Investigation of effects of circadian rhythm disruptive light exposure on contractile performance and fatigue in isolated rat soleus and extensor digitorum longus muscles

Circadian rhythms are endogenous oscillations that synchronize an organism's biological functions to the 24-hour day by adapting to the light–dark cycle. Although the central pacemaker is the suprachiasmatic nucleus (SCN) in the hypothalamus, many peripheral tissues also contain local circadian regulators. It is well established that diurnal variations influence muscle performance. This thesis aimed to evaluate, under ex vivo conditions, the effects of circadian rhythm disruption via altered light exposure on the contractile performance and fatigue profiles of the soleus (slow-twitch, oxidative) and extensor digitorum longus (EDL, fast-twitch, glycolytic) muscles in adult male Wistar rats (10 weeks old). In the experimental group, the 12-hour dark period was extended to reverse the circadian rhythm over eight days; the control group maintained the natural 12:12 light–dark cycle. Muscles were kept viable in a tissue bath at 30°C in oxygenated (95% O₂, 5% CO₂) Krebs-Henseleit solution and subjected to electrical stimulation protocols inducing twitch and fatigue (soleus: 100 Hz; EDL: 150 Hz). Maximal twitch force (Pt), specific twitch force (sPt), contraction–relaxation kinetics, and fatigue parameters were measured. Comparative analyses revealed that the eight-day reversal of the circadian rhythm significantly reduced absolute force production in both EDL and soleus muscles (p < 0.05). Furthermore, specific force was significantly decreased in the EDL muscle (p < 0.05), whereas no statistically significant change was observed in the soleus. Although fatigue analyses overall showed no significant differences, the experimental group exhibited greater force loss in the soleus at the 30-second mark compared to controls (80.60 ± 11.10% vs. 91.80 ± 7.70%, p = 0.045). These findings indicate that an eight-day reversal of circadian rhythm adversely affects muscle force-generating capacity, without directly altering contraction velocity or fatigue resistance. Moreover, they suggest that such effects on muscle function may arise at the peripheral level, independent of central contributions.