Effects of 12 Months of Caloric Restriction on Muscle Mitochondrial Function in Healthy Individuals Article

International Collaboration

cited authors

  • Sparks, Lauren M., Redman, Leanne M., Conley, Kevin E., Harper, Mary-Ellen, Yi, Fanchao, Hodges, Andrew, Eroshkin, Alexey, Costford, Sheila R., Gabriel, Meghan E., Shook, Cherie, Cornnell, Heather H., Ravussin, Eric, Smith, Steven R.

funding text

  • This work was supported by National Institutes of Health Grants R01 AG030226 (S.S.R. and E.R.) and U01 AG020478 (E.R.). Additional support for this work was supplied by Pennington/Louisiana NORC Grant P30 DK072476 and Louisiana Clinical and Translational Science Center Grant U54 GM104940.

abstract

  • Context: The effects of caloric restriction (CR) on in vivo muscle mitochondrial function in humans are controversial. Objective: We evaluated muscle mitochondrial function and associated transcriptional profiles in nonobese humans after 12 months of CR. Design: Individuals from an ancillary study of the CALERIE 2 randomized controlled trial were assessed at baseline and 12 months after a 25% CR or ad libitum (control) diet. Setting: The study was performed at Pennington Biomedical Research Center in Baton Rouge, LA. Participants: Study participants included 51 (34 female subjects, 25 to 50 years of age) healthy nonobese individuals randomized to 1 of 2 groups (CR or control). Intervention: This study included 12 months of a 25% CR or ad libitum (control) diet. Main Outcomes: In vivo mitochondrial function [ maximal ATP synthesis rate (ATPmax), ATPflux/O-2 (P/O)] was determined by 31P-magnetic resonance spectroscopy and optical spectroscopy, and body composition was determined by dual-energy X-ray absorptiometry. In a subset of individuals, a muscle biopsy was performed for transcriptional profiling via quantitative reverse transcription polymerase chain reaction and microarrays. Results: Weight, bodymass index (BMI), fat, and fat-freemass (P < 0.001 for all) significantly decreased at month 12 after CR vs control. In vivo ATPmax and P/O were unaffected by 12 months of CR. Targeted transcriptional profiling showed no effects on pathways involved inmitochondrial biogenesis, function, or oxidative stress. A subgroup analysis according to baseline P/O demonstrated that a higher (vs lower) P/O was associated with notable improvements in ATPmax and P/O after CR. Conclusions: In healthy nonobese humans, CR has no effect on muscle mitochondrial function; however, having a " more coupled" (versus "less coupled") phenotype enables CR-induced improvements in muscle mitochondrial function.

authors

Publication Date

  • January 1, 2017

webpage

published in

category

start page

  • 111

end page

  • 121

volume

  • 102

issue

  • 1

WoS Citations

  • 3

WoS References

  • 41