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World Journal of Sport Sciences 3 (S): 668-672, 2010
ISSN 2078-4724
© IDOSI Publications, 2010
Estimation of the Integrity of Vital Organs and the Balance Between
Catabolism and Anabolism in Athletes and Non-Athletes
1
H. Heshmat, 2A. Moussa and 3O. Emara
1
Department of Physiology, Faculty of Physical Education, Zagazig University, Egypt
2
Department of Training, Faculty of Physical Education, Kena University, Egypt
3
Department of Health Science, Faculty of Physical Education, Kena University, Egypt
Abstract: The purpose of this study was to estimate the integrity of vital organs and the balance between
catabolism and anabolism in athletes and non-athletes. 20 students in Kena University were divided to
two equal groups, athletes and non athletes and they were subjected to sub-maximal ergometric test.
Blood samples were obtained before and after the tests, maximal oxygen consumption values were
estimated after each test, also Creatine Kinase, Aminotransferases (ALT, AST), Cortisol and testosterone
levels were determined pre and post tests using commercial kits, spectrophotometer and Elisa techniques.
The results revealed significant increase in Creatine Kinase, ALT, AST, Cortisol and Testosterone in
both groups, in case of post tests. At rest, data revealed different results in the studied Parameters
as the CK, Cortisol and Testosterone rise in case of athletes indicated physical, mental stress. The results
indicated that the measurement of enzymes lets one estimate the integrity of vital organs (Liver, Muscle)
where as the Cortisol and Testosterone indicate the balance between catabolism and anabolism in athletes and
non-athletes.
Key words: Catabolism % Anabolism % Enzymes % Hormones
INTRODUCTION
Ferrando et al. [5] added that testosterone acts by
increasing muscle protein synthesis without having
any effect on protein breakdown, nor does testosterone
have any effect on the transport of amino acids into
muscle fibers. Wolfe et al. [6] reported that testosterone
acts via the genome by enhancing transcription and not
by accelerating translation. Thus, the aim of this study
was to estimate the integrity of vital organs (liver, muscle)
and the balance between catabolism and anabolism in
athletes and non athletes.
Creatine Kinase catalyzes the interconvention of
CP and ATP. The enzyme is present in almost all tissues
but is highest in muscle, the heart and in the brain. The
serum CK concentration rises when an organ that
contains the enzyme is damaged. The serum CK
concentration is probably the best biochemical marker of
muscle fiber damage [1]. Aminotransferases catalyze the
transfer of an amino group from " - amino acid to " keto
acid.
This transfer is necessary for amino acid
metabolism. The serum ALT and AST concentration are
low unless the organ that contain them are harmed [2].
Previous studies have established that an acute bout of
exercise stimulates hormonal responses in the
hypothalamic - pituitary - gonad - adrenal axis. They
reported acute increases in concentrations of cortisol
and testosterone in response to submaximal exercise [3].
Cortisol is often credited which being the principal
catabolic hormone because of its central role in
proteolysis. Also, cortisol’s importance for protein
turnover exceeds its importance for glucoregulation [4].
MATERIALS AND METHODS
Research Sample: 20 male volunteers students were
assigned to the study, 10 athletes and 10 non athletes.
Each subject gave informed written consent to participate
in the study. Subjects were not taking any medications
and had no history of any endocrine disorders. Subjects
characteristics were as follows (mean ± SD). Group 1 non
athletes n=10, age 19.6±4yr, height 172.4±7.3 cm and
weight 70.2±6.4 kg. Group 2 athletes n=10, age 20.1±4.2
yr., height 173.3±6.5 cm, weight 71.3±5.8 kg. No significant
Corresponding Author: H. Heshmat, Department of Physiology, Faculty of Physical Education, Zagazig University, Egypt
668
World J. Sport Sci., 3 (S): 668-672, 2010
Table 1: The effect of test determination on maximal oxygen consumption
differences were observed between the two groups for
the physical characteristics. Prior to the test, subjects
were familiarized with the procedures. A 5 min. warm up
was done before tests determinations on the bicycle
ergometer, submaximal intensity was performed according
to protocol of the American College of Sports Medicine.
