scholarly journals ARCAgRP/NPY Neuron Activity Is Required for Acute Exercise-Induced Food Intake in Un-Trained Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Wyatt Bunner ◽  
Taylor Landry ◽  
Brenton Thomas Laing ◽  
Peixin Li ◽  
Zhijian Rao ◽  
...  
Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1941 ◽  
Author(s):  
Christopher Gustafson ◽  
Nigina Rakhmatullaeva ◽  
Safiya Beckford ◽  
Ajai Ammachathram ◽  
Alexander Cristobal ◽  
...  

Acute exercise can induce either a compensatory increase in food intake or a reduction in food intake, which results from appetite suppression in the post-exercise state. The timing of food choice—choosing for immediate or later consumption—has been found to influence the healthfulness of foods consumed. To examine both of these effects, we tested in our study whether the timing of food choice interacts with exposure to exercise to impact food choices such that choices would differ when made prior to or following an exercise bout. Visitors to a university recreational center were equipped with an accelerometer prior to their habitual workout regime, masking the true study purpose. As a reward, participants were presented with a snack for consumption after workout completion. Participants made their snack choice from either an apple or chocolate brownie after being pseudo-randomly assigned to choose prior to (“before”) or following workout completion (“after”). Complete data were available for 256 participants (54.7% male, 22.1 ± 3.1 years, 24.7 ± 3.7 kg/m2) who exercised 65.3 ± 22.5 min/session. When compared with “before,” the choice of an apple decreased (73.7% vs. 54.6%) and the choices of brownie (13.9% vs. 20.2%) or no snack (12.4% vs. 25.2%) increased in the “after” condition (χ2 = 26.578, p < 0.001). Our results provide support for both compensatory eating and exercise-induced anorexia. More importantly, our findings suggest that the choice of food for post-exercise consumption can be altered through a simple behavioral intervention.


2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.


2015 ◽  
Vol 308 (9) ◽  
pp. C710-C719 ◽  
Author(s):  
Anna Vainshtein ◽  
Liam D. Tryon ◽  
Marion Pauly ◽  
David A. Hood

Regular exercise leads to systemic metabolic benefits, which require remodeling of energy resources in skeletal muscle. During acute exercise, the increase in energy demands initiate mitochondrial biogenesis, orchestrated by the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Much less is known about the degradation of mitochondria following exercise, although new evidence implicates a cellular recycling mechanism, autophagy/mitophagy, in exercise-induced adaptations. How mitophagy is activated and what role PGC-1α plays in this process during exercise have yet to be evaluated. Thus we investigated autophagy/mitophagy in muscle immediately following an acute bout of exercise or 90 min following exercise in wild-type (WT) and PGC-1α knockout (KO) animals. Deletion of PGC-1α resulted in a 40% decrease in mitochondrial content, as well as a 25% decline in running performance, which was accompanied by severe acidosis in KO animals, indicating metabolic distress. Exercise induced significant increases in gene transcripts of various mitochondrial (e.g., cytochrome oxidase subunit IV and mitochondrial transcription factor A) and autophagy-related (e.g., p62 and light chain 3) genes in WT, but not KO, animals. Exercise also resulted in enhanced targeting of mitochondria for mitophagy, as well as increased autophagy and mitophagy flux, in WT animals. This effect was attenuated in the absence of PGC-1α. We also identified Niemann-Pick C1, a transmembrane protein involved in lysosomal lipid trafficking, as a target of PGC-1α that is induced with exercise. These results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α. Anna Vainshtein received the AJP-Cell 2015 Paper of the Year award. Listen to a podcast with Anna Vainshtein and coauthor David A. Hood at http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/ .


2016 ◽  
Vol 88 (1) ◽  
pp. 15-25 ◽  
Author(s):  
Tegan E. Kastelein ◽  
Cheyne E. Donges ◽  
Amy E. Mendham ◽  
Rob Duffield

Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle


1999 ◽  
Vol 276 (1) ◽  
pp. E118-E124 ◽  
Author(s):  
S. M. Phillips ◽  
K. D. Tipton ◽  
A. A. Ferrando ◽  
R. R. Wolfe

We examined the effect of resistance training on the response of mixed muscle protein fractional synthesis (FSR) and breakdown rates (FBR) by use of primed constant infusions of [2H5]phenylalanine and [15N]phenylalanine, respectively, to an isolated bout of pleiometric resistance exercise. Trained subjects, who were performing regular resistance exercise (trained, T; n = 6), were compared with sedentary, untrained controls (untrained, UT; n = 6). The exercise test consisted of 10 sets (8 repetitions per set) of single-leg knee flexion (i.e., pleiometric muscle contraction during lowering) at 120% of the subjects’ predetermined single-leg 1 repetition maximum. Subjects exercised one leg while their contralateral leg acted as a nonexercised (resting) control. Exercise resulted in an increase, above resting, in mixed muscle FSR in both groups (UT: rest, 0.036 ± 0.002; exercise, 0.0802 ± 0.01; T: rest, 0.045 ± 0.004; exercise, 0.067 ± 0.01; all values in %/h; P< 0.01). In addition, exercise resulted in an increase in mixed muscle FBR of 37 ± 5% (rest, 0.076 ± 0.005; exercise, 0.105 ± 0.01; all values in %/h; P < 0.01) in the UT group but did not significantly affect FBR in the T group. The resulting muscle net balance (FSR − FBR) was negative throughout the protocol ( P < 0.05) but was increased in the exercised leg in both groups ( P < 0.05). We conclude that pleiometric muscle contractions induce an increase in mixed muscle protein synthetic rate within 4 h of completion of an exercise bout but that resistance training attenuates this increase. A single bout of pleiometric muscle contractions also increased the FBR of mixed muscle protein in UT but not in T subjects.


