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455
Journal of Strength and Conditioning Research, 2003, 17(3), 455–462
q 2003 National Strength & Conditioning Association
The Effects of L-Carnitine L-Tartrate
Supplementation on Hormonal Responses to
Resistance Exercise and Recovery
W
ILLIAM
J. K
RAEMER
,
1
J
EFF
S. V
OLEK
,
1
D
UNCAN
N. F
RENCH
,
1
M
ARTYN
R. R
UBIN
,
1
M
ATTHEW
J. S
HARMAN
,
1
A
NA
L. G
O
´
MEZ
,
1
N
ICHOLAS
A. R
ATAMESS
,
1
R
OBERT
U. N
EWTON
,
2
B
OZENA
J
EMIOLO
,
3
B
RUCE
W. C
RAIG
,
3
AND
K
EIJO
H
A
¨
KKINEN
4
1
Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, Connecticut
06269;
2
Exercise and Sport Science, Edith Cowan University, Joondalup, Western Australia, 6027 Australia;
3
Human Performance Laboratory, Ball State University, Muncie, Indiana 47306;
4
Department of Biology of
Physical Activity, The University of Jyva¨skyla¨, Jyva¨skyla¨, Finland.
ABSTRACT
The purpose of this investigation was to examine the influ-
ence of L-carnitine L-tartrate (LCLT) supplementation using
a balanced, cross-over, placebo-controlled research design on
the anabolic hormone response (i.e., testosterone [T], insulin-
like growth factor-I, insulin-like growth factor-binding pro-
tein-3 [IGFBP-3], and immunofunctional and immunoreac-
tive growth hormone [GHif and GHir]) to acute resistance
exercise. Ten healthy, recreationally weight-trained men
(mean 6 SD age 23.7 6 2.3 years, weight 78.7 6 8.5 kg, and
height 179.2 6 4.6 cm) volunteered and were matched, and
after 3 weeks of supplementation (2 g LCLT per day), fasting
morning blood samples were obtained on six consecutive
days (D1–D6). Subjects performed a squat protocol (5 sets of
15–20 repetitions) on D2. During the squat protocol, blood
samples were obtained before exercise and 0, 15, 30, 120, and
180 minutes postexercise. After a 1-week washout period,
subjects consumed the other supplement for a 3-week peri-
od, and the same experimental protocol was repeated using
the exact same procedures. Expected exercise-induced in-
creases in all of the hormones were observed for GHir, GHif,
IGFBP-3, and T. Over the recovery period, LCLT reduced the
amount of exercise-induced muscle tissue damage, which
was assessed via magnetic resonance imaging scans of the
thigh. LCLT supplementation significantly (p , 0.05) in-
creased IGFBP-3 concentrations prior to and at 30, 120, and
180 minutes after acute exercise. No other direct effects of
LCLT supplementation were observed on the absolute con-
centrations of the hormones examined, but with more un-
damaged tissue, a greater number of intact receptors would
be available for hormonal interactions. These data support
the use of LCLT as a recovery supplement for hypoxic ex-
ercise and lend further insights into the hormonal mecha-
nisms that may help to mediate quicker recovery.
Key Words: hypoxic stress, growth hormone, muscle
damage, testosterone, growth factors, IGFBP-3 binding
protein
Reference Data: Kraemer, W.J., J.S. Volek, D.N. French,
M.R. Rubin, M.J. Sharman, A.L. Go´mez, N.A. Rata-
mess, R.U. Newton, B. Jemiolo, B.W. Craig, and K.
Ha¨kkinen. The effects of L-carnitine L-tartrate supple-
mentation on hormonal responses to resistance excer-
cise and recovery. J. Strength Cond. Res. 17(3):455–462.
2003.