Exercise intensities for these tests were predetermined
for each subject in a time (– 10 min). The times of the test
between subjects were similar. This was important to help
separate out diurnal effects on hormonal responses to the
test. Maximal oxygen consumption (Vo2 max) was
determined using Astrand nomogram [7]. The tests were
performed at the same time of the day for all individuals at
several days, to reduce the effects of any diurnal variation
on the hormonal concentrations. Subjects refrained
from food for 8 h., 5 ml. Blood samples were obtained from
a superficial vein utilizing sterile syringe, before and
after the tests and then centrifuged 2000 xg for 15 min.,
serum was immediately frozen to -20°C until analyzed.
Creatinekinase, Aminotransferase (ALT, AST) and
Cortisol, Testosterone were analyzed using commercial
kits, spectrophotometer and Elisa technique.
Serum testosterone hormone was assayed by kits
supplied by Diagnostic System Lab, Texas and USA [8].
Serum cortisol hormone was assayed according to Foster
and Dunn [9]. Serum AST and ALT were assayed [10],
serum CPK was analyzed using colorimetric method [11].
Statistical evaluation of the data was accomplished
using SPSS; all data were expressed as mean ± SD. The
statistical significance was evaluated by using student
test, for comparison between athletes and non athletes.
P<0.05 was considered to indicated a significant
difference between the two groups.
and ALT, AST, CK, Cortisol and Testosterone (non athletes)
Group 1
Variables
Before
After
P value
Vo2max ml/kg/min
-
36.3±3.2
ALT (SGPT) IU/L
13.1±2.3
26.3±3.1
S
AST (SGOT) IU/L
14.2±2.6
32.3±5.1
S
CK IU/L
25.3±4.1
44.3±4.9
S
Cortisol ug/dl
11.6±2.1
26.4±3.6
S
Testosterone n mol/L
12±1.5
21±3.6
S
*P < 0.05 values mean ± standard deviation
Table 2: The effect of test determination on maximal oxygen consumption
and
ALT,
AST, CK, Cortisol and Testosterone (athletes)
Group 2
Variables
Before
After
P value
Vo2max ml/kg/min
-
63.3±6.2
ALT (SGPT) IU/L
13.6±1.9
24.2±3.3
S
AST (SGOT) IU/L
15.2±2.9
28.3±4.2
S
CK IU/L
28.3±3.4
42.1±4.4
S
Cortisol ug/dl
16.4±2.6
24.2±3.7
S
Testosterone n mol/L.
15±3.1
29.2±2.8
S
Values mean ± SD
*P < 0.05
Table 3: The effect of test determination on group (1) and (2):
Variables
After Group (1)
After Group (2)
Vo2max ml/kg/min
36.3±3.2
63.3±6.2
P value
S
ALT (SGPT) IU/L
26.3±3.1
24.2±3.3
NS
AST (SGPT) IU/L
32.3±5.1
28.3±4.2
NS
CK IU/L
44.3±4.9
42.1±4.4
NS
Cortisol ug/dl
26.4±3.6
24.2±3.7
NS
Testosterone n mol/L.
21±3.6
29.2±2.8
S
*P < 0.05 values mean ± standard deviation
RESULTS AND DISCUSSION
The increased in Vo2 max observed in case of
athletes compared to non athletes might be due to
increased mitochondrial volume and numbers,
together with cardiovascular adaptations and muscle
adaptations. The combination of an increased
mitochondrial v olume and mass results in increases
in the blood and muscle thresholds and the muscle
creatine phosphate threshold. Cogganet al. [14]
reported a high negative correlation (-0.63) between
muscle mitochondrial enzyme activity and shope of
the increase in Pi/crP, which indicates that an increased
mitochondrial capacity must also increase the rate of
ATP demand necessary to tax muscle creatine phosphate
stores.
Maximal oxygen consumption (Vo2 max) is the
maximal rate at which the body can consume oxygen
during exercise. Vo2 max values can be relative to body
mass (ml / kg / min) or expressed as an absolute volume of
oxygen per unit time (L/min) ( Tables 1-3 and Fig. 1-3).
Vo2 max values range in non athletes (36±3.2)
ml/kg/min as those trained (63.1±6.2 ml/kg/min). Jacobs
[12] reported the factors that influence. Vo2 max: are a high
proportion of slow twitch motor units, high central and
peripheral cardiovascular capacities and the quality
and duration of training. Saltin and Astrand [13] recorded
Vo2 max values in ill individuals (<20 ml/kg/min) to those
well trained and elite endurance (>80 ml/kg/min).
