Diabetology & Metabolic Syndrome (Feb 2018)

Acute vitamin C improves cardiac function, not exercise capacity, in adults with type 2 diabetes

  • Rebecca L. Scalzo,
  • Timothy A. Bauer,
  • Kylie Harrall,
  • Kerrie Moreau,
  • Cemal Ozemek,
  • Leah Herlache,
  • Shawna McMillin,
  • Amy G. Huebschmann,
  • Jennifer Dorosz,
  • Jane E. B. Reusch,
  • Judith G. Regensteiner

DOI
https://doi.org/10.1186/s13098-018-0306-9
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 9

Abstract

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Abstract Background People with type 2 diabetes (T2D) have impaired exercise capacity, even in the absence of complications, which is predictive of their increased cardiovascular mortality. Cardiovascular dysfunction is one potential cause of this exercise defect. Acute infusion of vitamin C has been separately shown to improve diastolic and endothelial function in prior studies. We hypothesized that acute vitamin C infusion would improve exercise capacity and that these improvements would be associated with improved cardiovascular function. Methods Adults with T2D (n = 31, 7 female, 24 male, body mass index (BMI): 31.5 ± 0.8 kg/m2) and BMI-similar healthy adults (n = 21, 11 female, 10 male, BMI: 30.4 ± 0.7 kg/m2) completed two randomly ordered visits: IV infusion of vitamin C (7.5 g) and a volume-matched saline infusion. During each visit peak oxygen uptake (VO2peak), brachial artery flow mediated dilation (FMD), reactive hyperemia (RH; plethysmography), and cardiac echocardiography were measured. General linear mixed models were utilized to assess the differences in all study variables. Results Acute vitamin C infusion improved diastolic function, assessed by lateral and septal E:E’ (P < 0.01), but did not change RH (P = 0.92), or VO2peak (P = 0.33) in any participants. Conclusion Acute vitamin C infusion improved diastolic function but did not change FMD, forearm reactive hyperemia, or peak exercise capacity. Future studies should further clarify the role of endothelial function as well as other possible physiological causes of exercise impairment in order to provide potential therapeutic targets. Trial registration NCT00786019. Prospectively registered May 2008

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