Introduction
E
ndogenous carnitine is a necessary component of
fat oxidation in cells. Specifically, carnitine acts in
a transport system at the level of the mitochondria that
facilitates the transport of fatty acids across the mito-
chondrial matrix for the subsequent metabolism and
energy production via beta-oxidation. As a result of
carnitine’s known role in fat oxidation, dietary supple-
mentation with the amino acid-like nutrient L-carni-
tine was examined extensively in the context of exer-
cise in the early to mid-1990s as a potential tool to
enhance fatty acid delivery to the mitochondria, thus
enhancing fat utilization during exercise (2, 4, 5, 12,
26, 28). Unfortunately, despite a logical theoretical ra-
tional for its use, carnitine supplementation proved to
be largely ineffective in improving exercise perfor-
mance and in enhancing fatty acid oxidation during
exercise, most likely because of the fact that supple-
mental carnitine in the diet has not proven to increase
the skeletal muscle content of carnitine in humans (28),
compared with rats (1).
More recent research on L-carnitine L-tartrate
456 Kraemer, Volek, French, Rubin, Sharman, Go´mez, Ratamess, Newton, Jemiolo, Craig, and Ha¨kkinen
(LCLT) supplementation in the context of exercise has
focused on a different hypothesis separate from the
previously examined role of L-carnitine in fat metab-
olism (27). Recent work from our laboratory involves
the examination of L-carnitine as a potential protective
mechanism to attenuate hypoxic-free radical tissue
damage during exercise and into recovery (27). L-car-
nitine, by accumulating in the capillary endothelial
cells, may enhance oxygen delivery to exercising mus-
cles via a vasodilatory effect on the capillary, thereby
reducing local muscular hypoxia normally observed
during high-intensity exercise and a cascade of events
leading to free radical formation and chemical-induced
tissue disruption and damage. In addition, blood flow
to other important tissues and glands in the body may
be enhanced and provide additional mechanisms be-
yond the circulatory flow to muscle to enhance recov-
ery (e.g., cells of the pituitary gland, liver, and testis
all have complex capillary systems that provide oxy-
gen and other nutrients to these endocrine glands and
provide a route for hormone transport into the circu-
lation). In general, the results from our prior study
provided the first data to support this hypothesis (27).
We found a favorable effect of LCLT supplementation
on endothelial blood flow regulation during and after
moderate-intensity squat exercise, as evidenced by sig-
nificantly less accumulation of markers of purine deg-
radation, free radical formation, tissue damage, and
muscle soreness. In addition, Giamberardino et al. (9)
had also indicated that supplementation with L-car-
nitine (3 g per day for 3 weeks) can attenuate the ex-
ercise-induced delayed onset of muscle soreness and
the accumulation of creatine kinase following eccentric
effort of the quadriceps muscle, but this study focused
more on its impact because of high levels of mechan-
ical damage in which optimal blood flow would not
be present. Thus, LCLT supplementation may provide
benefit in the recovery process from exercise stress, yet
more research is needed to elucidate the potential-me-
diating mechanisms of this process (7, 27).
The biochemical events that occur consequent to in-
tense exercise are numerous and complex and include
catabolism of purines, generation of reactive oxygen
species, and disruption of cell membranes and cyto-
skeleton (26, 27). To promote recovery from individual
exercise bouts, optimal conditions are necessary. Re-
covery involves the coordinated functioning of several
physiological processes that are heavily influenced by
the availability and actions of specific hormones (6, 10,
13–15). Of particular importance to the recovery fol-
lowing exercise-induced muscle damage and regener-
ation of cellular structure are the anabolic hormones
and growth factors, including testosterone, growth
hormone (GH), and insulin-like growth factor-I (IGF-
I) (6, 16–20). Interactions between these hormones and
their muscle cell receptors during the recovery phase
from exercise have the effect of stimulating repair and
promoting structural remodeling through processes of
protein synthesis (14, 15, 20). Enhanced protein turn-
over favors the repair and growth of damaged muscle
tissue and is acutely regulated by the homeostatic in-
teractions of these anabolic hormones. Strenuous ex-
ercise clearly disrupts or damages the structure of
muscle fibers, which later during recovery must un-
dergo a remodeling process. It may therefore be rea-
sonable to consider a link between circulating concen-
trations of anabolic hormones and increased rates of
protein synthesis leading to improved regeneration
and recovery.
