Aims To assess the frequency and severity of hypogonadal symptoms in male long-term anabolic-androgenic steroid (AAS) misusers who have discontinued AAS use. Design Cross-sectional, naturalistic. Setting Outpatient facility. Participants Twenty-four male former long-term AAS users and 36 non-AAS-using weightlifters, recruited by advertisement in Massachusetts, USA. Five of the former users were currently receiving treatment with physiologic testosterone replacement, leaving 19 untreated users for the numerical comparisons below. Measurements The Structured Clinical Interview for DSM-IV, questions regarding history of AAS use, physical examination, serum hormone determinations, and the International Index of Erectile Function (IIEF). Findings Compared with the 36 non-AAS-using weightlifters, the 19 untreated former AAS users displayed significantly smaller testicular volumes (estimated difference [95% confidence interval (CI)]: 2.3 [0.1, 4.5] ml; p = 0.042) and lower serum testosterone levels (estimated difference: 131 [25, 227] dL; p = 0.009), with five users showing testosterone levels below 200 ng/dL despite abstinence from AAS for 3–26 months. Untreated former users also displayed significantly lower scores on the IIEF Sexual Desire subscale (estimated difference: 2.4 [1.3, 3.5] points on a 10-point scale; p < 0.001). In the overall group of 24 treated plus untreated former users, 7 (29%) had experienced major depressive episodes during AAS withdrawal; 4 of these had not experienced major depressive episodes at any other time. Two men (8%) had failed to regain normal libidinal or erectile function despite adequate replacement testosterone treatment. Conclusions Among long-term anabolic-androgenic steroid misusers, anabolic-androgenic steroid-withdrawal hypogonadism appears to be common, frequently prolonged, and associated with substantial morbidity.

E xercise-induced cardiac remodeling (EICR) refers to changes in cardiac structure and function that occur in response to exercise training. Numerous structural aspects of EICR (ie, athlete's heart) including ventricular chamber enlargement 1 and hypertrophy 2 have been described, and several key determinants of the EICR process including age, 3 sex, 4 ethnicity, 5 and sporting discipline 6,7 have been established. However, contemporary understanding of EICR is based largely on cross-sectional data derived from competitive athletes and instructive but relatively short duration longitudinal studies of recreational exercisers. 8,9 Therefore, the temporal progression of EICR among competitive athletes remains incompletely understood. See Clincial Perspective See Editorial by D'Silva and SharmaThe myocardial response to hemodynamic perturbation occurs in discrete phases in numerous settings. Specifically, physiological remodeling after 12 months of exercise training in previously sedentary people 9 and cardiac adaptations during pregnancy 10 occurs in different stages. In addition, numerous cardiac disease states are defined by phasic adaptations in myocardial structural and function. 11,12 Whether the EICR that occurs among competitive athletes develops in a phasic sequence remains unknown because of the lack of long-term longitudinal data. Determining the time course of EICR represents a critical step in further defining the myocardial response Background-Contemporary understanding of exercise-induced cardiac remodeling is based on cross-sectional data and relatively short duration longitudinal studies. Temporal progression of exercise-induced cardiac remodeling remains incompletely understood. Methods and Results-A longitudinal repeated-measures study design using 2-dimensional and speckle-tracking echocardiography was used to examine acute augmentation phase (AAP; 90 days) and more extended chronic maintenance phase (39 months) left ventricular (LV) structural and functional adaptations to endurance exercise training among competitive male rowers (n=12; age 18.6±0.5 years). LV mass was within normal limits at baseline (93±9 g/ m 2 ), increased after AAP (105±7 g/m 2 ; P=0.001), and further increased after chronic maintenance phase (113±10 g/m 2 ; P<0.001 for comparison to post-AAP). AAP LV hypertrophy was driven by LV dilation (ΔLV end-diastolic volume, 9±3 mL/m 2 ; P=0.004) with stable LV wall thickness (ΔLV wall thickness, 0.3±0.1 mm; P=0.63). In contrast, chronic maintenance phase LV hypertrophy was attributable to LV wall thickening (Δ LV wall thickness, 1.1±0.4 mm; P=0.004) with stable LV chamber volumes (ΔLV end-diastolic volume, 1±1 mL/m 2 ; P=0.48). Early diastolic peak tissue velocity increased during AAP (−11.7±1.9 versus −13.6±1.3 cm/s; P<0.001) and remained similarly increased after chronic maintenance phase. Conclusions-In a small sample of competitive endurance athletes, exercise-induced cardiac remodeling follows a phasic response with increases in LV chamber size, early diastolic function, and sy...