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Exercise training differentially impacts 13 C 4 ‐octanoic acid oxidation in obese individuals with high and low intrahepatic lipid content‐ a pilot study
Author(s) -
Winn Nathan C,
Lee Nhan,
Kanaley Jill A,
Rector R. Scott,
Parks Elizabeth J,
Ibdah Jamal A
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1249.3
Subject(s) - steatosis , medicine , nonalcoholic fatty liver disease , meal , aerobic exercise , body mass index , fatty acid , fatty liver , endocrinology , chemistry , gastroenterology , physical therapy , disease , biochemistry
The beneficial adaptations to chronic physical activity (PA) reduce the risk of nonalcoholic fatty liver disease (NAFLD) and PA is a first line treatment for patients diagnosed with NAFLD. Accumulating evidence posits that increased utilization of lipid substrates may be one mechanism by which exercise reduces liver fat (LF); nonetheless there is paucity of data regarding the impact of exercise training on fatty acid oxidation (FAO) in individuals with differing levels of hepatic steatosis. Here, we determined whether the level of medium chain FAO is altered in individuals with varying contents of intrahepatic lipid (IHL) in response to exercise training. Methods Obese individuals (n=8, body mass index, 38.5±1.6 kg/m 2 ) with 1 H‐MRS‐measured hepatic steatosis underwent baseline and post‐training meal tests (3 h) with labeled 13 C 4 ‐octanoic acid to assess FAO. Frequent breath samples were taken and analyzed for 13 CO 2 enrichment (%). Subjects were stratified into Low‐ (IHL<15%; n=4) and High‐LF (IHL≥15%; n=4) and compared to non‐exercising controls (n=2). Exercise training was performed 4x/wk for 4 wks at 55–80% maximal oxygen consumption for a duration equivalent to ~400 kcal energy expenditure (30–70 min/session). Results At baseline, IHL was greater in High‐LF (27.0±4.3%) compared to both Low‐LF (10.1±1.4%) and controls (5.0±1.8%), P <0.05. Exercise training decreased IHL in High‐LF (−16.7±5.3%; P <0.05) with no statistically‐significant changes in Low‐LF (−11.3±10.1%) or non‐exercising controls (17.3±14.5%), P >0.05. Body weight, body fat percentage, and fat mass were unchanged with exercise training within groups. Baseline 13 CO 2 area under the curve (AUC) [Control, 9.7±2.0 AU; Low‐LF, 8.4±0.5 AU; High‐LF, 6.7±1.2 AU] and steady‐state (SS) 13 CO 2 [Control, 4.2±0.8%; Low‐LF, 3.7±0.2%; High‐LF, 2.9±0.5%] were not different among groups ( P >0.05). Neither 13 CO 2 AUC nor SS 13 CO 2 were changed with exercise training in High‐LF or non‐exercising controls. By contrast, 13 CO 2 AUC and SS 13 CO 2 were reduced in Low‐LF by 26.8±5.4% and 22.1±5.9%, respectively ( P <0.05). The change in SS 13 CO 2 was inversely associated with the change in IHL (r=−0.75, P <0.05). Conclusions Exercise‐induced reductions in IHL, without weight loss, were not accompanied by an increase in medium chain FAO in obese individuals with High‐LF, whereas, FAO was decreased in obese individuals with Low‐LF despite no changes in IHL following exercise training. Larger cohort studies are needed to confirm these findings.