Intrahepatic lipid accumulation
Conditions in which IHL accumulates
|
• Increased hepatic NEFA uptake due to higher fasting and/or postprandial plasma NEFA concentrations |
• Low partition of fatty acids to skeletal muscle (low chylomicron clearance by muscle and low NEFA uptake) |
• Elevated DNL; activated by elevated plasma glucose and insulin concentrations |
• Limited capacity to increase hepatic VLDL–TAG secretion and hepatic mitochondrial oxidation |
Effects of exercise training on IHL content
Study/participant type | Training protocol | Length of intervention | Intensity of exercise training protocol | Effect on IHL | Effect on other variables |
---|---|---|---|---|---|
van der Heijden et al (2010) [51] | |||||
Obese Hispanic adolescents | Supervised AET (n = 15) | 12 weeks | 4×/week, 30 min; 70% of \( \overset{.}{V}{\mathrm{O}}_{2\mathrm{peak}} \)
| ↓ | ↓FM, ↓VAT, ↑IS, ↓f-Ins, =f-Glu |
Lean Hispanic adolescents | Supervised AET (n = 14) | 12 weeks | 4×/week, 30 min; 70% of \( \overset{.}{V}{\mathrm{O}}_{2\mathrm{peak}} \)
| No change | =FM, =IS, =f-Ins, =f-Glu |
Sullivan et al (2012) [50] | |||||
Obese NAFL patients | Unsupervised AET (n = 12) | 16 weeks | 5×/week, 30–60 min; 45–55% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \)
| ↓ (vs non-exercising control) | =BW, =FM, =f-NEFA |
Pugh et al (2014) [49] | |||||
Obese NAFL patients | Supervised AET (n = 13) | 16 weeks | 3×/week; 30 min at 30% of HRR (weeks 1–4), 30 min at 45% of HRR (weeks 5–8), 45 min at 45% of HRR (weeks 9–12), 45 min at 60% of HRR (weeks 13–16) | ↓ | ↓f-Glu, =IS, =BW, =VAT, =f-Ins |
Lee et al (2012) [47] | |||||
Obese adolescent boys | Supervised AET n = 16) | 3 months | 3×/week; 40 min at 40% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \) (week 1), 60 min at 60–75% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \) (weeks 2–12) | ↓ (vs non-exercising control) | ↓BW, ↓FM, ↓VAT, =IS, =f-Glu, =f-Ins =2 h-Glu, =2 h-Ins |
Obese adolescent boys | Supervised RET (n = 16) | 3 months | 3×/week, 60 min, 10 exercises, 2× 8–12 repetitions; 60% of 1RM (weeks 1–4), to fatigue (week 5–12) | ↓ (vs non-exercising control) | ↓BW, ↓FM, ↓VAT, ↑IS, =f-Glu, =f-Ins, =2 h-Glu, =2 h-Ins |
Lee et al (2013) [48] | |||||
Obese adolescent girls | Supervised AET (n = 16) | 3 months | 3×/week; 40 min at 40% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \) (week 1), 60 min at 60–75% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \) (weeks 2–12) | ↓ (vs non-exercising control) | ↓FM, ↓VAT, ↑IS, ↓f-Ins, =f-Glu, =2 h-Glu, =2 h-Ins |
Obese adolescent girls | Supervised RET (n = 16) | 3 months | 3×/week, 60 min, 10 exercises, 2 × 8–12 repetitions; 60% of 1RM (weeks 1–4), to fatigue (weeks 5–12) | No change (vs non-exercising control) | ↓FM, =VAT, =IS, =f-Glu, =f-Ins, =2 h-Glu, =2 h-Ins |
Johnson et al (2009) [46] | |||||
Obese men and women | Supervised AET (n = 19) | 4 weeks | 3×/week, 30–45 min; 50% (week 1), 60% (week 2), 70% (weeks 3 and 4) of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \)
| ↓ (vs non-exercising control) | ↓VAT, ↓f-NEFA, =BW, =f-Glu, =f-Ins |
Hallsworth et al (2011) [45] | |||||
Men and women with NAFL | Supervised RET (n = 11) | 8 weeks | 3×/week, 8 exercises, 45–60 min; 50% (weeks 1–6), 70% (weeks 7 and 8) of 1RM | ↓ | ↑IS, ↓f-Glu, =BW, =FM, =VAT, =f-NEFA, =f-Ins |
Finucane et al (2010) [44] | |||||
Older men and women | Supervised AET (n = 50) | 12 weeks | 3×/week, 60 min; 50% (weeks 1–4), 60% (weeks 5–8), 70% (weeks 9–12) of Wmax
| ↓ (vs non-exercising control) | ↓BW, ↓f-Ins, ↓2 h-Glu, ↓2 h-Ins, =FM, =f-Glu |
Bacchi et al (2013) [43] | |||||
Patients with type 2 diabetes and NAFL | Supervised AET (n = 14) | 4 months | 3×/week, 60 min; 60–65% HRR | ↓ | ↓FM, ↓VAT, ↑IS |
Patients with type 2 diabetes and NAFL | Supervised RET (n = 17) | 4 months | 3×/week, 9 exercises, 3 × 10 repetitions; 70–80% of 1RM | ↓ | ↓FM, ↓VAT, ↑IS |
Shojaee-Moradie et al (2007) [54] | |||||
Overweight healthy men | Supervised AET (n = 10) | 6 weeks | 3×/week, 20 min; 60–85% of \( \overset{.}{V}{\mathrm{O}}_{2 \max } \)
| No change | ↑IS, ↓f-NEFA, ↓IS-NEFA, =BW, =FM |
Key effects of exercise training on pathways that influence IHL content
| |
Plasma NEFA | • Increase in plasma NEFA uptake by skeletal muscle |
• Some evidence for decrease in fasting and/or postprandial plasma NEFA | |
Dietary TAG | • Increase in LPL-mediated TAG uptake by skeletal muscle |
• Decrease in HL-mediated TAG uptake by liver | |
DNL | • Decrease in plasma insulin, a key player for the activation of DNL |
• In diabetes, exercise can decrease plasma glucose and hence decrease DNL | |
• Lower ACC and FAS protein content, indicative for decreased de novo lipolysis activity (rodent data) | |
VLDL metabolism | • Decrease in hepatic VLDL–ApoB-100 and VLDL–TAG secretion, possibly as a consequence of lower hepatic TAG accumulation |
Mitochondrial oxidation | • Increase in hepatic CS, β-HAD and Cyt c, indicative for increases in hepatic mitochondrial content and oxidative phosphorylation (rodent data) |