Joti Chauhan, Keith Hua 1
BPK 432: Physiological Basis of Temperature Regulation
Counter-Point Argument
Humans do not pant as a thermoregulatory response when they
become hyperthermic
Keith Hua
Joti Chauhan
Nov. 21st, 2016
Fall 2016
Joti Chauhan, Keith Hua 2
Humans Do Not Pant as a Thermoregulatory Response when Hyperthermic
Hypothesis
The hypothesis for the point presentation is that humans do not show panting as a
thermoregulatory response when they become hyperthermic.
Our hypothesis for our counter-point presentation is that humans do not show panting as a
thermoregulatory response when they become hyperthermic.
Evidence Supporting Our Counter-Point Argument
Panting is a controlled increase of respiratory frequency and decrease in tidal volume in
order to increase ventilation of the upper respiratory tract preserving alveolar ventilation, also
defined as thermal tachypnea.1 To contrast, Cabanac and White found that hyperthermic humans
showed an increase in ventilation with increased depth rather than rate representing thermal
hyperpnea.2 In Hiley et al’s study, on primates, they found that these animals showed thermal
tachypnea when exposed to heat stress while humans under the same conditions would have
utilized evaporative heat loss.1 In animals that displayed thermal panting, increases in ventilation
were restricted largely in the upper respiratory tracts.3 However, human dead space and alveoloar
ventilation are not separated, allowing for mixing of gases, due to increases in depth of breathing
versus rapid shallow breathing restricted to the upper respiratory tract. 3 To preserve pH
homeostasis, alveolar oxygen and carbon dioxide exchange should be regulated, but mixing of
gases and increased alveolar ventilation produce respiratory alkalosis.3 These changes are more
tolerable in panting animals such as sheep and dogs, while it provides great inefficiency in
humans because they would require regulation of both pH and gas exchange.3
White et al, demonstrated that the threshold for onset of hyperventilation is much greater
than the thresholds for sweating and cutaneous blood flow, engaging these responses before
Joti Chauhan, Keith Hua 3
hyperventilation or panting.2 Evaporative heat loss is a greater thermoregulatory mechanism for
humans than panting would be, as it would require much larger increases in core temperature.
Evaporative heat loss mechanisms are triggered early on, preventing the high thresholds to be
reached. In Robertshaw’s study, species that utilize sweating and panting, sweating is the
primary mechanism for heat loss. In larger animals, to dissipate heat by respiration would require
high energy demands. Therefore, maximal panting frequency is inversely related to body size.
Larger animals, including humans, dissipate heat mainly through cutaneous evaporation while
smaller animals utilized their respiratory tract for heat loss.4
Humans have a powerful sweating response while ventilatory heat loss is only a small
portion of total heat loss during stress.5. In Wilsmore’s study, spinal cord victims with loss of
sweating abilities as a thermoregulatory mechanism had significant increases in breathing
frequency under thermal stress. They observed this increase in breathing frequency to not be
rapid shallow breathing, therefore unable to conclude it was a true panting response.
Furthermore, the calculated respiratory response was equivalent to ~3g/h of evaporative sweat,
while ~160g/h of evaporative sweat is required to prevent a significant increase in core
temperature.5
Critique for Point Argument
In Nybo and Nielsen’s study, they concluded that hyperventilation may be a type of
thermoregulatory panting and heat loss from the upper respiratory tract can have a significant
cooling effect on the brain.6 Subjects observed in the study were put through exercise trials on
cycle ergometers. Since they are exercising under resistance, it can be explained that
hyperventilation could be induced in an effort to maintain motor output opposed to strictly
reducing core temperature.6 With prolonged exercise, there were small increases in anaerobic
Joti Chauhan, Keith Hua 4
metabolism observed, which may have stimulated ventilation to counteract acid-base disorders.6
Therefore, this study did not clearly demonstrate that hyperthermia lead to the increase in
ventilation.
A study conducted on 7 males by Cabanac and White, showed that during body warming,
higher than normal core temperatures were reached and elicited changes in ventilation known as
thermal hyperpnea. Although this is not the same as thermal tachypnea, this change in ventilation
is seen as a thermoregulatory response, because it was likely to participate in selective brain
cooling.7 The subjects were required to fast and refrain from exercise prior to undergoing body
warming. This is not representative of all individuals in hyperthermic situations. They also
observed an increase in sensitivity in CO2 and were unable to identify whether or not the
increase in ventilation was due to the CO2 sensitivity or increase in temperature.7 Therefore, the
results may not show the true mechanism for the increase in ventilation, and hyperthermia may
not be initiating the ventilatory response.
The evidence we show supports the counterpoint hypothesis that humans do not pant as a
thermoregulatory response when hyperthermic.
Joti Chauhan, Keith Hua 5
References
1. Hiley, P. G. (1976). The thermoreculatory responses of the galago (Galago
crassicaudatus), the baboon (Papio cynocephalus) and the chimpanzee (Pan stayrus) to
heat stress. The Journal of physiology, 254(3), 657-671.
2. White, M. D., Martin, D., & Hall, A. M. (2004, March). Core temperature thresholds for
ventilation, ecerine sweating and cutaneous blood flow in hyperthermic, exercising
humans. In FASEB JOURNAL (Vol. 18, No. 5, pp. A1300-A1300). 9650 ROCKVILLE
PIKE, BETHESDA, MD 20814-3998 USA: FEDERATION AMER SOC EXP BIOL.
3. Hales, J. R. S., & Webster, M. E. D. (1967). Respiratory function during thermal
tachypnoea in sheep. The Journal of physiology, 190(2), 241-260.
4. Robertshaw, D., & Taylor, C. R. (1969). A comparison of sweat gland activity in eight
species of East African bovids. The Journal of physiology, 203(1), 135-143.
5. Wilsmore, B. R., Cotter, J. D., Bashford, G. M., & Taylor, N. A. S. (2006). Ventilatory
changes in heat-stressed humans with spinal-cord injury. Spinal Cord, 44(3), 160-164 6. Nybo, L., & Nielsen, B. (2001). Middle cerebral artery blood velocity is reduced with
hyperthermia during prolonged exercise in humans. The Journal of Physiology, 534(1),
279- 286. Joti Chauhan, Keith Hua 6
7. Cabanac, M., & White, M. D. (1995). Core temperature thresholds for hyperpnea during
passive hyperthermia in humans. European Journal of Applied Physiology and
Occupational Physiology, 71(1), 71-76.