The importance of the anabolic hormones during
the recovery process has been highlighted by Mac-
Dougal et al. (20), who observed elevated protein syn-
thesis in trained muscle up to 36 hours after the com-
pletion of resistance exercise. Many studies have
shown that the circulating concentrations of anabolic
hormones are acutely increased following resistance
exercise (16–19). In addition, studies using supraphys-
iological doses of testosterone have further document-
ed its anabolic effect on muscle tissue (3, 15). Though
previous research has indicated L-carnitine may have
a protective mechanism during exercise and promotes
increased recovery following exercise (7, 27), no stud-
ies have examined the effects of L-carnitine supple-
mentation on anabolic hormones and growth factors
following resistance exercise. It therefore remains un-
known whether the improved recovery status reported
in previous studies (7, 9, 27) is the consequence of
changes in circulating concentrations of anabolic hor-
mones and their ability to augment cell-tissue repair
and regeneration. Therefore, the purpose of this inves-
tigation was to examine the influence of LCLT supple-
mentation on the anabolic hormone response to acute
resistance exercise.
Methods
Experimental Approach to the Problem
We wanted to further extend our understanding about
the recovery benefits and possible mechanisms related
to LCLT supplementation and hormonal factors me-
diating such anabolic repair have not been elucidated.
This study involved a balanced, cross-over, placebo-
controlled research design that examined the effects of
LCLT on markers of anabolic hormonal response after
concentric-eccentric squat exercise. Subjects were
matched for pretesting clinical values, activity back-
ground, nutritional patterns, and body size and then
randomly assigned to either an LCLT or placebo group
in a double-blind fashion. After 3 weeks of supple-
mentation (2 g LCLT per day), fasting morning blood
samples were obtained on 6 consecutive days (D1–D6).
Subjects performed a concentric-eccentric squat pro-
tocol (5 sets of 15–20 repetitions) on D2. During the
squat protocol, blood samples were obtained before
L-Carnitine L-Tartrate and Exercise Recovery
457
exercise and 0, 15, 30, 120, and 180 minutes after ex-
ercise. After a 1-week washout period, subjects con-
sumed the other supplement for a 3-week period, and
the same experimental protocol was repeated using
the exact same procedures.
Subjects
This study extended our work from our prior study
using the same 10 healthy, recreationally weight-
trained men with a mean 6 SD age 23.7 6 2.3 years,
weight 78.7 6 8.5 kg, and height 179.2 6 4.6 cm who
served as subjects. All subjects were required to be
engaged in a strength-training program that included
the squat exercise for 1 year before the study to exclude
individuals that would experience a high degree of
damage to the quadriceps in response to squatting for
the first time. Subjects continued their normal training
with the exception of the time period between D1 and
D6 during which they were not allowed to train. All
subjects were informed of the purpose and possible
risks of this investigation before signing an informed
consent document approved by the institutional re-
view board. A registered dietitian was utilized to
screen the potential subjects for dietary behaviors or
confounding supplement use. Dietary and activity logs
were used to standardize the behaviors under each ex-
perimental condition to remove the potential for con-
founding nutritional and behavioral influences.
Supplementation Protocol
Subjects were provided with capsules of either L-CAR-
NIPURE LCLT (Lonza, Fair Lawn, NJ) containing 736
mg LCLT (500 mg L-carnitine and 236 mg L-tartrate)
or an identical-looking placebo (powdered cellulose)
with written instructions to consume 2 capsules with
breakfast and lunch for a total dose of 2 g L-carnitine
per day. Supplementation commenced 3 weeks before
the squat protocol and continued through recovery.
