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Aerobic Capacity

The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform

Steven L. Britton – 1st expert on this subject based on the ideXlab platform

  • interactive effects of aging and Aerobic Capacity on energy metabolism related metabolites of serum skeletal muscle and white adipose tissue
    bioRxiv, 2020
    Co-Authors: Sira Karvinen, Steven L. Britton, Haihui Zhuang, Xiaobo Zhang, Xiaowei Ojanen, Timo Tormakangas, Vidya Velagapudi, Markku Alen, Lauren M Koch, Heikki Kainulainen

    Abstract:

    Aerobic Capacity is a strong predictor of longevity. With aging, Aerobic Capacity decreases concomitantly with changes in whole body metabolism leading to increased disease risk. To address the role of Aerobic Capacity, aging and their interaction on metabolism, we utilized rat models of low and high intrinsic Aerobic Capacity (LCRs/HCRs) and assessed the metabolomics of serum, muscle, and white adipose tissue (WAT). We compared LCRs and HCRs at two time points: Young rats were sacrificed at 9 months, and old rats were sacrificed at 21 months. Targeted and semi-quantitative metabolomics analysis was performed on ultra-pressure Liquid Chromatography Tandem Mass Spectrometry (UPLC-MS) platform. Interaction of Aerobic Capacity and aging was studied via regression analysis. Our results showed at young age, metabolites linked to amino acid metabolism differed in serum and muscle with Aerobic Capacity, whereas no difference were observed in WAT. In aged animals, most prominent changes in metabolites occurred in WAT. Aerobic Capacity and aging interactively affected seven metabolites linked to energy metabolism. Our results support previous findings that high Aerobic Capacity is associated with more efficient amino acid metabolism in muscle. While impaired branched chain amino acids (BCAAs) and fatty acid metabolism in the muscle may associate to the high risk of metabolic disorders and shorter lifespan previously observed in LCRs. The interactive effects of aging and Aerobic Capacity on energy metabolism-related metabolites were largely driven by HCRs, reflecting the importance of inherited Aerobic Capacity in the aging process. Our results highlight that dysfunctional mitochondrial {beta}-oxidation in WAT may be one key mechanism related to aging.

  • intrinsic high Aerobic Capacity in male rats protects against diet induced insulin resistance
    Endocrinology, 2019
    Co-Authors: Matthew E Morris, Lauren G. Koch, Steven L. Britton, Grace M Meers, Gregory N Ruegsegger, Umesh D Wankhade, Tommy Robinson, Scott R Rector, Kartik Shankar, John P Thyfault

    Abstract:

    : Low Aerobic Capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic Aerobic Capacity, that is, high-Capacity running (HCR) and low-Capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in Aerobic Capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic Aerobic Capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative Capacity, gene expression profile, and transcriptional adaptations to an HFD.

  • Inherent Aerobic Capacity-dependent differences in breast carcinogenesis
    Carcinogenesis, 2017
    Co-Authors: Henry J Thompson, Lee W. Jones, Lauren G. Koch, Steven L. Britton, Elizabeth S. Neil, John N Mcginley

    Abstract:

    Although regular physical activity is associated with improvement in Aerobic Capacity and lower breast cancer risk, there are heritable sets of traits that affect improvement in Aerobic Capacity in response to physical activity. Although Aerobic Capacity segregates risk for a number of chronic diseases, the effect of the heritable component on cancer risk has not been evaluated. Therefore, we investigated breast carcinogenesis in rodent models of heritable fitness in the absence of induced physical activity. Female offspring of N:NIH rats selectively bred for low (LIAC) or high (HIAC) inherent Aerobic Capacity were injected intraperitoneally with 1-methyl-1-nitrosurea (70 mg/kg body wt). At study termination 33 weeks post-carcinogen, cancer incidence (14.0 versus 47.3%; P < 0.001) and multiplicity (0.18 versus 0.85 cancers per rat; P < 0.0001) were significantly decreased in HIAC versus LIAC rats, respectively. HIAC had smaller visceral and subcutaneous body fat depots than LIAC and activity of two proteins that regulated the mammalian target of rapamycin, protein kinase B (Akt), and adenosine monophosphate-activated protein kinase were suppressed and activated, respectively, in HIAC. Although many factors distinguish between HIAC and LIAC, it appears that the protective effect of HIAC against breast carcinogenesis is mediated, at least in part, via alterations in core metabolic signaling pathways deregulated in the majority of human breast cancers.

