<p>Warming rate is regarded as a critical determinant of thermal tolerance. However, its role in shaping metabolic depression and the underlying molecular mechanisms remain poorly understood. Here, we examined how the fast and slow ramping rates influence cardiac performance and transcriptional and post-transcriptional regulations in the mudflat gastropod <i>Batillaria attramentaria</i>. Slow warming increased the prevalence of bimodal heart rate responses by driving transitions from unimodal cardiac performance, which is consistent with the deployment of metabolic depression. In contrast, fast warming predominantly produced unimodal responses and a stronger temperature dependence of heart rate. Despite similar cardiac breakpoints, the upper thermal limit of cardiac function was significantly lower under a slow warming rate, suggesting a trade-off between energy conservation and maximal performance. Transcriptomic analyses revealed that molecular stress responses were strongly warming rate-dependent. Rapid warming triggered early downregulation of peptide-mediated GPCR signaling, followed by induction of protein-folding chaperones and, at extreme temperatures, suppression of DNA repair and DNA duplex unwinding, consistent with accelerated regulatory breakdown. Under slow warming rate, translation-related processes were enriched near cardiac limits, while signatures of molecular dysfunction were largely absent. Alternative splicing analyses further revealed distinct regulatory strategies: gradual warming was associated with consistent enrichment of chromatin remodeling-related splicing, whereas rapid warming promoted spliceosome-related splicing and increased overlap between differentially expressed and spliced genes at high temperatures. Our findings demonstrate that warming rate determines the deployment of metabolic depression and its molecular regulation, thereby shapes thermal limits and vulnerability under climate change.</p>