Effects of melatonin on muscle and liver bioenergetic profiles: focus on acylcarnitines following endurance swimming exercise in rats

Melatonin (N-acetyl-5-methoxytryptamine) plays a key role in lipid metabolism regulation, directly influencing fatty acid oxidation and lipid transport and modulating pathways related to energy homeostasis.

This study aimed to evaluate its acute effects on tissue bioenergetics during post-exercise recovery.

Thirty Wistar rats performed a 60-min swimming at 90% of their individual maximal aerobic capacity and received melatonin (10 mg.kg^-¹) or vehicle immediately after exercise. The animals were euthanized at 1, 3, or 24 h post-exercise.

Melatonin did not alter the acylcarnitine pool in the muscle or liver, indicating no synergistic effect on β-oxidation. However, it significantly reduced serum glucose levels (F = 11.01; p < 0.001), increased glycogen levels in the red gastrocnemius (F = 82.81; p < 0.001), gluteus maximus (F = 19.55; p < 0.001), and liver (F = 6.24; p < 0.001), and decreased triglyceride content in several skeletal muscles. The integrated biomarker response (IBR) revealed time-dependent shifts in specific acylcarnitine species, although melatonin did not influence these shifts.

In conclusion, despite not modulating the acylcarnitine pool, melatonin induced favorable metabolic adaptations by enhancing glycogen replenishment and altering lipid availability in a tissue-specific manner. These findings suggest that melatonin may favor the transport or utilization of larger fatty acid molecules, potentially bypassing the conventional acylcarnitine-mediated oxidation pathways. This highlights its role as a modulator of post-exercise recovery and underscores the need for temporally resolved analyses to unravel its bioenergetic effects.