Acute exercise does not decrease liver fat in men with overweight or NAFLD

Abstract

Elevated hepatic lipid content (IntraHepatic Lipid, IHL) increases the risk of metabolic complications. Although prolonged exercise training lowers IHL, it is unknown if acute exercise has the same effect. Furthermore, hepatic ATP content may be related to insulin resistance and IHL. We aimed to investigate if acute exercise leads to changes in IHL and whether this is accompanied by changes in hepatic ATP. Twenty-one men (age 54.8 ± 7.2 years, BMI 29.7 ± 2.2 kg/m(2)) performed a 2 h cycling protocol, once while staying fasted and once while ingesting glucose. IHL was determined at baseline, 30 min post-exercise and 4 h post-exercise. Additionally ATP/Total P ratio was measured at baseline and 4 h post-exercise. Compared with baseline values we did not observe any statistically significant changes in IHL within 30 min post-exercise in neither the fasted nor the glucose-supplemented condition. However, IHL was elevated 4 h post-exercise compared with baseline in the fasted condition (from 8.3 ± 1.8 to 8.7 ± 1.8%, p = 0.010), an effect that was blunted by glucose supplementation (from 8.3 ± 1.9 to 8.3 ± 1.9%, p = 0.789). Acute exercise does not decrease liver fat in overweight middle-aged men. Moreover, IHL increased 4 h post-exercise in the fasted condition, an increase that was absent in the glucose-supplemented condition. These data suggest that a single bout of exercise may not be able to lower IHL.

Figure 1. Hepatic lipid content at baseline for each individual subject given as percentage (w/w) of fat relative to wet tissue, n = 18.

Figure 2. (a) Respiratory quotient during and after 2 h of cycling at 50% of maximal power output (Wmax) (n = 17) and plasma concentrations of (b) free fatty acids (FFA), (c) glucose, (d) and triglycerides (TG), with (open square) and without (filled square) glucose supplementation.

* p < 0.05 compared with glucose-supplemented condition. # p < 0.05 compared with baseline (t = −60). Data are mean ± SE.

Figure 3. (a) Hepatic lipid content within 30 min after cessation of exercise (30 min post-exercise) and 4 h post-exercise, (because the subjects had a wide variety of liver fat content data was normalized to baseline values), n = 18, and (b) delta (Δ) IHL between baseline and 4 h post-exercise in the fasted condition in subjects with low (<5.6%) and high (>5.6%) liver fat content * p < 0.05.

Data are mean ± SE.

Figure 4. Hepatic ATP/Total P ratio (the relative amount of total phosphorous in the liver) at baseline and 4 h post-exercise as (a) group average and individual data with (b) and without (c) glucose supplementation.

In the fasted condition (without glucose-supplementation) it was a trend to a lower hepatic ATP/Total P ratio 4 h post-exercise compared with baseline.

Figure 5. The experimental design of the study.

All subjects performed the protocol twice, one time in the fasted state consuming water and one time with glucose supplementation. MRS: hepatic magnetic resonance spectroscopy.