scholarly journals Energy Status Differentially Modifies Feeding Behavior and POMCARC Neuron Activity After Acute Treadmill Exercise in Untrained Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Taylor Landry ◽  
Daniel Shookster ◽  
Alec Chaves ◽  
Katrina Free ◽  
Tony Nguyen ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Food Intake ◽  
Feeding Behavior ◽  
Exercise Intensity ◽  
High Intensity ◽  
Treadmill Exercise ◽  
High Intensity Exercise ◽  
Neuron Activity ◽  
Energy Status ◽  
Post Exercise

Emerging evidence identifies a potent role for aerobic exercise to modulate activity of neurons involved in regulating appetite; however, these studies produce conflicting results. These discrepancies may be, in part, due to methodological differences, including differences in exercise intensity and pre-exercise energy status. Consequently, the current study utilized a translational, well-controlled, within-subject, treadmill exercise protocol to investigate the differential effects of energy status and exercise intensity on post-exercise feeding behavior and appetite-controlling neurons in the hypothalamus. Mature, untrained male mice were exposed to acute sedentary, low (10m/min), moderate (14m/min), and high (18m/min) intensity treadmill exercise in a randomized crossover design. Fed and 10-hour-fasted mice were used, and food intake was monitored 48h. post-exercise. Immunohistochemical detection of cFOS was performed 1-hour post-exercise to determine changes in hypothalamic NPY/AgRP, POMC, tyrosine hydroxylase, and SIM1-expressing neuron activity concurrent with changes in food intake. Additionally, stains for pSTAT3tyr705 and pERKthr202/tyr204 were performed to detect exercise-mediated changes in intracellular signaling. Results demonstrated that fasted high intensity exercise suppressed food intake compared to sedentary trials, which was concurrent with increased anorexigenic POMC neuron activity. Conversely, fed mice experienced augmented post-exercise food intake, with no effects on POMC neuron activity. Regardless of pre-exercise energy status, tyrosine hydroxylase and SIM1 neuron activity in the paraventricular nucleus was elevated, as well as NPY/AgRP neuron activity in the arcuate nucleus. Notably, these neuronal changes were independent from changes in pSTAT3tyr705 and pERKthr202/tyr204 signaling. Overall, these results suggest fasted high intensity exercise may be beneficial for suppressing food intake, possibly due to hypothalamic POMC neuron excitation. Furthermore, this study identifies a novel role for pre-exercise energy status to differentially modify post-exercise feeding behavior and hypothalamic neuron activity, which may explain the inconsistent results from studies investigating exercise as a weight loss intervention.

Exercise Increases NPY/AgRP and TH Neuron Activity in the Hypothalamus of Female Mice

2021 ◽  
Author(s):  
Taylor Landry ◽  
Daniel Shookster ◽  
Alec Chaves ◽  
Katrina Free ◽  
Tony Nguyen ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Food Intake ◽  
Aerobic Exercise ◽  
High Intensity ◽  
Treadmill Exercise ◽  
High Intensity Exercise ◽  
Neuron Activity ◽  
Post Exercise ◽  
Female Mice ◽  
Neuron Populations

Recent evidence identifies a potent role for aerobic exercise to modulate activity of hypothalamic neurons related to appetite; however, these studies have been primarily performed in male rodents. Since females have markedly different neuronal mechanisms regulating food intake, the current study aimed to determine the effects of acute treadmill exercise on hypothalamic neuron populations involved in regulating appetite in female mice. Mature, untrained female mice were exposed to acute sedentary, low (10m/min), moderate (14m/min), and high (18m/min) intensity treadmill exercise in a randomized crossover design. Mice were fasted 10-hours before exercise and food intake was monitored for 48-hours after bouts. Immunohistochemical detection of cFOS was performed 3-hours post-exercise to determine changes in hypothalamic NPY/AgRP, POMC, tyrosine hydroxylase, and SIM1-expressing neuron activity concurrent with changes in food intake. Additionally, stains for pSTAT3tyr705 and pERKthr202/tyr204 were performed to detect exercise-mediated changes in intracellular signaling. Briefly, moderate and high intensity exercise increased 24-hour food intake by 5.9% and 19%, respectively, while low intensity exercise had no effects. Furthermore, increases in NPY/AgRPARC, SIM1PVN, and tyrosine hydroxylase neuron activity were observed 3-hours after high intensity exercise, with no effects on POMCARC neurons. While no effects of exercise on pERKthr202/tyr204 were observed, pSTAT3tyr705 was elevated specifically in NPY/AgRP neurons 3-hours post-exercise. Overall, aerobic exercise increased activity of several appetite-stimulating neuron populations in the hypothalamus of female mice, which may provide insight into previously reported sexual dimorphisms in post-exercise feeding.

