The role of spinal thermosensitive structures in the respiratory heat loss during exercise

Clough, D.P.; Jessen, Claus

doi:10.1007/bf00592600

Cited by 11 publications

(11 citation statements)

References 15 publications

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“…At variance with this notion is the findings that hyperthermic hyperventilation in humans usually leads to hypocapnia and reduced cerebral blood flow (10,15,36), which in turn induces a reduction in heat exchange in the brain and thus increases in brain temperature (34). In the present study, humans exhibited a core temperature threshold for hyperventilation during submaximal exercise in the heat that was similar to well-known thermoregulatory responses such as sweating and skin vasodilation in humans (20,22), as well as the ventilatory response in panting animals (7,28), which supports the notion of White (41). Further studies comparing the characteristics of core temperature thresholds between human hyperthermic hyperventilation and the aforementioned well-known thermoregulatory responses in humans and animals may provide a better understanding of the physiological significance of human hyperthermic hyperventilation.…”

Section: Perspectives and Significancesupporting

confidence: 66%

“…In their study; however, the functions relating V E/V O 2 and V E/V CO 2 to core temperature included data collected at two body temperature levels (36.5-37.5°C and 38.4 -38.7°C), which may have diminished the precision of the estimated threshold. A core temperature threshold for hyperventilation is reportedly seen both during exercise at a constant workload and at rest in animals (7,28,29). Clough and Jessen (7) showed that, in dogs the core (spinal) temperature threshold for an increase in respiratory evaporative heat loss during exercise is lower than at rest.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, animal studies suggest there is a core temperature threshold for the increase in respiratory evaporative heat loss (an index of ventilation) during exercise both at a constant workload and rest, and the threshold during exercise is lower than at rest (7,28,29). This suggests that if the initial resting core temperature were to be lowered by cooling, a core temperature threshold for hyperventilation like that seen in animals (7,28) and during incremental exercise in humans (37,43) might be detected around 37°C during exercise at a constant workload in humans.…”

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confidence: 99%

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Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Tsuji

Honda

Fujii

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Nishiyasu T. Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat. Am J Physiol Regul Integr Comp Physiol 302: R94 -R102, 2012. First published September 28, 2011 doi:10.1152/ajpregu.00048.2011.-We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (Tes). Initial Tes was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). Tes after the water immersion was significantly higher in the Preheating trial (37.5 Ϯ 0.3°C) and lower in the Precooling trial (36.1 Ϯ 0.3°C) than in the Control trial (36.9 Ϯ 0.3°C). In the Precooling trial, minute ventilation (V E) showed little change until Tes reached 37.1 Ϯ 0.4°C. Above this core temperature threshold, V E increased linearly in proportion to increasing Tes. In the Control trial, V E increased as Tes increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, V E increased from the initially elevated levels of Tes (from 37.6 to 38.6°C) and V E. The sensitivity of V E to increasing Tes above the threshold for hyperventilation (the slope of the Tes-V E relation) did not significantly vary across trials (Precooling trial ϭ 10.6 Ϯ 5.9, Control trial ϭ 8.7 Ϯ 5.1, and Preheating trial ϭ 9.2 Ϯ 6.9 L·min Ϫ1 ·°C Ϫ1 ). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.hyperpnea; hyperthermia; thermoregulation; precooling; preheating WHEN HUMANS ARE EXPOSED TO a hot environment, heat dissipation through cutaneous vasodilation and sweating increases in response to rising body core and skin temperatures. In addition to these thermoregulatory responses, Haldane found in 1905 that an increase in ventilation is also induced by a rise in body core temperature (13). Since that early report, many studies have confirmed the existence of hyperthermia-induced hyperventilation (5, 9 -11, 16, 26, 32, 38, 43) although its characteristic and significance remain unclear.When ventilation is expressed as a function of core temperature in passively-heated humans at rest, there is no significant change until core temperature reaches a temperature threshold for hyperventilation, ϳ37.8 -38.5°C. Above this threshold, ventilation increases linearly in proportion to increasing core temperature with minimal change in oxygen consumption (5, 10). As in resting subjects, metabolic factors contribute minimally to ventilation during prolo...

