In view of the complex statements that have been made concerning load errors, variable thermoregulatory setpoints, etc, it sounds overly simplistic to suggest that the elevation in T(c) during exercise may be a result of a high background bias of SNA that reduces SkBF in order to maintain MAP. Yet, this might explain, for example, why T(c) is more closely related to the percent of maximal VO2
... [Show full abstract] required during exercise (and thus to total SNA) than to absolute heat production. One thing is clear, CO and SkBF cannot be driven upward without bounds by thermoregulatory drives to meet demands for heat loss. I have tried to explain this by showing that the T(c) we maintain is often the result of competing nervous influences on the skin vasculature. These influences compete with thermoregulatory needs for SkBF so that the full potential of the cutanous vasodilator system is not realized. Blood pressure regulation and metabolic demands appear to have precedence, unless T