Modulation of feeding by endogenous sugar acids acting as hunger or satiety factors

1984 ◽  
Vol 246 (4) ◽  
pp. R542-R550 ◽  
Author(s):  
N. Shimizu ◽  
Y. Oomura ◽  
T. Sakata
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Food Consumption ◽  
Single Neuron ◽  
Cerebral Ventricle ◽  
Neuron Activity ◽  
Hypothalamic Area ◽  
The Third ◽  
Single Neuron Activity ◽  
Fasted Rats

Endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid, 3-DPA), have been identified in the serum of fasted rats. Effects of these sugar acids on rat feeding behavior and neuron activity were investigated. Injections of 2-DTA (2.5 mumol) into the third cerebral ventricle of chronic rats suppressed food intake and single-neuron activity in the lateral hypothalamic area (LHA). Food consumption was reduced for 24 h, even in 72-h food-deprived rats. The same amounts of 3-DPA elicited feeding and increased LHA single-neuron activity with latencies of 6-8 min. Electrophoretically applied 2-DTA significantly and specifically suppressed activity of glucose-sensitive neurons in the LHA, whereas 3-DPA facilitated the activity. Nonglucose-sensitive LHA neurons were not affected by these sugar acids. The high correlation between modulation of feeding behavior and changes in LHA neuron activity after injection of these sugar acids suggested that 2-DTA may act as an endogenous satiety substance and 3-DPA as a hunger substance. The effects may be mediated through glucose-sensitive neurons in the LHA.

scholarly journals Antioxidants Facilitate High–intensity Exercise IL–15 Expression in Skeletal Muscle

2018 ◽  
Vol 40 (01) ◽  
pp. 16-22 ◽  
Author(s):  
Alberto Pérez-López ◽  
Marcos Martin-Rincon ◽  
Alfredo Santana ◽  
Ismael Perez-Suarez ◽  
Cecilia Dorado ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Acute Hypoxia ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Post Exercise ◽  
Sprint Exercise

AbstractInterleukin (IL)-15 stimulates mitochondrial biogenesis, fat oxidation, glucose uptake and myogenesis in skeletal muscle. However, the mechanisms by which exercise triggers IL-15 expression remain to be elucidated in humans. This study aimed at determining whether high-intensity exercise and exercise-induced RONS stimulate IL-15/IL-15Rα expression and its signaling pathway (STAT3) in human skeletal muscle. Nine volunteers performed a 30-s Wingate test in normoxia and hypoxia (PIO2=75 mmHg), 2 h after placebo or antioxidant administration (α-lipoic acid, vitamin C and E) in a randomized double-blind design. Blood samples and muscle biopsies (vastus lateralis) were obtained before, immediately after, and 30 and 120 min post-exercise. Sprint exercise upregulated skeletal muscle IL-15 protein expression (ANOVA, P=0.05), an effect accentuated by antioxidant administration in hypoxia (ANOVA, P=0.022). In antioxidant conditions, the increased IL-15 expression at 120 min post-exercise (33%; P=0.017) was associated with the oxygen deficit caused by the sprint (r=–0.54; P=0.020); while, IL-15 and Tyr705-STAT3 AUCs were also related (r=0.50; P=0.036). Antioxidant administration promotes IL-15 protein expression in human skeletal muscle after sprint exercise, particularly in severe acute hypoxia. Therefore, during intense muscle contraction, a reduced PO2 and glycolytic rate, and possibly, an attenuated RONS generation may facilitate IL-15 production, accompanied by STAT3 activation, in a process that does not require AMPK phosphorylation.

scholarly journals Exercise training intensity determination in cardiovascular rehabilitation: Should the guidelines be reconsidered?

2019 ◽  
Vol 26 (18) ◽  
pp. 1921-1928 ◽  
Author(s):  
Dominique Hansen ◽  
Kim Bonné ◽  
Toon Alders ◽  
Ann Hermans ◽  
Katrien Copermans ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Heart Rate ◽  
Exercise Intensity ◽  
High Intensity ◽  
Ventilatory Threshold ◽  
Cardiopulmonary Exercise Test ◽  
High Intensity Exercise ◽  
Cardiovascular Rehabilitation ◽  
Correct Determination ◽  
Low Intensity Exercise

