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1Exercise Science Program, University of Rhode Island, Kingston, Rhode Island 02881; and 2The Schwartz Center for Metabolism and Nutrition, Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio 44109
Submitted 11 November 2002 ; accepted in final form 9 June 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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-adrenoreceptor
activity has previously been shown to mediate amino acid metabolism (Lamont
LS, McCullough AJ, and Kalhan SC. Am J Physiol Endocrinol Metab 268:
E910-E916, 1995; Lamont LS, Patel DG, and Kalhan SC. J Appl Physiol
67: 221-225, 1989). This study was a gender comparison of leucine and lysine
kinetics during a -adrenoreceptor blockade
(1,2-blockade) and a placebo control by
using a double-blind crossover protocol. Subjects exercised at 50% of their
trial-specific maximal O2 consumption (1 h) after 7 days of dietary
control. During exercise with -blockade, men had an increased nonprotein
respiratory exchange ratio (P < 0.001), whereas women had an
increased circulation of free fatty acids (P < 0.001). The genders
also displayed distinct differences in exercise amino acid kinetics. The men,
but not the women, increased leucine oxidation (P < 0.005) and
lysine rate of appearance (P < 0.009) when exercising during
-adrenergic blockade. This study indicates that during -blockade,
exercising men increase their need for amino acids (and carbohydrate) to fuel
energy needs, whereas women increase their mobilization of fat, thereby
requiring less alternative fuels such as carbohydrate and amino acids.
Gender-specific fuel preferences during exercise are regulated by
-adrenergic-receptor activity. Substrate availability during exercise
appears to modulate the amino acid oxidation differences between genders.
L-[1-13C] leucine; L-[
-15N] lysine; prolonged exercise; -adrenergic blockade
-adrenergic-receptor activity has not been studied.
Men may typically have heightened -adrenergic-receptor stimulation
during exercise due to a greater circulating epinephrine and norepinephrine
level that has been reported in some
(7,
13,
21) but not all studies
(15,
18). Despite these reports of
gender differences in -receptor stimulation during exercise, there are
no comparative studies of -adrenergic regulation of amino acid
metabolism. However, previous human studies do indicate that whole body amino
acid metabolism can be mediated with an inhibition of
-adrenergic-receptor activity
(8,
10). Specifically, when
subjects of both genders were exercised in the presence of a
-adrenergic-receptor blockade, there were dramatic increases in leucine
oxidation and lysine rate of appearance
(8). These previous studies did
not compare or isolate specific gender responses
(8,
10). Therefore, the purpose of
this experiment was to determine whether there are gender differences in the
-adrenergic-receptor regulation of leucine and, for comparison purposes,
lysine metabolism.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max; women = 43
± 5.4 vs. men = 48 ± 6.0 ml · kg-1
· min-1; P = not significant (NS)] as
well as body weight (see Table
2). Our human experimentation review board approved this project,
and written, informed consent was obtained from each subject before
participation.
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Dietary and pharmacological procedures. A registered dietitian
designed standardized 1-wk meal plans for all subjects using dietary exchange
procedures (4). An exchange
list for meal planning was given to each subject along with specific menu
ideas. The subjects repeated this weekly meal plan twice: once while ingesting
a placebo (twice a day) and once while ingesting a
1,2-adrenergic blocking agent (propranolol,
80 mg twice a day). Both pills were formulated to be the same color and size
and were distributed in a random, double-blind manner. A drug washout period
of a minimum of 1 wk was interspersed between trials.
These meal plans were designed to be weight maintaining and employed standard metabolic equations to determine daily energy needs (2, 5). The specific Harris-Benedict equation used to determine resting energy expenditure was as follows: women = 655 + (9.6 x weight) + (1.8 x height) - (4.7 x age) and men = 66 + (13.7 x weight) + (5 x height) - (6.8 x age). Each subject was required to maintain a daily dietary logbook. The dietary macronutrient composition was controlled in both genders and was 58-60% carbohydrate, 30% fat, and 10-12% protein. Daily caloric intake was 1,753 ± 89 kcal in the women (7,339 ± 373 kJ) and 2,563 ± 108 kcal in the men (10,731 ± 452 kJ). The dietary protein content was 1 g protein · kg-1 · day-1 for both groups. Compliance with these dietary procedures was evaluated with a written 1-wk dietary logbook.
