Effect of Body Temperature on Steady State Ventilation and Metabolism in Exercise

Petersen, E. Strange; Vejby-Christensen, H

doi:10.1111/j.1748-1716.1973.tb05529.x

Cited by 29 publications

(15 citation statements)

References 24 publications

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Section: Discussionsupporting

confidence: 83%

“…3) is in agreement with results from previous studies (2,25). Petersen and Vejby-Christensen (25) suggested that a core temperature threshold for ventilation existed around 38°C above which a significant hyperpnea was evident. These core temperature thresholds were subsequently defined for passively or actively induced hyperthermia (2,37), and above these thresholds, ventilation increased proportionately to core temperatures (2,37).…”

Section: Discussionsupporting

confidence: 83%

“…Furthermore, during the hypoxic hyperthermic phase, it would be expected that pH may increase in response to the hypoxic hyperventilation; however, PET CO 2 was clamped at isocapnic value (Fig. 5), which should have prevented increases in pH (25). This last suggestion, however, needs to be expressed with the reservation that CO 2 buffering capacity may also be diminished and that pH may decrease during hyperthermia (32).…”

Section: Discussionmentioning

confidence: 99%

“…oxygen consumption; isocapnia; hyperpnea; chemosensitivity; immersion THERE HAVE BEEN SEVERAL PROPOSED mechanisms for the hyperpnea that occurs during exercise (16,25,37). A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2,37).…”

mentioning

confidence: 99%

“…In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors. oxygen consumption; isocapnia; hyperpnea; chemosensitivity; immersion THERE HAVE BEEN SEVERAL PROPOSED mechanisms for the hyperpnea that occurs during exercise (16,25,37). A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2, 37).…”

mentioning

confidence: 99%

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The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

Chu¹,

Jay²,

White³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This study assessed whether the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (Tes). Eleven males volunteered for two exercise sessions on an underwater, headout cycle ergometer at a steady-state rate of oxygen consumption (V O 2) of ϳ0.87 l/min (SD 0.07). In one exercise session, 31.5°C (SD 1.4) water held Tes at a normothermic level of ϳ37.1°C, and in the other exercise session, water at 38.2°C (SD 0.1) maintained a hyperthermic Tes of ϳ38.5°C. After a 30-min rest and 20-min warm-up, exercising participants inhaled air for 10 min [Euoxia 1 (E1)], an isocapnic hypoxic gas mixture with 12% O2 in N2 (H1) for the next 10 min and air again [Euoxia 2 (E2)] for the last 10 min. A significant increase in V E during all hyperthermia conditions (0.01Ͻ P Ͻ 0.048) was evident; however, during hyperthermic hypoxia, there was a disproportionate and significant (P ϭ 0.017) increase in V E relative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction (P ϭ 0.012) for V E. Significant effects of hyperthermia, isocapnic hypoxia, and their positive interaction remained evident after removing the influence of V O2 on V E. Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermic and hyperthermic-hypoxic conditions. In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors. oxygen consumption; isocapnia; hyperpnea; chemosensitivity; immersion THERE HAVE BEEN SEVERAL PROPOSED mechanisms for the hyperpnea that occurs during exercise (16,25,37). A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2, 37). It suggests that increases in core temperature could increase pulmonary ventilation by several mechanisms. One proposed mechanism suggests an increase in core temperature is associated with an increase in carbon dioxide sensitivity (30), while another suggests a direct physical effect of increased temperature in the respiratory control center and the peripheral chemoreceptors (5). The increased sensitivity to carbon dioxide (CO 2 ) appears to be evident during exercise (35), and during postexercise hyperthermia (28). Another hypothesis suggests a direct effect of an increase in core temperature causing a change in the equilibrium constants of the CO 2 buffer system, resulting in a diminished capacity to buffer CO 2 by body fluids (32). Pulmonary ventilation is then elevated after hydrogen ion (H ϩ ) concentration is increased in the regions of the central respiratory centers in the medulla oblongata.Hypoxia is another well-established modulator of pulmonary ventilation. Low inspired O 2 parti...

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

Chu¹,

Jay²,

White³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Metabolism, Temperature, and Ventilation

Mortola

Maskrey

2011

Comprehensive Physiology

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In mammals and birds, all oxygen used (VO2) must pass through the lungs; hence, some degree of coupling between VO2 and pulmonary ventilation (VE) is highly predictable. Nevertheless, VE is also involved with CO2 elimination, a task that is often in conflict with the convection of O2. In hot or cold conditions, the relationship between VE and VO2 includes the participation of the respiratory apparatus to the control of body temperature and water balance. Some compromise among these tasks is achieved through changes in breathing pattern, uncoupling changes in alveolar ventilation from VE. This article examines primarily the relationship between VE and VO2 under thermal stimuli. In the process, it considers how the relationship is influenced by hypoxia, hypercapnia or changes in metabolic level. The shuffling of tasks in emergency situations illustrates that the constraints on VE-VO2 for the protection of blood gases have ample room for flexibility. However, when other priorities do not interfere with the primary goal of gas exchange, VE follows metabolic rate quite closely. The fact that arterial CO2 remains stable when metabolism is changed by the most diverse circumstances (moderate exercise, cold, cold and exercise combined, variations in body size, caloric intake, age, time of the day, hormones, drugs, etc.) makes it unlikely that VE and metabolism are controlled in parallel by the condition responsible for the metabolic change. Rather, some observations support the view that the gaseous component of metabolic rate, probably CO2, may provide the link between the metabolic level and VE.

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