Journal of Strength and Conditioning Research, 2005, 19(1), 6–8
q 2005 National Strength & Conditioning Association
PRECONDITIONING OF THE PERFORMANCE IN POWER
EVENTS BY ENDOGENOUS TESTOSTERONE: in memory of professor Carmelo Bosco
ATKO VIRU1 AND MEHIS VIRU2
1Institute of Exercise Biology and 2Institute of Sports Pedagogy, University of Tartu, Estonia.
Prove convincenti sono state ottenute che il testosterone è un potente induttore della sintesi di proteine contrattili nei muscoli scheletrici. Nella formazione, il ruolo del testosterone endogeno è un amplificatore dell’azione induttrice dei metaboliti accumulati durante gli esercizi di resistenza (RT). Pertanto, il testosterone è essenziale per ipertrofia miofibrillare (vedi 13, 24, 37). La maggior parte delle prove emerse per questa esclusione dell’ Ipertrofia muscolare da training specifico si basano sul blocco farmacologico del recettore cellulare specifico del testosterone (22). Tuttavia, i dati ottenuti da Bosco e dei suoi collaboratori ha mostrato che la performance degli atleti sui test di potenza muscolare si correla con il loro livello sanguigno di testosterone. In professionisti giocatori di calcio l’altezza del salto con cotromovimento è positivamente correlato con livello basale del testosterone nel sangue (11). La relazione specifica tra testosterone e il livello della forza esplosiva dei muscoli delle gambe erano supportato dal fatto che la resistenza aerobica, determinata dal test di 12 minuti di Cooper, ha mostrato una correlazione negativa con il livello di testosterone (11). Comparazioni tra i livelli di testosterone della mattina e le concentrazioni sono più alte, e l’ascesa del centro di gravità nel test jump con contromovimento in 97 atleti di alto livello indicano i valori più alti del test sono degli sprinters, il valori più bassi di questi parametri negli sciatori di fondo, e valori intermedi nei giocatori di calcio (12). In conformità, Kraemer et al. (25) segnalano una correlazione positiva tra livello di testosterone e esercizi di estensione a doppio ginocchio. Sono state trovate anche correlazioni significative tra Potenza media e potenza altezza media di salto durante un salto continuo per 60 secondi ed un cambio della concentrazione nel sangue sangue del testosterone durante questo test (10). È impossibile presumere che alcuni secondi siano abbastanza da attivare la secrezione di un ormone, per il trasporto la quantità aumentata di un ormone a un muscolo di lavoro, e per attualizzare l’effetto metabolico di questo ormone. Tuttavia, la performance della concorrenza è preceduta dal riscaldamento su. Gli atleti sono influenzati dal stato anticipatorio. Durante la competizione, ogni atleta può utilizzare 3 o 6 prove. Quindi, gli esercizi in competizioni di potenza vengono eseguiti con livelli di ormone alterati nel sangue. Il significato di queste alterazioni ormonali per le prestazioni dipende dal tempo richiesto per l’attualizzazione degli effetti sul metabolismo di questi ormoni. Gli ormoni che sono legati sulla membrana cellulare e agiscono attraverso la formazione di Adenosina-monofosfato ciclico AMPc.(ad esempio, catecolammina) hanno bisogno solo di un paio di secondi per evocare effetti sul metabolismo. Gli ormoni che si legano ai recettori specifici nel citoplasma e agiscono attraverso l’induzione della proteina di sintesi (ad esempio, testosterone e altri ormoni steroidi) richiedono in diversi casi più di 1 ora per mostrare effetti metabolici. Di conseguenza, la performance negli esercizi di tipo esplosivo di potenza può essere influenzato solo da cambiamenti ormonali prima delle prestazioni principali. Questi cambiamenti ormonali contribuiscono alle precondizioni dell’all’azione. Lo scopo del presente editoriale è di puntare l’attenzione sull’ipotesi del precondizionamento, esplorando il significato del testosterone per le prestazioni negli eventi di potenza. L’ipotesi precondizionata presuppone che nell’individuo il tasso di produzione del testosterone sia in relazione causale con (a) lo sviluppo di fibre muscolari a contrazione rapida (FT), (b) funzionamento delle unità motorie veloci. Pertanto, 2 tipi di precondizionamento nelle prestazioni negli eventi di potenza sono correlati al testosterone endogeno. Il precondizionamento a lungo termine è legato all’influenza del testosterone sullo sviluppo dei muscoli FT. Principalmente, è correlato a il periodo di pubertale. Il precondizionamento a breve termine dovrebbe essere correlato all’influenza del testosterone sul sistema nervoso centrale. Il risultato vede “girare” nel sistema nervoso centrale il motore per prestazione di tipo esplosivo
Long-Term Preconditioning.
