Genetics of the Adaptation to Exercise

2011 ◽  
pp. 144-149
Author(s):  
Theodore J. Angelopoulos ◽  
Joshua Lowndes ◽  
Richard L. Seip
Keyword(s):  
Adaptation To Exercise

scholarly journals Molecular Mechanisms Underlying Cardiac Adaptation to Exercise

2017 ◽  
Vol 25 (5) ◽  
pp. 1012-1026 ◽  
Author(s):  
Rick B. Vega ◽  
John P. Konhilas ◽  
Daniel P. Kelly ◽  
Leslie A. Leinwand
Keyword(s):  
Molecular Mechanisms ◽  
Cardiac Adaptation ◽  
Adaptation To Exercise

Early postnatal overnutrition impairs VO2max gains with moderate exercise and increase post-exercise muscle damage in adult male rats

2021 ◽  
pp. 1-5
Author(s):  
Douglas Lopes Almeida ◽  
Gabriel Sergio Fabricio ◽  
Laize Peron Tófolo ◽  
Tatiane Aparecida Ribeiro ◽  
Camila Cristina Ianoni Matiusso ◽  
...  
Keyword(s):  
Early Life ◽  
Male Rats ◽  
Moderate Intensity ◽  
Moderate Exercise ◽  
Moderate Intensity Exercise ◽  
Post Exercise ◽  
Reduced Body ◽  
Male Wistar Rats ◽  
The Impact ◽  
Adaptation To Exercise

Abstract Exercise counteracts obesity effects, but information on how early-life obesity may affect long-term adaptation to exercise is lacking. This study investigates the impact of early-life postnatal overfeeding (PO) on animals’ adaptation to exercise. Only male Wistar rats were used. On postnatal day (PN) 30, rats from control (NL-9 pups) or PO (SL-3 pups) litters were separated into four groups: NL-sedentary (NL-Se), NL-exercised (NL-Ex), SL-sedentary (SL-Se), and SL-exercised (SL-Ex). Exercised groups performed moderate-intensity exercise, running on a treadmill, from PN30 to PN90. Further experiments were carried out between PN90 and PN92. PO promoted obesity in SL versus NL rats (P < 0.05). Exercise reduced body weight (P < 0.001), body fat (P < 0.01), and improved glucose homeostasis in SL-Ex versus SL-Se. SL-Ex presented lower VO2max (P < 0.01) and higher post-exercise LDH (P < 0.05) compared to NL-Ex rats. Although moderate exercise counteracted obesity in SL rats, early-life overnutrition restricts fitness gains in adulthood, indicating that early obesity may impair animals’ adaptation to exercise.

Abstract 431: Mitochondrial Fission in the Heart is an Adaptation to Increased Energetic Demands: The Role of Physiologic Fragmentation

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Michael Coronado ◽  
Giovanni Fajardo ◽  
Kim Nguyen ◽  
Mingming Zhao ◽  
Kristina Bezold Kooiker ◽  
...  
Keyword(s):  
Cell Death ◽  
Exercise Capacity ◽  
Mitochondrial Function ◽  
Adrenergic Receptor ◽  
Mitochondrial Fission ◽  
Physiological Adaptation ◽  
Mitochondrial Fragmentation ◽  
Energetic Demand ◽  
Adaptation To Exercise

Mitochondria play a dual role in the heart, responsible for meeting energetic demands and regulating cell death. Current paradigms hold that mitochondrial fission and fragmentation are the result of pathologic stresses such as ischemia, are an indicator of poor mitochondrial health, and lead to mitophagy and cell death. However, recent studies demonstrate that inhibiting fission also results in cardiac impairment, suggesting that fission is important for maintaining normal mitochondrial function. In this study, we identify a novel role for mitochondrial fragmentation as a normal physiological adaptation to increased energetic demand. Using two models of exercise, we demonstrate that “physiologic” mitochondrial fragmentation occurs, results in enhanced mitochondrial function, and is mediated through beta 1-adrenergic receptor signaling. Similar to pathologic fragmentation, physiologic fragmentation is induced by activation of Drp1; however, unlike pathologic fragmentation, membrane potential is maintained and regulators of mitophagy are downregulated. To confirm the role of fragmentation as a physiological adaptation to exercise, we inhibited the pro-fission mediator Drp1 in mice using the peptide inhibitor P110 and had mice undergo exercise. Mice treated with P110 had significantly decreased exercise capacity, decreased fragmentation and inactive Drp1 vs controls. To further confirm these findings, we generated cardiac-specific Drp1 KO mice and had them undergo exercise. Mice with cardiac specific Drp1 KO had significantly decreased exercise capacity and abnormally large mitochondria compared to controls. These findings indicate the requirement for physiological mitochondrial fragmentation to meet the energetic demands of exercise and support the still evolving conceptual framework, where fragmentation plays a role in the balance between mitochondrial maintenance of normal physiology and response to disease.

