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Cells
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Physical Activity and Energy Metabolism in Animal Models
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Physical Activity and Energy Metabolism in Animal Models

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7308

Special Issue Editor

Dr. Julia Brenmoehl

E-Mail Website
Guest Editor
Institute for Genome Biology, Research Institute for Farm Animal Biology (FBN), Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany
Interests: exercise; metabolic diseases; energy metabolism; mitochondria; animal models

Special Issue Information

Dear Colleagues,

Physical inactivity leads to metabolic adaptations and promotes a variety of metabolic diseases, such as obesity, cardiovascular disease, or type II diabetes, which can lead to premature death. On the other hand, physical activity increases energy metabolism and can thus contribute significantly to the maintenance of mental and physical health, and has beneficial effects even in the presence of existing diseases. In this regard, various exercise concepts exist to support metabolic health, ranging from voluntary to forced, moderate- to high-intensity, short- to long-term, and endurance to resistance concepts. Animal models are useful in exploring the positive effects of different training and exercise approaches on energy metabolism, including energy production, storage, and utilization. With them, a holistic view of the effects of exercise on the organism is possible, as well as detailed organ-, metabolite-, hormone-, gene- or even pathway-specific views. In this Special Issue, new findings and insights regarding exercise-related energy metabolism in different animal models are presented, aiming to provide new approaches to efficiently improve metabolic health through exercise and shed light on its relevance for counteracting metabolic disorders. 

Dr. Julia Brenmoehl 
Guest Editor

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Keywords

  • metabolic diseases
  • physical activity
  • animal models
  • energy metabolism

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Published Papers (4 papers)