O2
max· O2
max was determined on day 4 or 5 of each trial with
the use of a graded, cycle ergometry protocol. Therefore, each subject was
O2 max tested twice to
calculate a trial-specific submaximal workload for the subsequent infusion
study. O2 max was
assessed with a metabolic cart that was calibrated with a standard gas mixture
(model 2900, Sensor Medics, Yorba Linda, CA).
O2 max was assumed if
there was a plateau in oxygen uptake
(O2) and/or a respiratory
exchange ratio (RER) that exceeded one at maximal exercise.
Tracer infusion studies. To avoid an acute exercise recovery
effect on leucine or lysine kinetics, the subjects were instructed to refrain
from physical activity for 2 days before each infusion. The subjects reported
to the Clinical Research Center (Case Western Reserve University) in a
postabsorptive state (
15 h) on the morning of day 7 for both
trials. Before each infusion, an intravenous cannula was placed into a
superficial vein in each hand. One cannula was used for the tracer infusions
of L-[1-13C]leucine (99 atom %excess of 13C),
L-[-15N]lysine (99 atom %excess of
15N), and sodium bicarbonate NaH[13C]O3 (99
atom %excess of 13C) (Merck, Dorval, Canada). All tracers were
tested for sterility and pyrogenicity before the infusion and were weighed,
dissolved in normal saline, and filtered (Micropore filter, 0.22 µm). The
second intravenous cannula was used for blood sample collections and was kept
patent with a saline infusion (10 ml/h). This sampling site was warmed to
obtain arterialized venous blood.
Priming doses of the isotopes were administered to reach an early isotopic
steady-state and were 1.2 µmol/kg of NaH13CO3, 4.0
µmol/kg of L-[1-13C]leucine, and 6.8 µmol/kg of
L-[-15N]lysine. These priming doses were followed
by a constant-rate infusion of labeled leucine at 5.0 µmol ·
kg-1 · h-1 and of lysine at
7.0 µmol · kg-1 ·
h-1. A background sample of expired air and venous blood
was obtained from each subject before both experiments were begun. A weighed
amount of labeled water [H218O, 99 atom %excess of
18O; MSD Isotopes] was orally given to assess total body water.
Tracer infusion during rest. The first 3 h of each infusion
protocol included a supine rest that was used to obtain an isotopic plateau
for the determination of resting leucine and lysine kinetics
(8,
9). During this rest period,
the venous blood samples were withdrawn every 30 min. These blood samples were
immediately centrifuged, and the plasma was stored at -70°C for later
biochemical analyses. Breath samples were collected every 30 min by using a
Hans-Rudolph, one-way non-rebreathing valve that was connected to a 5-liter
anesthesia bag. An aliquot of each breath sample was trapped in an evacuated
glass tube for the subsequent analysis of 13CO2.
CO2 production
(CO2) and
O2 were determined
continuously throughout rest. Leucine and lysine kinetics were calculated by
using an averaged isotopic enrichment value (180 min of rest).
Tracer infusion during exercise. After 3 h of supine rest, each
subject began exercising at 50% of his or her trial-specific
O2 max (workloads were
specific for the placebo and -blockade trial). A constant-load,
pan-weight Monark cycle ergometer was used (Varberg, Sweden). Blood samples
were withdrawn at 0, 15, 30, 45, 50, 55, and 60 min of exercise. Heart rates
were determined during rest and throughout exercise at 20, 30, 40, 45, 50, and
60 min. O2 and
CO2 were continuously
monitored with a Hans-Rudolph adult face mask that was interfaced with the
metabolic cart. Aliquots of breath samples were trapped in an evacuated glass
tube at 0, 5, 13, 27, 43, 50, 55, and 57 min of exercise for the subsequent
determination of 13CO2 enrichment. With this
steady-state exercise procedure, there was an isotopic plateau in plasma
[-13C]ketoisocaproate (-KIC) enrichments between 40
and 60 min of exercise (see Table
1). An averaged isotopic enrichment value was used to calculate
amino acid kinetics during exercise (40-60 min of exercise).