669
World J. Sport Sci., 3 (S): 668-672, 2010
Before
After
45
40
35
30
25
20
15
10
5
0
Vo2 max
ALT
AST
CK
Cortisol
Testost.
Fig. 1: The effect of test determination on maximal oxygen consumption and ALT, AST, CK (non athletes)
Before
After
70
60
50
40
30
20
10
0
Vo2 max
ALT
AST
CK
Cortisol
Testost.
Fig. 2: The effect of test determination on maximal oxygen consumption and ALT, AST, CK, Cortisol and Testosterone
(athletes)
Before
After
70
60
50
40
30
20
10
0
Vo2 max
ALT
AST
Fig. 3: The effect of test determination on group (1) and (2):
670
CK
Cortisol
Testost.
World J. Sport Sci., 3 (S): 668-672, 2010
Table 1-3 and Fig. 1-3 revealed an increased CK post
tests in the two groups, with a slight increase for the favor
of non athletes, At rest, CK was higher in case of athletes
compared to non athletes cases.
Athletes, as a rule, have higher serum CK
concentrations than non athletes because of the regular
strain imposed by training on their muscles. In fact, CK is
one of the parameters affected the most by training.
On the other hand, the increase in the serum CK after
a bout of exercise is lower in athletes than non athletes.
This might be due to adaptation. Vassilis [1] reported that
the most probable mechanisms of the adaptation by
neural hypothesis, repetition of exercise increases the
number of muscle fibers that are activated; as a result,
more muscle fibers share a certain load and damage is
less. It may be due to connective tissue hypothesis as
their rupture leads to their reconstruction, their increase
during recovery, or both leading to increased tolerance
to damage or due to cellular hypothes, is due to increase
sarcomeres number along the myofibrils increases, which
mitigates sarcomere strain and damage as the muscle is
stretched.
Tables 1-3 and Fig. 1-3, the serum aminotransferase
concentrations increase after the exercise bout in case of
non athletes more than athletes because of more muscle
fiber damage and that AST increases more than ALT as
its muscle concentration is higher. Newsholme [15]
reported that ALT and AST increase also in case of liver
disease such as cirrhosis and hepatitis and serve as
indices of the integrity of liver as a vital organ together
with the muscle fibers.
As for cortisol and testosterone, both are steroid
hormones, they are derivatives of cholesterol, they both
are useful in biochemical assessment of exercising
persons and estimation of the balance between catabolism
and anabolism. Tables 1-3 and Fig. 1-3 indicated that
athletes have higher resting concentrations of cortisol
than non athletes, while exercise affect increase cortisol
response in non athletes more than athletes. So, in
measuring cortisol at rest may aid in estimating physical
or mental stress, while measuring cortisol after exercise
may show that the subject receives a particular load.
In case of testosterone at rest, the results indicated
an increased testosterone concentration in case of
athletes compared to non athletes, also exercise elevated
testosterone concentration in case of athletes than non
athletes. The cause of testosterone rise in case of athletes
might be to promote protein synthesis and curbs
proteolysis in muscle, so high concentration is desirable.
Warner [16] stated that testosterone level is
subjected to diurnal variation, the highest levels occur
between 6-9AM; with a 15-40% decrement in the
afternoon. Ferrando [5] reported that testosterone acts
by increasing muscle protein synthesis without having
any effect on protein breakdown, nor have any effect on
the transport of amino acids into muscle fibers. Wolfe [6]
added that testosterone acts via the genome by
enhancing transcription and not accelerating translation.
The cortisol and testosterone share an important
feature, their production is controlled by the
hypothalamus, which synthesizes two peptide hormones
(CRH) corticotropin - releasing hormone and (GNRH)
gonadotropin - releasing hormone. They are secreted to
the pituitary gland. The cortisol and testosterone
concentrations
are
controlled
by
reciprocal
communication of the brain with the adrenal and the
testis. So cortisol and testosterone are controlled by
feedback mechanism. There is no doubt that skeletal
muscle is a target organ for sex hormones and both
classes of hormones, cortisol and testosterone share the
same intra muscular receptor. He also added that
testosterone exert an anabolic action on skeletal muscle
where as cortisol causes muscle waste and atrophy,
especially in the type II muscle [17, 18]. Thus, in males
growth and hypertrophy in skeletal muscle are, among
others induced by testosterone and counteracted by
cortisol. This is also reported by previous studies [19-22]
which added that athletes have higher anabolic hormone
than non athletes and higher ability to recovery after an
exhaustive exercise test.
