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Voluntary control of breathing and cerebral blood flow during prolonged exercise in the heat
Author(s) -
Tsuji Bun,
Honda Yasushi,
Ikebe Yusuke,
Fujii Naoto,
Kondo Narihiko,
Nishiyasu Takeshi
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1201.25
Subject(s) - hyperventilation , cerebral blood flow , ventilation (architecture) , medicine , anesthesia , tidal volume , middle cerebral artery , hyperthermia , respiratory minute volume , respiratory rate , blood flow , breathing , blood pressure , respiratory system , cardiology , heart rate , ischemia , mechanical engineering , engineering
Hyperthermia during prolonged exercise leads to hyperventilation (hyperthermic hyperventilation), which causes a decrease in arterial CO 2 pressure (Pa CO2 ), resulting in reduced cerebral blood flow. Here we examined whether humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise and, if so, are reductions in Pa CO2 and cerebral blood flow attenuated by this suppression. Eight male subjects performed two exercise trials at 50% of peak oxygen uptake in the heat (37°C). The subjects breathed normally (normal breathing) and tried to control respiratory frequency and tidal volume to their levels of 5 min of exercise (controlled breathing). Minute ventilation increased with rising esophageal temperature (T es ) in normal breathing, whereas controlled breathing attenuated the increased ventilation (increase from the onset of controlled breathing: 11.5 vs. 3.6 L/min at +1.3°C T es , P < 0.05). Normal breathing resulted in a decrease in end‐tidal CO 2 pressure (P ETCO2 ) and middle cerebral artery mean blood velocity (MCAV mean ) with rising T es , whereas controlled breathing attenuated the reductions (P ETCO2 −4.8 vs. −1.4 mmHg; MCAV mean −15.7 vs. −6.6 cm/s at +1.3°C T es , P < 0.05, respectively). Our results indicate that humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise, and this suppression leads to smaller changes in Pa CO2 and cerebral blood flow.