Jong Sam Lee

Interaction of Diet and Training on Endurance Performance in Rats

We determined the interaction of diet and training on metabolic adaptations in skeletal muscle and liver, and the consequences of these adaptations for endurance. Eighty rats performed a baseline treadmill run to exhaustion at 16 m min−1 (RUN1) and were then divided into two groups and given one of two diets: high carbohydrate (CHO) or high fat (FAT). Each dietary group was then divided into one of four subgroups: sedentary control that performed no training (NT); low‐intensity running (8 m min−1; LOW) and two groups who trained at their maximal voluntary running speed without electrical stimulation (28 m min−1; VMAX). Training volume was identical for LOW and VMAX (1000 m session−1) and animals ran 4 days week−1 for 8 weeks. To assess the interaction of the higher intensity exercise with diet, a second endurance test (RUN2) was undertaken after 6 weeks at either 16 m min−1 or 28 m min−1. The NT group ran for a longer duration (increase of 77%) after FAT than CHO (239 ± 28 vs. 135 ± 30 min, P < 0.05) at 16 m min−1. There were no differences in RUN2 for the LOW group when rats ran at 16 m min−1 (454 ± 86 vs. 427 ± 75 min for CHO and FAT groups, respectively), but rats in the VMAX group fed FAT ran longer than rats fed CHO at 28 m min−1 (100 ± 28 vs. 58 ± 11 min, respectively, P < 0.05). FAT increased the activities of the enzymes citrate synthase, β‐hydroxyacyl‐CoA dehydrogenase and carnitine palmitoyl‐transferase compared to CHO (P < 0.01), but there was no systematic effect of training. We conclude: (1) there was no additive effect of a high‐fat diet on endurance performance when rats performed low‐intensity training; (2) running performance at 28 m min−1 was only enhanced by a high‐fat diet after more intense training; (3) diet‐induced and training‐induced adaptations that increase exercise capacity may be under independent control.

Effect Of Training On Activation Of Extracellular Signal-Regulated Kinase 1/2 And P38 Mitogen-Activated Protein Kinase Pathways In Rat Soleus Muscle

1. The effect of a chronic programme of either low‐ or moderate‐to‐high‐intensity treadmill running on the activation of the extracellular‐signal regulated protein kinase (ERK1/2) and the p38 mitogen‐activated protein kinase (MAPK) pathways was determined in rat muscle.

Skeletal muscle respiratory capacity is enhanced in rats consuming an obesogenic Western diet

Obesity-induced lipid oversupply promotes skeletal muscle mitochondrial biogenesis. Previous investigations have utilized extreme high-fat diets (HFD) to induce such mitochondrial perturbations despite their disparity from human obesogenic diets. Here, we evaluate the effects of Western diet (WD)-induced obesity on skeletal muscle mitochondrial function. Long-Evans rats were given ad libitum access to either a WD [40% energy (E) from fat, 17% protein, and 43% carbohydrate (30% sucrose); n = 12] or a control diet (CON; 16% of E from fat, 21% protein, and 63% carbohydrate; n = 12) for 12 wk. Rats fed the WD consumed 23% more E than CON (P = 0.0001), which was associated with greater increases in body mass (23%, P = 0.0002) and adiposity (17%, P = 0.03). There were no differences in fasting blood glucose concentration or glucose tolerance between diets, although fasting insulin was increased by 40% (P = 0.007). Fasting serum triglycerides were also elevated in WD (86%, P = 0.001). The maximal capacity of the electron transfer system was greater following WD (37%, P = 0.02), as were the maximal activities of several mitochondrial enzymes (citrate synthase, β-hydroxyacyl-CoA dehydrogenase, carnitine palmitoyltransferase). Protein expression of citrate synthase, UCP3, and individual respiratory complexes was greater after WD (P < 0.05) despite no differences in the expression of peroxisome proliferator-activated receptor (PPAR)α, PPARδ, or PPARγ coactivator-1 mRNA or protein abundance. We conclude that the respiratory capacity of skeletal muscle is enhanced in response to the excess energy supplied by a WD. This is likely due to an increase in mitochondrial density, which at least in the short term, and in the absence of increased energy demand, may protect the tissue from lipid-induced impairments in glycemic control.

The Effect of Exercise on the Skeletal Muscle Phospholipidome of Rats Fed a High-Fat Diet

The aim of this study was to examine the effect of endurance training on skeletal muscle phospholipid molecular species from high-fat fed rats. Twelve female Sprague-Dawley rats were fed a high-fat diet (78.1% energy). The rats were randomly divided into two groups, a sedentary control group and a trained group (125 min of treadmill running at 8 m/min, 4 days/wk for 4 weeks). Forty-eight hours after their last training bout phospholipids were extracted from the red and white vastus lateralis and analyzed by electrospray-ionization mass spectrometry. Exercise training was associated with significant alterations in the relative abundance of a number of phospholipid molecular species. These changes were more prominent in red vastus lateralis than white vastus lateralis. The largest observed change was an increase of ~30% in the abundance of 1-palmitoyl-2-linoleoyl phosphatidylcholine ions in oxidative fibers. Reductions in the relative abundance of a number of phospholipids containing long-chain n-3 polyunsaturated fatty acids were also observed. These data suggest a possible reduction in phospholipid remodeling in the trained animals. This results in a decrease in the phospholipid n-3 to n-6 ratio that may in turn influence endurance capacity.