• Brothers R Matthew RM Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, TX, USA Department of Internal Medicine, University of, Rebekah A I Lucas, Yong-Sheng Zhu, Craig G Crandall, and Rong Zhang.
• Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, TX, USA Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA Department of Kinesiology and Health Education, University of Texas at Austin, TX, USA r.m.brothers@mail.utexas.edu.
• Exp. Physiol. 2014 Nov 1; 99 (11): 1499-510.

AbstractCerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal carbon dioxide tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P < 0.01) and CVCI versus P ET , CO 2 (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2 is similar regardless of the employed methodology to induce changes in P aCO 2 and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. © 2014 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.

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