Liver HSP70 was not induced under control conditions (Fig. 4A); however, a significant interaction was observed with time and temperature treatment (F12, 160 = 9.68, P < 0.001), indicating that the pattern of induction depended on thermal regime. Liver HSP70 was induced in the 18–27°C and 22–27°C groups at the pre-thermal stress sampling point after exposure to 23°C (t = 48 h; P < 0.001 & P = 0.02, respectively). The peak of the first day of heat exposure induced a significant increase in liver HSP70 in all three high thermal cycles compared to the 16–21°C group (t = 60 h; P < 0.001; Fig. 4); however, HSP70 was not significantly different among the temperature treatments. Although the specific pattern of liver HSP70 induction varied among temperature treatments, levels remained elevated throughout the duration of the 3-day heat event (t = 60–120 h; P < 0.001 in all cases). After the onset of the event, treatments did not vary from one another statistically (P = 0.07–0.99), with the exceptions of the diel minima following the first and third heat cycles (t = 72 and 120 h) where HSP70 levels in the 18–27°C were significantly greater than in the 22–27°C group (P = 0.018 and 0.008, respectively; Fig. 4). Figure 4:Liver HSP70 in juvenile salmon exposed to diel cycles: (A) 16–21°C only; or multi-day thermal stress (closed symbols; 60–120 h) of (B) 18–27°C; (C) 20–27°C; (D) 22–27°C. Data are presented as mean ± SEM (n = 5–9). Pre-thermal stress sampling (open symbols; t = 12 & 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.