ACC1 deficiency in platelets had an impact on both mitochondrial reserve capacity and glycolytic activity. OCR was measured in washed murine platelets from ACC1^flx/flx or pKO mice. (A-B) OCR was assessed under basal conditions, after stimulation with 1 U/mL Thr, and after sequential treatment with 1 μM oligomycin (O), 0.4 μM carbonyl cyanide p-trifluoromethoxyphenylhydrazone (F), and a mix of 1 μM AtA/R. (A) Representative OCR profiles are shown as mean ± SEM (n = 4). (B) Quantification of mitochondrial respiratory parameters including basal (baseline OCR – R/AtA-sensitive OCR), Thr (Thr response − baseline OCR), ATP-linked (thrombin response − oligomycin sensitive OCR), maximal (FCCP [carbonyl cyanide-p-trifluoromethoxyphenylhydrazone]-sensitive – R/AtA-sensitive OCR), reserve capacity (FCCP-sensitive – Thr-responsive OCR), proton leak (oligomycin-sensitive – R/AtA-sensitive OCR), and nonmitochondrial (R/AtA-sensitive OCR). Results are expressed as mean ± SEM (n = 4). (C-D) ECAR, used as an indirect indicator of glycolytic activity, was measured in the same experimental conditions. (C) Representative ECAR profiles are shown as mean ± SEM (n = 4). (D) Quantification of basal and Thr-induced ECAR. Results are expressed as mean ± SEM (n = 4). ∗P ≤ .05 relative to unstimulated conditions. #P ≤ .05 relative to ACC1^flx/flx mice. Statistical analysis was performed using 2-way ANOVA. Ata, antimycin A; DMEM, Dulbecco’s modified eagle medium; NS, nonstimulated; R, rotenone; Thr, thrombin.