A low‐glycemic diet lifestyle intervention improves fat utilization during exercise in older obese humans
Objective: To determine the influence of dietary glycemic index on exercise training‐induced adaptations in substrate oxidation in obesity. Design and Methods: Twenty older, obese individuals undertook 3 months of fully supervised aerobic exercise and were randomized to low‐ (LoGIX) or high‐glycemic...
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Published in | Obesity (Silver Spring, Md.) Vol. 21; no. 11; pp. 2272 - 2278 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.11.2013
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Subjects | |
Online Access | Get full text |
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Summary: | Objective: To determine the influence of dietary glycemic index on exercise training‐induced adaptations in substrate oxidation in obesity.
Design and Methods: Twenty older, obese individuals undertook 3 months of fully supervised aerobic exercise and were randomized to low‐ (LoGIX) or high‐glycemic (HiGIX) diets. Changes in indirect calorimetry (VO2; VCO2) were assessed at rest, during a hyperinsulinemic‐euglycemic clamp, and during submaximal exercise (walking: 65% VO2max, 200 kcal energy expenditure). Intramyocellular lipid (IMCL) was measured by 1H‐magnetic resonance spectroscopy.
Results: Weight loss (−8.6 ± 1.1%) and improvements (P < 0.05) in VO2max, glycemic control, fasting lipemia, and metabolic flexibility were similar for both LoGIX and HiGIX groups. During submaximal exercise, energy expenditure was higher following the intervention (P < 0.01) in both groups. Respiratory exchange ratio during exercise was unchanged in the LoGIX group but increased in the HiGIX group (P < 0.05). However, fat oxidation during exercise expressed in relation to changes in body weight was increased in the LoGIX group (+10.6 ± 3.6%; P < 0.05). Fasting IMCL was unchanged, however, extramyocellular lipid was reduced (P < 0.05) after LoGIX.
Conclusions: A LoGIX/exercise weight‐loss intervention increased fat utilization during exercise independent of changes in energy expenditure. This highlights the potential therapeutic value of low‐glycemic foods for reversing metabolic defects in obesity. |
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Bibliography: | Funding Agencies This research was supported by NIH grant RO1 AG12834 (JPK), and was supported in part by the National Institutes of Health, National Center for Research Resources, CTSA 1UL1RR024989, Cleveland, OH. JMH was supported by National Institutes of Health grant T32 HL00787. TPJS, JMH, CAF, and JPK designed the research; TPJS, JMH, MAC, CAF, and JPK conducted the research; TPJS, JMH, CAF, and JPK analyzed the data; TPJS, JMH, and JPK discussed the data; TPJS and JMH wrote the paper; and JPK had primary responsibility for the final content. All authors read and approved the final manuscript. TPJS and JMH contributed equally to this work. Author Contributions ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Undefined-3 Current address for TPJS: Thomas Solomon, Ph.D., Centre of Inflammation and Metabolism, Rigshospitalet, Section 7641 Blegdamsvej 9, 2100 København Ø Denmark : thomas.solomon@inflammation-metabolism.dk TPJS and JMH contributed equally to this work |
ISSN: | 1930-7381 1930-739X |
DOI: | 10.1002/oby.20411 |