Are the reductions in triacylglycerol and insulin levels after exercise related?

2002 ◽  
Vol 102 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Jason M.R. GILL ◽  
Sara L. HERD ◽  
Natassa V. TSETSONIS ◽  
Adrianne E. HARDMAN
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Response ◽  
Insulin Concentration ◽  
Moderate Intensity ◽  
Fasting Insulin ◽  
Prior Exercise ◽  
Exercise Induced ◽  
Induced Changes ◽  
Postprandial Insulin Response ◽  
Postprandial Insulin

Moderate exercise improves insulin sensitivity and reduces triacylglycerol (triglyceride; TG) concentrations. We hypothesized that changes in insulin sensitivity are an important determinant of exercise-induced changes in postprandial TG concentrations. Altogether, 38 men and 43 women, all of whom were normotriglyceridaemic and normoglycaemic, each underwent two oral fat tolerance tests with different pre-conditions: control (no exercise) and prior exercise (90min of exercise at 60% of maximal O2 uptake the day before). Venous blood samples were obtained in the fasting state and for 6h after a high-fat mixed meal. In the control trial there were significant correlations between log fasting TG concentration and log fasting insulin concentration (r = 0.42, P < 0.0005) and between log postprandial TG response (area under the curve) and log postprandial insulin response (r = 0.48, P < 0.0005). Prior exercise reduced the fasting TG concentration by 18.2±2.2% (mean±S.E.M.) (P < 0.0005), the postprandial TG response by 21.5±1.9% (P < 0.0005), the fasting insulin concentration by 3.8±3.1% (P < 0.01) and the postprandial insulin response by 11.9±2.5% (P < 0.0005). However, there was no relationship between the exercise-induced changes in log fasting TG and log fasting insulin (r = 0.08, P = 0.50), nor between the exercise-induced changes in log postprandial TG response and log postprandial insulin response (r = 0.04, P = 0.70). These data suggest that the reductions in fasting and postprandial TG levels elicited by a session of moderate-intensity exercise are not mediated by an increase in insulin sensitivity.

scholarly journals Characterization of extracellular redox enzyme concentrations in response to exercise in humans

2019 ◽  
Vol 127 (3) ◽  
pp. 858-866 ◽  
Author(s):  
Alex J. Wadley ◽  
Gary Keane ◽  
Tom Cullen ◽  
Lynsey James ◽  
Jordan Vautrinot ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Resistance Exercise ◽  
High Intensity ◽  
Redox Balance ◽  
Moderate Intensity ◽  
Redox Enzymes ◽  
Redox Enzyme ◽  
Systemic Oxidative Stress ◽  
Exercise Induced ◽  
Induced Changes

Redox enzymes modulate intracellular redox balance and are secreted in response to cellular oxidative stress, potentially modulating systemic inflammation. Both aerobic and resistance exercise are known to cause acute systemic oxidative stress and inflammation; however, how redox enzyme concentrations alter in extracellular fluids following bouts of either type of exercise is unknown. Recreationally active men ( n = 26, mean ± SD: age 28 ± 8 yr) took part in either: 1) two separate energy-matched cycling bouts: one of moderate intensity (MOD) and a bout of high intensity interval exercise (HIIE) or 2) an eccentric-based resistance exercise protocol (RES). Alterations in plasma (study 1) and serum (study 2) peroxiredoxin (PRDX)-2, PRDX-4, superoxide dismutase-3 (SOD3), thioredoxin (TRX-1), TRX-reductase and interleukin (IL)-6 were assessed before and at various timepoints after exercise. There was a significant increase in SOD3 (+1.5 ng/mL) and PRDX-4 (+5.9 ng/mL) concentration following HIIE only, peaking at 30- and 60-min post-exercise respectively. TRX-R decreased immediately and 60 min following HIIE (−7.3 ng/mL) and MOD (−8.6 ng/mL), respectively. In non-resistance trained men, no significant changes in redox enzyme concentrations were observed up to 48 h following RES, despite significant muscle damage. IL-6 concentration increased in response to all trials, however there was no significant relationship between absolute or exercise-induced changes in redox enzyme concentrations. These results collectively suggest that HIIE, but not MOD or RES increase the extracellular concentration of PRDX-4 and SOD3. Exercise-induced changes in redox enzyme concentrations do not appear to directly relate to systemic changes in IL-6 concentration. NEW & NOTEWORTHY Two studies were conducted to characterize changes in redox enzyme concentrations after single bouts of exercise to investigate the emerging association between extracellular redox enzymes and inflammation. We provide evidence that SOD3 and PRDX-4 concentration increased following high-intensity aerobic but not eccentric-based resistance exercise. Changes were not associated with IL-6. The results provide a platform to investigate the utility of SOD3 and PRDX-4 as biomarkers of oxidative stress following exercise.