This dose of carnitine was chosen to maximize plasma
carnitine concentrations without exceeding the renal
threshold for carnitine (11, 25). Blood concentrations
acted as the internal marker of adherence to the pro-
tocol. This dose has also been shown to be safe (24).
Exercise Protocol
The squat exercise protocol was performed on a Ply-
ometric Power System (PPS, Lismore, Australia) pre-
viously described in detail (29). Briefly, the PPS allows
only vertical movement of the bar. Linear bearings at-
tached to either end of the bar allow it to slide up and
down 2 steel shafts with a minimum of friction. We
determined each subject’s 1 repetition maximum
(1RM) in the squat exercise 1 week before any supple-
mentation using standard procedures in our labora-
tory (17). Pilot studies involving different exercise
loads and magnetic resonance imaging (MRI) scans
were performed to determine an exercise intensity that
would elicit muscle tissue disruption but not severe
damage to maximize the potential for LCLT to reduce
hypoxia-mediated biochemical responses to exercise
stress. The exercise protocol was performed in the af-
ternoon 3 hours after lunch (reproduced by each sub-
ject during both exercise days) and 3 hours after the
last dose of carnitine on D2. After a standardized
warm-up (5 minutes of cycling), subjects performed 5
sets of 15–20 repetitions of squat with a load equal to
50% of their previously determined 1RM squat. There
was a 2-minute recovery between each set. The load
was decreased if ,15 repetitions were performed.
Muscle Tissue Disruption
Direct assessment of muscle tissue disruption and re-
pair was evaluated using MRI cross-sections and spin-
spin relaxation time of the thigh muscles before the
exercise test and 1 and 4 days postexercise using meth-
ods previously described by Dudley et al. (8) in detail.
The same investigator did all of the measurements
with a reliability of R 5 0.99. Scans were collected
using a 0.3-Tesla open MRI magnet (AIRIS II, Hitachi
Medical Systems America, Twinsburg, OH), and areas
were measured with the National Institutes of Health
(NIH) Macintosh computer program, NIH Image
1.55b 20, a MacIntosh Quadra 800 computer (Apple
Computer, Inc., Cupertino, CA), and a scanner
(ArtixScan 1100, Microtek Laboratories, Inc., Redondo
Beach, CA). NIH Image 1.55b 20 uses pixels of light to
determine the area of skeletal muscle where damage
occurs.
Blood Collections
Blood samples were obtained on 6 consecutive days at
the same time of the morning after a 12-hour overnight
fast and abstinence from alcohol and strenuous exer-
cise. The last dose of carnitine was consumed during
lunch the day before each morning blood draw (;18–
20 hours earlier). Subjects reported to the laboratory
between 7:00 and 9:00
AM
and rested quietly for 10
minutes in the supine position, and ;30 ml of blood
were obtained from an antecubital vein with a 20-
gauge needle and Vacutainers. On exercise days, a flex-
ible catheter was inserted into a forearm vein, which
was kept patent with a constant saline drip (60 ml·h
21
).
Before all blood collections, 3 ml of blood were with-
drawn and discarded to avoid dilution of the sample,
and ;30 ml were subsequently withdrawn and placed
in 2 10-ml tubes with a clot activator and 1 10-ml tube
containing EDTA. Within 15 minutes, whole blood
was centrifuged (1,200g for 15 minutes at 108 C), and
the resultant serum-plasma was divided into aliquots
and stored frozen at 2808 C. Subjects rested quietly in
a seated position during the 3-hour postexercise re-
covery period.
Biochemical Analyses
Circulating immunoreactive plasma GH was mea-
sured via the Nichols immunoradiometric assay
458 Kraemer, Volek, French, Rubin, Sharman, Go´mez, Ratamess, Newton, Jemiolo, Craig, and Ha¨kkinen
Figure 1. Responses of immunoreactive growth hormone
to the squat exercise protocol. Significant increases (p ,
0.05) above rest at 0, 15, and 30 minutes postexercise with
no differences between placebo (dashed line) and L-
carnitine L-tartrate (solid line).
