Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

1994 ◽  
Vol 69 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Estelle V. Lambert ◽  
David P. Speechly ◽  
Steven C. Dennis ◽  
Timothy D. Noakes
2017 ◽  
Vol 95 (6) ◽  
pp. 667-674 ◽  
Author(s):  
Bing Wang ◽  
Jing Zeng ◽  
Qi Gu

In the gold standard treatment for nonalcoholic fatty liver disease (NAFLD), exercise training has been shown to effectively improve nonalcoholic steatohepatitis (NASH). However, limited data are available about the underlying mechanisms involved. This work was undertaken to investigate the mechanisms underlying the beneficial effect of exercise training on high-fat diet (HFD)-induced NAFLD in mice. Male mice were fed with HFD and given moderate-intensity exercise for 24 weeks. Exercise training lowered mass gain, attenuated systemic insulin resistance and glucose intolerance, and mitigated hepatic steatosis and fibrosis in mice fed with HFD. Exercise training improved mitochondrial function and enhanced mitochondrial β-oxidation in livers of HFD-fed mice. Exercise training enhanced hydrogen sulfide (H2S) levels in plasma and livers, and mRNA expression of cystathionine β-synthase (CBS), cystathionine γ-lyase (CES), and 3-mercaptopyruvate sulfurtransferase (3-MST) in livers of HFD-fed mice. Exercise training had no significant effect on the ratio of LC3-II/LC3-I, but decreased p62 protein expression in livers of HFD-fed mice. Additionally, exercise training reduced formation of malondialdehyde, enhanced ratio of GSH/GSSG, and down-regulated expression of TNF-α and IL-6 in livers of HFD-fed mice. Exercise training restored bioavailability of H2S and promoted autophagy influx in livers, which might contribute to its benefit on HFD-induced NAFLD.


2009 ◽  
Vol 2 (7) ◽  
pp. 641-649 ◽  
Author(s):  
Kristen A. Baltgalvis ◽  
Franklin G. Berger ◽  
Maria Marjorette O. Peña ◽  
J. Mark Davis ◽  
James A. Carson

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Yi Yan ◽  
Chunyu Liang ◽  
Rui Xu

Objective To observe the effect of high fat diet on the hypothalamic expression of KiSS-1and the G-protein coupled receptor (GPR) 54 mRNA and explore the modulatory role of moderate-intensity exercise in the diet induced obesity male rats. Methods After 8 weeks high fat feeding, 20 obesity 11-weeks SD rats were randomly assigned to high-fat diet sedentary (FS, n=8) and high-fat diet exercise (FE, n=8) groups, 20 normal diet 11-weeks SD rats also were randomly assigned to sedentary (SS, n=8) and exercise (SE, n=8) groups. During the following 8 weeks, obesity rats were continued expose to high-fat-diet. SE and FE groups did the 60%-70%V(•)O2max treadmill training (5 days/week, 1 hour/day). The V(•)O2 max of exercise groups were remeasured every two weeks. The hypothalamic expression of KiSS-1 and GPR54 mRNA were tested in each group. Results After the first 8-weeks high fat feeding, the obesity rats were heavier than normal diet group (491.74±26.19g vs. 410.05±45.77g, p<0.01). After 8-weeks training, the FE group was lighter than FS group (590.23±35.74g vs. 681±52.56, p<0.01). The FS group had higher hypothalamic expression of KiSS-1 mRNA (1.51±0.66 vs 0.75±0.27, p<0.05) and GPR54 mRNA (2.45±0.38 vs 0.61±0.15, p<0.01) than SS group. The FE group had lower hypothalamic expression of KiSS-1 mRNA (0.69±0.13, p>0.05) and GPR54 mRNA (0.58±0.10, p<0.01) than FS group. Conclusions There is stimulating effect of high-fat diet induced obesity on hypothalamic expression of KiSS-1and GPR54 mRNA. 8-weeks 60%-70%V (•) O2max treadmill training could cure this effect.  


