A 2-week training camp resulted in 30% decrease of blood testosterone levels with a simultaneous increase in CK creatine-kinase activity in the wrestlers. Several weeks' preparatory training was reported to have increased testosterone level by 5% to 14% in canoeists, and runners, and tennis players. Exercise intensifies the synthesis of testosterone and increases its concentration in blood circulation, but the changes depend on the intensity and duration of exercise. Also, cortisol and IGF-1 are both involved in the inflammatory response and exist on opposite sides of the anabolic-catabolic balance at skeletal muscle tissue. Additionally, IGF-1 levels eventually dropped for the athletes, with an increase in creatine kinase a marker used to assess tissue damage, suggesting a combination of extensive training-induced muscle damage and exhaustive depletion of these endocrine systems. With aging, there is also evidence for motor unit denervation/reinnervation and declines in motor nerve conduction velocity (Kanda and Hashizume, 1989). Furthermore, compared to normal untreated specimens, saporin causes 63% dendrite morphology reduction in quadriceps motor neurons of treated female rats. With facial nerve crush, animals display unilateral facial paralysis with drooping of one corner of the mouth, flattened and paralyzed vibrissae, and loss of eyeblink reflex, but testosterone treatment in these rodents results in a return of movement during a 2–3 week postoperative period, indicating a functional recovery with the androgen-mediated neuroregeneration (Jones, 1994). Accordingly, studies in rodent facial nerves may be a useful translational model for age-related issues with strength and motor performance in humans.