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Analytic methods. Plasma free fatty acid (FFA) concentrations were determined according to Laurell and Tebbling (12). Total plasma protein concentration was measured with a refractometer (model SPR-T2, Atago). The percent increase in plasma protein concentration during exercise was used to correct FFA concentrations for fluid volume shifts (19). Total 24-h urine volumes were collected on day 6 of each experiment, and urinary urea nitrogen excretion was determined with a colorimetric assay (640A, Sigma Chemical).
The method of Adams (1) was
used to perform plasma derivatizations, and the n-propyl
N-acetyl ester was used for the subsequent quantitative analyses
(1). The analytic methods
employed to determine the [13C]leucine and expired
13CO2 enrichments have been described elsewhere
(8-10).
Plasma -KIC and lysine enrichments were measured with a Hewlett-Packard
model 5985A gas chromatograph-mass spectrometer with selective ion-monitoring
software. Selected ion monitoring was performed at a mass-to-charge ratio of
273/274 for lysine and of 174/175 for -KIC. The expired CO2
was separated from each breath sample by cryogenic distillation, and the
13CO2- o-12CO2 ratio was measured
on an isotope ratio mass spectrometer
(8-10).
Calculations. Leucine kinetic calculations were corrected for
background enrichment of expired CO2 as well as for bicarbonate
retention. The background enrichment of expired 13CO2
was measured before each infusion. This background enrichment was subtracted
from the isotopic plateau to calculate leucine kinetics
(10). -Blockade had no
measurable effect on the 13C enrichment of CO2
(%13Cplacebo = 1.0871 ± 0.0005 vs.
%13C-blockade = 1.0878 ± 0.0005)
(n = 8). Therefore, no correction was made to breath CO2
because of -blockade. Leucine oxidation was corrected for bicarbonate
retention as previously described
(8). Body composition measures
were determined by using the H218O tracer dilution
method (20). Total body water
and fat-free mass (FFM) were calculated with this labeled-water technique. An
isotopic plateau for expired C18O2 was achieved within 3
h (9,
20).
Data analyses. Steady-state tracer kinetic equations were used to
calculate leucine and lysine kinetics. The reciprocal pool model was used for
the leucine kinetic calculations. The statistical analyses for this study
included the three-way analysis of variance (gender x treatment x
time) for leucine and lysine metabolism, RER, and blood measures. Time was a
repeated measure. Statistical techniques also included the two-way analysis of
variance for O2 max,
resting heart rates, and urinary urea nitrogen (gender x treatment).
When a significant main effect was found, pairwise comparisons were performed
with a Newman-Keuls post hoc test. A probability value of P < 0.05
was considered statistically significant. The statistical power for these data
at an of 0.05 included leucine kinetics (0.81), lysine kinetics
(0.98), indirect calorimetry (0.96), urinary urea nitrogen (0.95), and
circulating free fatty acids (0.96). Values are means ± SE.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max did not change due
to the administration of the -blocking drug (womenplacebo =
42.8 ± 5.42 and women-blocked = 36.0
± 4.24; menplacebo = 47.7 ± 6.04 and
men-blocked = 43.4 ± 3.74
ml·kg-1·min-1;
P = NS). All subjects exhibited a significant reduction in
-adrenergic stimulation during the -blockade trial as demonstrated
by the decrease in resting heart rate (menplacebo = 65.7 ±
2.45 and men-blocked = 50.5 ± 1.32
beats/min; womenplacebo = 65.5 ± 6.3 and
women-blocked = 56.5 ± 3.0 beats/min;
P < 0.002). When both groups exercised in the presence of a
-blockade, the heart rates were significantly lower at all exercise time
points (P < 0.001).
