Effects of Melatonin Administration on Physical Performance and Biochemical Responses Following Exhaustive Treadmill Exercise

Abstract

Exercise, despite being a beneficial activity for health, can also be a source of oxidative imbalance, which can lead to a decrease in performance. Furthermore, melatonin is an endogenous molecule that may counteract exercise-induced oxidative stress. The aim of this study was to evaluate the potential ergogenic and antioxidant capacity of melatonin administered for a maximal effort test. A total of 30 rats were divided into three groups-control, exercise, and exercise + melatonin (intraperitoneal administration of 10 mg/kg)-to assess the effects of an exhaustive incremental protocol in the two exercise groups (with and without melatonin) on the treadmill-running performance (final speed reached), lipid and protein oxidation markers (malondialdehyde + 4-hidroxyalkenals and carbonyl content, respectively), and cellular and mitochondrial membranes' fluidity in skeletal muscle, brain, and liver tissues. Our results show an ergogenic effect of melatonin (31 ± 4 vs. 36 ± 4 cm/s), which may be due to its antioxidant properties being significantly stronger than its protective effect when performing increasing exercise on a treadmill until exhaustion. Melatonin reverted the membrane rigidity in the brain caused by exercise (with no effect on muscle or liver), prevented lipid oxidation in muscle, and prevented lipid and protein oxidation in the liver. Differences between tissues' responses to exercise and melatonin need to be investigated in the future to elucidate other possible mechanisms that explain melatonin's ergogenic effect.

Keywords: brain; ergogenic; lipid peroxidation; liver; membrane fluidity; muscle; protein oxidation; tissue biomarkers.

Figure 1

Summary of the experimental design.

Figure 2

Final speed (cm/s) reached at the end of the incremental ergometry by each animal in group Exercise (without melatonin) and in group Exercise + aMT (animals with melatonin). * means p < 0.05.

Figure 3

Muscle. (a) Malondialdehyde + 4 hydroxyalkenals (nM/mg proteins), (b) carbonyl content (nM/mg protein), (c) Membrane fluidity (1/P) and (d) mitochondrial membrane fluidity (1/P) in group Control (without exercise or melatonin), at the end of the incremental ergometry in group Exercise (without melatonin) and in group Exercise + aMT (animals with melatonin). * means p < 0.05 vs. Control. *** means p < 0.001 vs. Control. ### means p < 0.001 vs. Exercise.

Figure 3

Muscle. (a) Malondialdehyde + 4 hydroxyalkenals (nM/mg proteins), (b) carbonyl content (nM/mg protein), (c) Membrane fluidity (1/P) and (d) mitochondrial membrane fluidity (1/P) in group Control (without exercise or melatonin), at the end of the incremental ergometry in group Exercise (without melatonin) and in group Exercise + aMT (animals with melatonin). * means p < 0.05 vs. Control. *** means p < 0.001 vs. Control. ### means p < 0.001 vs. Exercise.

Figure 4

Brain. (a) Malondialdehyde + 4 hydroxyalkenals (nM/mg proteins), (b) carbonyl content (nM/mg protein), (c) membrane fluidity (1/P) and (d) mitochondrial membrane fluidity (1/P) in group Control (without exercise or melatonin), at the end of the incremental ergometry in group Exercise (without melatonin) and in group Exercise + aMT (animals with melatonin). * means p < 0.05 vs. Control. *** means p < 0.001 vs. Control. ### means p < 0.001 vs. Exercise.

Figure 5

Liver. (a) Malondialdehyde + 4 hydroxyalkenals (nM/mg proteins), (b) carbonyl content (nM/mg protein), (c) membrane fluidity (1/P) and (d) mitochondrial membrane fluidity (1/P) in group Control (without exercise or melatonin), at the end of the incremental ergometry in group Exercise (without melatonin) and in group Exercise + aMT (animals with melatonin). * means p < 0.05 vs. Control. ** means p < 0.01 vs. Control. *** means p < 0.001 vs. Control. # means p < 0.05 vs. Exercise. ### means p < 0.001 vs. Exercise.