(IRMA) (Nichols Institute Diagnostics, San Juan Cap-
istrano, CA). This commercially available assay uses
two monoclonal antibodies of high affinity and spec-
ificity for GH. Each antibody detects a different epi-
tope on the GH molecule. One antibody is labeled
with
125
I for detection and the other is coupled to bi-
otin. The sensitivity for this assay is 0.04 dn·ml. Intra-
assay variances were less than 5%.
Immunofunctional plasma GH was determined in
an assay using an amplified 2-step sandwich-type as-
say requiring an anti-GH monoclonal antibody and
biotinylated recombinant GH binding protein (GHBP)
that bind, respectively, to GH receptor-binding site 2
and site 1 present on all ‘‘biologically active’’ GH mol-
ecules (Diagnostics Systems Laboratories, Inc. [DSL],
Webster, TX). Plasma samples were incubated sequen-
tially (with intervening wash steps) with (a) an im-
mobilized anti-GH antibody, (b) biotinylated GHBP
followed by streptavidin-labeled with horseradish per-
oxidase, and finally (c) tetramethylbenzidine substrate.
After addition of an acidic stop solution, enzyme turn-
over was determined by dual-wavelength absorbency
measurements at 450 and 630 nm. The absorbancy
measured is directly proportional to the concentration
of biologically active ‘‘intact’’ GH that possesses both
GH receptor-binding sites. The sensitivity for this as-
say, when the B
0
6 2 SD method was used, was 0.20
ng·ml
21
. Intra-assay variances for low, medium, and
high GH concentrations were less than 9%.
Total serum IGF-I was determined via 2-site IRMA
(DSL). This assay includes a simple ethanol extraction
procedure in which IGF-I is separated from its binding
protein in the serum sample, a step considered to be
essential for accurate IGF-I measurement. This is a
noncompetitive, sandwich-type assay in which the an-
alyte is sandwiched between 2 antibodies, 1 immobi-
lized to the wall of the tube and the other radiolabeled
with
125
I for detection. The sensitivity of this assay is
0.03 ng·ml
21
. Intra-assay variances were less than 5%.
Measurement of circulating IGFBP-3 was per-
formed using a 2-site coated-tube IRMA (DSL). This
IRMA is a noncompetitive assay in which the analyte
to be measured is sandwiched between 2 antibodies.
The first antibody is immobilized on the inside walls
of the tube, and the other is radiolabeled for detection.
The sensitivity of this assay is 0.5 ng·ml
21
. Intra-assay
variances were less than 5%.
Total serum testosterone was assayed in duplicate
using a sold-phase
125
I-labeled radioimmunoassay
with a sensitivity of 0.278 nmol·L
21
(DSL). Intra-assay
variances were less than 5%.
Statistical Analyses
A 2-way repeated-measures analysis of variance (AN-
OVA) was used to evaluate changes over time and be-
tween the L-carnitine and placebo conditions. Trape-
zoidal analysis over the data collection time points was
used to determine area under the curve values. Tests
for normality of distribution (Kolmogorov-Smirnov
chi-square test) and homogeneity of variance (Levene’s
test) were used on all data sets prior to ANOVAs. Post
hoc comparisons were accomplished via a Fisher’s
least significant difference (LSD) test or Tukey test
when appropriate. Statistical power was determined to
be .0.80 for all measures for the sample size used at
the 0.05 alpha level (nQuery Advisor software, Statis-
tical Solutions, Saugus, MA). All statistical significance
in this study was set at p # 0.05.
Results
The responses of immunoreactive GH (Figure 1) and
immunofunctional GH (Figure 2) demonstrated iden-
tical responses with significant increases above rest at
0, 15, and 30 minutes postexercise. The magnitude of
the concentrations of immunoreactive GH was all
greater than the immunofunctional GH values. No dif-
ferences were observed between the LCLT and placebo
conditions.
