Oxygen plays a critical role in aerobic metabolism. Accordingly, low oxygen conditions (hypoxia) can impair essential physiological processes and cause cellular damage and death, such as is observed as a result of stroke and cardiovascular disease. However, hypoxic preconditioning, in which a non-injurious hypoxic exposure precedes the damaging hypoxic insult, has been shown to be effective at attenuating the cellular damage caused by hypoxia, suggesting that there are cellular mechanisms that can protect against hypoxic damage. We have found that specific concentrations of hypoxia cause a disruption of protein homeostasis in C. elegans, as measured by increased aggregation of polyglutamine proteins in the body wall muscles. Here, we show that nutritional cues regulate the effect of hypoxia on proteostasis. Animals that are fasted develop dramatically fewer protein aggregates compared to their fed counterparts when exposed to hypoxia. Polyglutamine and amyloid-beta protein aggregation in the body wall muscles is thought to be cytotoxic, resulting in age-dependent uncoordination and eventual paralysis. In support of this, fed animals exposed to hypoxia have an accelerated rate of paralysis compared to controls maintained in room air. However, animals that are fasted prior to hypoxia are partially rescued from this expedited paralysis rate. We also demonstrate that fasted animals are resistant to the long-term effects of hypoxia on proteostasis. When animals are exposed to hypoxia for a short period of time, they do not display increased polyglutamine aggregation. Yet, as the animals continue to grow and develop in room air, the appearance of aggregates is accelerated in fed animals exposed to hypoxia, whereas fasted animals accumulate aggregates at a rate identical to room air controls. Taken together, our results underscore the influential role of nutritional state on both the immediate and long-term effects of hypoxia on proteostasis.