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Section: Perspectives and Significancesupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Tsuji

Honda

Fujii

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In two studies, however, the relationship between core temperature and ventilatory response was obtained at rest and during submaximal, moderate-intensity exercise and was compared using the same animals (dogs and goats) (4,22). Those studies showed that the slope of the regression line relating core temperature and respiratory evaporative water loss (E res , an index of the panting response) was smaller during exercise than at rest.…”

mentioning

confidence: 99%

“…Those studies showed that the slope of the regression line relating core temperature and respiratory evaporative water loss (E res , an index of the panting response) was smaller during exercise than at rest. Furthermore, it was suggested that there is a core temperature threshold for the increase in E res at rest and during exercise and that the threshold is lower during exercise than at rest (4,22). Moreover, separately reported core temperature thresholds for hyperthermic hyperpnea during incremental exercise (37.4 -37.9°C) (27,34,35) were lower than those during passively induced hyperthermia (38.1-38.6°C) (3,29) in humans.…”

mentioning

confidence: 99%

Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise

Fujii

Honda²,

Hayashi³

et al. 2008

Journal of Applied Physiology

102

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yasu T. Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise. J Appl Physiol 104: 998-1005, 2008. First published January 3, 2008 doi:10.1152/japplphysiol.00146.2007.-We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a waterperfused suit were used to increase esophageal temperature (T es) in 19 healthy male subjects; in the exercise trial, T es was increased by prolonged submaximal cycling [50% peak O 2 uptake (V O2)] in the heat (35°C). Minute ventilation (V E), ventilatory equivalent for V O2 (V E/V O2) and CO2 output (V E/V CO2), tidal volume (VT), and respiratory frequency (f) were plotted as functions of T es. In the exercise trial, V E increased linearly with increases (from 37.0 to 38.7°C) in Tes in all subjects; in the rest trial, 14 of the 19 subjects showed a Tes threshold for hyperpnea (37.8 Ϯ 0.5°C). Above the threshold for hyperpnea, the slope of the regression line relating V E and Tes was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating V E/V O2, V E/V CO2, and Tes were significantly greater for the rest than the exercise trial. The increase in V E reflected increases in VT and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to VT. Finally, the slope of the regression line relating Tes and VT or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity. thermoregulation; evaporative heat loss; ventilatory pattern IN MANY SPECIES OF MAMMALS and birds, an elevation in body temperature stimulates ventilation and increases evaporative heat loss for thermoregulation with a two-phase panting response (26,33). In animals such as the sheep and dog, this panting response can include two distinct patterns of breathing, often referred to as first-and second-phase panting (7,12,13,26,33). In the first phase, respiratory frequency (f) is maximized, while tidal volume (VT) is minimized, and arterial blood gases are not perturbed (33). The second phase is only evident with an increase in core temperature, and VT and f are increased, so that alveolar ventilation is increased, resulting in hypocapnia and respiratory alkalosis (33). In 1905, Haldane (11) was the first to report that hyperthermia also increases ventilation in humans. The recent review by White (33) suggested that since increased ventilation by hyperthermia in humans increases alveolar ventilation so that respiratory alkalosis occurs, a hyperthermia-induced increase in ventilation in humans is likely to be the second phase of panting. However, the mechanisms and the physiological significance of this response in humans are not fully understood.When body tem...

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Neurophysiological Aspects of Thermoregulation

Boulant¹,

Currás²,

Dean

1989

Advances in Comparative and Environmental Physiology

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The role of spinal thermosensitive structures in the respiratory heat loss during exercise

Cited by 11 publications

References 15 publications

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise

Neurophysiological Aspects of Thermoregulation

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