Adaptation to exercise: role of hemoglobin affinity for oxygen and 2,3-diphosphoglycerate

1971 ◽  
Vol 30 (6) ◽  
pp. 827-832 ◽  
Author(s):  
S. D. Shappell ◽  
J. A. Murray ◽  
A. J. Bellingham ◽  
R. D. Woodson ◽  
J. C. Detter ◽  
...  
Keyword(s):  
Hemoglobin Affinity For Oxygen ◽  
Adaptation To Exercise

scholarly journals Osteocalcin in the adaptation to exercise

2016 ◽  
Vol 12 (8) ◽  
pp. 434-434 ◽  
Author(s):  
Claire Greenhill
Keyword(s):  
Adaptation To Exercise

scholarly journals Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis

2010 ◽  
Vol 299 (4) ◽  
pp. R1059-R1067 ◽  
Author(s):  
I. Mark Olfert ◽  
Richard A. Howlett ◽  
Peter D. Wagner ◽  
Ellen C. Breen
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Exercise Training ◽  
Metabolic Adaptation ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Running Speed ◽  
Endothelial Growth Factor ◽  
Adaptation To Exercise

We have previously shown, using a Cre-LoxP strategy, that vascular endothelial growth factor (VEGF) is required for the development and maintenance of skeletal muscle capillarity in sedentary adult mice. To determine whether VEGF expression is required for skeletal muscle capillary adaptation to exercise training, gastrocnemius muscle capillarity was measured in myocyte-specific VEGF gene-deleted (mVEGF−/−) and wild-type (WT) littermate mice following 6 wk of treadmill running (1 h/day, 5 days/wk) at the same running speed. The effect of training on metabolic enzyme activity levels and whole body running performance was also evaluated in mVEGF−/− and WT mice. Posttraining capillary density was significantly increased by 59% ( P < 0.05) in the deep muscle region of the gastrocnemius in WT mice but did not change in mVEGF−/− mice. Maximal running speed and time to exhaustion during submaximal running increased by 20 and 13% ( P < 0.05), respectively, in WT mice after training but were unchanged in mVEGF−/− mice. Training led to increases in skeletal muscle citrate synthase (CS) and phosphofructokinase (PFK) activities in both WT and mVEGF−/− mice ( P < 0.05), whereas β-hydroxyacyl-CoA dehydrogenase (β-HAD) activity was increased only in WT mice. These data demonstrate that skeletal muscle capillary adaptation to physical training does not occur in the absence of myocyte-expressed VEGF. However, skeletal muscle metabolic adaptation to exercise training takes place independent of myocyte VEGF expression.

Abstract 165: Saxagliptin Restores Vascular Mitochondrial Exercise Response in Diabetes

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Amy C Keller ◽  
Leslie A Knaub ◽  
Matthew W Miller ◽  
Jane E Reusch
Keyword(s):  
Exercise Intervention ◽  
Cvd Risk ◽  
Dipeptidyl Peptidase 4 ◽  
Gk Rats ◽  
Mitochondrial Complexes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
The Impact ◽  
Mitochondrial Adaptation ◽  
Adaptation To Exercise

Exercise decreases cardiovascular disease (CVD) risk and all-cause mortality. We and others have defined that exercise stimulates mitochondrial biogenesis via upstream signaling through endothelial nitric oxide synthase (eNOS), sirtuins (SIRTs), and/or PPARγ co-activator alpha (PGC1-α). Further, this response is absent in diabetes and hypertension. We tested the hypothesis that pharmacological restoration of vascular signaling with the dipeptidyl peptidase-4 (DPP-4) inhibitor saxagliptin will improve vascular mitochondrial adaptation to exercise through activation of eNOS, SIRTs, and/or PGC1-α. We examined the impact of an 8 day treadmill exercise intervention in the Goto-Kakizaki (GK) rat, a model of lean, type 2 diabetes (T2DM), and Wistar control rats. Four groups were examined: sedentary or exercise groups with or without saxagliptin. Twenty-four hours post-bout, aortas were probed for mitochondrial complexes I-V, as well upstream signaling molecules. In Wistar rats, the expression of mitochondrial complexes III, IV, and V, along with SIRT3 (p<0.05), eNOS, and PCG1-α, increased with exercise. Conversely, in GK animals, exercise led to a decrease of complexes I, III, and IV, a decrease in the expression of COX IV (p<0.05) and AMPK, and no effect on eNOS or SIRT3. In exercised GK rats treated with saxagliptin, the expression of all mitochondrial complexes increased, complex IV significantly (p<0.05). Significant increases (p<0.05) were also observed in cytochrome c, eNOS and nNOS, PGC1-α, and UCP3 protein content in GK rats treated with both exercise and saxagliptin. Body weight and insulin and glucose concentrations were not significantly different in GK animals across experimental groups, indicating that the effects observed are independent of changes in these parameters. In addition, saxagliptin added to a three week exercise intervention improved running time significantly compared to an exercise intervention alone. In summary, our data suggest that saxagliptin restores vascular mitochondrial adaptation to exercise in a rodent model of diabetes. In conclusion, these data are proof of concept of a targetable mitochondrial defect in the diabetic vasculature.

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