Background and aims: Anabolic androgenic steroids (AAS) have been associated with coronary artery disease (CAD). AAS abuse leads to a remarkable decrease in high-density lipoprotein (HDL) plasma concentration, which could be a key factor in the atherosclerotic process. Moreover, not only the concentration of HDL, but also its functionality, plays a pivotal role in CAD. We tested the functionality of HDL by cholesterol efflux and antioxidant capacity. We also evaluated the prevalence of CAD in AAS users. Methods: Twenty strength-trained AAS users (AASU) age 29 ± 5 yr, 20 age-matched strength-trained AAS nonusers (AASNU), and 10 sedentary controls (SC) were enrolled in this cross-sectional study. Functionality of HDL was evaluated by 14 C-cholesterol efflux and the ability of HDL in inhibiting LDL oxidation. Coronary artery was evaluated with coronary computed tomography angiography. Results: Cholesterol efflux was lower in AASU compared with AASNU and SC (20 vs. 23 vs. 24%, respectively, p < 0.001). However, the lag time for LDL oxidation was higher in AASU compared with AASNU and SC (41 vs 13 vs 11 min, respectively, p < 0.001). We found at least 2 coronary arteries with plaques in 25% of AASU. None of the AASNU and SC had plaques. The time of AAS use was negatively associated with cholesterol efflux. Conclusions: This study indicates that AAS abuse impairs the cholesterol efflux mediated by HDL. Long-term AAS use seems to be correlated with lower cholesterol efflux and early subclinical CAD in this population.

Disturbed shear rate (SR), characterized by increased retrograde and oscillatory SR in the brachial artery, is associated with inflammation, atherosclerosis, endothelial dysfunction, and sympathetic hyperactivity. Young subjects do not have disturbed SR; however, elderly subjects do, which seems to be associated with sympathetic hyperactivity. Anabolic androgenic steroids (AAS) abuse in young is associated with increased muscle sympathetic nerve activity (MSNA). We hypothesized that AAS users might have disturbed SR. We tested the association between retrograde and oscillatory SR with MSNA. In addition, we measured the high-sensitivity C-reactive protein (hs-CRP). We evaluated 10 male AAS users, age 27 ± 4 years, and 10 agematched AAS nonusers, age 29 ± 5 years. At rest, retrograde and oscillatory SR were evaluated by Doppler ultrasound, MSNA was measured with microneurography, and hs-CRP was measured in blood sample. Flow-mediated dilation (FMD) was also assessed. AAS users had higher retrograde SR (24.42 ± 17.25 vs 9.15 ± 6.62 s −1 , P = 0.01), oscillatory SR (0.22 ± 0.13 vs 0.09 ± 0.07 au P = 0.01), and MSNA (42 ± 9 vs 32 ± 4 bursts/100 heart beats, P = 0.018) than nonusers. MSNA (bursts/100 heart beats) was correlated with retrograde SR (r = 0.50, P = 0.050) and oscillatory SR (r = 0.51, P = 0.042). AAS users had higher hs-CRP [1.17 (0.44-3.63) vs 0.29 (0.17-0.70) mg/L, P = 0.015] and decreased FMD (6.42 ± 2.07 vs 8.28% ± 1.53%, P = 0.035) than nonusers. In conclusion, AAS abuse is associated with retrograde and oscillatory SR which were associated with augmented sympathetic outflow. In addition, AAS seems to lead to inflammation characterized by increased hs-CRP. These alterations may have the potential of increasing the early risk of atherosclerotic disease in young AAS users. K E Y W O R D S anabolic steroid, muscle sympathetic nervous activity, retrograde shear rate [Correction added on 7 December 2018, after first online publication: The panel A in figure 1 has been updated.]

During muscle mechanoreflex activation (isometric exercise), AASU have normal MSNA and FBF responses, whereas during central command (mental stress) stimulation, AASU have exacerbated MSNA and blunted vasodilation. Therefore, mental stress seems to exacerbate neurovascular control throughout stress reaction situations in AASU.