Results of several studies provide evidence that explosive contractile activity of
muscles (jumping, sprinting, etc.) is related to the percentage
of FT fibers in leg muscles (9, 15, 20). Thus, the
capacity for muscular activities of explosive type depends
on development of FT fiber and fast motor units. Results
of other studies indicate that testosterone is responsible
for improved anaerobic enzyme systems and structural
development of FT fibers in muscles. Bass et al. (4) established
that in the temporalis muscle of the guinea pig,
sexual differentiation of the enzyme pattern is related to
testosterone. Dux et al. (16) demonstrated that pubertal
castration alters the structure of skeletal muscle; the development
of FT muscles suffers most of all. Krotiewski
et al. (26) confirmed castration effects in male rats. Testosterone
substitution restored development of FT muscles
in male castrates. According to these results, it is
possible to assume that during puberty, interindividual
differences in testosterone production rate are decisive for
the formation and development of FT fibers.
Several studies in male adolescents support this assumption.
Already at the onset of puberty (in 11- to 12-
year-old boys), the area of FT fibers as well as blood lactate
level after 15 seconds of all-out exercise correlated
significantly with testosterone level (31). In circumpubertal
boys testosterone levels in blood or saliva correlated
with maximal anaerobic power (19, 32), maximal power
output in incremental exercise (18), blood lactate level after
Wingate test (32), and maximal voluntary strength
(31). Bosco (7) indicated that in the age period between
8.5 and 14.5 years the rise of the center of gravity in the
countermovement jump increases linearly in children of
both genders. From the age of 14.5 years differentiation
of boys appeared. At this age there is typically a pronounced
increase in blood testosterone concentration.
Thus in the pubertal period, enhanced rate of increase
of testosterone concentration in blood obviously favors the
development of a phenotype characterized by high testosterone
level and effective performance in exercise of explosive
application of forces.
Inherent high levels of testosterone may enhance
myofibrillar hypertrophy in resistance training. However,
in power events even more important is the possible influence
of high testosterone levels on central nervous
structures. In early postnatal life certain neurons of the
central nervous system become sensitive to steroids, for
example, the spinal nucleus of the bulbocavernosus becomes
highly androgen sensitive. In adulthood testosterone
regulates both the size of motoneurons of the spinal
nucleus of bulbocavernosus and the related muscle (1, 27,
28). This neuromuscular subsystem plays an important
role in male copulatory behavior. There is still no evidence
that testosterone influences the neural adaptations
in strength training, including the adjustments at the level
of spinal motoneurons. Nevertheless, data have been
collected suggesting that androgens are able to influence
structure of neurons, including dendritic branching and
synapse formation in the adult brain (2, 29). Testosterone
also influences the regenerative properties of injured cranial
motoneurons (23). The contribution of testosterone in
training-induced long-term neural adaptivity waits investigation.
Short-Term Preconditioning.
Another way of understanding
the significance of testosterone in power exercises
is the short-term preconditioning effect. Testosterone
is known to play a role in preconditioning of aggressive
behavior (34, 35). By analogy, it is possible to assume
that testosterone promotes changes in neurons that are
related not only to increased aggressiveness but also to
mobilization of neuromuscular capacity for explosive performance
in power events.
A study of a sample of normal male adolescents (15 to
17 years old) showed that a positive relationship exists
between circulating plasma testosterone levels and certain
forms of aggressive behavior (34). To extend this
study, the same team investigated another contingent of
58 healthy boys. Results suggested that circulating levels
of testosterone in the blood had a direct causal influence
on provoked aggressive behavior. A high level of testosterone
was related to readiness to respond vigorously and
assertively to provocations and threats. High levels of testosterone
made the boys more impatient and irritable,
which in turn increased their propensity to engage in aggressive-
destructive behavior (35). Results also indicated
the possibility that the testosterone effect is a permissive
one and that the sensitivity of the central nervous system
to testosterone varies interindividually (33). Castration of
adult male mice resulted in the decrease of aggressive
behavior, which was restored after testosterone replacement
(3). Experiments on rodents also showed that a differential
degree of local conversion of testosterone to estradiol
by the enzyme aromatase in the brain preoptic
area might be involved in the expression of aggressive
behavior (14).
In male sprinters after a hard training session, power
output in full squats and half squats was significantly
decreased and the ratio of electromyogram to power increased,
indicating fatigue. These changes were associated
with a decrease in the testosterone concentration in
blood (8). The developing fatigue might simultaneously
and independently impair neuromuscular function and
suppress testosterone production. However, the possibility
that the cause of impaired neuromuscular function
was a decreased testosterone level cannot be excluded.
Accordingly, the neuromuscular function may have been
impaired because of the lack of necessary preconditioning
by testosterone.
