The preoptic area in the hypothalamus is the source of the additional respiratory drive at raised body temperature in anaesthetised rats

Boden, A. G.; Harris, Mary; Parkes, Michael A.

doi:10.1017/s0958067000020534

Cited by 16 publications

(5 citation statements)

References 30 publications

(53 reference statements)

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“…However, the precise physiological mechanisms responsible for this hyperthermia-induced hyperventilation in humans are poorly understood. Potential causative factors include increases in (i) rectal temperature (White, 2006), (ii) temperature of the hypothalamus (Boden et al 2000), (iii) peripheral chemoreceptor sensitivity, possibly specific to O 2 (Fujii et al 2008a). Although hyperthermia increases peripheral chemoreceptor ventilatory O 2 drive in resting humans, the relative contribution of this drive to hyperthermia-induced hyperventilation is small (ß20%), and appears to be unaffected by increasing deep body temperature (Fujii et al 2008a).…”

Section: Results: Ventilatory Responsesmentioning

confidence: 99%

The human ventilatory response to stress: rate or depth?

Tipton

Harper

Paton

et al. 2017

The Journal of Physiology

165

166

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Many stressors cause an increase in ventilation in humans. This is predominantly reported as an increase in minute ventilation (V̇E). But, the same V̇E can be achieved by a wide variety of changes in the depth (tidal volume, V ) and number of breaths (respiratory frequency, ƒ ). This review investigates the impact of stressors including: cold, heat, hypoxia, pain and panic on the contributions of ƒ and V to V̇E to see if they differ with different stressors. Where possible we also consider the potential mechanisms that underpin the responses identified, and propose mechanisms by which differences in ƒ and V are mediated. Our aim being to consider if there is an overall differential control of ƒ and V that applies in a wide range of conditions. We consider moderating factors, including exercise, sex, intensity and duration of stimuli. For the stressors reviewed, as the stress becomes extreme V̇E generally becomes increased more by ƒ than V . We also present some tentative evidence that the pattern of ƒ and V could provide some useful diagnostic information for a variety of clinical conditions. In The Physiological Society's year of 'Making Sense of Stress', this review has wide-ranging implications that are not limited to one discipline, but are integrative and relevant for physiology, psychophysiology, neuroscience and pathophysiology.

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Section: Results: Ventilatory Responsesmentioning

confidence: 99%

The human ventilatory response to stress: rate or depth?

Tipton

Harper

Paton

et al. 2017

The Journal of Physiology

165

166

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“…The exact mechanisms responsible for the hyperventilatory response during hyperthermia in humans have not been fully delineated. It is likely that a medullar integration of skin, and deep tissue temperature, principally hypothalamic temperature (Ingram and Whittow, 1962; Boden et al, 2000), primarily determine the magnitude of hyperventilatory response to hyperthermia. Temperature reception at the carotid bodies may also play an independent role (Zapata et al, 1994).…”

Section: Cerebral Blood Flowmentioning

confidence: 99%

Cerebral oxygenation and hyperthermia

2014

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Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution remains a point of contention, and probably depends on the experimental condition (e.g., posture and degree of hyperthermia). The hyperthermia-induced hyperventilatory response reduces arterial CO2 pressure (PaCO2) causing cerebral vasoconstriction and subsequent reductions in flow. During supine passive hyperthermia, the majority of recent data indicate that reductions in PaCO2 may be the primary, if not sole, culprit for reduced CBF. On the other hand, during more dynamic conditions (e.g., hemorrhage or orthostatic challenges), an inability to appropriately decrease peripheral vascular conductance presents a condition whereby adequate cerebral perfusion pressure may be compromised secondary to reductions in systemic blood pressure. Although studies have reported maintenance of pre-frontal cortex oxygenation (assessed by near-infrared spectroscopy) during exercise and severe heat stress, the influence of cutaneous blood flow is known to contaminate this measure. This review discusses the governing mechanisms associated with changes in CBF and oxygenation during moderate to severe (i.e., 1.0°C to 2.0°C increase in body core temperature) levels of hyperthermia. Future research directions are provided.

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“…During prolonged moderate exercise, for instance, oxygen uptake and blood lactate concentrations remain virtually constant and are similar under hot and thermoneutral conditions, but V E increases when core temperature rises (20,33). This increase in V E during hyperthermia is possibly due to elevated brain temperature [e.g., medulla and hypothalamus (5,9)] and increased chemoreceptor activity (10,12). This heat-induced hyperventilation can lead to excessive elimination of CO 2 from the body, reduced arterial CO 2 pressure, and, in turn, cerebral hypoperfusion (19,33), which may eventually lead to elevated brain temperature (34).…”

mentioning

confidence: 99%

Diurnal variation in the control of ventilation in response to rising body temperature during exercise in the heat

Tsuji

Honda

Kondo

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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We investigated whether heat-induced hyperventilation during exercise is affected by time of day, as diurnal variation leads to higher core temperatures in the evening. Nineteen male subjects were divided into two experiments (protocol 1, n = 10 and protocol 2, n = 9). In protocol 1, subjects performed cycle exercise at 50% peak oxygen uptake in the heat (37°C and 50% RH) in the morning (0600) and evening (1800). Results showed that baseline resting and exercising esophageal temperature (Tes) were significantly (0.5°C) higher in the evening than morning. Minute ventilation (V̇e) increased from 54.3 ± 7.9 and 54.9 ± 6.8 l/min at 10 min to 71.4 ± 8.1 and 76.5 ± 11.8 l/min at 48.5 min in the morning and evening, respectively (both P < 0.01). Time of day had no effect on V̇e (P = 0.44). When V̇e as the output response was plotted against Tes as thermal input, the Tes threshold for increases in V̇e was higher in the evening than morning (37.2 ± 0.7 vs. 36.6 ± 0.6°C, P = 0.009), indicating the ventilatory response to the same core temperature is smaller in the evening. In protocol 2, the circadian rhythm-related higher resting Tes seen in the evening was adjusted down to the same temperature seen in the morning by immersing the subject in cold water. Importantly, the time course of changes in V̇e during exercise were smaller in the evening, but the threshold for V̇e remained higher in the evening than morning (P < 0.001). Collectively, those results suggest that time of day has no effect on time course hyperventilation during exercise in the heat, despite the higher core temperatures in the evening. This is likely due to diurnal variation in the control of ventilation in response to rising core temperature.

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The preoptic area in the hypothalamus is the source of the additional respiratory drive at raised body temperature in anaesthetised rats

Cited by 16 publications

References 30 publications

The human ventilatory response to stress: rate or depth?

The human ventilatory response to stress: rate or depth?

Cerebral oxygenation and hyperthermia

Diurnal variation in the control of ventilation in response to rising body temperature during exercise in the heat

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