Control of local and total sweating during exercise transients.
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Biomedical subjects
Publications and source records attributed to E R Nadel.
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This study was undertaken to determine if the observed increase in ventilation during passive limb movement was a reflex hyperventilation or a response to an increased metabolic need for oxygen. Experiments on human volunteers were designed to test the hypothesis that the rapid increase of ventilation at the onset of exercise was due to stimulation of the joints. Results of these studies showed significant increases in ventilation, oxygen consumption, carbon dioxide production, ventilation/oxygen consumption ratio, and heart rate compared to rest and recovery values. The data lead to the conclusion that the rapid increase of ventilation at the onset of exercise is a true hyperventilation and that stimulation of the joints can be a significant contributor to increased pulmonary ventilation.
During exercise, circulatory reflexes ensure that the cardiac output is sufficiently elevated to meet the oxygen delivery requirements of the contracting skeletal muscles and the heat delivery requirements of the body to the skin. The latter requirements are met by increasing skin blood flow. These increases are largely driven by elevations in the body temperatures, although non-thermal effects on the control of skin blood flow occur in certain conditions. These effects are largely the consequence of high and/or low baroreflex stimulation. Even in the face of such non-thermal effects, which occur during exercise in the heat, the body's requirements for heat transfer from core to skin are largely met by the increased skin blood flow. Thus, non-thermal effects on the control of skin blood flow are relatively unimportant in the body's overall regulatory response to exercise.
Because diabetics are prone to the development of neuropathy and microvascular disease, abnormalities of cardiovascular reactivity and capillary permeability in response to acute exercise and/or an increase in environmental temperature might presage the development of clinically overt complications. In the present study insulin-dependent diabetics without evidence of microangiopathy or neuropathy and controls matched for the same level of physical fitness performed cycle ergometer exercise for 20 minutes at 65 percent VO2 max in a temperature maintained at 35 percent C. Ther rise in heart rate (82-85 beats min-1), the fall in plasma volume (11-13 percent), and the increase in total serum proteins (13-16 percent) induced by exercise were the same in the two groups. Furthermore, comparable increments in skin blood flow (two- to threefold) and in core and skin temperatures were observed. The relationship between increases in body core temperature and increases in skin blood flow and the vasodilatory threshold (37.0 percent C) were also the same in the diabetics and controls.
Seven healthy adult volunteers underwent 30-second facial immersions in ice water before and during 36 minutes exposure to intense ambient heat (68 degrees C) on separate, non-consecutive days: one normovolemic and the second with thiazide-induced, 10% hypovolemia. The normovolemic, preheat immersion induced a heart rate (H.R.) decrease from 74 +/- 6 to 48 +/- 5 bpm (-35%) and a forearm blood flow (F.B.F.) decrease from 3.5 +/- 1.6 to 0.8 +/- 0.3 ml/(100 ml min) (-77%). Pre-heat changes were similar for hypovolemic subjects. After 36 minutes of heat exposure there was a 07 degrees C increase in esophageal temperature and a four-fold increase in F.B.F. for normovolemic and a two-fold increase in F.B.F. for hypovolemic subjects. Heating reduced diving bradycardia more than did superimposed hypovolemia. Four subjects had diving tachycardia after hypovolemic heating. We concluded that the bradycardia response to facial immersion can be overridden by reducing the central circulating blood volume by heat and that this effect is enhanced by hypovolemia.