{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cree-Green M"],"funding":["BLRD VA","NCATS NIH HHS","NICHD NIH HHS","NCRR NIH HHS","NIDDK NIH HHS","American Diabetes Association","NIH HHS","CSRD VA"],"pagination":["1369-1379"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6463751"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["67(7)"],"pubmed_abstract":["Type 2 diabetes is associated with impaired exercise capacity. Alterations in both muscle perfusion and mitochondrial function can contribute to exercise impairment. We hypothesized that impaired muscle mitochondrial function in type 2 diabetes is mediated, in part, by decreased tissue oxygen delivery and would improve with oxygen supplementation. Ex vivo muscle mitochondrial content and respiration assessed from biopsy samples demonstrated expected differences in obese individuals with (<i>n</i> = 18) and without (<i>n</i> = 17) diabetes. Similarly, in vivo mitochondrial oxidative phosphorylation capacity measured in the gastrocnemius muscle via <sup>31</sup>P-MRS indicated an impairment in the rate of ADP depletion with rest (27 ± 6 s [diabetes], 21 ± 7 s [control subjects]; <i>P</i> = 0.008) and oxidative phosphorylation (<i>P</i> = 0.046) in type 2 diabetes after isometric calf exercise compared with control subjects. Importantly, the in vivo impairment in oxidative capacity resolved with oxygen supplementation in adults with diabetes (ADP depletion rate 5.0 s faster, <i>P</i> = 0.012; oxidative phosphorylation 0.046 ± 0.079 mmol/L/s faster, <i>P</i> = 0.027). Multiple in vivo mitochondrial measures related to HbA<sub>1c</sub> These data suggest that oxygen availability is rate limiting for in vivo mitochondrial oxidative exercise recovery measured with <sup>31</sup>P-MRS in individuals with uncomplicated diabetes. Targeting muscle oxygenation could improve exercise function in type 2 diabetes."],"journal":["Diabetes"],"pubmed_title":["Supplemental Oxygen Improves In Vivo Mitochondrial Oxidative Phosphorylation Flux in Sedentary Obese Adults With Type 2 Diabetes."],"pmcid":["PMC6463751"],"funding_grant_id":["BX002046","P30 DK048520","R56 DK088971","I01 BX002046","T32 DK063687","K23 DK107871","1-12-CT-64","I01 CX001532","S10 OD018435","UL1 TR001082","K23 RR020038","K12 HD057022"],"pubmed_authors":["Newcomer BR","Orlicky D","Knaub L","McClatchey PM","Schauer IE","Huebschmann AG","Reusch JEB","Brown MS","McMillin S","Nadeau KJ","Cree-Green M","Harrall K","Scalzo RL","Regensteiner JG","Bauer TA"],"additional_accession":[]},"is_claimable":false,"name":"Supplemental Oxygen Improves In Vivo Mitochondrial Oxidative Phosphorylation Flux in Sedentary Obese Adults With Type 2 Diabetes.","description":"Type 2 diabetes is associated with impaired exercise capacity. Alterations in both muscle perfusion and mitochondrial function can contribute to exercise impairment. We hypothesized that impaired muscle mitochondrial function in type 2 diabetes is mediated, in part, by decreased tissue oxygen delivery and would improve with oxygen supplementation. Ex vivo muscle mitochondrial content and respiration assessed from biopsy samples demonstrated expected differences in obese individuals with (<i>n</i> = 18) and without (<i>n</i> = 17) diabetes. Similarly, in vivo mitochondrial oxidative phosphorylation capacity measured in the gastrocnemius muscle via <sup>31</sup>P-MRS indicated an impairment in the rate of ADP depletion with rest (27 ± 6 s [diabetes], 21 ± 7 s [control subjects]; <i>P</i> = 0.008) and oxidative phosphorylation (<i>P</i> = 0.046) in type 2 diabetes after isometric calf exercise compared with control subjects. Importantly, the in vivo impairment in oxidative capacity resolved with oxygen supplementation in adults with diabetes (ADP depletion rate 5.0 s faster, <i>P</i> = 0.012; oxidative phosphorylation 0.046 ± 0.079 mmol/L/s faster, <i>P</i> = 0.027). Multiple in vivo mitochondrial measures related to HbA<sub>1c</sub> These data suggest that oxygen availability is rate limiting for in vivo mitochondrial oxidative exercise recovery measured with <sup>31</sup>P-MRS in individuals with uncomplicated diabetes. Targeting muscle oxygenation could improve exercise function in type 2 diabetes.","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jul","modification":"2024-02-15T09:54:17.329Z","creation":"2019-07-25T07:13:56Z"},"accession":"S-EPMC6463751","cross_references":{"pubmed":["29643061"],"doi":["10.2337/db17-1124"]}}