Figure 3.

Ventilatory responses to hypoxia in wild type (NTS-HIF-1α^+/+, squares and solid lines) and NTS-HIF-1α^−/− null mice (triangles and dashed lines) during normoxic control conditions (filled symbols) and after 7 days of chronic hypoxia (CH, open symbols). A. For V̇_I, the 3-way interaction between acute O₂ level, chronic O₂ level and genotype by ANOVA was significant (p=0.044) and all of the 2-way interactions were significant (p≤0.0025). In acute normoxia (21% O₂), V̇_I was significantly greater after CH regardless of genotype (p ≤ 0.0003, Fisher’s test after multivariate ANOVA, n=11 to 14 for the 4 groups of mice). In acute hypoxia (10% O₂), however, the increase in V̇_I with CH was significantly greater in wild-type (NTS-HIF-1α^+/+) than in NTS-HIF1-α^−/− mice (*p ≤ 0.05, Fisher’s test after multivariate ANOVA, n=11 to 14 for the 4 groups of mice). This was mainly due to similar effects on f_R (B) while V_T increased similarly with CH independent of genotype (C). D. The magnitude of the HVR increased significantly more with CH in wild-type versus NTS-HIF1-α^−/− null mice (2-way interaction p=0.044 with multivariate ANOVA, *p ≤ 0.05 Fisher’s post-hoc test, n=11 to 14 for the 4 groups of mice). The effects of CH on f_R (E) and V_T (F) responses to hypoxia showed similar trends with genotype but were not significant (p=0.056 and 0.429, respectively, for 2-way interaction with ANOVA).