Expired gas measurements during submaximal exercise.
Figure 1 displays the mean
nonprotein RER values for both trials and both genders. The RER was found to
exhibit a significant gender (P < 0.001), a significant treatment
(P < 0.04), and a significant exercise effect (P <
0.01). Therefore, the RER values were significantly greater in the men
compared with the women and significantly increased as a result of
-blocker administration. In the men, the RER during exercise was
increased from rest during the -blockade trial (P < 0.05).
There was no significant gender x exercise interaction for the RER
(P = NS).
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FFA and urinary urea nitrogen concentrations. There was a
significant gender (P < 0.001) and treatment (P <
0.03) effect on FFA concentration. Figure
2 indicates that, during both trials, the FFA concentrations were
greater in the women compared with the men (P < 0.05).
Additionally, during the -blockade trial, the women had a heightened FFA
concentration compared with their placebo control trial (P <
0.05). There was no gender x treatment interaction effect for FFAs
(P = NS).
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Urinary urea nitrogen excretion displayed a significant treatment effect.
There was a significant increase in urinary urea nitrogen excretion during the
-blockade trial (placebo = 0.12 ± 0.02 vs. -blockade = 0.17
± 0.02 g · kg body wt-1 · 24
h-1; P < 0.005). There was no gender
difference in urinary urea nitrogen excretion (P = NS).
Leucine kinetics. The leucine rate of appearance data (whole body
protein breakdown) is located in Table
3. We found no significant gender, treatment, or exercise effect
for leucine rate of appearance (P = NS). However, there was a
significant gender (P < 0.005), treatment (P < 0.05),
and exercise effect (P < 0.001) for leucine oxidation (displayed
in Fig. 3). There was also a
significant gender x time interaction effect for this measure
(P < 0.04). Hence, leucine oxidation was significantly greater in
men compared with women and was greater in exercise compared with rest. Women
showed no change in exercise leucine oxidation when placebo control was
compared with -blockade, but the men had a heightened exercise leucine
oxidation when their -blockade and control trials were compared
(P < 0.05). In addition, leucine oxidation during the
-blockade exercise trial in the men was greater compared with the female
-blockade exercise trial (P < 0.05). Nonoxidative leucine
disposal (protein synthesis) demonstrated no gender or treatment effects.
However, there was a significant exercise effect (P < 0.002).
Table 3 indicates that
nonoxidative leucine disposal was significantly reduced during exercise
compared with rest (P < 0.05).
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Lysine kinetics. Figure
4 illustrates the lysine rate of appearance data for both genders
during both trials. There was a significant gender effect (P <
0.009) and a gender x treatment interaction for lysine rate of
appearance (P < 0.001). During resting conditions, the
-blocked women had a decrease in lysine rate of appearance (P
< 0.05), but no change was observed in the men, thereby explaining the
gender x treatment interaction. A difference between genders in the
direction of change for exercise lysine rate of appearance accounts for the
significant gender x treatment interaction. When exercising during
-blockade, the women had a diminished lysine rate of appearance
(P < 0.05), but the men had an increased lysine rate of appearance
(P < 0.05).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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-adrenergic-receptor blockade and a placebo control in pair-matched men
and women. These gender pairs were matched on age, aerobic fitness, exercise
habits, and body weight. Our subjects were more lean and aerobically fit than
average, two factors that are known to influence gender-specific fuel
utilization during exercise
(15). To eliminate confounding
influences on exercise metabolism, the preexperimental diet of our subjects
was controlled. A gender difference in the -adrenergic regulation of
whole body amino acid metabolism during moderate-intensity, long-term exercise
was found. Specifically, when exercising during a
1,2-adrenergic-receptor blockade, the men
increased their whole body leucine oxidation and lysine rate of appearance,
whereas women exhibited no change in leucine oxidation and decreased their
lysine rate of appearance.
