(A and B) 2-week application of cerivastatin (A) and lovastatin (B) at increasing doses significantly reduced tetanus force, normalized to untreated or vehicle treated (DMSO for Lovastatin) control (n = 4 myobundles per donor). (C) Accumulation of lipids in myobundles, evaluated by Oil Red O stain, was absent from controls, moderate at lower concentrations, and considerable at higher concentrations of both statins (scale bar = 50 µm). (D–F) 1-week exposure of myobundles to chloroquine resulted in dose-dependent decrease of contractile force (n = 4 myobundles per donor) (D) as well as increased expression of the autophagic pathway marker LC3B-II and decreased expression of contractile protein sarcomeric α-actinin (SAA) (E–F, n = 4 myobundles per donor). (A–F) (*p < 0.05 vs 0 µM, #p < 0.05 vs all other concentrations). (G) Acute (30-min) and (H) chronic (2-week) application of clenbuterol to myobundles (shown in different donors) results in a dose-dependent increase in contractile force with peak effects observed at 1 µM (acute) and 0.1 µM (chronic) and significant reduction in force generation observed at 100 µM (acute, n = 3 myobundles; chronic, n = 4 myobundles). (I) Chronic administration of 0.1 µM Clenbuterol induced hypertrophy of myofibers as evident from a rightward shift in their diameter distribution and significant increase in the average myofiber diameter (untreated, 15.7 ± 0.3 µm vs 0.1 µM clenbuterol, 17.1 ± 0.6 µm, *p < 0.05, n ≥ 55 myofibers per myobundle, pooled for 3 myobundles).