2010 ◽  
Vol 105 (4) ◽  
pp. 506-516 ◽  
Author(s):  
Nicholas M. Hurren ◽  
Frank F. Eves ◽  
Andrew K. Blannin

Moderate-intensity exercise can lower the TAG response to a high-fat meal; however, the British diet is moderate in fat, and no study to date has compared the effect of such exercise on responses to high-fat and moderate-fat meals. The present work investigated the effect of brisk walking performed 13 h before intake of both high-fat and moderate-fat meals on postprandial plasma TAG concentrations. Eight inactive, overweight men completed four separate 2 d trials, i.e. rest (Con) or a 90-min treadmill walk (Ex) on the evening of day 1, followed by the ingestion of a moderate-fat (Mod) or high-fat (High) meal on the morning of day 2. High-fat meals contained 66 % of total energy as fat, while the percentage was 35 % for moderate-fat meals; both the meals were, however, isoenergetic. On day 2, venous blood was sampled in the fasted state, 30 and 60 min after ingesting the test meal and then hourly until 6 h post-meal. Exercise reduced plasma TAG concentrations significantly (P < 0·001), with no exercise × meal interaction (P = 0·459). Walking reduced the total TAG response to a high-fat meal by 29 % (relative to High Con); the same bout of exercise performed before ingesting a moderate-fat meal lowered total TAG by 26 % (compared with Mod Con). The ability of a single moderate-intensity aerobic exercise bout to lower postprandial TAG concentrations is just as great, in percentage terms, when the test meal ingested is of a moderate rather than a high fat content.


2020 ◽  
Vol 29 (2) ◽  
pp. 178-187
Author(s):  
Dong-Hyun Kim ◽  
In-Jae Kim

PURPOSE: The purpose of this study was to analyze the effects of aerobic exercise on the expression of synaptic vesicle transporter and antioxidant enzymes in obesity and to investigate the feasibility of exercise training to reduce AD pathogenesis in the 3xTg-AD mice fed a high fat diet.METHODS: Male 3 month old 3xTg-AD mice were divided into standard chow(SC, n=10), standard chow+exercise (SC-EXE, n=10), high fat diet (HFD, n=10), and high fat diet+exercise (HFD-EXE, n=10) groups. EXE mice were subjected to treadmill running at a moderate intensity with duration of 30 minutes per day and frequency of 5 days per week for 12 weeks. HFD mice were fed a 60% fat HFD during the same period. Mice were sacrificed and immunohistology and western blot analysis were performed.RESULTS: Compared with the SC mice, the HFD mice had significantly higher levels of Aβ (<i>p</i><.01), p-tau/t-tau (<i>p</i><.01) and defects of Vglut1 (<i>p</i><.05), VGAT (<i>p</i><.05), postsynaptic density 95 (<i>p</i><.01) and GPX (<i>p</i><.05) in the hippocampus. On the other hand, we found that treadmill running attenuated HFD-induced exacerbations of Aβ (<i>p</i><.01), p-tau/t-tau (<i>p</i><.05) and defects of Vglut1 (<i>p</i><.01), Synaptophysin (<i>p</i><.05), SOD1 (<i>p</i><.05) in the hippocampus.CONCLUSIONS: High fat diet-induced obesity resulted in increased AD neuropathology and decreased synaptic vesicle transporter and antioxidant enzyme in the hippocampus of 3xTg-AD mice. However, aerobic exercise delayed AD-like disease progression, alleviated impaired synaptic function and the decreased expression of antioxidant enzymes in the hippocampus.


2014 ◽  
Vol 117 (11) ◽  
pp. 1371-1379 ◽  
Author(s):  
J. A. Raper ◽  
L. K. Love ◽  
D. H. Paterson ◽  
S. J. Peters ◽  
G. J. F. Heigenhauser ◽  
...  