Elias (17) and Booth et al. (6) showed that during
sports competition in judo or tennis, winners have higher
levels of testosterone than losers. Therefore, Mazur and
Booth (30) suggested that testosterone prepared winners
for more effective performance.
On the background of extended experimental material,
Ingle (21) affirmed that the permissive effect of hormones
consists in making the changes in body function
or metabolic processes possible even though the hormone
itself is not the direct cause of the change. The supposed
permissive action of testosterone is obviously related to
the indirect effect of testosterone, which is actualized
without participation of androgen receptor (36). The manifestations
of the indirect effect of testosterone are the
production of insulin-like growth factor 1, competition for
the specific binding sites for glucocorticoids, autocrine release
of andromedins, transmembrane influx of extracellular
calcium, and activation of extracellular signal-related
kinase cascade via binding to a yet-unidentified extracellular
receptor (5).
Conclusion.
The hypothesis of preconditioning of performance
in power events by endogenous testosterone
opens a wide spectrum of tasks for further research. The
perspectives include testing various aspects of the hypothesis
as well as deep investigations in order to establish
the cellular-metabolic foundations of testosterone actions
on nervous structures and muscle fibers of various
types related to power performance.
REFERENCES
1. ARAKI, I., Y. HARADA, AND M. KUNO. Target-dependent hormonal
control of neuron size in the rat spinal nucleus of the
bulbocavernosus. J. Neurosci. 11:3025–3033. 1991.
2. ARNOLD, A., AND M. BREEDLOVE. Organizational and activational
effects of sex steroids on brain and behavior: A reanalysis.
Horm. Behav. 19:469–498. 1985.
3. BARKLEY, M.S., AND B.D. GOLDMAN. The effect of castration
and silastic implants of testosterone in internal aggression in
the mouse. Horm. Behav. 9:32–48. 1977.
4. BASS, A., E. GUTMANN, V. HANZLIKOVA, AND I. SYROVY. Sexual
differentiation of enzyme pattern and its conversion by testosterone
in temporalis muscle of the guinea pig. Physiol. Bohemoslov.
20:423–431. 1971.
5. BERARDI, J.M. Androgen action and the androgen receptor.
Available at: http://www.mesomorphosis.com/articles/beraldi/
androgen-action-and-the-androgen-recepter.htm. Accessed
January 26, 2005.
6. BOOTH, A., G. SHELLY, A. MAZUR, G. THORP, AND R. KITTOK.
Testosterone, winning and losing in human competition. Hum.
Behav. 23:556–571. 1989.
7. BOSCO, C. Test di valutazione della donna nella practica del
calcio. In: Confegno Nazionale ‘‘Il Calcio Femminile’’ Aspetti
Medici e Tecnici. R. Cambri and M. Paterni, eds. Rome: FIGC,
1993. pp. 219–230.
8 VIRU AND VIRU
8. BOSCO, C., R. COLLI, R. BONOMI, S.P. VON DUVILLARD, AND A.
VIRU. Monitoring of strength training: Neuromuscular and hormonal
profile. Med. Sci. Sports Exerc. 32:202–208. 2000.
9. BOSCO, C., AND P. KOMI. Mechanical characteristics and fiber
composition of human leg extensor muscles. Eur. J. Appl. Physiol.
41:275–284. 1979.
10. BOSCO, C., J. TIHANYI, L. RIVALTA, G. PARLATO, C. TRANQUILLI,
G. PULVERENTI, C. FOTI, AND M. VIRU. Hormonal responses in
strenuous jumping effort. Jpn. J. Physiol. 46:93–98. 1996.
11. BOSCO, C., J. TIHANYI, AND A. VIRU. Relationship between field
fitness test and basal serum testosterone and cortisol levels in
soccer players. Clin. Physiol. 16:317–322. 1996.
12. BOSCO, C., AND A. VIRU. Testosterone and cortisol levels in
blood of male sprinters, soccer players and cross-country skiers.
Biol. Sport 15:3–8. 1988.
13. BOSCO, C., AND A. VIRU. Biologia dell’allenamento. Rome: Societa
Stampa Sportiva, 1996.
14. COMPAAN, J.C., A. WOZNIAK, A.J.H. DERUITER, J.M. KOOLHAAS,
AND J.B. HUTCHISON. Aromatase activity in the preoptic
area differs between aggressive and nonaggressive male house
mice. Brain Res. Bull. 35:1–7. 1994.
15. COSTILL, D.L., J. DANIELS, W. EVANS, W. FINK, G. KRAHENBUHL,
AND B. SALTIN. Skeletal muscle enzymes and fiber composition
in male and female track athletes. J. Appl. Physiol. 40:
149–154. 1976.