scholarly journals Bread making technology influences postprandial glucose response: a review of the clinical evidence

2017 ◽  
Vol 117 (7) ◽  
pp. 1001-1012 ◽  
Author(s):  
Nikoleta S. Stamataki ◽  
Amalia E. Yanni ◽  
Vaios T. Karathanos
Keyword(s):  
Insulin Response ◽  
Postprandial Glucose ◽  
Daily Basis ◽  
Physical Structure ◽  
Bread Making ◽  
Glucose Response ◽  
Insulin Responses ◽  
Baking Conditions ◽  
Postprandial Insulin Response ◽  
Postprandial Insulin

AbstractLowering postprandial glucose and insulin responses may have significant beneficial implications for prevention and treatment of metabolic disorders. Bread is a staple food consumed worldwide in a daily basis, and the use of different baking technologies may modify the glucose and insulin response. The aim of this review was to critically record the human studies examining the application of different bread making processes on postprandial glucose and insulin response to bread. Literature is rich of results which show that the use of sourdough fermentation instead of leavening with Saccharomyces cerevisiae is able to modulate glucose response to bread, whereas evidence regarding its efficacy on lowering postprandial insulin response is less clear. The presence of organic acids is possibly involved, but the exact mechanism of action is still to be confirmed. The reviewed data also revealed that the alteration of other processing conditions (method of cooking, proofing period, partial baking freezing technology) can effectively decrease postprandial glucose response to bread, by influencing physical structure and retrogradation of starch. The development of healthier bread products that benefit postprandial metabolic responses is crucial and suggested baking conditions can be used by the bread industry for the promotion of public health.

scholarly journals Associations between postprandial insulin and blood glucose responses, appetite sensations and energy intake in normal weight and overweight individuals: a meta-analysis of test meal studies

2007 ◽  
Vol 98 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Anne Flint ◽  
Nikolaj T. Gregersen ◽  
Lise L. Gluud ◽  
Bente K. Møller ◽  
Anne Raben ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Blood Glucose ◽  
Meta Analysis ◽  
Insulin Response ◽  
Normal Weight ◽  
Appetite Regulation ◽  
Short Term ◽  
Healthy Participants ◽  
Postprandial Insulin Response ◽  
Postprandial Insulin