The responses of IGF-I to the squat exercise proto-
col (Figure 3) demonstrated no significant exercise-in-
duced changes or any differences between the placebo
and LCLT treatment conditions.
The responses of IGFBP-3 to the squat exercise pro-
tocol (Figure 4) demonstrated a significant increase
above rest at 0 minutes after exercise. There were sig-
nificant differences between the placebo and LCLT
treatment conditions on D1 and D2 as well as at 30,
120, and 180 minutes after the exercise protocol with
the LCLT treatment responding with higher binding
protein. In addition, the LCLT treatment demonstrated
a significantly higher area under the curve concentra-
tions than the placebo treatment.
The responses of testosterone to the squat exercise
L-Carnitine L-Tartrate and Exercise Recovery
459
Figure 2. Responses of immunofunctional growth
hormone to the squat exercise protocol. Significant
increases (p , 0.05) above rest at 0, 15, and 30 minutes
postexercise with no differences between placebo (dashed
line) and L-carnitine L-tartrate (solid line).
Figure 3. Responses of total insulin-like growth factor-I to
the squat exercise protocol. No significant (p . 0.05)
changes with exercise and no differences between placebo
(dashed line) and L-carnitine L-tartrate (solid line).
Figure 4. Responses of insulin-like growth factor-binding
protein-3 to the squat exercise protocol. Significant
increases (p , 0.05) above rest at 0 minutes postexercise
with significant differences between placebo (dashed line)
and L-carnitine L-tartrate (solid line) at D1 and D2 and at
30, 120, and 180 minutes after exercise.
Figure 5. Responses of testosterone to the squat exercise
protocol. Significant increases (p , 0.05) above rest at 15
minutes postexercise with no significant differences
between placebo (dashed line) and L-carnitine L-tartrate
(solid line) treatment groups.
protocol (Figure 5) demonstrated significant increases
above rest at 15 minutes postexercise. There were no
differences between the placebo and LCLT treatment
conditions.
Using a control resting MRI cross-sectional scan of
the midthigh as the baseline for comparison with post-
exercise changes to determine the effects of the resis-
tance exercise stress, the percentage of muscle tissue
disruption-damage assessed at D3 and D6 were 23 6
8and166 5% for LCLT and 39 6 5and296 6% for
placebo, respectively. The percent muscle tissue dis-
ruption was significantly greater during placebo treat-
ment condition. The delta damage from D3 to D6 was
significantly less in the LCLT treatment condition.
Discussion
Accumulation of LCLT in the capillary endothelial
cells appears to have enhanced the oxygen delivery to
exercising muscles via a vasodilatory effect on the cap-
illary, resulting in a reduced local muscular hypoxia
typically observed during exercise stress. This appears
to have reduced the magnitude of damage related to
prevented to free radical formation and chemical-in-
duced tissue disruption and damage (27). Important
to this investigation was the finding that LCLT sup-
plementation significantly reduced the amount of
damage by 7–10% of the area allowing for greater
numbers of stabilized cellular receptors available for
binding interactions and cellular signals for increased
protein synthesis or anticatabolic effects at the receptor
level. This finding may provide key insights into the
mechanisms of action and the response patterns of the
anabolic hormones in circulation. Thus, the greater
amount of undamaged tissue may have preserved the
ability for hormonal interactions with muscle tissue
460 Kraemer, Volek, French, Rubin, Sharman, Go´mez, Ratamess, Newton, Jemiolo, Craig, and Ha¨kkinen
and help to explain the reduced progression of chem-
ical tissue damage that occurred from D3 to D6, com-
pared with the placebo treatment conditions.
Discovered in 1957, the evolution of the study of
the IGF-I system has been shown to be an important
hormonal interface for metabolic, mitogenic, and an-
abolic cellular dynamics in response to exercise stress
(23). With the use of 3 weeks of LCLT supplementa-
tion, increases in IGFP-3 were observed on D1 and D2
and from 30 to 180 minutes during the recovery period
following the acute squat exercise protocol. Concomi-
tantly no increases or supplement effects were ob-
served with IGF-I concentrations. The interpretation of
these findings needs to be examined in unison because
of the intimate interrelationships of their cybernetic
function.
