Liver glycogen levels in the 16–21°C group remained relatively stable at a mean of 67.4 ± 4.8 mg g−1 throughout the experimental sampling period (Fig. 3). Although liver glycogen decreased over time in all but the 16–21°C group, a significant interaction was observed between time and temperature treatment (F12, 160 = 2.63, P < 0.003; Table 2) indicating that the pattern of decline was different in each thermally cycled group. No significant differences in glycogen were observed prior to the first heat cycle in any temperature treatment (t = 48 h; F3, 27 = 1.08, P = 0.37; Fig. 3). Differences among thermally cycled groups were apparent at the peak of the first heat cycle (t = 60 h). The 20–27°C and 22–27°C groups experienced the most pronounced decline in liver glycogen, but by the end of the experiment (t = 120 h) only the 22–27°C group was significantly different than the 16–21°C group (19.1 ± 4.0 mg·g−1, P = 0.006). One noteworthy exception to the overall pattern is the observed spike in liver glycogen at t = 72 h in the 20–27°C group (Fig. 3C) that was significantly greater than the 16–21°C and 22–27°C groups (P = 0.04 and P < 0.001, respectively). Figure 3:Liver glycogen in juvenile salmon exposed to diel cycles: (A) 16–21°C (control group); or multi-day thermal stress (60–120 h) of (B) 18–27°C; (C) 20–27°C; (D) 22–27°C. Data are presented as mean ± SEM (n = 6–9). Pre-thermal stress sampling (t = 12 and 24 h) assessed the effect of ‘trial’ and was not included in the analysis. Letters indicate significant differences among treatments (P < 0.05) within sampling time points.