Hyperthermic-induced hyperventilation and associated respiratory alkalosis in humans

Abbiss, Chris R.; Nosaka, Kazunori; Laursen, Paul B.

doi:10.1007/s00421-007-0405-z

Cited by 19 publications

(13 citation statements)

References 27 publications

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“…2D), which suggests that hyperthermic hyperpnea occurs with increases in alveolar ventilation, leading to respiratory alkalosis. The same observation was made in earlier human (1,19,26) and animal (14) studies. If hyperthermic hyperpnea is induced by thermoregulatory drive in exercising humans, we suggest that thermoregulatory drive (increase in ventilation) overrides chemoregulation (e.g., arterial CO 2 pressure) in hyperthermic exercising humans.…”

Section: Discussionsupporting

confidence: 64%

Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

Fujii

Honda²,

Hayashi³

et al. 2008

Journal of Applied Physiology

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Nishiyasu T. Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men. J Appl Physiol 105: 1509-1518. First published September 11, 2008 doi:10.1152/japplphysiol.01206.2007.-We tested the hypothesis that, in humans, hypohydration attenuates hyperthermic hyperpnea during exercise in the heat. On two separate occasions, thirteen male subjects performed a fluid replacement (FR) and a no-fluid replacement (NFR) trial in random order. The subjects performed two bouts of cycle exercise (Ex1 and Ex2, 30 -60 min) at 50% peak oxygen uptake (V O2 peak) in 35°C separated by a 70-to 80-min rest period, during which they drank water containing 25 mosmol/l sodium in the FR trial but not the NFR trial. The drinking in the FR trial nearly restored the body fluid to the euhydrated condition, so that the body fluid status differed between the trials before Ex2 (the difference in plasma osmolality before Ex2 was 9.4 mosmol/kgH 2O; plasma volume was 7.6%, and body weight was 2.5%). The slopes of the linear relationships between ventilatory variables (minute ventilation, ventilatory equivalents for oxygen uptake and carbon dioxide output, tidal volume, respiratory frequency, and end-tidal CO 2 pressure) and esophageal temperature (Tes) did not significantly differ between Ex1 and Ex2, or between the FR and NFR trials. On the other hand, during Ex2 in the NFR trial, the Tes threshold for the onset of increased forearm vascular conductance (FVC) was higher, and the slope and peak values of the relationship between FVC and Tes were lower than during Ex1 in the NFR trial and during Ex2 in the FR trial. These findings suggest that hypohydration does not affect the hyperthermic hyperpnea during exercise, although it markedly attenuates the cutaneous vasodilatory response. thermoregulation; respiration; ventilation; skin circulation IN MANY SPECIES of mammals and birds, an elevation in body temperature stimulates ventilation and increases evaporative heat loss for thermoregulation (the so-called panting response) (42). In 1905, Haldane (25) was the first to report that hyperthermia also increases ventilation in humans, and the recent review by White (53) suggested that the hyperthermic hyperventilatory response provides countercurrent cooling of blood perfusing the brain (selective brain cooling). However, the mechanism and the physiological significance of this response in humans are not fully understood.Hayashi et al. (26) and Nybo and Nielsen (37) recently reported that during prolonged submaximal exercise [50 -57% peak oxygen uptake (V O 2 peak )] in the heat in humans, minute ventilation (V E) increases linearly with increasing esophageal temperature (T es ), but this ventilatory response appears independent of skin temperature (T sk ) and the rate of increase in core temperature (26). Such prolonged exercise in the heat usually leads to profuse sweating, which can lead to hypohydration. Indeed, body weight was reduced by 1.5% in Hayashi's study (unpublished data), and by 0.7% in Nybo and Ni...

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Section: Discussionsupporting

confidence: 64%

Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

Fujii

Honda²,

Hayashi³

et al. 2008

Journal of Applied Physiology

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“…Even though arterial pH decreased between t 0 and t 10 (p <0.05), it increased slightly after t 10 , whereas paCO 2 decreased and [HCO 3 − ] did not change (table 2), suggesting a ventilatory compensation for a mild exercise-induced metabolic acidosis15 or hyperthermically induced hyperventilation 38. Furthermore, arterial pH at the termination of exercise (∼7.37 units) was much above values considered to cause fatigue by a direct effect in the exercising muscles 39 40…”

Section: Discussionmentioning

confidence: 97%

Why does exercise terminate at the maximal lactate steady state intensity?

Baron¹,

et al. 2007

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“…Ventilation rose linearly with increasing Tc during passive heating, such that it had doubled from baseline values at T-LIM. This increased respiratory drive has been consistently reported during hyperthermia, and although its causation or function is not fully understood, it has been suggested to be integral to the thermoregulatory response (1,6,38). An elevated Tc is seemingly a more potent stimulus to ventilation than the inhibition brought about by the ensuing hypocapnia, and this increased ventilation may play a role in "selective brain cooling" through respiratory evaporative heat loss and countercurrent heat exchange in the cranial vessels (38).…”

Section: Respiratory Changes During Passive Heatingmentioning

confidence: 95%

Cerebrovascular and corticomotor function during progressive passive hyperthermia in humans

Ross

Cotter²,

Wilson

et al. 2012

Journal of Applied Physiology

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The present study examined the integrative effects of passive heating on cerebral perfusion and alterations in central motor drive. Eight participants underwent passive hyperthermia [0.5°C increments in core temperature (Tc) from normothermia (37 ± 0.3°C) to their limit of thermal tolerance (T-LIM; 39.0 ± 0.4°C)]. Blood flow velocity in the middle cerebral artery (CBFv) and respiratory responses were measured continuously. Arterial blood gases and blood pressure were obtained intermittently. At baseline and each Tc level, supramaximal femoral nerve stimulation and transcranial magnetic stimulation (TMS) were performed to assess neuromuscular and cortical function, respectively. At T-LIM, measures were (in a randomized order) also made during a period of breathing 5% CO(2) gas to restore eucapnia (+5% CO(2)). Mean heating time was 179 ± 51 min, with each 0.5°C increment in Tc taking 40 ± 10 min. CBFv was reduced by ∼20% below baseline from +0.5°C until T-LIM. Maximal voluntary contraction (MVC) of the knee extensors was decreased at T-LIM (-9 ± 10%; P < 0.05), and cortical voluntary activation (VA), assessed by TMS, was decreased at +1.5°C and T-LIM by 11 ± 8 and 22 ± 23%, respectively (P < 0.05). Corticospinal excitability (measured as the EMG response produced by TMS) was unaltered. Reductions in cortical VA were related to changes in ventilation (Ve; R(2) = 0.76; P < 0.05) and partial pressure of end-tidal CO(2) (Pet(CO(2)); R(2) = 0.63; P < 0.05) and to changes in CBFv (R(2) = 0.61; P = 0.067). Interestingly, although CBFv was not fully restored, MVC and cortical VA were restored towards baseline values during inhalation of 5% CO(2). These results indicate that descending voluntary drive becomes progressively impaired as Tc is increased, presumably due, in part, to reductions in CBFv and to hyperthermia-induced hyperventilation and subsequent hypocapnia.

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Hyperthermic-induced hyperventilation and associated respiratory alkalosis in humans

Cited by 19 publications

References 27 publications

Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

Why does exercise terminate at the maximal lactate steady state intensity?

Cerebrovascular and corticomotor function during progressive passive hyperthermia in humans

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