Here’s the state of knowledge on the role of anabolic steriods on connective tissue. Realize that the ligs and tunica are both examples of connective tissues, so I think this article certainly applies to penile tissue.
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Anabolic SteroidsAthletes have used anabolic/androgenic steroids for decades with the intent to enhance performance or increase muscle mass. Steroids (testosterone analogs) that athletes use vary in their anabolic and androgenic activity; they are referred to as anabolic steroids (AS) for sake of simplicity in this article. Although their primary activity is anabolic and androgenic, AS influence other cellular and tissue functions. Their impact on connective tissue is discussed based on the research that is available.
As expected, the studies of AS impact on connective tissue is conflicting due to many factors: methodology, lack of dependable information submitted by human subjects, poor control of variables (diet, training, other drug use, etc), and subjective bias. The most reliable information is studies on animal models; however, extrapolation to humans is limited for obvious reasons. Haupt comprehensively reviews the literature on athletic steroid use and connective tissue as well as some of the animal studies (25). He rightly comments; "Extrapolating from current research provides some insight, but whether anabolic steroid use is beneficial or not remains unclear."
Much of the literature focusing on athletic AS use case studies reporting increased injury rate, especially with concomitant use of corticosteroids. Few mention the dosage levels used by many of these athletes, which are generally supra-physiological and for long durations. Although AS have a reputation within the athletic arena as promoting recovery from injuries, there are no human studies to support accelerated healing of connective tissue. Some of the animal studies suggest that short-term low-dose AS administration may increase the collagen fibril diameter and thus strength of new collagen (2930,30). Inhofe et al. demonstrated that a 6-week course of AS (at doses comparable to the typical athlete’s administration) produced a stiffer tendon in exercised rats that failed with less elongation and energy than in control groups (26). The ultrastructural changes in tendon morphology of the AS+exercise subjects varied with an insignificant trend towards larger fibril diameters. These results contrast those reported by other authors (27,28) who observed changes in collagen fibril crimp angle and fibril length.
Inhofe et al. also examined the biomechanical and ultrastructural changes at 6 weeks after cessation of AS administration. Since the observed differences in the AS+exercise group were eliminated at 12 weeks, apparently effects induced by AS are reversible with drug withdrawal. Based on these results, AS use may have accelerated the same changes in mechanical properties that ultimately occurred in the control groups. However, this has limited extrapolation to repairing connective tissues in humans. *
