Molecular markers of skeletal muscle hypertrophy following 10 wk of resistance training in oral contraceptive users and nonusers.

The objective was to determine whether skeletal muscle molecular markers and SC number were influenced differently in users and nonusers of oral contraceptives (OCs) following 10 wk of resistance training. Thirty-eight young healthy untrained users (n = 20) and nonusers of OC (n = 18) completed a 10-wk supervised progressive resistance training program. Before and after the intervention, a muscle tissue sample was obtained from the vastus lateralis muscle for analysis of muscle fiber cross-sectional area (fCSA) and satellite cell (SC) and myonuclei number using immunohistochemistry, gene expression using PCR, protein expression, and myosin heavy chain composition. Following the training period, quadriceps fCSA (P < 0.05), SCs/type I fiber (P = 0.05), and MURF-1 mRNA (P < 0.01) were significantly increased with no difference between the groups. However, SCs/total fiber and SCs/type II fiber increased in OC users only, and SCs/type II fCSA tended (P = 0.055) to be greater in the OC users. Furthermore, in OC users there were a fiber type shift from myosin heavy chain (MHC) IIx to MHC IIa (P < 0.01), and expression of muscle regulatory factor 4 (MRF4) mRNA (P < 0.001) was significantly greater than in non-OC users. Use of second-generation OCs in young untrained women increased skeletal muscle MRF4 expression and SC number following 10 wk of resistance training compared with nonusers.NEW & NOTEWORTHY The effect of oral contraceptive use on the skeletal muscle regulatory pathways in response to resistance training has not been investigated previously. Here we present novel data, demonstrating that use of second-generation oral contraceptives in young untrained women increased skeletal muscle regulatory factor 4 expression and satellite cell number following 10 wk of resistance training compared with nonusers.

To switch or not to switch: results of a nationwide guideline of mandatory switching from originator to biosimilar etanercept. One-year treatment outcomes in 2061 patients with inflammatory arthritis from the DANBIO registry.

OBJECTIVES: Real-world evidence on effectiveness of switching to biosimila r etanercept is scarce. In Denmark, a nationwide guideline of mandatory switch from 50 mg originator (ETA) to biosimilar (SB4) etanercept was issued for patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (AxSpA) in 2016. Clinical characteristics and treatment outcomes were studied in ETA-treated patients, who switched to SB4 (switchers) or maintained ETA (non-switchers). Retention rates were compared with that of a historic cohort of ETA-treated patients. Switchers who resumed ETA treatment (back-switchers) were characterised. METHODS: Observational cohort study based on the DANBIO registry. Treatment retention was explored by Kaplan-Meier plots and Cox regression (crude, adjusted). RESULTS: 1621 (79%) of 2061 ETA-treated patients switched to SB4. Disease activity was unchanged 3 months' preswitch/postswitch. Non-switchers often received 25 mg ETA (ETA 25 mg pens/syringes and powder solution were still available). One-year adjusted retention rates were: non-switchers: 77% (95% CI: 72% to 82%)/switchers: 83% (79% to 87%)/historic cohort: 90% (88% to 92%). Patients not in remission had lower retention rates than patients in remission, both in switchers (crude HR 1.7 (1.3 to 2.2)) and non-switchers (2.4 (1.7 to 3.6)). During follow-up, 120 patients (7% of switchers) back-switched to ETA. Back-switchers' clinical characteristics were similar to switchers, and reasons for SB4 withdrawal were mainly subjective. CONCLUSION: Seventy-nine per cent of patients switched from ETA to SB4. After 1 year, adjusted treatment retention rates were lower in switchers versus the historic ETA cohort, but higher than in non-switchers. Withdrawal was more common in patients not in remission. The results suggest that switch outcomes in routine care are affected by patient-related factors and non-specific drug effects.