Aims In the rehabilitation of cardiovascular disease patients a correct determination of the endurance-type exercise intensity is important to generate health benefits and preserve medical safety. It remains to be assessed whether the guideline-based exercise intensity domains are internally consistent and agree with physiological responses to exercise in cardiovascular disease patients. Methods A total of 272 cardiovascular disease patients without pacemaker executed a maximal cardiopulmonary exercise test on bike (peak respiratory gas exchange ratio >1.09), to assess peak heart rate (HRpeak), oxygen uptake (VO2peak) and cycling power output (Wpeak). The first and second ventilatory threshold (VT1 and VT2, respectively) was determined and extrapolated to %VO2peak, %HRpeak, %heart rate reserve (%HRR) and %Wpeak for comparison with guideline-based exercise intensity domains. Results VT1 was noted at 62 ± 10% VO2peak, 75 ± 10% HRpeak, 42 ± 14% HRR and 47 ± 11% Wpeak, corresponding to the high intensity exercise domain (for %VO2peak and %HRpeak) or low intensity exercise domain (for %Wpeak and %HRR). VT2 was noted at 84 ± 9% VO2peak, 88 ± 8% HRpeak, 74 ± 15% HRR and 76 ± 11% Wpeak, corresponding to the high intensity exercise domain (for %HRR and %Wpeak) or very hard exercise domain (for %HRpeak and %VO2peak). At best (when using %Wpeak) in only 63% and 72% of all patients VT1 and VT2, respectively, corresponded to the same guideline-based exercise intensity domain, but this dropped to about 48% and 52% at worst (when using %HRR and %HRpeak, respectively). In particular, the patient’s VO2peak related to differently elicited guideline-based exercise intensity domains ( P < 0.05). Conclusion The guideline-based exercise intensity domains for cardiovascular disease patients seem inconsistent, thus reiterating the need for adjustment.

Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity

1987 ◽  
Vol 63 (2) ◽  
pp. 654-658 ◽  
Author(s):  
M. S. Sothmann ◽  
A. B. Gustafson ◽  
M. Chandler
Keyword(s):  
Oxygen Consumption ◽  
Exercise Intensity ◽  
High Intensity ◽  
Maximal Oxygen Consumption ◽  
High Intensity Exercise ◽  
The Relationship ◽  
Circulating Levels

Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.

Effect of Exercise Intensity on Exogenous Glucose Requirements to Maintain Stable Glycemia At High Insulin Levels in Type 1 Diabetes

2020 ◽  
Vol 106 (1) ◽  
pp. e83-e93
Author(s):  
Vinutha B Shetty ◽  
Paul A Fournier ◽  
Nirubasini Paramalingam ◽  
Wayne Soon ◽  
Heather C Roby ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Exercise Intensity ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Moderate Intensity ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Exogenous Glucose ◽  
High Insulin

Abstract Context Under basal insulin levels, there is an inverted U relationship between exercise intensity and exogenous glucose requirements to maintain stable blood glucose levels in type 1 diabetes (T1D), with no glucose required for intense exercise (80% V̇O2 peak), implying that high-intensity exercise is not conducive to hypoglycemia. Objective This work aimed to test the hypothesis that a similar inverted U relationship exists under hyperinsulinemic conditions, with high-intensity aerobic exercise not being conducive to hypoglycemia. Methods Nine young adults with T1D (mean ± SD age, 22.6 ± 4.7 years; glycated hemoglobin, 61 ± 14 mmol/mol; body mass index, 24.0 ± 3.3 kg/m2, V̇O2 peak, 36.6 ± 8.0 mL·kg–1 min–1) underwent a hyperinsulinemic-euglycemic clamp to maintain stable glycemia (5-6 mmol·L−1), and exercised for 40 minutes at 4 intensities (35%, 50%, 65%, and 80% V̇O2peak) on separate days following a randomized counterbalanced study design. Main Outcome Measures Glucose infusion rates (GIR) and glucoregulatory hormones levels were measured. Results The GIR (± SEM) to maintain euglycemia was 4.4 ± 0.4 mg·kg–1 min–1 prior to exercise, and increased significantly by 1.8 ± 0.4, 3.0 ± 0.4, 4.2 ± 0.7, and 3.5 ± 0.7 mg·kg–1 min–1 during exercise at 35%, 50%, 65%, and 80% V̇O2 peak, respectively, with no significant differences between the 2 highest exercise intensities (P &gt; .05), despite differences in catecholamine levels (P &lt; .05). During the 2-hour period after exercise at 65% and 80% V̇O2 peak, GIRs did not differ from those during exercise (P &gt; .05). Conclusions Under hyperinsulinemic conditions, the exogenous glucose requirements to maintain stable glycemia during and after exercise increase with exercise intensity then plateau with exercise performed at above moderate intensity ( &gt; 65% V̇O2 peak). High-intensity exercise confers no protection against hypoglycemia.

Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1α mRNA: a role of β2-adrenergic receptor activation

2011 ◽  
Vol 300 (2) ◽  
pp. E341-E349 ◽  
Author(s):  
Miki Tadaishi ◽  
Shinji Miura ◽  
Yuko Kai ◽  
Emi Kawasaki ◽  
Keiichi Koshinaka ◽  
...  
Keyword(s):  
Exercise Intensity ◽  
High Intensity ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Receptor Activation ◽  
High Intensity Exercise ◽  
Treadmill Running ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Exercise Induced

There are three isoforms of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA, which promotes mitochondrial biogenesis in skeletal muscles. Compared with PGC-1α-a mRNA, PGC-1α-b or PGC-1α-c mRNA is transcribed by a different exon 1 of the PGC-1α gene. In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were investigated. All isoforms were increased in proportion to exercise intensity of treadmill running (10–30 m/min for 30 min). Preinjection of β2-adrenergic receptor (AR) antagonist (ICI 118551) inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs, but not the increase in PGC-1α-a mRNA, in response to high-intensity exercise. Although high-intensity exercise activated α2-AMP-activated protein kinase (α2-AMPK) in skeletal muscles, inactivation of α2-AMPK activity did not affect high-intensity exercise-induced mRNA expression of all PGC-1α isoforms, suggesting that activation of α2-AMPK is not mandatory for an increase in PGC-1α mRNA by high-intensity exercise. A single injection in mice of AICAR, an AMPK activator, increased mRNAs of all PGC-1α isoforms. AICAR increased blood catecholamine concentrations, and preinjection of β2-AR antagonist inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs but not the increase in PGC-1α-a mRNA. Direct exposure of epitrochlearis muscle to AICAR increased PGC-1α-a but not the -b isoform. These data indicate that exercise-induced PGC-1α expression was dependent on the intensity of exercise. Exercise or AICAR injection increased PGC-1α-b and PGC-1α-c mRNAs via β2-AR activation, whereas high-intensity exercise increased PGC-1α-a expression by a multiple mechanism in which α2-AMPK is one of the signaling pathways.

Plasma glycerol during the acute post-exercise recovery period: influence of exercise intensity

2013 ◽  
Vol 9 (2) ◽  
pp. 103-108
Author(s):  
R.J. Bloomer ◽  
T.M. Farney
Keyword(s):  
Aerobic Exercise ◽  
High Intensity ◽  
Recovery Period ◽  
Area Under The Curve ◽  
Fat Oxidation ◽  
High Intensity Exercise ◽  
Exercise Session ◽  
Exercise Recovery ◽  
Post Exercise ◽  
Post Exercise Recovery

Intensity of exercise can influence substrate utilization, with increasing intensity resulting in lower rates of fat oxidation and the reliance on carbohydrate as the preferred fuel. Fat oxidation (or more specifically, mobilization) can be assessed via the measurement of circulating glycerol, with most prior research focusing on aerobic exercise and measurements obtained during the actual exercise bout. The present study determined the degree of fat oxidation/mobilization by measuring plasma glyctierol concentrations during the one hour post-exercise recovery period following three difference exercise bouts. On four different days, exercise trained men (n=12; 23.7±1.1 years) either rested quietly or performed aerobic cycle exercise (60 min at 70% heart rate reserve), 60 s cycle sprints at 100% max wattage obtained during graded exercise testing (GXT) - a total of five, or 15 s cycle sprints at 200% max wattage obtained during GXT - a total of 10. Blood was collected before and at 1, 30 and 60 min post-exercise. Haematocrit and haemoglobin were measured to correct for changes in plasma volume. Glycerol was analysed in plasma and the area under the curve was calculated. Glycerol increased across time (P<0.0001) from pre-exercise (8.4±0.3 μg/dl) to 1 min (13.1±0.7 μg/dl), 30 min (11.3±0.6 μg/dl) and 60 min (9.1±0.5 μg/dl) post-exercise, with 1 min and 30 min post-exercise greater than pre-exercise and 60 min post-exercise (P<0.05). Area under the curve was greater (P=0.0004) for aerobic exercise (24.7±2.0 μg/dl/h), 60 second sprints (23.4±1.9 μg/dl/h) and 15 sec sprints (24.4±1.5 μg/dl/h), as compared to rest (15.3±0.8 μg/dl/h), with no differences noted between exercise bouts (P≯0.05). All exercise bouts increase circulating glycerol, with no differences noted between bouts. Although previous data indicate that low intensity aerobic exercise results in greater fat oxidation than high intensity exercise (when assessed during the actual exercise session), our findings suggest that high intensity exercise may result in similar fat oxidation/mobilization as compared to aerobic exercise during the acute post-exercise period.

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