A single bout of whole-body resistance exercise augments basal VLDL-triacylglycerol removal from plasma in healthy untrained men

2008 ◽  
Vol 116 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Yiannis E. Tsekouras ◽  
Faidon Magkos ◽  
Konstantinos I. Prentzas ◽  
Konstantinos N. Basioukas ◽  
Stergoula G. Matsama ◽  
...  

A single bout of prolonged aerobic exercise lowers plasma TAG (triacylglycerol) concentrations the next day by increasing the efficiency of VLDL (very-low-density lipoprotein)-TAG removal from the circulation. The effect of resistance exercise on VLDL-TAG metabolism is not known. Therefore we evaluated VLDL-TAG kinetics by using stable isotope-labelled tracers in eight healthy untrained men (age, 25.3±0.8 years; body mass index, 24.5±0.6 kg/m2) in the post-absorptive state in the morning on two separate occasions: once after performing a single 90-min bout of strenuous isokinetic resistance exercise (three sets×ten repetitions, 12 exercises at 80% of maximum peak torque production, with a 2-min rest interval between exercises) on the preceding afternoon and once after an equivalent period of rest. Fasting plasma VLDL-TAG concentrations in the morning after exercise were significantly lower than in the morning after rest (0.23±0.04 compared with 0.33±0.06 mmol/l respectively; P=0.001). Hepatic VLDL-TAG secretion rate was not different (P=0.31), but plasma clearance rate of VLDL-TAG was significantly higher (by 26±8%) after exercise than rest (31±3 compared with 25±3 ml/min respectively; P=0.004), and the mean residence time of VLDL-TAG in the circulation was significantly shorter (113±10 compared with 144±18 min respectively; P=0.02). Fasting plasma NEFA (non-esterified fatty acid; ‘free’ fatty acid) and serum β-hydroxybutyrate concentrations were both significantly higher after exercise than rest (P<0.05), whereas plasma glucose and serum insulin concentrations were not different (P>0.30). We conclude that, in healthy untrained men, a single bout of whole-body resistance exercise lowers fasting plasma VLDL-TAG concentrations by augmenting VLDL-TAG removal from plasma. The effect appears to be qualitatively and quantitatively similar to that reported previously for aerobic exercise.

2013 ◽  
Vol 38 (8) ◽  
pp. 823-829 ◽  
Author(s):  
Elena Bellou ◽  
Faidon Magkos ◽  
Tonia Kouka ◽  
Eirini Bouchalaki ◽  
Dimitra Sklaveniti ◽  
...  

A single bout of high-intensity interval aerobic exercise has been shown to produce the same or greater metabolic benefits as continuous endurance exercise with considerably less energy expenditure, but whether this applies to very low density lipoprotein (VLDL) metabolism is not known. We sought to examine the effect of a single bout of high-intensity interval aerobic exercise on basal VLDL-triglyceride (TG) kinetics 14 and 48 h after exercise cessation to determine the acute and time-dependent effects of this type of exercise on VLDL-TG metabolism. Eight healthy sedentary men (age, 23.6 ± 6.1 years; body mass index, 23.1 ± 2.2 kg·m−2, peak oxygen consumption (V̇O2peak), 36.3 ± 5.5 mL·kg−1·min−1) participated in three stable isotopically labeled tracer infusion studies: (i) 14 h and (ii) 48 h after a single bout of high-intensity aerobic interval exercise (60% and 90% of V̇O2peak in 4 min intervals for a total of 32 min; gross energy expenditure ∼500 kcal) and (iii) after an equivalent period of rest, in random order. Fasting plasma VLDL-TG concentration was 20% lower at 14 h (P = 0.046) but not at 48 h (P = 1.000) after exercise compared with the resting trial. VLDL-TG plasma clearance rate increased by 21% at 14 h (P < 0.001) but not at 48 h (P = 0.299) after exercise compared with rest, whereas hepatic VLDL-TG secretion rate was not different from rest at any time point after exercise. We conclude that high-intensity interval exercise reduces fasting plasma VLDL-TG concentrations in non-obese men the next day by augmenting VLDL-TG clearance, just like a single bout of continuous endurance exercise. This effect is short-lived and abolished by 48 h after exercise.


