["The Journal of Physiology, EarlyView. ", "\nAbstract figure legend Diet‐induced obesity induced fibro‐adipogenic remodelling of the muscle–tendon unit, characterized by increased fibrosis, reduced specific force, impaired relaxation kinetics, elevated hysteresis, and reduced aerobic capacity and glucose tolerance. Here, we compared two commonly used lifestyle interventions to counteract these detrimental effects: caloric restriction and aerobic exercise. Following a 6 week intervention, caloric restriction (30% reduction in energy intake) decreased body mass, normalized glucose tolerance and reduced fibrosis, and was associated with improvements in muscle contractile function. By contrast, aerobic exercise improved aerobic capacity and partially enhanced mechanical behaviour (reduced hysteresis), but had limited effects on body mass, fibrosis and muscle contractile function. These findings indicate that caloric restriction and exercise promote distinct and only partially overlapping adaptations, suggesting that metabolic and mechanical pathways differentially contribute to the recovery of muscle–tendon function in obesity.\n\n\n\n\n\n\n\n\n\nAbstract\nObesity profoundly impairs musculotendinous structure and function, but the extent to which these alterations can be reversed remains unclear. This study compared the effects of aerobic exercise (EX) and caloric restriction (CR) on the recovery of muscle–tendon structural integrity, contractile performance and passive mechanical properties in high‐fat diet‐induced obese mice. Male C57BL/6J mice were fed a high‐fat diet for 28 weeks and remained on this diet during a subsequent 6 week intervention of either treadmill training (OBEX, 5 days week−1 at 45–65% V̇O2max${{\\dot{V}}_{{{{\\mathrm{O}}}_{\\mathrm{2}}}{\\mathrm{max}}}}$) or 30% caloric restriction (OBCR), whereas controls received standard chow with (CNEX) or without exercise (CN). Muscle [soleus, extensor digitorum longus (EDL)] and Achilles tendon mechanical properties, morphology and composition were assessed alongside circulating and tissue‐specific remodelling markers. OB had higher circulating transforming growth factor beta 1, periostin and advanced glycation end products, accompanied by higher muscle and tendon fibrosis. These molecular and structural alterations coincided with slower contraction–relaxation kinetics, lower specific force and increased tissue viscosity. EX but not CR increased tissue energy storage capacity. OBCR but not OBEX had lower muscle AGEs and muscle collagen fraction than OB. In CR, this was associated with significant improvements in muscle‐specific force. However, tendon properties remained largely unaffected following CR. In summary, a 6 week CR decreased body mass, normalized glucose tolerance, reduced fibrosis and improved muscle contractility. By contrast, EX enhanced aerobic capacity and modestly improved tissue mechanical behaviour, but had limited effects on body mass, fibrosis, and muscle contractile function. These findings indicate that caloric restriction and exercise induce distinct, only partially overlapping adaptations, highlighting differential contributions of metabolic and mechanical pathways to the recovery of muscle–tendon function in obesity.\n\n\n\n\n\n\n\n\n\nKey points\n\nObesity is known to induce skeletal muscle dysfunction, but it is unclear to what extent this can be reversed by lifestyle interventions such as exercise or reduced food intake.\nUsing a mouse model of diet induced obesity, we compared aerobic exercise with caloric restriction to assess recovery of muscle–tendon structure and function.\nObesity caused excess connective tissue to accumulate in muscles and tendons, leading to lower specific force, slower contraction and relaxation, and a stiffer and more viscous muscle‐tendon complex.\nCompared to exercise, caloric restriction more effectively restored muscle specific force and tissue composition than exercise, whereas tendon recovery remained limited.\nCaloric restriction and exercise elicit distinct, partly overlapping adaptations, suggesting that metabolic and mechanical pathways differentially drive muscle–tendon recovery following diet‐induced obesity.\n\n\n"]