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Background:Although sympathetic overactivity at rest and impaired parasympathetic reactivation after exercise have been described in patients with heart failure (HF), their interaction in sarcopenic patients with HF is still unknown. Purpose: The aim of this study was to evaluate the impact of the autonomic modulation assessed by muscle sympathetic nerve activity (MSNA) and heart rate recovery (HRR) after exercise in sarcopenic and non-sarcopenic patients with HF, and to determine their possible screening to detect sarcopenia. Methods: We enrolled 80 male stable patients with HF in New York Heart Association functional class I-IV (NYHA) and left ventricular ejection fraction (LVEF) <40%. All patients underwent a maximal cardiopulmonary exercise testing on cycle ergometer. Maximal heart rate was recorded and HRR was assessed at 1st and 2nd minutes immediately after exercise. MSNA was measured using microneurography. The sum of the lean mass of the arms and the legs divided by the height in meters squared was assessed by dual energy x-ray absorptiometry (DXA). Sarcopenia was defined as the appendicular muscle mass ≤7.26 kg/m 2 and maximal voluntary contraction by handgrip <30 kg. Blood samples were also drawn in the morning after an overnight fasting. Results: Sarcopenia was identified in 21 patients (26.25%). Patients with sarcopenia were older (58±8 vs. 53±9 years, p=0.015) and presented higher MSNA than those without (45±11 vs. 39±10 bursts/min, p=0.012). In addition, sarcopenic patients showed lower HRR at 1st min (13±8 vs. 20±10 beats/min, p=0.008), but at 2nd min, both sarcopenic and non-sarcopenic showed similar response (25±14 vs. 30±14 beats/min, p=0.104). Absolute peak VO2 (1.073±0.32 vs. 1.543±0.48 L/min, p<0.001), absolute peak VO2/lean mass (23.9±7.0 vs. 28.9±9.9 ml/kg/min, p=0.016), peak ventilation (51.7±12.6 vs. 65.6±17.5 L/min, p=0.001) and power output (67±27 vs. 108±50 watts, p<0.001) were also lower in patients with sarcopenia than those without. Logistic regression showed age (hazard ratio, 0.908; 95% confidence interval, 0.831-0.991; p=0.031), MSNA (hazard ratio, 3.441; 95% confidence interval, 1.032-11.480; p=0.044) and HRR at 1st min (hazard ratio, 3.455; 95% confidence interval, 1.089-10.961; p=0.035) to be independently associated with sarcopenia adjusted for hemoglobin, creatinine, LVEF, NYHA and aetiology (Chagas, Yes/No). Using receiver operating characteristics (ROC), we calculated the optimal MSNA value to identify patients with sarcopenia as >39 bursts/min, which had a sensitivity of 76.19% and a specificity of 54.24%. The area under the ROC curve was 0.67 (95% confidence interval, 0.55-0.77). Conclusion: MSNA shows a good sensitivity for the detection of sarcopenia in patients with HF. In addition, HRR after exercise can be clinically used to detect an impaired parasympathetic activity in sarcopenic patients with HF. Background: Cardiac cachexia is a serious and life-threatening complication of heart failure with reduced ejection fraction (HFrEF). Purpose: The aims of the study wer...

PurposeExacerbated sympathetic nerve activity and increased blood pressure have been documented in anabolic androgenic steroid users (AASU). We tested the hypothesis that arterial baroreflex sensitivity (BRS) and carotid distensibility would be reduced in AASU.MethodsTen AASU and 10 age‐paired anabolic androgenic steroid nonusers (AASNU) were studied. Both groups were involved in strength training (90% 1MR) and AASU were self‐administered anabolic steroids for at least 2 years. The use of AAS was proved by urine. Heart rate (HR) was evaluated by EKG and blood pressure non‐invasively on a beat to beat. BRS was analyzed by time domain through spontaneous fluctuations between systolic blood pressure (SBP) and HR. Carotid artery distensibility was measured by doppler (M‐mode).ResultsHR was higher in AASU compared to AASNU (69±3 vs. 59±3 bpm, P≤0.05). Systolic (123±4 vs. 118±2 mmHg, P=0.29), diastolic (72±2 vs. 67±2 mmHg, P=0.12) and mean blood pressure (90±3 vs. 85±2 mmHg, P=0.15) were not different between groups. BRS for increases (14.2±2 vs. 22.8±3 msec/mmHg, P=0.05) and decreases (13.3±1 vs. 19.2±2 msec/mmHg, P=0.04) were lower in AASU. Carotid distensibility was reduced in AASU (7±1 vs. 9±1 %, P≤0.05).ConclusionImpaired BRS and reduced carotid distensibility may prematurely lead to increased cardiovascular risk in AASU.

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