IGFBP-3 is the predominant IGF-binding protein in
adult serum and more than 75% of IGF-I circulates in
a 150 kD ternary complex comprised of IGF-I–IGFBP-
3 and an acid labile subunit. Smaller proportions of
IGF-I are bound to smaller-molecular-weight–binding
proteins or in free form. It appears that IGFBP-3 is
independent of GH regulation and inhibits IGF-I ac-
tions implying that the IGFBP-3 can modulate IGF-I
binding to its receptor and thereby affect and titrate
biological actions. This essentially allows the seques-
tering of IGF-I away from its cellular receptor when
increases of the binding protein occur. It is the free
and nonternary complex that has the acceptable mo-
lecular size to pass through the capillary fenestrations
and into the extracellular fluid to interact with the cel-
lular membrane to exert its effects. The IGFBP-3 can
increase and extend the half-life of the IGF-I–IGFBP-3
complex by 1–2 hours before degradation of the ter-
nary complex occurs. Thus, this binding protein helps
to provide a mechanism for a longer period of time in
which IGF-I concentrations can be biologically dosed
to enhance the cellular interactive environment with
free IGF-I. This may be one of the hormonal mecha-
nisms that provides for more optimal trophic interac-
tions that would positively influence protein metabo-
lism and enhance muscle tissue repair. Thus, although
no changes in the IGF-I concentrations were observed,
the use of LCLT supplementation apparently enhances
viability, half-life, and biocompartment kinetics of IGF-
I. Such findings extend the supplementation construct
of LCLT to affecting the partitioning of the IGF-I sys-
tem in a manner that can be enhance cellular interac-
tions.
The lack of an exercise-induced increase in IGF-I
concentrations in response to acute exercise stress may
well be related to the already highly conditioned na-
ture of our subjects in this study. This is supported by
findings that resistance training has been shown to
have the ability to increase resting serum concentra-
tions of IGF-I (21). In prior studies by our laboratory
groups, we have observed increases or no changes in
response to a resistance exercise protocol. Although
many factors related to composition of the exercise
stress might be put forth as to possible reasons for a
lack of change with acute exercise, one important ob-
servation is the fact that the starting concentrations of
IGF-I may be the most important factor related to the
potential to observe an exercise-induced increase in
the circulatory blood (16, 18, 19). Higher starting con-
centrations may inhibit the ability to stimulate a fur-
ther increase in IGF-I with exercise stress because of
negative feedback mechanisms or at least mask the
small changes that may occur within a very narrow
biological window of the maximal endogenous con-
centrations possible with exercise stress. The concen-
trations found in the current study were similar to our
group’s prior study in which no increases in response
to acute resistance exercise stress were observed (16,
19) and were much higher than earlier research dem-
onstrating increases (17, 18).
No changes were observed in immunoreactive GH
or immunofunctional GH in response to LCLT supple-
mentation. Although only a few studies have exam-
ined resistance exercise and immunofunctional GH re-
sponses concomitant with immunoreactive GH con-
centrations, expected increases with acute exercise
stress were observed and the lower magnitude of con-
centrations of immunofunctional GH, compared with
immunoreactive GH were consistent with the findings
in our prior research team’s reports (13, 22). The in-
crease in GH is important for the somatogenic and
metabolic actions following resistance exercise and has
been thought to be one of the major influences of an-
abolic actions including influencing the IGF system
and testosterone. The immunofunctional assay used in
this investigation was designed on the basis that this
assay detects only those intact molecules that possess
both sites 1 and 2, which are required to induce signal
transduction. Conversely, the Nichols IRMA used to
determine immunoreactive GH concentrations utilizes
monoclonal antibodies that interact with epitopes of
unknown specificity.
