Respiratory Physiology & Neurobiology 155 (2007) 71–81 Cerebral and muscle tissue oxygenation in acute hypoxic ventilatory response test Juha E. Peltonen a,b,∗ , John M. Kowalchuk b , Donald H. Paterson b , Darren S. DeLorey b,c , Gregory R. duManoir b , Robert J. Petrella b,d , J. Kevin Shoemaker e a Unit for Sports and Exercise Medicine, Institute of Clinical Medicine, University of Helsinki, Helsinki 00250, Finland b Canadian Centre for Activity and Aging, School of Kinesiology, The University of Western Ontario, London, Ont., Canada N6G 2M3 c Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53295, USA d Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ont., Canada N6A 5C1 e Neurovascular Research Laboratory, School of Kinesiology, The University of Western Ontario, London, Ont., Canada N6A 3K7 Accepted 28 March 2006 Abstract Eight men were exposed to progressive isocapnic hypoxia for 10 min to test the hypothesis that (i) cerebral and muscle tissue would follow similar deoxygenation profiles during an acute hypoxic ventilatory response (AHVR) test; and (ii) strong cerebrovascular responsiveness to hypoxia would be related to attenuated cerebral deoxygenation. End-tidal O 2 concentration was reduced from normoxia (∼102 mmHg) to ∼45 mmHg while arterial oxygen saturation (Sp O 2 %) declined from 98 ± 1% to 77 ± 7% (P < 0.001). Near-infrared spectroscopy (NIRS)-derived local cerebral tissue (frontal lobe) deoxyhemoglobin increased 5.55 ± 2.22 M, while oxyhemoglobin and tissue oxygenation index decreased 2.57 ± 1.99 M and 6.2 ± 3.4%, respectively (all P < 0.001). In muscle (m. vastus lateralis) the NIRS changes from the initial normoxic level were non-significant. Cerebral blood velocity (V mean , transcranial Doppler) in the middle cerebral artery increased from 53.4 ± 10.4 to 60.6 ± 11.6 cm s -1 (P < 0.001). In relation to the decline in Sp O 2 % the mean rate of increase of V mean and AHVR were 0.33 ± 0.19 cm s -1 % -1 and 0.52 ± 0.20 l min -1 % -1 , respectively. We conclude that cerebral, but not muscle, tissue shows changes reflecting a greater deoxygenation during acute hypoxia. However, the changes in NIRS parameters were not related to cerebrovascular responsiveness or ventilatory chemosensitivity during graded hypoxia. © 2006 Elsevier B.V. All rights reserved. Keywords: Near-infrared spectroscopy; Cerebral blood flow; Transcranial Doppler; Hypoxia; Acute; Chemosensitivity; Ventilation 1. Introduction Sufficient oxygenation and perfusion of brain tissue is vital for avoidance of hazardous symptoms while at hypoxia/altitude or after effects of chronic hypoxia (Hornbein, 2001). Previous studies indicate that with exposure to acute hypoxia, cerebral blood flow (CBF) (Cohen et al., 1967) and CBF velocity (Jensen et al., 1996; Kolb et al., 2004b) increase to maintain O 2 delivery. It has been suggested that cerebral O 2 supply is well protected in acute hypoxia (Roach and Hackett, 2001). Thus, whole brain O 2 consumption is unaffected even with severe degrees of hypox- emia (Cohen et al., 1967) and the energy state of the brain tissue remains remarkably normal by arterial O 2 tensions (Pa O 2 ) as low as 56 mmHg, although intracellular energy state is compromised ∗ Corresponding author. Tel.: +358 9 43 42 100; fax: +358 9 49 08 09. E-mail address: Juha.Peltonen@helsinki.fi (J.E. Peltonen). when Pa O 2 is further reduced to 40 mmHg (Rolett et al., 2000; Raichle and Hornbein, 2001). In contrast, the turnover of several cerebral neurotransmitters, e.g. acetylcholine, is reduced even by mild hypoxia (Gibson et al., 1981; Raichle and Hornbein, 2001). The recent papers, however, indicate a drop in regional cerebral oxygen saturation in acute hypoxia. Kolb et al. (2004b) reported cerebral tissue saturation reduction from an average of 74% to approximately 66% during an acute hypoxic ventilatory response (AHVR) test. In the study of Imray et al. (2003) not only was regional cerebral saturation reduced from 70% at 150 m to 66% after a night at 3459 m but also muscle tissue saturation decreased from 73% to 68%. In the acute ventilatory response to hypoxia the afferent impulses from the carotid body reach the nucleus tractus soli- tarius leading to the stimulation of ventilation ( ˙ V E )(Burton and Kazemi, 2000). The chemosensitivity of this ventilatory response to lowered arterial O 2 tensions is monitored with an AHVR test, while end-tidal CO 2 tension is clamped to iso- 1569-9048/$ – see front matter © 2006 Elsevier B.V. All rights reserved. doi:10.1016/j.resp.2006.03.008