Mitochondrial pyruvate dehydrogenase (PDH) regulates the delivery of carbohydrate-derived substrate to the mitochondrial tricarboxylic acid cycle and electron transport chain. PDH activity at rest and its activation during exercise is attenuated following high-fat (HFAT) compared with high-carbohydrate (HCHO) diets. Given the reliance on carbohydrate-derived substrate early in transitions to exercise, this study examined the effects of HFAT and HCHO on phase II pulmonary O2 uptake (V̇o2p) kinetics during transitions into the moderate-intensity (MOD) exercise domain. Eight active adult men underwent dietary manipulations consisting of 6 days of HFAT (73% fat, 22% protein, 5% carbohydrate) followed immediately by 6 days of HCHO (10% fat, 10% protein, 80% carbohydrate); each dietary phase was preceded by a glycogen depletion protocol. Participants performed three MOD transitions from a 20 W cycling baseline to work rate equivalent to 80% of estimated lactate threshold on days 5 and 6 of each diet. Steady-state V̇o2p was greater ( P < 0.05), and respiratory exchange ratio and carbohydrate oxidation rates were lower ( P < 0.05) during HFAT. The phase II V̇o2p time constant (τV̇o2p) [HFAT 40 ± 16, HCHO 32 ± 19 s (mean ± SD)] and V̇o2p gain (HFAT 10.3 ± 0.8, HCHO 9.4 ± 0.7 ml·min−1·W−1) were greater ( P < 0.05) in HFAT. The overall adjustment (effective time constant) of muscle deoxygenation (Δ[HHb]) was not different between diets (HFAT 24 ± 4 s, HCHO 23 ± 4 s), which coupled with a slower τV̇o2p, indicates a slowed microvascular blood flow response. These results suggest that the slower V̇o2p kinetics associated with HFAT are consistent with inhibition and slower activation of PDH, a lower rate of pyruvate production, and/or attenuated microvascular blood flow and O2 delivery.


2012 ◽  
Vol 123 (5) ◽  
pp. 313-321 ◽  
Author(s):  
Brendan Gabriel ◽  
Aivaras Ratkevicius ◽  
Patrick Gray ◽  
Michael P. Frenneaux ◽  
Stuart R. Gray

Regular exercise can reduce the risk of CVD (cardiovascular disease). Although moderate-intensity exercise can attenuate postprandial TAG (triacylglycerol), high-intensity intermittent exercise might be a more effective method to improve health. We compared the effects of high-intensity intermittent exercise and 30 min of brisk walking on postprandial TAG, soluble adhesion molecules and markers of oxidative stress. Nine men each completed three 2-day trials. On day 1, subjects rested (control), walked briskly for 30 min (walking) or performed 5×30 s maximal sprints (high-intensity). On day 2, subjects consumed a high-fat meal for breakfast and 3 h later for lunch. Blood samples were taken at various times and analysed for TAG, glucose, insulin, ICAM-1 (intracellular adhesion molecule-1), VCAM-1 (vascular adhesion molecule-1), TBARS (thiobarbituric acid- reactive substances), protein carbonyls and β-hydroxybutyrate. On day 2 of the high-intensity trial, there was a lower (P<0.05) incremental TAG AUC (area under the curve; 6.42±2.24 mmol/l per 7 h) compared with the control trial (9.68±4.77 mmol/l per 7 h) with no differences during day 2 of the walking trial (8.98±2.84 mmol/l per 7 h). A trend (P=0.056) for a reduced total TAG AUC was also seen during the high-intensity trial (14.13±2.83 mmol/l per 7 h) compared with control (17.18±3.92 mmol/l per 7 h), walking showed no difference (16.33±3.51 mmol/l per 7 h). On day 2 of the high-intensity trial plasma TBARS and protein carbonyls were also reduced (P<0.05) when compared with the control and walking trials. In conclusion, high-intensity intermittent exercise attenuates postprandial TAG and markers of oxidative stress after the consumption of a high-fat meal.


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