2014 ◽  
Vol 6 (2) ◽  
pp. 29-34
Author(s):  
Nirmala Limbu ◽  
Ramanjan Sinha ◽  
Meenakshi Sinha ◽  
Bishnu Hari Paudel

Objective: We aimed to investigate how EEG frequency bands change in females in response to acute exercise compared to males.Methods: Consenting healthy adult females (n=15) & males (n=15) bicycled an ergometer at 50% HRmax for 20 min. EEG was recorded using 10-20 system from mid-frontal (F4 & F3), central (C4 & C3), parietal (P4 & P3), temporal (T4 & T3) & occipital (O2 & O1) regions. Exercise-induced EEG changes were compared between two sexes by Mann Whitney test. EEG power (μV2) is presented as median & interquartile range.Results: In females, as compared to males, resting right side delta, alpha, and beta activities were more in almost all recorded sites [delta: F4= 49.82 (44.23-63.56) vs. 35.5 (32.70-44.44), p < 0.001; etc], [alpha F4: 127.62 (112.89-149.03) vs. 49.36 (46.37-52.98), p < 0.001; etc], [beta F4= 18.96 (15.83-25.38)  vs. 14.77 (10.34-17.55), p < 0.05; C4= 21.16 (18.4-25.9) vs. 15.48 (9.66-19.40), p < 0.01; etc]. Similarly, females resting right theta activity was more in parietal [P4= 33.04 (25.1-42.41) vs. 22.3 (18.36-34.33), p < 0.05] & occipital [O2= 50.81 (30.64-66.8) vs. 26.85 (22.18-34.42), p < 0.001] regions than in males. They had similar picture on the left side also. The delta values of right alpha power was less in female in frontal [F4= -11.61 (-45.24 -3.64) vs. 9.48 (1.05-16.58), p < 0.01] and central [C4= -72 (-32.98-9.48) vs. 22.69 (13.03-33.05), p < 0.01] regions compared to males. Also, they had less delta values of left central alpha [C3= -8.32 (-32.65-6.1) vs. 16.5 (0.36-36.36), p < 0.01] and temporal beta [T3= -6.29 (-10.09- -1.49) vs. 1.24 (-0.84- 2.8), p < 0.001] power compared to males.Conclusion: At rest females may have high EEG powers in different bands. In response to acute exercise, they respond in reverse way as compared to males.DOI: http://dx.doi.org/10.3126/ajms.v6i2.11116Asian Journal of Medical Sciences Vol.6(2) 2015 30-35


2001 ◽  
Vol 91 (3) ◽  
pp. 1099-1104 ◽  
Author(s):  
François Désy ◽  
Yan Burelle ◽  
Patrice Bélanger ◽  
Marielle Gascon-Barré ◽  
Jean-Marc Lavoie

The present study was conducted to examine the effect of a single bout of exercise (rodent treadmill, 60 min at 26 m/min, 0% grade) on the gluconeogenic activity of periportal hepatocytes (PP-H) and perivenous hepatocytes (PV-H) in fasted (18 h) rats. Isolated PP-H and PV-H, obtained by selective destruction following liver perfusion with digitonin and collagenase, were incubated with saturating concentrations of alanine (Ala; 20 mM) or a mixture of lactate and pyruvate (Lac+Pyr; 20:2 mM) to determine the glucose production flux ( J glucose) in the incubation medium. Results show that, in the resting conditions, J glucose from all exogenous substrates was significantly higher ( P < 0.01) in PP-H than in PV-H. Exercise, compared with rest, resulted in a higher J glucose ( P < 0.01) from Lac+Pyr substrate in the PV-H but not in the PP-H, resulting in the disappearance of the difference in J glucosebetween PP-H and PV-H. Exercise, compared with rest, led to a higher J glucose ( P < 0.01) from Ala substrate in both PP-H and PV-H. However, the exercise-induced increase in J glucose (gluconeogenic activity) from Ala substrate was higher in PV-H than in PP-H, resulting, as from Lac+Pyr substrate, in the disappearance ( P > 0.05) of the difference of J glucose between PP-H and PV-H. It is concluded that exercise differentially stimulates the gluconeogenic activity of PV-H to a larger extent than PP-H, indicative of a heterogenous metabolic response of hepatocytes to exercise.


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