No abstract

Horses were exercised at 40, 65, and 90% of their maximum O2 uptake (VO2max) until moderately fatigued (approximately 38, 15, and 9 min, respectively) to assess heat loss through different routes. Approximately 4,232, 3,195, and 2,333 kcal of heat were generated in response to exercise at these intensities. Of this, approximately 7, 16, and 20% remained as stored heat 30 min postexercise. Respiratory heat loss, estimated from the temperature difference between blood in the pulmonary and carotid arteries and the cardiac output, was estimated to be 30, 19, and 23% of the heat produced during exercise at the three intensities. The kinetics of the increases in muscle and blood temperature were similar, with the greatest change in temperature occurring in muscle (+3.8, 5.2, and 6.1 degrees C after exercise at 40, 65, and 90% of VO2max, respectively). The temperature of blood in the superficial thoracic vein was approximately 2 degrees C below that of arterial blood at rest. This difference had increased to approximately 3 degrees C during the last minute of exercise. The rate of sweating at sites on the back and neck increased with exercise intensity to a common peak of approximately 40 ml.m-2.min-1. If complete evaporation had occurred, water loss in response to exercise (estimated to be 12, 10, and 7.7 liters for the different intensities of exercise) greatly surpassed that required for dissipation of the metabolic heat load.

SUMMARY

In 11 normal men, central circulatory responses were measured while skin temperature was changed in a square-wave pattern during uninterrupted exercise (26% to 64% maximal oxygen consumption). Skin temperature was changed at 30-minute intervals, beginning at 32°C. On raising it to 38.2°C at low oxygen consumption (Vo 2 ), cardiac output increased 2.5 liters/min, and central blood volume, aortic mean pressure, and stroke volume fell (7%, 7%, and 11%, respectively). Right atrial mean pressure fell 2.2 and 2.3 mm Hg during control and heating periods, respectively. All variables returned to control levels when skin temperature was reduced toward 26.9°C. Raising it to 40°C reproduced these changes with a more clear-cut drop in right atrial mean pressure. Results indicated reduced peripheral venous tone and cutaneous pooling of blood during heating and rapid reversal on cooling. On raising skin temperature to 38.7°C at high Vo 2 , cardiac output increased 19% (3.1 liters/min), stroke volume decreased 14%, and central blood volume rose slightly. Aortic mean pressure fell during the control period and was maintained or rose during heating periods. On cooling, central blood volume and stroke volume rose, cardiac output remained elevated, and aortic mean pressure fell. Increases in cardiac output during heating were related to skin temperature and not to Vo 2 or body temperature. At high Vo 2 , circulatory adjustments favor metabolic rather than thermoregulatory demands. This work was supported in part by U. S. Public Health Service Grant HE-09773 from the National Heart Institute. A part of this study was conducted through the Clinical Research facility of the University of Washington, supported by the National Institutes of Health (Grant FR-37). ADDITIONALDr. Rowell was an Established Investigator of the American Heart Association and was supported by the Washington State Heart Association.A preliminary report of this work was presented at the annual meeting of the American Heart Association, November 23, 1968, Miami, Florida. Received August 19, 1968. Accepted for publication March 25, 1969. thermal and metabolic stresses have depended upon manipulation of environmental temperature rather than skin temperature. But, where natural conditions are simulated, skin temperature may vary throughout the exposure (1). It will also vary over the body surface and may well be reduced, the more severe the exercise, due to an increased sweating response (1). In short, skin temperature is not tightly controlled by exposing subjects to controlled environments, but it is important in both direct local control and reflex control of the vasoactive state of the skin (2). Accordingly, it is important to control this variable when attempting to understand the mechanisms governing human cardiovascular responses to metabolic and thermal stresses. Our experimental design was based on controlling skin temperature as closely as possible and manipulating it in a square-wave pattern between extremes during uninterrupted exercise. It ...

In humans, matching of heat loss and heat production in the "neutral" zone, defined operationally in terms of a range of skin temperatures (Tsk), is accomplished by regulation of skin blood flow (SkBF). Our studies were designed to reveal the characteristics of control of SkBF [from measurements of forearm blood flow (FBF)] in this zone. We controlled the temperature of water sprayed on most of the body of supine men and women at 33 or 35 degrees C in a square-wave pattern (15 min at each temperature) or a step pattern (60 min at 33 degrees C separated by short periods at 35 degrees C). FBF followed Tsk (0.5 ml.min-1.degrees C-1). Esophageal temperature changed approximately 0.11 degrees C with each 2 degrees C change in Tsk, falling with Tsk increase and vice versa. Little influence on FBF, < 0.1 ml.min-1.100 ml-1. degrees C-1, was observed when only the forearm was sprayed with 33 and 35 degrees C water. We conclude that SkBF control in the 33-35 degree C range of Tsk is dominated by the feedforward reflex influence of Tsk on SkBF. The reflex response overcompensates for the effect of Tsk on thermal balance in the neutral zone, so that equilibrium core temperature has an inverse relationship to Tsk.