No effect of skin temperature on human ventilation response to hypercapnia during light exercise with a normothermic core temperature

Abstract

Hyperthermia potentiates the influence of CO(2) on pulmonary ventilation (.V(E)). It remains to be resolved how skin and core temperatures contribute to the elevated exercise ventilation response to CO(2). This study was conducted to assess the influences of mean skin temperature (_T(SK)) and end-tidal PCO(2) (P(ET)CO(2)) on .V(E) during submaximal exercise with a normothermic esophageal temperature (T(ES)). Five males and three females who were 1.76 +/- 0.11 m tall (mean +/- SD), 75.8 +/- 15.6 kg in weight and 22.0 +/- 2.2 years of age performed three 1 h exercise trials in a climatic chamber with the relative humidity (RH) held at 31.5 +/- 9.5% and the ambient temperature (T (AMB)) maintained at one of 25, 30, or 35 degrees C. In each trial, the volunteer breathed eucapnic air for 5 min during a rest period and subsequently cycle ergometer exercised at 50 W until T (ES) stabilized at approximately 37.1 +/- 0.4 degrees C. Once T (ES) stabilized in each trial, the volunteer breathed hypercapnic air twice for approximately 5 min with P(ET)CO(2) elevated by approximately +4 or +7.5 mmHg. The significantly (P < 0.05) different increases of P(ET)CO(2) of +4.20 +/- 0.49 and +7.40 +/- 0.51 mmHg gave proportionately larger increases in .V(E) of 10.9 +/- 3.6 and 15.2 +/- 3.6 L min(-1) (P = 0.001). This hypercapnia-induced hyperventilation was uninfluenced by varying the _T(SK) to three significantly different levels (P < 0.001) of 33.2 +/- 1.2 degrees C, to 34.5 +/- 0.8 degrees C to 36.4 +/- 0.5 degrees C. In conclusion, the results support that skin temperature between approximately 33 and approximately 36 degrees C has neither effect on pulmonary ventilation nor on hypercapnia-induced hyperventilation during a light exercise with a normothermic core temperature.

Essential genes from Arctic bacteria used to construct stable, temperature-sensitive bacterial vaccines

“…The temperature of the human body is dependent on a number of variables, but there is a significant difference between the temperature of the skin (∼32-36°C) and the body core (∼37-40°C) (19,20). TS viral vaccines, such as FluMist, take advantage of the anatomical differences in human body temperatures (11,13,14).…”

Ventilatory response to increasing body temperature: Characteristics and effect on central fatigue

“…By contrast, our findings suggest that changes in skin temperature have no effect on the ventilatory response to increasing body temperature during moderate intensity exercise 3) . Similarly, Greiner et al 23) reported that changes in skin temperature do not influence ventilation during light intensity exercise. And, whereas hypohydration attenuates the cutaneous vasodilatory response and sweating 24,25) , we found that hypohydration (2.5% of body weight) does not influence hyperthermia-induced hyperventilation, though the Tes threshold for cutaneous vasodilation is increased, and the sensitivity of cutaneous vasodilation is reduced 11) .…”

Evolutionarily Conserved Essential Genes from Arctic Bacteria: A Tool for Vaccination

“…In accordance with the above mentioned facts, the human body temperature varies depending upon the body parts, temperature of the skin varies between 32 and 36°C whereas the body core is about 37–42°C. [78] Over decades, attempts have been made to develop TS bacterial strains and viral strains,[9–12] yet bacterial strains were not adapted for human vaccination,[13] for example, the TS version of Yersinia pestis [14] and because of their reversion this strain was not further developed. [13] Further, small numbers of TS bacterial strain vaccines (developed by chemical mutagenesis) were developed for veterinary use; but it is uncertain whether the TS nature is primary attenuating phenotype or merely a coincidental phenotype.…”