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This Article Full Text Full Text (PDF) All Versions of this Article: 90/6/909    most recent expphysiol.2005.031294v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Low, D. Articles by Cable, N. T. Search for Related Content PubMed PubMed Citation Articles by Low, D. Articles by Cable, N. T.

¹ Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, 15–21 Webster Street, Liverpool L3 2ET, UK ² School of Sport and Leisure Management, Sheffield Hallam University, Sheffield, SH10 2BP, UK

The aim of this study was to compare the prolactin and blood pressure responses at identical core temperatures during active and passive heat stresses, using prolactin as an indirect marker of central fatigue. Twelve male subjects cycled to exhaustion at 60% maximal oxygen uptake () in a room maintained at 33°C (active). In a second trial they were passively heated (passive) in a water bath (41.56 ± 1.65°C) until core temperature was equal to the core temperature observed at exhaustion during the active trial. Blood samples were taken from an indwelling venous cannula for the determination of serum prolactin during active heating and at corresponding core temperatures during passive heating. Core temperature was not significantly different between the two methods of heating and averaged 38.81 ± 0.53 and 38.82 ± 0.70°C (data expressed as means ± S.D.) at exhaustion during active heating and at the end of passive heating, respectively (P > 0.05). Mean arterial blood pressure was significantly lower throughout passive heating (active, 73 ± 9 mmHg; passive, 62 ± 12 mmHg; P < 0.01). Despite the significantly reduced blood pressure responses during passive heating, during both forms of heating the prolactin response was the same (active, 14.9 ± 12.6 ng ml^–1; passive, 13.3 ± 9.6 ng ml^–1; n.s.). These results suggest that thermoregulatory, i.e. core temperature, and not cardiovascular afferents provide the key stimulus for the release of prolactin, an indirect marker of central fatigue, during exercise in the heat.

(Received 10 June 2005; accepted after revision 12 September 2005; first published online 12 September 2005)
Corresponding author D. Low: Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, Dallas, Texas, TX 75231, USA. Email: davidlow{at}texashealth.org

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