Microbial electrosynthesis (MES) enables certain microorganisms to utilize electrical energy (electrons) to produce valuable compounds using CO2 as a carbon source. It is closely related to gas fermentation in which hydrogen gas (H2) is used as the energy source, rather than in-situ electrochemically produced H2 in MES. Despite its potential for energy and carbon storage and the hype created around it, MES persists to face major limitations, such as low efficiency, unattractive products, and poor microbial growth. In this study, we compare the physiology of the model acetogen Clostridium ljungdahlii cultivated in gas fermenters and H-type electrobioreactors to identify the key stress factors limiting MES. We observed severe cellular stress and distinct physiological changes in MES through transcriptomics, proteomics, and electron microscopy analysis, showing that the electrochemical operation directly affects cellular metabolism. Most impressively, cell integrity was strongly impaired during growth in MES. Our results strongly indicate that this is because of a struggle to maintain the membrane potential and ATP synthesis. MES significantly impacted the central metabolic flux of the Wood-Ljungdahl pathway for CO₂ fixation and a diversion towards the glycine synthase-reductase pathway (GSRP), resulting in a broader spectrum of reduced products, including two amino compounds that appeared exclusively under MES conditions, ethanolamine, and glycine. We show that this struggle for ATP is compensated by the activation of the arginine metabolism to produce ATP. Multiple evidences indicate that this reaction could be fueled by the degradation of internal cyanophycin storage compounds, which have not been reported for C. ljungdahlii before. Additionally, our research highlights the expression of bacterial microcompartments (BMCs), which raises questions about their role during MES. This work demonstrates that MES drives C. ljungdahlii into a distinct physiological state and challenges its fitness, reshaping how we view MES process development. Our findings highlight the need to design MES strategies that mitigate the effects of the electrochemical environment on cellular physiology.