We previously reported that there were no gender differences in lysine rate
of appearance during rest, exercise, or exercise recovery
(9). The present study
indicates, however, that gender and -adrenergic activity interact in
their regulation of lysine kinetics. During -adrenergic blockade and
rest, lysine rate of appearance decreases in women but remains unchanged in
men, thereby explaining the gender x treatment interaction effect. When
the subject exercises in the presence of a -adrenergic blockade, the
lysine rate of appearance increases in men but decreases in women, again
explaining the gender x treatment interaction. The likely explanation
for these findings is that the regulation of lysine kinetics occurs through an
interaction between gender-specific sex hormones and
-adrenergic-receptor activity.
These distinct differences in lysine kinetics were accompanied by gender
differences in leucine metabolism. Leucine rate of appearance or whole body
protein breakdown remained unaffected by gender, -blockade treatment, or
exercise time. Nonoxidative leucine disposal showed a significant main effect
for time. Hence, there was a significant decrease in protein synthesis rate in
both genders due to exercise. As has previously been reported, we found that
the genders differ in whole body leucine oxidation
(9,
14,
17). These men, compared with
women, had a greater rate of leucine oxidation during endurance exercise.
Leucine oxidation further increased in these men but not women when they
exercised in the presence of a -blockade. Exercise in combination with
-adrenergic-receptor blockade has previously been shown to heighten
leucine oxidation rate in humans when studied without regard to gender
(8,
10). It was concluded that
-adrenergic stimulation downregulates whole body leucine oxidation and
that both the 1- and 2-adrenoreceptors
mediate this downregulation (8,
10). The present data indicate
that in men, compared with women, there was heightened branched-chain amino
acid sensitivity to -adrenergic-receptor inhibition. Whereas men doubled
their rate of leucine oxidation when exercising in the presence of a
-blockade, women showed no -adrenergic effect. This gender
dimorphism in leucine oxidation might indicate that there are differences in
the regulation of branched-chain 2-oxoacid dehydrogenase. However, previous
research has failed to show a gender difference in skeletal muscle activation
of branched-chain 2-oxoacid dehydrogenase activation due to exercise
(17). To our knowledge, a
gender comparison of -adrenergic-receptor sensitivity of branched-chain
2-oxoacid dehydrogenase activation has not been done. Alternatively, this
increased whole body leucine oxidation in our -blocked men may be a
metabolic compensation for the lack of other primary fuel sources
(16). Our laboratory
previously postulated that increased exercise leucine oxidation during
-blockade might be due to a fuel-mediated effect on whole body
metabolism (8,
10). That is, leucine
oxidation will be heightened during -blockade in response to a reduction
in other fuel sources such as FFA and glucose
(8,
10). Subsequently, another
research group has found an increased use of alternative fuels when humans
exercised during -adrenoreceptor blockade
(16). They reported a
suppression of lipolysis and FFA availability and an increase in glucose rate
of disposal (carbohydrate oxidation) when humans exercise in the presence of a
-blockade (16).
Unfortunately, a gender comparison was not made in any of these experiments
(8,
10,
16). The present study extends
previous findings to indicate that men, but not women, have a reduction in
lipolysis and hence fat oxidation during -blockade, thereby increasing
their need for alternative fuels such as carbohydrate and amino acids.
This study and others have reported a significant main effect of gender on
exercise energy metabolism (3,
7,
9,
13-15,
17,
18,
21,
22). Both animal and human
studies have linked gender differences in carbohydrate, fat, and amino acid
metabolism during exercise to the female sex hormones (see Ref.
