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Background: MicroRNAs (miRNAs) are small non-coding RNAs involved in post-transcriptional gene regulation. miRNAs are taken in by intracellular exosomes, secreted into circulation, and taken up by other cells, where they regulate cellular functions. We hypothesized that muscle-enriched miRNAs existing in circulation mediate beneficial metabolic responses induced by exercise. To test this hypothesis, we measured changes in muscle-enriched circulating miRNAs (c-miRNAs) in response to acute and chronic aerobic exercise.Methods: Eleven healthy young men (age, 21.5 ± 4.5 y; height, 168.6 ± 5.3 cm; and body weight, 62.5 ± 9.0 kg) performed a single bout of steady-state cycling exercise at 70% VO2max for 60 min (acute exercise) and cycling training 3 days per week for 4 weeks (chronic exercise). Blood samples were collected from the antecubital vein before and after acute and chronic exercise. RNA was extracted from serum, and the levels of muscle-enriched miRNAs (miR-1, miR-133a, miR-133b, miR-206, miR-208b, miR-486, and miR-499) were measured.Results: All of these miRNAs, except for miR-486, were found at too low copy numbers at baseline to be compared. miR-486 was significantly decreased by both acute (P = 0.013) and chronic exercise (P = 0.014). In addition, the change ratio of miR-486 due to acute exercise showed a significant negative correlation with VO2max for each subject (R = 0.58, P = 0.038).Conclusion: The reduction in circulating miR-486 may be associated with metabolic changes during exercise and adaptation induced by training.

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Substance P (SP) is implicated in transmission of primary afferent nociceptive signals. In primary neurons, SP is colocalized with calcitonin gene-related peptide (CGRP), which is another neuropeptide marker for small to medium primary neurons. CGRP coreleased with SP augments the postsynaptic effect of SP and thereby modulates the nociceptive transmission. This study demonstrates the distribution of CGRP-like immunoreactivity (-ir) and SP-ir in the lower brainstem of normal rats and after trigeminal rhizotomy or tractotomy at the level of subnucleus interpolaris (Vi). By comparing the results obtained from normal and deafferented rats, we analyzed the central projection of trigeminal primary nociceptors. The CGRP-immunoreactive (-ir) trigeminal primaries projected to the entire rostrocaudal extent of the spinal trigeminal nucleus, the principal nucleus (PrV), the paratrigeminal nucleus (paraV), and the lateral subnucleus of solitary tract nucleus (STN) on the ipsilateral side. The trigeminal primaries projecting to the spinal trigeminal nucleus, paraV and STN also contained SP-ir. The ipsilateral trigeminal primaries were the exclusive source of CGRP-ir terminals in the PrV, the Vi and the dorsomedial nucleus within the subnucleus oralis (Vo). The medullary dorsal horn (MDH) and the lateral edge of Vo received convergent CGRP-ir projection from the ipsilateral trigeminal primaries and other neurons. The glossopharyngeal and vagal primaries are candidates for the source of CGRP-ir projection to the Vo and the MDH, while the dorsal root axons supply the MDH with CGRP-ir terminals. In addition, contralateral primary neurons crossing the midline appear to contain CGRP and to terminate in the MDH.

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