Fig. 4. Comparison of the ability of preconditioning (5 min ofhypoxic pre-exposure) to protect (A) hypoxia-sensitive (Gamperl et al., 2001) and (B) hypoxia-tolerant (Gamperl et al., 2004) trout hearts from the myocardial dysfunction that follows more prolonged exposure to hypoxia. In A, 5 min of hypoxic pre-exposure completely eliminated the loss of myocardial function that normally followed the `Hypoxia-high workload' protocol. In B, preconditioning with 5 min of hypoxia either did not affect, or increased, the amount of myocardial dysfunction following exposure to `30 min of hypoxia'. Top panels, maximum cardiac output; middle panels, maximum stroke volume; bottom panels, heart rate. Note that the hypoxia-tolerant trout hearts in B required twice the duration of hypoxia (15 vs 30 min), and 6 times the workload, as compared with hypoxia-sensitive hearts (A) to achieve a comparable (15–20%) decrease in post-hypoxic myocardial function. Values were obtained by comparing maximum in situ cardiac function before and after the treatment protocols. All values are means ± S.E.M. (N=7–9). Dissimilar letters indicate a significant difference at P<0.05, as determined by one-way ANOVA. Hypoxia in these experiments was defined as perfusate P_O2=5–10 mmHg. Control hearts were only exposed to oxygenated saline.