23 for review). It has been
reported numerous times that the genders differ in their relative contribution
of fat and carbohydrate to exercise energy needs
(3,
7,
9,
13-15,
17,
18,
21,
22). Women have a greater
reliance on fat, and men a greater reliance on carbohydrate, to fuel
long-duration exercise when conducted at similar relative intensities. These
data build on those previous studies to indicate that gender-specific fuel
regulation can be mediated by -adrenergic-receptor activity. Men
increase their reliance on carbohydrate when exercising in the presence of a
-adrenergic blockade. On the other hand, women are able to increase
circulating FFA and fat availability during similar conditions (exercise with
-blockade). Therefore, when -adrenergic-receptor activity is
inhibited, men and women will increase their reliance on their gender-specific
preferred fuels (i.e., carbohydrate in men and fat in women). Mittendorfer et
al. (15) recently reported
that whole body lipolytic rate and plasma FFA availability and uptake are
greater in exercising women compared with men. These researchers employed a
different methodological approach than ours, however, and matched their
subjects according to body fat (adiposity)
(15). They speculated that
there could be three possible explanations for the higher lipolytic rates in
women: increased adipose tissue sensitivity to -adrenergic stimulation,
a decreased -adrenergic stimulation, or a combination of these two
mechanisms (15). Our data show
that women have increased adipose tissue sensitivity to adrenergic-receptor
stimulation. It should be noted, however, that there is evidence of
-adrenergic-receptor activity inhibiting lipolysis during exercise in
men but not women (6).
Therefore, sexual dimorphism in fat availability during exercise appears to be
at least partially mediated by -adrenergic-receptor activity.
The significance of this study is that it, for first time, indicates that
gender-specific preferences for amino acid oxidation during exercise are
regulated by -adrenergic activity. It has been known that amino acids
provide a small percentage of energy needs during exercise and that men
oxidize more amino acids than women, and these data now indicate that amino
acids become an important alternative fuel for men (but not women) during
times of substrate deficits. Our data also indicate that women do not need to
draw on amino acids as an alternative fuel during -adrenergic blockade
because of an enhanced lipolytic responsiveness.
In summary, there is a sexual dimorphism in the regulation of whole body
amino acid metabolism during exercise. Leucine oxidation and lysine rate of
appearance during exercise showed a heightened sensitivity to
-adrenergic-receptor blockade in men but not women. This gender
dimorphism was probably a compensation for a reduction in primary fuel sources
in the men, notably circulating FFA. Moreover, women display an enhanced
lipolytic responsiveness to -adrenergic blockade, thereby sparing
alternative fuels. To conclude, gender-specific fuel preferences during
exercise are regulated by -adrenergic-receptor activity. Substrate
availability during exercise appears to modulate the amino acid oxidation
differences between genders.
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DISCLOSURES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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-Adrenergic blockade heightens the
exercise-induced increase in leucine oxidation. Am J Physiol
Endocrinol Metab 268:
E910-E916, 1995.-Adrenergic blockade alters whole-body
leucine metabolism in humans. J Appl Physiol
67: 221-225,
1989.-adrenergic receptor stimulation and blockade on substrate
metabolism during submaximal exercise. Am J Physiol Endocrinol
Metab 280:
E752-E760, 2001.This article has been cited by other articles:
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  S. Fujita, B. B. Rasmussen, J. A. Bell, J. G. Cadenas, and E. Volpi Basal muscle intracellular amino acid kinetics in women and men Am J Physiol Endocrinol Metab, January 1, 2007; 292(1): E77 - E83. [Abstract] [Full Text] [PDF]
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 S. K. Sundaram, O. Muzik, D. C. Chugani, F. Mu, T. J. Mangner, and H. T. Chugani Quantification of Protein Synthesis in the Human Brain Using L-[1-11C]-Leucine PET: Incorporation of Factors for Large Neutral Amino Acids in Plasma and for Amino Acids Recycled from Tissue J. Nucl. Med., November 1, 2006; 47(11): 1787 - 1795. [Abstract] [Full Text] [PDF]
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 J S Volek, C E Forsythe, and W J Kraemer Nutritional aspects of women strength athletes Br. J. Sports Med., September 1, 2006; 40(9): 742 - 748. [Abstract] [Full Text] [PDF]
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 M. J. Hamadeh, M. C. Devries, and M. A. Tarnopolsky Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3592 - 3599. [Abstract] [Full Text] [PDF]
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