Christos S. Katsanos

This study was designed to evaluate the effects of enriching an essential amino acid (EAA) mixture with leucine on muscle protein metabolism in elderly and young individuals. Four (2 elderly and 2 young) groups were studied before and after ingestion of 6.7 g of EAAs. EAAs were based on the composition of whey protein [26% leucine (26% Leu)] or were enriched in leucine [41% leucine (41% Leu)]. A primed, continuous infusion of l-[ ring-²H₅]phenylalanine was used together with vastus lateralis muscle biopsies and leg arteriovenous blood samples for the determinations of fractional synthetic rate (FSR) and balance of muscle protein. FSR increased following amino acid ingestion in both the 26% (basal: 0.048 ± 0.005%/h; post-EAA: 0.063 ± 0.007%/h) and the 41% (basal: 0.036 ± 0.004%/h; post-EAA: 0.051 ± 0.007%/h) Leu young groups ( P < 0.05). In contrast, in the elderly, FSR did not increase following ingestion of 26% Leu EAA (basal: 0.044 ± 0.003%/h; post-EAA: 0.049 ± 0.006%/h; P > 0.05) but did increase following ingestion of 41% Leu EAA (basal: 0.038 ± 0.007%/h; post-EAA: 0.056 ± 0.008%/h; P < 0.05). Similar to the FSR responses, the mean response of muscle phenylalanine net balance, a reflection of muscle protein balance, was improved ( P < 0.05) in all groups, with the exception of the 26% Leu elderly group. We conclude that increasing the proportion of leucine in a mixture of EAA can reverse an attenuated response of muscle protein synthesis in elderly but does not result in further stimulation of muscle protein synthesis in young subjects.

The objective of this study was to examine the effects of the timing of exercise relative to the consumption of a fat-rich meal (81% fat) on postprandial hypertriglyceridemia. A single bout of exercise was either completed 30 minutes before the fat meal (EM trial) or initiated 90 minutes after the fat meal (ME trial). A third trial, fat meal only, served as a control (CON trial). The trials performed in a random order, and venous blood samples were drawn before and 1.5, 3.5, 5.5, and 7.5 hours after the meal for the determination of triglycerides, glycerol, insulin, glucose, and free fatty acids. Ten untrained healthy males 25.2 ± 0.9 years old (mean ± SE) with maximal oxygen uptake (VO2max) of 46.6 ± 3.0 mL · kg−1 · min−1. Walking exercise performed at 50% VO2max for 90 minutes. Postprandial hypertriglyceridemia, which was quantified by calculating the area under the triglycerides curve over the 7.5-hour postprandial period. The mean incremental area under the curve (total area adjusted to baseline) describing postprandial hypertriglyceridemia was lower both in the EM trial (3.16 ± 0.99 mmol · L−1 · 8 h) and in the ME trial (2.96 ± 0.69 mmol · L−1 · 8 h) compared with CON trial (6.18 ± 1.10 mmol · L−1 · 8 h; P < 0.05). The corresponding areas under the curve describing the postprandial insulinemia were not different between trials (ME: 38.56 ± 8.36 uIU · mL−1 · 8 h; EM: 21.65 ± 3.80 uIU · mL−1 · 8 h; CON: 25.06 ± 5.15 uIU · mL−1 · 8 h; P > 0.05). A single bout of moderate intensity exercise decreases postprandial hypertriglyceridemia irrespective of the timing of the exercise relative to a high-fat meal.

Hepatic lipid accumulation may be a result of one or several of the following factors: increased delivery of adipose tissue or dietary fatty acids to the liver, increased de novo synthesis of fatty acids in the liver, decreased rate of hepatic fatty-acid oxidation, or decreased rate in the exit of fatty acids from the liver in the form of triglycerides. Delivery of fatty acids to the liver appears to be the most potent mechanism for hepatic lipid accumulation. Hepatic lipid accumulation is linked to the development of hepatic insulin resistance, which is demonstrated by the impaired suppression of hepatic glucose output by insulin. Current evidence suggests that defects associated with the molecular mechanisms responsible for the propagation of the insulin signal in the liver cells are responsible for the impaired insulin effect and that these defects can develop secondary to lipid accumulation in the liver. Hepatic lipid accumulation appears to affect the activity of phosphatidylinositol 3-kinase, which has a central role in mediating the insulin action in hepatocytes. Generally, exercise has been shown to enhance the insulin action in the liver. Although an exercise-related mechanistic link between attenuation in hepatic lipid accumulation and enhancement in insulin action in the liver has not been described yet, the benefits of exercise on hepatic insulin action may relate to the potential effects of exercise on regulating/preventing hepatic lipid accumulation. However, direct effects of exercise on insulin action in the liver, independent of any effects on hepatic lipid metabolism, cannot currently be excluded. Further research is needed to evaluate the relative importance of exercise in the treatment of hepatic insulin resistance, specifically as it relates to lipid accumulation in the liver.

This study was designed to assess differences in the intensity of exercise to attenuate postprandial lipemia (PPL). Thirteen healthy men (age 23.8 ± 0.9 yr) participated in three random-ordered trials: in low-(25% peak oxygen consumption; Low) and moderate-intensity (65% peak oxygen consumption; Mod) exercise trials, which were completed 1 h before a high-fat meal (1.3 g fat/kg body mass), and a control (Con), fat meal only, trial. Venous blood samples were obtained before the fat meal, and at 2, 4, 6, 8, and 20 h after the fat meal. PPL in the Mod trial (267 ± 50 mg·dl^-1·8 h) was lower compared with that in either Con (439 ± 81 mg·dl^-1·8 h) or Low (403 ± 91 mg·dl^-1·8 h) trials ( P < 0.05), whereas there was no difference in PPL between Con and Low trials ( P > 0.05). High-density lipoprotein cholesterol (HDL-C) and HDL subtype 2 cholesterol were not different between or within trials ( P > 0.05). Postprandial insulinemia was lower in the Mod trial (20.5 ± 5.7 μIU·ml^-1·8 h; P < 0.05), but not in the Low trial (31.4 ± 4.7 μIU·ml^-1·8 h), compared with that in the Con trial (34.9 ± 5.0 μIU·ml^-1·8 h). Postheparin lipoprotein lipase activity at 8 h was higher in the Low trial compared with that in either Con or Mod trials, whereas there were no differences between trials at 20 h. These results suggest that, when exercise is performed 1 h before a fat meal, only exercise of moderate but not of low intensity attenuates PPL and that this effect is not associated with changes in postheparin lipoprotein lipase activity.