16. DUX, L., E. DUX, AND F. GUBA. Further data on the androgenic
dependence of the skeletal musculature: Effect of pubertal castration
on the structure of the skeletal muscle. Horm. Metab.
Res. 14:191–194. 1982.
17. ELIAS, M. Serum cortisol, testosterone, and testosterone-binding
globulin response to competitive fighting in human males.
Aggress. Behav. 7:215–224. 1981.
18. FAHEY, D.T., A.D. VALLE-ZURIS, G. OEHLSEN, M. TRIEB, AND J.
SEYMOUR. Pubertal stage differences in hormonal and hematological
responses to maximal exercise in males. J. Appl. Physiol.
46:823–827. 1979.
19. FALGAIRETTE, G., M. BEDU, N. FELLMANN, E. VANPRAAGH, AND
J. COUDERT. Bioenergetic profile in 144 boys aged 6 to 15 years
with special reference to sexual maturation. Eur. J. Appl. Physiol.
62:151–156. 1991.
20. FROESE, E.A., AND M.E. HOUSTON. Torque-velocity characteristics
and muscle fiber type in human vastus lateralis. J. Appl.
Physiol. 59:309–314. 1985.
21. INGLE, D.J. The role of the adrenal cortex in homeostasis. J.
Endocrinol. 8:xxii–xxxvii. 1952.
22. INOUE, K., S. YAMASAKI, T. FUSHIKI, Y. OKADA, AND E. SUGIMOTO.
Androgen receptor agonist suppresses exercise-induced
hypotrophy of skeletal muscle. Eur. J. Appl. Physiol. 69:88–91.
1994.
23. JONES, K.J. Androgenic enhancement of motor neuron regeneration.
Ann. N. Y. Acad. Sci. 743:141–161. 1994.
24. KRAEMER, W.J., S.J. FLECK, AND W.J. EVANS. Strength and
power training: Physiological mechanisms of adaptation. Exerc.
Sports Sci. Rev. 24:363–397. 1996.
25. KRAEMER, W.J., K. HA¨ KKINEN, R.U. NEWTON, J. PATTON, E.A.
HARMAN, K. DOHI, I. BUSH, AND J.E. DZIADOS. Factors in various
strength and power performance in man. In: Proceedings
of the XVth Congress of the International Society of Biomechanics.
University of Jyva¨skyla¨, Jyva¨skyla¨ , Finland, 1995. pp. 508–
509.
26. KROTIEWSKI, M., J.G. KRAL, AND J. KARLSSON. Effects of castration
and testosterone substitution on body composition and
muscle metabolism in rats. Acta Physiol. Scand. 109:233–237.
1980.
27. KURTZ, E.M., D.R. SENGELAUB, AND A.P. ARNOLD. Androgens
regulate the dendritic length of mammalian motoneurons in
adulthood. Science 232:395–398. 1986.
28. LUBISHER, J.L., AND A.P. ARNOLD. Evidence for target regulation
of the development of androgen sensitivity in rat spinal
motoneurons. Dev. Neurosci. 17:106–117. 1995.
29. MATSUMOTO, A. Sex steroid induction of synaptic reorganization
in adult neuroendrine brain. Rev. Neurosci. 3:287–306.
1992.
30. MAZUR, A., AND A. BOOTH. Testosterone and dominance in human
males. Behav. Brain Sci. 21:353–397. 1998.
31. MERO, A. Blood lactate production and recovery from anaerobic
exercise in trained and untrained boys. Eur. J. Appl. Physiol.
57:660–666. 1988.
32. MERO, A., L. JAAKOLA, AND P.V. KOMI. Serum hormones and
physical performance capacity in young boy athletes during 1-
year training period. Eur. J. Appl. Physiol. 60:32–37. 1990.
33. MEYER-BAHLBURG, H.F.L. Sex hormones in human aggression:
Models and methodology. Sociol. Abstr. 43(Suppl.):143. 1974.
34. OLWEUS, D., A°
. MATTSON, D. SCHALLING, AND H. LO¨ W. Testosterone,
aggression, physical and personality dimensions in normal
adolescent males. Psychosom. Med. 42:253–269. 1980.
35. OLWEUS, D., A°
. MATTSON, D. SCHALLING, AND H. LO¨ W. Circulating
testosterone levels and aggression in adolescent males:
A causal analysis. Psychosom. Med. 50:261–272. 1988.
36. ROMMERTS, F.F.G. Testosterone action. In: Testosterone Action,
Deficiency, and Substitution. E. Nieschlag and H.M. Behre, eds.
New York: Springer-Verlag, 1998. pp. 1–31.
37. VIRU, A. Adaptation in Sports Training. Boca Raton, FL: CRC
Press, 1995.