CONCLUSION
According to the study aim and sample the following
could be concluded:
1.
2.
3.
4.
Vo2max might be used as fitness index.
CPK is an important marker of tissue healing.
AST, ALT together with CPK are very important for
estimation of the integrity of vital organs (Liver,
Muscle and Heart).
Cortisol and testosterone act as basal hormones in
the balance between catabolism and anabolism.
REFERENCES
1.
671
Vassilis, M., 2006. Exercise biochemistry. Human
Kinetics, USA.
World J. Sport Sci., 3 (S): 668-672, 2010
2.
Murray, R., D. Bender and P. Kennely, 2009. Harper’s
illustrated biochemistry, 28th Ed., Lange, USA.
3. Kraemer, W., F. Steven and C. Robin, 1989. Training
responses
of
plasma
bEndorphin
Adrenocorticotrophin and cortisol. Med. and Sc. In
Sports and Exer., 21: 146-153.
4. Van Canter, E., E. Shapiro and H. Tillil, 1992.
Circardian modulation of glucose and insulin
responses to meals: relationship to cortisol rhythm.
Am. J. Physiol., 262: 470.
5. Ferrando, A., K. Tipton and D. Doyle, 1998.
Testosterone injection stimulate, net protein
synthesis but not tissue amino acid transport. Am. J.
Physiol., 275: 864-871.
6. Wolfe, R., A. Ferrando and M. Sheffield, 2000.
Testosterone and muscle protein metabolism.
Mayo Clin Proc., pp: 55-59.
7. Astrand, P., 1960. The Astrand - Rhyming nomogram.
Acta Physiologica Scandinavia, 49: 51.
8. Delacerda, L., A. Kowarski and C. Migeon, 1978.
Integrated Concentration and circadian variation of
plasma testosterone in normal men. J. Clin End.
Metab, 37: 366-371.
9. Foster, L. and R. Dunn, 1979. Cortisol determination
Clin Chem., 20: 365-367.
10. Reitman, S. and S. Frankel, 1957. A colorimetric
method for determination of glutamic pyruvic
transaminase. Am J. Clin Pathol., 25: 56-60.
11. SCE, 1974. Recommended methods for determination
of enzymes. Scand. J. Clin Lab Invest, 33: 291.
12. Jacobs, I., 1983. Lactate in human skeletal muscle
after 10 and 30 seconds of supramaximal exercise. J.
Appl. Physiol., 55: 365-367.
13. Saltin, B. and P. Astrand, 1967. Maximal oxygen
uptake in athletes. J. Appl. Physiol., 25: 353.
14. Coggan, A., A. Abduljilil and S. Swansson, 1993.
Muscle metabolism during exercise in young and
older untrained and endurance trained men. J. Appl.
Physiol., 75: 2125-2133.
15. Newsholme, E., 2004. Enzymes, Energy and
endurance: In J.R. Poortmans, ed. Karger, Ba Sel.,
pp: 1-35.
16. Warner, M., 1992. Endorinology. Williams and
Wilkins, USA.
17. Boissean, N. and P. Delamcarche, 2000. Metabolic
and hormonal responses to exercise in children and
adolescents. Sports Med., 30: 405-422.
18. Renstrom, P., 1993. Sports injuries. Blackwell Sc.
Publ., London.
19. Consitt, L., J. Compeland and M. Trembley, 2002.
Exercise Biochemistry. Human Kinetics, USA.
20. Mac Laren, D., T. Reilly and T. Camplell, 1999.
Hormonal and metabolic responses to maintain
hyperglycemia during prolonged exercise J. Appl.
Physiol., 87: 127-128.
21. Branderberger, G. and M. Follenius, 1975. Influence
of timing and intensity of muscular exercise on
temporal patterns of cortisol levels. J. Clin
Endocrinol. Metab., 40: 845-849.
22. Lin, T., W. Chia and L.Ying, 2008. The effects of the
exhaustive exercise on testosterone and cortisol
and T/C ratio in college students and athletes.
50th Ichper World Congress, pp: 241.
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