Acute melatonin administration enhances aerobic tolerance: an analysis of biochemical and hematological parameters

Aims: This study is aimed at testing the acute melatonin administration (oral; 6 mg) on aerobic tolerance at cycloergometer and analyzing the consequences on biochemical and hematological parameters. Methods: The maximal aerobic capacity intensity (iMAC) at cycloergometer of eleven male healthy men (24.18±3.92 years-old; 87.07±12.48 kg; 1.82±0.05 m; 26.18±3.63 kg/m2; and 16.28±5.77 % of fat) was individually determined and used to perform a time to exhaustion (tlim) trial of 30 minutes after melatonin or placebo administration. We observed 48-72h interval between tests, performed in a double-blind experiment design. In order to determine hematological and biochemical parameters we collected venous blood samples before and after tlim. Statistical significance was set at 5%. Results The intensity and the lactatemia corresponding to the maximal aerobic capacity were 120.88±18.78 W and 3.32±1.03 mmol.L-1, respectively. The tlim with placebo (33.94±15.26 min, confidence interval = 24.92 - 42.95) was significantly lower than the tlim with melatonin (41.94±17.22 min; CI = 31.76 - 52.12; p = 0.03; 19.06%; effect size = 0.49). All of the 21 analyzed blood physiological variables resulted in no significant variation after tlim when placebo was compared to melatonin, except for total sera cholesterol (lower after exercise with melatonin). Conclusion: Acute melatonin administration enhanced aerobic tolerance at iMAC in 19% at cycloergometer; however, the biochemical and hematological variables assessed were not significantly modulated.(AU)

Involvement of melatonin metabolites in the long-term inhibitory effect of the hormone on rat spinal nociceptive transmission.

There is evidence that melatonin and its metabolites could bind to nuclear sites in neurones, suggesting that this hormone is able to exert long-term functional effects in the central nervous system via genomic mechanisms. This study was designed to investigate (i) whether systemically administered melatonin can exert long-term effects on spinal cord windup activity, and (ii) whether blockade of melatonin degradation with eserine could prevent this effect. Rats receiving melatonin (10 mg/kg ip), the same dose of melatonin plus eserine (0.5 mg/kg ip), or saline were studied. Seven days after administration of the drugs or saline, spinal windup of rats was assessed in a C-fiber reflex response paradigm. Results show that rats receiving melatonin exhibited a reduction in spinal windup activity. This was not observed in the animals receiving melatonin plus eserine or saline, suggesting a role for melatonin metabolites in long-term changes of nociceptive transmission in the rat spinal cord.

Chronobiology of indoleamines in the dinoflagellate Gonyaulax polyedra: metabolism and effects related to circadian rhythmicity and photoperiodism.

The marine bioluminescent dinoflagellate Gonyaulax polyedra is capable of producing various indoleamines. The first enzyme in their formation, tryptophan hydroxylase, exhibits a high-amplitude circadian rhythm with a maximum during photophase. Hydroxyindole-O-methyltransferase shows a biphasic pattern with a major maximum during scotophase. 5-Methoxylated indoleamines, such as melatonin and 5-methoxytryptamine, peak at the beginning and in the second half of scotophase, respectively. A drop in temperature from 20 to 15 degrees C leads to dramatic increases of melatonin, up to more than 50 ng/mg protein. This effect may explain why a lower temperature sensitizes this organism to photoperiodic, indoleamine-mediated induction of asexual cysts. Melatonin can be catabolized either enzymatically or non-enzymatically. The non-enzymatic pathway involves free radicals, e.g., photooxidant cation radicals, and leads to the formation of N1-acetyl-N2- formyl-5-methoxykynuramine. Enzymatic catabolism comprises deacetylation to 5-methoxytryptamine and formation of 5-methoxytryptophol. 5-Methoxytryptamine represents a key substance acting as a stimulator of bioluminescence and a mediator of the encystment response. It opens proton channels in the membrane of an intracellular acidic vacuole system which is loaded by the action of a V-type ATPase, as shown by experiments using bafilomycin A1.