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Aoki, K1; Stephens, D P.1; Johnson, J M.1
1Graduate School of Science, Tokyo Metropolitan Univ., Tokyo, Japan. Univ. of Texas Health Science Center at San Antonio, TX 78229-3900
This study was designed to find the roles of the vasoconstrictor and active vasodilator systems in the diurnal variation of control of the cutaneous circulation and whether those changes could be mimicked by exogenous melatonin.
Skin blood flow was monitored at control sites and at the sites pretreated with bretylium (BT) to block noradrenergic nerve function. In experiment 1, we conducted whole body heating (skin temperature of 38°C; water-perfused suits) at 0630 hours (AM) and 1630 hours (PM). In experiment 2, two periods of whole body heating started at 1600 hours: one following melatonin administration (MEL), the other control (CON).
In experiment 1, the internal temperature threshold for cutaneous vasodilation was significantly higher in PM than AM at both control (P < 0.01) and BT treated sites (P < 0.01). The sensitivity (slope of cutaneous vascular conductance with respect to internal temperature) was significantly lower in AM than PM at control sites only (control sites: P < 0.05; BT treated sites: P > 0.1). In experiment 2, the internal temperature threshold for cutaneous vasodilation was significantly lower in MEL than CON at both control (P < 0.05) and BT treated sites (P < 0.05). The sensitivity of cutaneous vasodilation was also lower in MEL than CON at both control (P < 0.05) and BT treated sites (P < 0.05).
These results indicate the diurnal variation in the reflex thermoregulatory control of skin blood flow can be partially reproduced by exogenous melatonin. For both, the shift in threshold for cutaneous vasodilation is via the active vasodilator system. However, the lower sensitivity of cutaneous vasodilation relative to internal temperature in MEL is dependent on the active vasodilator system whereas the lower sensitivity of cutaneous vasodilation in the AM is dependent on a diurnal variation in sympathetic noradrenergic vasoconstrictor function. (Supported by NIH Grant HL 59166)
©2003The American College of Sports Medicine
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