It is unclear whether postprandial blood glucose or insulin exerts a regulatory function in short-term appetite regulation in humans. The aim of this study was to investigate, by use of meta-analysis, the role of blood glucose and insulin in short-term appetite sensation and energy intake (EI) in normal weight and overweight participants. Data from seven test meal studies were used, including 136 healthy participants (ALL) (92 normal weight (NW) and 44 overweight or obese (OW)). All meals were served as breakfasts after an overnight fast, and appetite sensations and blood samples were obtained frequently in the postprandial period. Finally, an ad libitum lunch was served. Data were analysed by fixed effects study level (SL) meta-regression analysis and individual participant data (IPD) regression analysis, using STATA software. In SL analysis, postprandial insulin response was associated with decreased hunger in ALL, NW and OW (P < 0·019), and with increased satiety in NW (P = 0·004) and lower subsequent EI in OW (P = 0·022). Multivariate IPD analysis showed similar associations, but only in NW for hunger, satiety and EI (P < 0·028), and in ALL for EI (P = 0·016). The only association involving blood glucose was the multivariate IPD analysis showing an inverse association between blood glucose and EI in ALL (P = 0·032). Our results suggest that insulin, but not glucose, is associated with short-term appetite regulation in healthy participants, but the relationship is disrupted in the overweight and obese. We conclude that the postprandial insulin response may be an important satiety signal, and that central nervous system insulin resistance in overweight might explain the blunted effect on appetite.

Effects of PYY1–36and PYY3–36on appetite, energy intake, energy expenditure, glucose and fat metabolism in obese and lean subjects

2007 ◽  
Vol 292 (4) ◽  
pp. E1062-E1068 ◽  
Author(s):  
Birgitte Sloth ◽  
Jens Juul Holst ◽  
Anne Flint ◽  
Nikolaj Ture Gregersen ◽  
Arne Astrup
Keyword(s):  
Heart Rate ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Peptide Yy ◽  
Fat Metabolism ◽  
Insulin Response ◽  
Well Being ◽  
Postprandial Glucose ◽  
Postprandial Insulin Response ◽  
Postprandial Insulin

Peptide YY (PYY)3–36has been shown to produce dramatic reductions in energy intake (EI), but no human data exist regarding energy expenditure (EE), glucose and fat metabolism. Nothing is known regarding PYY1-36. To compare effects of PYY1–36and PYY3–36on appetite, EI, EE, insulin, glucose and free fatty acids (FFA) concentrations, 12 lean and 12 obese males participated in a blinded, randomized, crossover study with 90-min infusions of saline, 0.8 pmol·kg−1·min−1PYY1–36and PYY3–36. Only four participants completed PYY3–36infusions because of nausea. Subsequently, six lean and eight obese participants completed 0.2 pmol·kg−1·min−1PYY3–36and 1.6 pmol·kg−1·min−1PYY1–36infusions. PYY3–36at 0.8 pmol·kg−1·min−1produced reduced EI, lower ratings of well-being, increases in FFA, postprandial glucose (only 0.8 pmol·kg−1·min−1PYY3–36) and insulin concentrations, as well as heart rate and EE (only 0.8 pmol·kg−1·min−1PYY3–36). PYY1–36at 1.6 pmol·kg−1·min−1produced increased heart rate and postprandial insulin response. Ratings of appetite were opposite with infusions of 0.8 and 1.6 pmol·kg−1·min−1PYY1–36and seemed to depend on subjects being lean or obese. PYY3–36caused increased thermogenesis, lipolysis, postprandial insulin and glucose responses, suggestive of increased sympathoadrenal activity. PYY1–36had no effect on EI and no clear effects on appetite but resulted in increased heart rate and postprandial insulin response. However, highest tolerable dose of PYY1–36was probably not reached in the present study.

Improved insulin sensitivity after a single bout of exercise is curvilinearly related to exercise energy expenditure

2007 ◽  
Vol 114 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Faidon Magkos ◽  
Yannis Tsekouras ◽  
Stavros A. Kavouras ◽  
Bettina Mittendorfer ◽  
Labros S. Sidossis
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Energy Expenditure ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Moderate Intensity ◽  
Model Assessment ◽  
Single Bout ◽  
Exercise Energy Expenditure ◽  
Exercise Induced