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Research

22 pages, 3333 KiB  
Article
Exercise Training Differentially Affects Skeletal Muscle Mitochondria in Rats with Inherited High or Low Exercise Capacity
by Estelle Heyne, Susanne Zeeb, Celina Junker, Andreas Petzinna, Andrea Schrepper, Torsten Doenst, Lauren G. Koch, Steven L. Britton and Michael Schwarzer
Cells 2024, 13(5), 393; https://doi.org/10.3390/cells13050393 - 24 Feb 2024
Cited by 1 | Viewed by 1536
Abstract
Exercise capacity has been related to morbidity and mortality. It consists of an inherited and an acquired part and is dependent on mitochondrial function. We assessed skeletal muscle mitochondrial function in rats with divergent inherited exercise capacity and analyzed the effect of exercise [...] Read more.
Exercise capacity has been related to morbidity and mortality. It consists of an inherited and an acquired part and is dependent on mitochondrial function. We assessed skeletal muscle mitochondrial function in rats with divergent inherited exercise capacity and analyzed the effect of exercise training. Female high (HCR)- and low (LCR)-capacity runners were trained with individually adapted high-intensity intervals or kept sedentary. Interfibrillar (IFM) and subsarcolemmal (SSM) mitochondria from gastrocnemius muscle were isolated and functionally assessed (age: 15 weeks). Sedentary HCR presented with higher exercise capacity than LCR paralleled by higher citrate synthase activity and IFM respiratory capacity in skeletal muscle of HCR. Exercise training increased exercise capacity in both HCR and LCR, but this was more pronounced in LCR. In addition, exercise increased skeletal muscle mitochondrial mass more in LCR. Instead, maximal respiratory capacity was increased following exercise in HCRs’ IFM only. The results suggest that differences in skeletal muscle mitochondrial subpopulations are mainly inherited. Exercise training resulted in different mitochondrial adaptations and in higher trainability of LCR. HCR primarily increased skeletal muscle mitochondrial quality while LCR increased mitochondrial quantity in response to exercise training, suggesting that inherited aerobic exercise capacity differentially affects the mitochondrial response to exercise training. Full article
(This article belongs to the Special Issue Physical Activity and Energy Metabolism in Animal Models)
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21 pages, 2126 KiB  
Article
Metabolic Pathway Modeling in Muscle of Male Marathon Mice (DUhTP) and Controls (DUC)—A Possible Role of Lactate Dehydrogenase in Metabolic Flexibility
by Julia Brenmoehl, Elli Brosig, Nares Trakooljul, Christina Walz, Daniela Ohde, Antonia Noce, Michael Walz, Martina Langhammer, Stefan Petkov, Monika Röntgen, Steffen Maak, Christina E. Galuska, Beate Fuchs, Björn Kuhla, Siriluck Ponsuksili, Klaus Wimmers and Andreas Hoeflich
Cells 2023, 12(15), 1925; https://doi.org/10.3390/cells12151925 - 25 Jul 2023
Viewed by 1818
Abstract
In contracting muscles, carbohydrates and fatty acids serve as energy substrates; the predominant utilization depends on the workload. Here, we investigated the contribution of non-mitochondrial and mitochondrial metabolic pathways in response to repeated training in a polygenic, paternally selected marathon mouse model (DUhTP), [...] Read more.
In contracting muscles, carbohydrates and fatty acids serve as energy substrates; the predominant utilization depends on the workload. Here, we investigated the contribution of non-mitochondrial and mitochondrial metabolic pathways in response to repeated training in a polygenic, paternally selected marathon mouse model (DUhTP), characterized by exceptional running performance and an unselected control (DUC), with both lines descended from the same genetic background. Both lines underwent three weeks of high-speed treadmill training or were sedentary. Both lines’ muscles and plasma were analyzed. Muscle RNA was sequenced, and KEGG pathway analysis was performed. Analyses of muscle revealed no significant selection-related differences in muscle structure. However, in response to physical exercise, glucose and fatty acid oxidation were stimulated, lactate dehydrogenase activity was reduced, and lactate formation was inhibited in the marathon mice compared with trained control mice. The lack of lactate formation in response to exercise appears to be associated with increased lipid mobilization from peripheral adipose tissue in DUhTP mice, suggesting a specific benefit of lactate avoidance. Thus, results from the analysis of muscle metabolism in born marathon mice, shaped by 35 years (140 generations) of phenotype selection for superior running performance, suggest increased metabolic flexibility in male marathon mice toward lipid catabolism regulated by lactate dehydrogenase. Full article
(This article belongs to the Special Issue Physical Activity and Energy Metabolism in Animal Models)
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13 pages, 2828 KiB  
Article
Establishment of a Murine Chronic Anorexia Nervosa Model
by Anna Staffeld, Sadaf Gill, Annelie Zimmermann, Natalie Böge, Katharina Schuster, Stephan Lang, Markus Kipp, Rupert Palme and Linda Frintrop
Cells 2023, 12(13), 1710; https://doi.org/10.3390/cells12131710 - 24 Jun 2023
Cited by 2 | Viewed by 1497
Abstract
Anorexia nervosa (AN) is associated with hyperactivity, amenorrhea, and brain atrophy. The underlying pathophysiology is mostly unknown, and new targets for therapeutic interventions are needed. This study aimed to systematically establish a murine AN model with the parameter extent of starvation, animal age, [...] Read more.
Anorexia nervosa (AN) is associated with hyperactivity, amenorrhea, and brain atrophy. The underlying pathophysiology is mostly unknown, and new targets for therapeutic interventions are needed. This study aimed to systematically establish a murine AN model with the parameter extent of starvation, animal age, and length of starvation for functional studies. The activity-based anorexia (ABA) model combines food restriction with running wheel access. Early adolescent and adolescent mice received 40% of their baseline food intake until a 20% or 25% weight reduction was reached (acute starvation). To mimic chronic starvation, body weight loss was maintained for another two weeks. Running activity was examined using wheel sensors, while amenorrhea was investigated by analysis of vaginal smears. Brain sections were used to analyze cerebral cortex volumes. Acute starvation did not lead to either AN-related symptoms, whereas chronic starvation led to hyperactivity and amenorrhea except in the adolescent cohort with 20% weight reduction. Only ABA mice with 25% weight reduction revealed a cortex volume reduction. The optimal parameters to mirror AN-related symptoms included a 25% weight reduction, early adolescent or adolescent mice, and chronic starvation. The ABA model enables functional analysis of the impact of chronic AN on the underlying hormonal, behavioral, and brain pathophysiology. Full article
(This article belongs to the Special Issue Physical Activity and Energy Metabolism in Animal Models)
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16 pages, 3129 KiB  
Article
Effect of Metabolic Adaptation by Voluntary Running Wheel Activity and Aldosterone Inhibition on Renal Function in Female Spontaneously Hypertensive Rats
by Felix Atmanspacher, Rolf Schreckenberg, Annemarie Wolf, Ivica Grgic and Klaus-Dieter Schlüter
Cells 2022, 11(24), 3954; https://doi.org/10.3390/cells11243954 - 7 Dec 2022
Viewed by 1557
Abstract
Metabolic effects of physical activity may be reno-protective in the context of hypertension, although exercise stresses kidneys. Aldosterone participates in renal disease in hypertension, but exercise affects the plasma concentration of aldosterone. This study was designed to evaluate whether physical activity and pharmacological [...] Read more.
Metabolic effects of physical activity may be reno-protective in the context of hypertension, although exercise stresses kidneys. Aldosterone participates in renal disease in hypertension, but exercise affects the plasma concentration of aldosterone. This study was designed to evaluate whether physical activity and pharmacological treatment by aldosterone have additive effects on renal protection in hypertensive rats. Female spontaneously hypertensive rats (SHR) or normotensive Wistar rats performed voluntary running wheel activity alone or in combination with aldosterone blockade (spironolactone). The following groups were studied: young and pre-hypertensive SHR (n = 5 sedentary; n = 10 running wheels, mean body weight 129 g), 10-month-old Wistar rats (n = 6 sedentary; n = 6 running wheels, mean body weight 263 g), 10-month-old SHRs (n = 18 sedentary, mean body weight 224 g; n = 6 running wheels, mean body weight 272 g; n = 6 aldosterone, mean body weight 219 g; n = 6 aldosterone and running wheels, mean body weight 265 g). Another group of SHRs had free access to running wheels for 6 months and kept sedentary for the last 3 months (n = 6, mean body weight 240 g). Aldosterone was given for the last 4 months. SHRs from the running groups had free access to running wheels beginning at the age of 6 weeks. Renal function was analyzed by microalbuminuria (Alb/Cre), urinary secretion of kidney injury molecule-1 (uKim-1), and plasma blood urea nitrogen (BUN) concentration. Molecular adaptation of the kidney to hypertension and its modification by spironolactone and/or exercise were analyzed by real-time PCR, immunoblots, and histology. After six months of hypertension, rats had increased Alb/Cre and BUN but normal uKim-1. Voluntary free running activity normalized BUN but not Alb/Cre, whereas spironolactone reduced Alb/Cre but not BUN. Exercise constitutively increased renal expression of proprotein convertase subtilisin/kexin type 9 (PCSK9; mRNA and protein) and arginase-2 (mRNA). Spironolactone reduced these effects. uKim-1 increased in rats performing voluntary running wheel activity exercise irrespectively of blood pressure and aldosterone blockade. We observed independent but no additive effects of aldosterone blockade and physical activity on renal function and on molecules potentially affecting renal lipid metabolism. Full article
(This article belongs to the Special Issue Physical Activity and Energy Metabolism in Animal Models)
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