Middle cerebral artery blood velocity is reduced with hyperthermia during prolonged exercise in humans

Nybo, Lars; Nielsen, Bodil

doi:10.1111/j.1469-7793.2001.t01-1-00279.x

Cited by 213 publications

(242 citation statements)

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“…During the hyperthermic hypoxic exercise condition, V T increased in a relatively equal magnitude as during the normothermic hypoxic condition, yet the HVR was enhanced. This can be attributed primarily to the elevated f v as a result of the increased T es , which has been described as a thermal tachypnea (2,22). This supports the suggestion that an elevated T es influences the sensitivity of the peripheral chemoreceptors and helps explain the elevated HVR during hyperthermic exercise (Fig.…”

Section: Discussionsupporting

confidence: 70%

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: 70%

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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“…Rasmussen et al (30) suggested that the observed increase in CO 2 reactivity, coupled with decreases in PET CO 2 , provides a mechanistic basis for previously observed reductions in cerebral blood flow when subjects exercised in the heat (25,26). The most obvious reason for conflicting findings with respect to cerebral vascular CO 2 reactivity between the present study and that of Rasmussen et al (30) is the absence of exercise in the present study.…”

Section: Discussioncontrasting

confidence: 57%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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“…3 In addition, it is well known that heat stress modifies distribution of blood flow toward cutaneous circulation while decreasing renal and splanchnic blood flows by enhanced vasoconstriction. 15,19 Maintained or decreased cerebral blood velocity during heat stress has been reported [10][11][12][20][21][22][23] but the mechanism remains unclear. The present study demonstrated that CBF conductance in MCAV mean , ICA, and VA gradually decreased during whole body heating, whereas CVC forehead and ECA conductance increased by 3 times and 2.5 times from the baseline, respectively.…”

Section: Modified Blood Distribution In Hyperthermic Conditionmentioning

confidence: 99%

Blood Flow Distribution during Heat Stress: Cerebral and Systemic Blood Flow

Ogoh

Sato

Okazaki

et al. 2013

J Cereb Blood Flow Metab

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The purpose of the present study was to assess the effect of heat stress-induced changes in systemic circulation on intra-and extracranial blood flows and its distribution. Twelve healthy subjects with a mean age of 22 ± 2 (s.d.) years dressed in a tube-lined suit and rested in a supine position. Cardiac output (Q), internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) blood flows were measured by ultrasonography before and during whole body heating. Esophageal temperature increased from 37.0 ± 0.21C to 38.4 ± 0.21C during whole body heating. Despite an increase in Q (59 ± 31%, Po0.001), ICA and VA decreased to 83 ± 15% (P ¼ 0.001) and 87 ± 8% (P ¼ 0.002), respectively, whereas ECA blood flow gradually increased from 188 ± 72 to 422±189 mL/minute ( þ 135%, Po0.001). These findings indicate that heat stress modified the effect of Q on blood flows at each artery; the increased Q due to heat stress was redistributed to extracranial vascular beds.

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Middle cerebral artery blood velocity is reduced with hyperthermia during prolonged exercise in humans

Cited by 213 publications

References 50 publications

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

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

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Blood Flow Distribution during Heat Stress: Cerebral and Systemic Blood Flow

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