A single bout of moderate-intensity exercise increases whole-body insulin sensitivity for 12–48 h post-exercise; however, the relationship between exercise energy expenditure and the improvement in insulin sensitivity is not known. We hypothesized that the exercise-induced increase in whole-body insulin sensitivity, assessed with HOMAIR (homoeostasis model assessment of insulin resistance), is directly related to the energy expended during exercise. We studied 30 recreationally active non-obese men (age, 27±5 years; body mass index, 24±2 kg/m2) in the post-absorptive state on two separate occasions: once after exercising at 60% of V̇O22peak (peak oxygen consumption) for 30–120 min on the preceding afternoon (expending a total of 1.28–5.76 MJ) and once after an equivalent period of rest. Blood samples were obtained the following morning. Exercise-induced changes in HOMAIR were curvilinearly related to exercise energy expenditure (r=−0.666, P=0.001) with a threshold of approx. 3.77 MJ (900 kcal) for improvements in HOMAIR to be manifested. In particular, HOMAIR was reduced by 32±24% (P=0.003) in subjects who expended more than 3.77 MJ during exercise, but did not change for those who expended fewer than 3.77 MJ (−2±21%; P=0.301). Furthermore, the magnitude of change in HOMAIR after exercise was directly associated with baseline (i.e. resting) HOMAIR (r=−0.508, P=0.004); this relationship persisted in multivariate analysis. We conclude that improved whole-body insulin resistance after a single bout of exercise is curvilinearly related to exercise energy expenditure, and requires unfeasible amounts of exercise for most sedentary individuals.

scholarly journals Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans

2019 ◽  
Vol 126 (2) ◽  
pp. 305-313
Author(s):  
Naoto Fujii ◽  
Miki Kashihara ◽  
Glen P. Kenny ◽  
Yasushi Honda ◽  
Tomomi Fujimoto ◽  
...  
Keyword(s):  
Young Men ◽  
Progressive Increase ◽  
Peak Oxygen Uptake ◽  
Body Core Temperature ◽  
Moderate Intensity ◽  
Esophageal Temperature ◽  
Moderate Intensity Exercise ◽  
Carotid Chemoreceptors ◽  
Exercise Induced ◽  
Induced Changes

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.

Glycogen depletion and increased insulin sensitivity and responsiveness in muscle after exercise

1986 ◽  
Vol 251 (6) ◽  
pp. E664-E669 ◽  
Author(s):  
A. Zorzano ◽  
T. W. Balon ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Utilization ◽  
Treadmill Exercise ◽  
Moderate Intensity ◽  
Glycogen Depletion ◽  
Increase Insulin Sensitivity ◽  
Enhanced Sensitivity ◽  
Prior Exercise ◽  
Insulin Responsiveness ◽  
The Relationship

As judged by its ability to stimulate glucose uptake and alpha-aminoisobutyric acid (AIB) transport, the sensitivity and the responsiveness of perfused rat muscle to insulin are enhanced after moderately intense treadmill exercise. In fed rats, these enhanced effects of insulin are predominantly restricted to muscles that performed work as evidenced by glycogen depletion. The present study was designed to examine the relationship between glycogen depletion per se and the postexercise changes in insulin action. Toward this end, fed and 48-h starved rats were run on a treadmill for 45 min at moderate intensity, and glucose and AIB uptake were then assessed using the isolated perfused hindquarter preparation. Glycogen is depleted in red muscles such as the soleus and red fibers of the gastrocnemius in fed rats immediately after such exercise, whereas, in starved rats, muscle glycogen is unchanged. As previously shown, the stimulation by insulin of glucose utilization by the hindquarter and AIB transport into red muscles was substantially increased in fed rats after the treadmill run. This was due to increases in both insulin sensitivity and responsiveness. In starved rats, the treadmill run also enhanced the ability of insulin to stimulate these processes; however, this was solely due to an increase in insulin sensitivity. No change in insulin responsiveness was observed. The results indicate that the enhanced sensitivity of muscle to insulin after exercise is not dependent on glycogen depletion, whereas increased insulin responsiveness does not occur in its absence. They also suggest that the mechanisms by which prior exercise acts to increase insulin sensitivity and responsiveness are different.

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