Hypoxia is common in aquatic environments and has substantial effects on development, metabolism and survival of aquatic organisms. To understand the physiological effects of hypoxia and its dependence on temperature, metabolic rate (ṀO2) and cardiorespiratory function were studied in response to acute hypoxia (21 → 5 kPa) at different measurement temperatures (Ta; 4, 8 and 12 °C) in Salmo salar alevins that were incubated under normoxic conditions (PO2 = 21 kPa) or following hypoxic acclimation (PO2 = 10 kPa) as well as two different temperatures (4 °C or 8 °C). Hypoxic acclimation lead to a developmental delay manifested through slower yolk absorption. The general response to acute hypoxia was metabolic depression (~ 60%). Hypoxia acclimated alevins had higher ṀO2s when measured in normoxia than alevins acclimated to normoxia. ṀO2s were elevated to the same degree (~ 30% per 4 °C change) irrespective of Ta. Under severe, acute hypoxia (~ 5 kPa) and irrespective of Ta or acclimation, ṀO2s were similar between most groups. This suggests that despite different acclimation regimes, O2 transport was limited to the same degree. While cardiorespiratory function (heart-, ventilation rate) was unchanged in response to acute hypoxia after normoxic acclimation, hypoxic acclimation led to cardiorespiratory changes predominantly in severe hypoxia, indicating earlier onset and plasticity of cardiorespiratory control mechanisms. Although ṀO2 in normoxia was higher after hypoxic acclimation, at the respective acclimation PO2, ṀO2 was similar in normoxia and hypoxia acclimated alevins. This is indicative of metabolic compensation to an intrinsic ṀO2 at the acclimation condition in hypoxia-acclimated alevins after re-exposure to normoxia.