Interestingly, the immunofunctional concentrations
were almost 10-fold lower in response to this specific
resistance exercise protocol, compared with our prior
work using 10RM at a minimal of 75% of 1RM. This
may support the importance of load to anabolic hor-
monal signals. However, as we have previously theo-
rized the biological importance of other GH variants
not able to dimerize receptors cannot be dismissed as
these forms may have important inhibitory and mod-
ulatory roles in the regulation cellular events (22). The
reproducibility of the hormonal fingerprints of GH as
well as the other hormones in this study again show
that one can examine circulatory hormones with great
sensitivity (19). The molar concentrations of GH hor-
mone(s) had a greater amount of undamaged area of
muscle tissues to interact with during the LCLT treat-
L-Carnitine L-Tartrate and Exercise Recovery
461
ment condition, potentially leading to a greater ana-
bolic effect (6). This may be a vital factor for the op-
timal muscle tissue interactions of both biologically
potent immunofunctional GH and potentially potent
immunoreactive GH. How aggregates as measured by
other bioassays (13) (i.e., higher-molecular-weight iso-
forms) of such GH monomers respond to such LCLT
supplementation remains a missing perspective in the
study of the pituitary function and exercise responses.
Different from peptide hormone interfaces with the
cell myonuclei, testosterone as a steroid hormone has
a more direct interaction on the DNA regulatory ele-
ment in skeletal muscle. Increases in serum testoster-
one were observed with exercise stress under both the
LCLT and placebo treatment conditions at 15 minutes
of recovery, demonstrating as with immunofunctional
GH a reduced magnitude of the response pattern most
likely caused by the loading used in the study design
(16, 17, 19). No absolute effect of LCLT supplementa-
tion was observed, but again more undamaged muscle
tissue was available for hormonal interactions during
the LCLT treatment condition. The importance of this
fact lies in the greater number of receptors that are
stabilized leading to greater transcription and ulti-
mately to greater protein synthesis (15). Thus, the im-
portance of optimizing tissue interfaces for hormonal
interactions may play an important role in optimizing
the recovery patterns of muscle tissue as demonstrated
with LCLT supplementation in this study and our pri-
or work.
In summary, the anabolic hormones examined in
this study showed amazing reproducibility over the
course of the investigation. The LCLT supplementation
had been previously shown to reduce the hypoxic
stress and chemical damage related to such exercise
and in addition had reduced soreness levels most like-
ly caused by less tissue damage. IGFBP-3 concentra-
tions were most dramatic in their response patterns to
the LCLT supplementation with our volunteers acting
as their own controls. The net result appears to be a
greater preservation of IGF-I concentrations in recovery
as well as the days leading up to the exercise stress.
The time course for the increase in IGFBP-3 with LCLT
supplementation after an exercise stress remains spec-
ulative and in need of further research. Each of the
hormones would seem to benefit from reduced muscle
tissue damage allowing greater numbers of intact and
viable receptors for both direct (steroid) and indirect
(peptide hormones) interactions with the DNA regu-
latory elements related to protein synthesis.
Practical Applications
LCLT supplementation was demonstrated to reduce
the amount of muscle tissue damage most likely me-
diated though a reduction in hypoxia-related damage
from free radicals resulting in the typical chemical
damage days after the mechanical events associated
with the resistance exercise protocol. Hormonal mech-
anisms appear to be enhanced because of the greater
viability of receptors to successfully interact with the
anabolic hormonal signals. The concentrations used in
the current study have been shown to be safe, and
these data provide additional support for positive ef-
fects of LCLT use as a recovery supplement for hyp-
oxic exercise stress.
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Acknowledgments
We would like to thank a dedicated group of test subjects
that made this work possible and laboratory staff for their
help with this project. This study was supported in part by
a grant from Lonza Inc., Fair Lawn, NJ.
Address correspondence to William J. Kraemer, Ph.D.,
kraemer@uconnvm.uconn.edu.
