Due to the ever‐expanding functions attributed to autophagy, there is widespread interest in understanding its contribution to human physiology; however, its specific cellular role as a stress‐response mechanism is still poorly defined. To investigate autophagy's role in this regard, we repeatedly subjected cultured mouse myoblasts to two stresses with diverse impacts on autophagic flux: amino acid and serum withdrawal (Hank's balanced salt solution [HBSS]), which robustly induces autophagy, or low‐level toxic stress (staurosporine, STS). We found that intermittent STS (int‐STS) administration caused cell cycle arrest, development of enlarged and misshapen cells/nuclei, increased senescence‐associated heterochromatic foci and senescence‐associated β‐galactosidase activity, and prevented myogenic differentiation. These features were not observed in cells intermittently incubated in HBSS (int‐HB). While int‐STS cells displayed less DNA damage (phosphorylated H2A histone family, member X content) and caspase activity when administered cisplatin, int‐HB cells were protected from STS‐induced cell death. Interestingly, STS‐induced senescence was attenuated in autophagy related 7‐deficient cells. Therefore, while repeated nutrient withdrawal did not cause senescence, autophagy was required for senescence caused by toxic stress. These results illustrate the context‐dependent effects of different stressors, potentially highlighting autophagy as a distinguishing factor.