We know that temperatures >22°C will induce HSP70 in wild juvenile Atlantic salmon in the Miramichi River (Lund et al., 2002). Diel temperature stress induced an upregulation of six heat shock genes in redband trout (Oncorhynchus mykiss gairdneri) (Narum et al., 2013) and HSP70 in several tissues of Atlantic salmon (Tunnah et al., 2017). Given this information, the current temperature conditions of the Miramichi River, and regulations regarding recreational angling (closure when T ≥ 20°C for two consecutive nights; DFO, 2012), our prediction was that juveniles experiencing higher nighttime temperatures would display a higher magnitude heat shock response (HSR) than those experiencing a lower diel Tmin. Instead, our data indicated that exposure to diel, environmentally relevant, sub-lethal heat stress, had cellular level consequences but the nature of high temperature cycling (i.e. nighttime temperature) had minor effects on the HSR. Thus, the magnitude of the thermal stress, regardless of diel cycle, was consistent with the magnitude of the HSR. Assuming that thermally induced protein denaturation/damage triggers the HSR (Ananthan et al., 1986), our data suggest that protein damage is similar among our different diel cycles. In support of this, induction of Ub occurred at the peak of the first heat cycle and remained elevated throughout the heating event, regardless of thermal cycle, as was the case with HSP70. Tunnah et al. (2017) also demonstrated consistency of the HSR with Ub induction in thermally cycled Atlantic salmon.