2013 ◽  
Vol 38 (8) ◽  
pp. 900-904 ◽  
Author(s):  
Brett A. Gordon ◽  
Stephen R. Bird ◽  
Richard J. MacIsaac ◽  
Amanda C. Benson

The glycemic response to aerobic exercise is well understood; however, the response to resistance exercise is not. Eight inactive males (61.0 ± 7.2 years) with insulin-treated type 2 diabetes randomly completed single sessions of whole-body resistance exercise or cycling, 7 days apart. There were different 24-h glucose responses (p < 0.001) between the resistance exercise and the aerobic exercise, with short-term (24-h) impairment of glycemic control following the resistance exercise (p = 0.004). Cycling did not reduce glucose concentrations (p > 0.05), which contrasts with previous findings.


2016 ◽  
Vol 4 (15) ◽  
pp. e12893 ◽  
Author(s):  
Lindsay S. Macnaughton ◽  
Sophie L. Wardle ◽  
Oliver C. Witard ◽  
Chris McGlory ◽  
D. Lee Hamilton ◽  
...  

2003 ◽  
Vol 23 (16) ◽  
pp. 5780-5789 ◽  
Author(s):  
Brandee L. Wagner ◽  
Annabel F. Valledor ◽  
Gang Shao ◽  
Chris L. Daige ◽  
Eric D. Bischoff ◽  
...  

ABSTRACT Liver X receptors (LXRs) regulate the expression of genes involved in cholesterol and fatty acid homeostasis, including the genes for ATP-binding cassette transporter A1 (ABCA1) and sterol response element binding protein 1 (SREBP1). Loss of LXR leads to derepression of the ABCA1 gene in macrophages and the intestine, while the SREBP1c gene remains transcriptionally silent. Here we report that high-density-lipoprotein (HDL) cholesterol levels are increased in LXR-deficient mice, suggesting that derepression of ABCA1 and possibly other LXR target genes in selected tissues is sufficient to result in enhanced HDL biogenesis at the whole-body level. We provide several independent lines of evidence indicating that the repressive actions of LXRs are dependent on interactions with the nuclear receptor corepressor (NCoR) and the silencing mediator of retinoic acid and thyroid hormone receptors (SMRT). While dissociation of NCoR and SMRT results in derepression of the ABCA1 gene in macrophages, it is not sufficient for derepression of the SREBP1c gene. These findings reveal differential requirements for corepressors in the regulation of genes involved in cholesterol and fatty acid homeostasis and raise the possibility that these interactions may be exploited to develop synthetic ligands that selectively modulate LXR actions in vivo.


2020 ◽  
Vol 11 ◽  
Author(s):  
Katsumi Iizuka ◽  
Ken Takao ◽  
Daisuke Yabe

Carbohydrate response element-binding protein (ChREBP) plays an important role in the development of type 2 diabetes, dyslipidemia, and non-alcoholic fatty liver disease, as well as tumorigenesis. ChREBP is highly expressed in lipogenic organs, such as liver, intestine, and adipose tissue, in which it regulates the production of acetyl CoA from glucose by inducing Pklr and Acyl expression. It has recently been demonstrated that ChREBP plays a role in the conversion of gut microbiota-derived acetate to acetyl CoA by activating its target gene, Acss2, in the liver. ChREBP regulates fatty acid synthesis, elongation, and desaturation by inducing Acc1 and Fasn, elongation of long-chain fatty acids family member 6 (encoded by Elovl6), and Scd1 expression, respectively. ChREBP also regulates the formation of very low-density lipoprotein by inducing the expression of Mtp. Furthermore, it plays a crucial role in peripheral lipid metabolism by inducing Fgf21 expression, as well as that of Angptl3 and Angptl8, which are known to reduce peripheral lipoprotein lipase activity. In addition, ChREBP is involved in the production of palmitic-acid-5-hydroxystearic-acid, which increases insulin sensitivity in adipose tissue. Curiously, ChREBP is indirectly involved in fatty acid β-oxidation and subsequent ketogenesis. Thus, ChREBP regulates whole-body lipid metabolism by controlling the transcription of lipogenic enzymes and liver-derived cytokines.


Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3029
Author(s):  
Mariwan H. Sayda ◽  
Bethan E. Phillips ◽  
John P. Williams ◽  
Paul L. Greenhaff ◽  
Daniel J. Wilkinson ◽  
...  

Leucine, isoleucine and valine (i.e., the branched chain amino acids, BCAA) play a key role in the support of tissue protein regulation and can be mobilized as energy substrates during times of starvation. However, positive relationships exist between elevated levels of BCAA and insulin resistance (IR). Thus, we sought to investigate the links between fasting plasma BCAA following a progressive resistance exercise training (RET) programme, an intervention known to improve metabolic health. Fasting plasma BCAA were quantified in adults (young: 18–28 y, n = 8; middle-aged: 45–55 y, n = 9; older: 65–75 y, n = 15; BMI: 23–28 kg/m2, both males and females (~50:50), in a cross-sectional, intervention study. Participants underwent 20-weeks whole-body RET. Measurements of body composition, muscle strength (1-RM) and metabolic health biomarkers (e.g., HOMA-IR) were made at baseline and post-RET. BCAA concentrations were determined by gas-chromatography mass spectrometry (GC-MS). No associations were observed across age with BCAA; however, RET elicited (p < 0.05) increases in plasma BCAA (all age-groups), while HOMA-IR scores reduced (p < 0.05) following RET. After RET, positive correlations in lean body mass (p = 0.007) and strength gains (p = 0.001) with fasting BCAA levels were observed. Elevated BCAA are not a robust marker of ageing nor IR in those with a healthy BMI; rather, despite decreasing IR, RET was associated with increased BCAA.


1989 ◽  
Vol 66 (3) ◽  
pp. 1430-1435 ◽  
Author(s):  
P. M. Young ◽  
M. S. Rose ◽  
J. R. Sutton ◽  
H. J. Green ◽  
A. Cymerman ◽  
...  

To examine the effect of hypobaric hypoxia on plasma lipid profiles, fasting blood samples were collected from six men (21–31 yr) at 760 Torr and periodically during a 40-day exposure to decreasing barometric pressure culminating in a final ambient pressure of 282 Torr. Preascent plasma total cholesterol concentration ([TC]) was decreased by 25% after the 40-day exposure (P less than 0.01). High-density lipoprotein concentrations ([HDL-C]) decreased 32% (P less than 0.001) with no alteration in the TC-to-HDL-C weight ratio. Plasma triglyceride concentration increased twofold during this period (P less than 0.01). There were no significant differences in fasting plasma free fatty acid concentrations or free fatty acid-to-albumin molar ratio throughout the study. Fasting plasma insulin levels were increased approximately twofold with no significant changes in glucagon concentration or the insulin-to-glucagon molar ratio. Plasma norepinephrine concentrations were increased threefold on reaching 282 Torr (P less than 0.01), with no significant changes in plasma epinephrine concentrations. Mean energy intake (kcal/day) decreased 42%, whereas mean body weights decreased by 8.9 +/- 0.8% (P less than 0.01) with exposure. Increased concentrations of insulin may lead to increased hepatic production of triglyceride-rich lipoproteins, thus eliciting metabolic changes independent of weight loss and dietary intake.


2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 42
Author(s):  
Tommy Lundberg ◽  
Rodrigo Fernandez-Gonzalo ◽  
Thomas Gustafsson ◽  
Per A. Tesch

2003 ◽  
Vol 94 (6) ◽  
pp. 2212-2216 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
Emily M. Downs ◽  
William H. Cooke

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 ± 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure ( n = 12; automated sphygmomanometer) and MSNA ( n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 ± 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups ( P < 0.001), and it significantly decreased systolic (130 ± 3 to 121 ± 2 mmHg; P = 0.01), diastolic (69 ± 3 to 61 ± 2 mmHg; P = 0.04), and mean (89 ± 2 to 81 ± 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 ± 2 to 67 ± 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.


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