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Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease

View Article: PubMed Central - PubMed

ABSTRACT

Aim: To investigate the independent effects of 6-mo of dietary energy restriction or exercise training on whole-body and hepatic fat oxidation of patients with non-alcoholic fatty liver disease (NAFLD).

Methods: Participants were randomised into either circuit exercise training (EX; n = 13; 3 h/wk without changes in dietary habits), or dietary energy restriction (ER) without changes in structured physical activity (ER; n = 8). Respiratory quotient (RQ) and whole-body fat oxidation rates (Fatox) were determined by indirect calorimetry under basal, insulin-stimulated and exercise conditions. Severity of disease and steatosis was determined by liver histology; hepatic Fatox was estimated from plasma β-hydroxybutyrate concentrations; cardiorespiratory fitness was expressed as VO2peak. Complete-case analysis was performed (EX: n = 10; ER: n = 6).

Results: Hepatic steatosis and NAFLD activity score decreased with ER but not with EX. β-hydroxybutyrate concentrations increased significantly in response to ER (0.08 ± 0.02 mmol/L vs 0.12 ± 0.04 mmol/L, P = 0.03) but remained unchanged in response to EX (0.10 ± 0.03 mmol/L vs 0.11 ± 0.07 mmol/L, P = 0.39). Basal RQ decreased (P = 0.05) in response to EX, while this change was not significant after ER (P = 0.38). VO2peak (P < 0.001) and maximal Fatox during aerobic exercise (P = 0.03) improved with EX but not with ER (P > 0.05). The increase in β-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis (r = -0.56, P = 0.04).

Conclusion: ER and EX lead to specific benefits on fat metabolism of patients with NAFLD. Increased hepatic Fatox in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

No MeSH data available.


Maximal fat oxidation before and after six months of energy restriction (n = 6) or exercise training (n = 10); individual data. aP < 0.05 between pre and post intervention.
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Figure 4: Maximal fat oxidation before and after six months of energy restriction (n = 6) or exercise training (n = 10); individual data. aP < 0.05 between pre and post intervention.

Mentions: VO2peak and MFO improved significantly (by 18% and 71%, respectively) in response to EX but did not change in the ER group (Table 4 and Figure 4). Fatmax increased by 72% in response to EX when expressed in absolute terms (45 ± 20 vs 76 ± 46 Watts, P = 0.03), whereas it remained unchanged after both interventions when expressed in relative terms (%VO2peak). Within the EX group, the increase in VO2peak (mL/kgFFM per minute) was correlated with the increase in ∆RQ (r = 0.73, P = 0.02) and the reduction in systolic blood pressure (r = -0.81, P = 0.01). The improvement in VO2peak was not related with the change in steatosis (r = 0.14, P = 0.73), NAS (P = 0.40) or basal RQ (r = -0.18, P = 0.62). Similarly, the change in MFO was not related to changes in hepatic steatosis (r = 0.03, P = 0.91), or changes in NAS (P = 0.63).


Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease
Maximal fat oxidation before and after six months of energy restriction (n = 6) or exercise training (n = 10); individual data. aP < 0.05 between pre and post intervention.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037327&req=5

Figure 4: Maximal fat oxidation before and after six months of energy restriction (n = 6) or exercise training (n = 10); individual data. aP < 0.05 between pre and post intervention.
Mentions: VO2peak and MFO improved significantly (by 18% and 71%, respectively) in response to EX but did not change in the ER group (Table 4 and Figure 4). Fatmax increased by 72% in response to EX when expressed in absolute terms (45 ± 20 vs 76 ± 46 Watts, P = 0.03), whereas it remained unchanged after both interventions when expressed in relative terms (%VO2peak). Within the EX group, the increase in VO2peak (mL/kgFFM per minute) was correlated with the increase in ∆RQ (r = 0.73, P = 0.02) and the reduction in systolic blood pressure (r = -0.81, P = 0.01). The improvement in VO2peak was not related with the change in steatosis (r = 0.14, P = 0.73), NAS (P = 0.40) or basal RQ (r = -0.18, P = 0.62). Similarly, the change in MFO was not related to changes in hepatic steatosis (r = 0.03, P = 0.91), or changes in NAS (P = 0.63).

View Article: PubMed Central - PubMed

ABSTRACT

Aim: To investigate the independent effects of 6-mo of dietary energy restriction or exercise training on whole-body and hepatic fat oxidation of patients with non-alcoholic fatty liver disease (NAFLD).

Methods: Participants were randomised into either circuit exercise training (EX; n = 13; 3 h/wk without changes in dietary habits), or dietary energy restriction (ER) without changes in structured physical activity (ER; n = 8). Respiratory quotient (RQ) and whole-body fat oxidation rates (Fatox) were determined by indirect calorimetry under basal, insulin-stimulated and exercise conditions. Severity of disease and steatosis was determined by liver histology; hepatic Fatox was estimated from plasma &beta;-hydroxybutyrate concentrations; cardiorespiratory fitness was expressed as VO2peak. Complete-case analysis was performed (EX: n = 10; ER: n = 6).

Results: Hepatic steatosis and NAFLD activity score decreased with ER but not with EX. &beta;-hydroxybutyrate concentrations increased significantly in response to ER (0.08 &plusmn; 0.02 mmol/L vs 0.12 &plusmn; 0.04 mmol/L, P = 0.03) but remained unchanged in response to EX (0.10 &plusmn; 0.03 mmol/L vs 0.11 &plusmn; 0.07 mmol/L, P = 0.39). Basal RQ decreased (P = 0.05) in response to EX, while this change was not significant after ER (P = 0.38). VO2peak (P &lt; 0.001) and maximal Fatox during aerobic exercise (P = 0.03) improved with EX but not with ER (P &gt; 0.05). The increase in &beta;-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis (r = -0.56, P = 0.04).

Conclusion: ER and EX lead to specific benefits on fat metabolism of patients with NAFLD. Increased hepatic Fatox in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

No MeSH data available.