss of acyl groups in urine. The energy intake was consistently higher in the S2 group followed by the S1 and placebo group (data not shown). We hypothesize that the sequence of choline/carnitine loading degrades the pathway of complete oxidation of energy substrates to carbon dioxide, resulting in certain waste of energy, and the latter is accentuated and sustained by a mild exercise regimen. The evidence presented here in humans is in concert with the observations in animal models and allows the conclusion that choline promotes carnitine conservation and accretion by tissues that favor incomplete oxidation of fatty acids and disposal of fatty acid carbons in urine as acylcarnitines.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AC, acetylcarnitine; AIAC, acid-insoluble acylcarnitine; ASAC, acid-soluble acylcarnitine; BIA, bioelectrical impedance analysis; BMI, body mass index; NEC, nonesterified carnitine; RQ, respiratory quotient; S1, supplement 1; S2, supplement 2; WHR, waist-to-hip ratio.
Manuscript received 17 July 2002. Initial review completed 19 August 2002. Revision accepted 23 October 2002.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Bremer, J. (1997) The role of carnitine in cell metabolism. De Simone, C. Famularo, G. eds. Carnitine Today 1997:1-37 Landes Bioscience Austin, TX. .
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5. Neumann, G. (1996) Effects of L-carnitine on athletic performance. Seim, H. Loster, H. eds. Carnitine: Pathophysiological Basics and Clinical Applications 1996:61-71 Ponte Press Bochum, Germany. .
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20. Hongu, N. & Sachan, D. S. (2000) Caffeine, carnitine and choline supplementation of rats decreases body fat and serum leptin concentration as does exercise. J. Nutr. 130:152-157.
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29. Daily, J. W., III, Park, E.-S., Hongu, N. & Sachan, D. S. (2002) Choline-induced carnitine conservation by increased fractional tubular reabsorption of carnitine in guinea pigs. Nutr. Res. 22:1219-1230.
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