HUMAN PANTING? TIM AINGE & KATE MCKINNON

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1 PANTING? TIM AINGE & KATE MCKINNON 1

2 POINT COUNTERPOI NT Humans, when they become hyperthermic, do not have panting as a thermoregulatory response Humans, when they become hyperthermic, do have panting as a thermoregulatory response 2

3 D BY COUNTERACTS VIA EVAPORATION Temp C Time (minutes) Figure 1: Temperature of blood in the pulmonary artery of horses at low (open circles), medium (closed circles), and high (closed squares) exercise intensities Adapted from Hodgson et al,

4 D BY COUNTERACTS VIA EVAPORATION Hyperventilation is an inefficient method of evaporative heat loss in humans Metabolic work done by the respiratory muscles counteracts the energy lost as heat via respiratory evaporation Totel,

5 D BY COUNTERACTS VIA EVAPORATION Figure 2: Whole body, metabolic, pulmonary, and dermal water loss via evaporation Borrowed from Totel,

6 INCREASES IN Figure 3: Minute ventilation as end-tidal CO 2 increases for normothermic (o) and hyperthermic (x) individuals Borrowed from House & Holmes,

7 INCREASES IN Figure 4: Phrenic nerve amplitude as temperature and P A CO 2 increase Borrowed from White,

8 S PREFERENTIALLY UNDERGO EVAPORATIVE THROUGH SWEATING Figure 5: Body surface area of adult men and women Borrowed from Sacco et al, 2010 Harkema et al determined that the surface area of human nasal cavities is only cm 2. Figure 3 shows that skin surface area is cm 2, approximately 100 times larger than the nasal cavity Harkema et al, 2006 Therefore, the respiratory system has a relatively insignificant potential for evaporative heat loss compared to eccrine sweating 8

9 S PREFERENTIALLY UNDERGO EVAPORATIVE THROUGH SWEATING Figure 6: Onset of sweating as core temperature passively increased by immersion in hot water Adapted from White & Mekjavic,

10 S PREFERENTIALLY UNDERGO EVAPORATIVE THROUGH SWEATING Figure 7: Ventilatory flow as core temperature passively increased by immersion in hot water Borrowed from Cabanac & White, 1995 Sweating occurred within Δ0.5 C, whereas increases in ventilation rate did not occur until Δ2 C à Therefore, increases in breathing rate are a consequence of dysregulation, not a mechanism of thermoregulation 10

11 HYPERTHERMIA IN S INFLUENCES Figure 8: Breathing frequency as mean body temperature increased in spinal-cord injured (circles) and able-bodied (triangles) individuals Borrowed from Wilsmore et al,

12 CRITICISMS OF WILSMORE ET AL, 2006 PANTING IS Only breathing frequency increased, there were not changes in tidal volume This is not consistent with White s description of second phase panting, where changes in the pattern of breathing including an increased tidal volume are defining features White, 2006 Therefore we maintain that panting is not a thermoregulatory response in hyperthermic humans 12

13 CRITICISMS OF WILSMORE ET AL, 2006 HYPERVENTILATION DOES NOTHING TO REGULATE CORE TEMPERATURE Increases in breathing rate occurred at lower core temperatures in spinal-cord injured individuals, but still occurred at higher temperatures than the eccrine sweating response Recall that the extra work of breathing during hyperventilation counteracts heat lost via respiratory evaporation Totel, 1974 Therefore we maintain that panting is not a thermoregulatory response in hyperthermic humans 13

14 Respiratory muscles produce heat that counteracts any cooling accomplished by respiratory evaporation Hypercapnia, not core temperature, control hyperventilation Sweating is the primary method of heat loss in hyperthermic humans Panting heat loss occurs in humans at high core temperatures We conclude that humans, when they become hyperthermic, do not have panting as a thermoregulatory response 14

15 ? 15

16 1. Hodgson D, McCutcheon L, Byrd S, et al. Dissipation of metabolic heat in the horse during exercise. Journal of Applied Physiology. March 1993;74(3): Totel G. Physiological responses to heat of resting man with impaired sweating capacity. Journal of Applied Physiology. September 1974;37(3): House J, Holmes C. Respiratory Responses of Hyperthermic Subjects. Paper presented at: The Fifth International Conference on Environmental Ergonomics;November 1992; Maastricht. 4. White M. Components and mechanisms of thermal hyperpnea. Journal of Applied Physiology. August 2006;101(2): Sacco J, Botten J, Macbeth F, Bagust A, Clark P. The average body surface area of adult cancer patients in the UK: a multicentre retrospective study. PloS One. January 2010;5(1):

17 6. Harkema J, Carey S, Wagner J. The nose revisited: a brief review of the comparative structure, function, and toxicologic pathology of the nasal epithelium. Toxicologic Pathology. May 2006;34(3): White M, Mekjavic I. Comparison of core threshold temperatures for forehead sweating based on esophageal and rectal temperatures. Canadian Journal of Physiology and Pharmacology. August 1993;71(8): Cabanac M, White M. Core temperature thresholds for hyperpnea during passive hyperthermia. European Journal of Applied Physiology. January 1995;71(1): Wilsmore B, Cotter J, Bashford G, Taylor N. Ventilatory changes in heat-stressed humans with spinal-cord injury. Spinal Cord. March 2006;44(3):

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