Tim Takken – 2nd expert on this subject based on the ideXlab platform

  • Are persons with rheumatoid arthritis deconditioned? A review of physical activity and Aerobic Capacity
    BMC Musculoskeletal Disorders, 2012
    Co-Authors: Tjerk Munsterman, Tim Takken, Harriët Wittink

    Abstract:

    Background: Although the general assumption is that patients with rheumatoid arthritis (RA) have decreased levels of physical activity, no review has addressed whether this assumption is correct. Methods: Our objective was to systematically review the literature for physical activity levels and Aerobic Capacity (VO2max). in patients with (RA), compared to healthy controls and a reference population. Studies investigating physical activity, energy expenditure or Aerobic Capacity in patients with RA were included. Twelve studies met our inclusion criteria. Results: In one study that used doubly labeled water, the gold standard measure, physical activity energy expenditure of patients with RA was significantly decreased. Five studies examined Aerobic Capacity. Contradictory evidence was found that patients with RA have lower VO2max than controls, but when compared to normative values, patients scored below the 10 th percentile. In general, it appears that patients with RA spend more time in light and moderate activities and less in vigorous activities than controls. Conclusion: Patients with RA appear to have significantly decreased energy expenditure, very low Aerobic Capacity compared to normative values and spend less time in vigorous activities than controls.

  • Aerobic Capacity in children and adolescents with cerebral palsy
    Research in Developmental Disabilities, 2010
    Co-Authors: Olaf Verschuren, Tim Takken

    Abstract:

    Abstract This study described the Aerobic Capacity [VO2peak (ml/kg/min)] in contemporary children and adolescents with cerebral palsy (CP) using a maximal exercise test protocol. Twenty-four children and adolescents with CP classified at Gross Motor Functional Classification Scale (GMFCS) level I or level II and 336 typically developing children were included. All children performed a progressive exercise test on a treadmill with respiratory gas-exchange analysis. The results are compared with normative values for age and gender-matched controls. Aerobic Capacity of children and adolescents with CP, who are classified at GMFCS level I or II was significantly lower than that of typically developing controls. Especially in girls with CP, the Aerobic Capacity deteriorated with age. The Aerobic Capacity of contemporary children and adolescents with CP, who are classified at GMFCS level I or II is significantly lower than that of typically developing controls.

  • Aerobic Capacity in children with hemophilia
    The Journal of Pediatrics, 2008
    Co-Authors: Raoul H H Engelbert, Martine Plantinga, Frank R Van Genderen, Marijke Van Den Berg, Paul J M Helders, Tim Takken

    Abstract:

    Objective To determine whether Aerobic Capacity is normal in boys with different types of hemophilia compared with healthy peers and whether the level of Aerobic Capacity correlates with the amount of physical activity, joint health status, muscle strength, and anthropometrics. Study design 47 patients (mean [SD] age, 12.9 [3.2] years; age range, 8.2-17.4 years) from the “Van Creveldkliniek” of the University Medical Center Utrecht, participated. Anthropometry, muscle strength, joint impairment, functional ability, and Aerobic Capacity were measured. The amount of energy expenditure during daily living was assessed. Results All boys were able to perform at maximal or near-maximal level on exercise tests, and none of them reported bleeds or other adverse events. Relative peak oxygen, peak heart rate, and peak working capaicty were significantly lower compared with healthy control subjects. 30% had Z-scores >2 for weight. Total muscle strength was normal, and almost no joint impairment and no decrease in functional ability were found. Conclusion The Aerobic Capacity of children with hemophilia is still lower than the normal population, whereas their overall muscle strength is comparable with healthy peers. The functional ability does not differ from healthy peers, and joint health status showed very minor impairments. A substantial proportion of Dutch children with hemophilia was overweight, without showing a reduction in the amount of self-reported physical activities.

Lauren G. Koch – 3rd expert on this subject based on the ideXlab platform

  • intrinsic high Aerobic Capacity in male rats protects against diet induced insulin resistance
    Endocrinology, 2019
    Co-Authors: Matthew E Morris, Lauren G. Koch, Steven L. Britton, Grace M Meers, Gregory N Ruegsegger, Umesh D Wankhade, Tommy Robinson, Scott R Rector, Kartik Shankar, John P Thyfault

    Abstract:

    : Low Aerobic Capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic Aerobic Capacity, that is, high-Capacity running (HCR) and low-Capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in Aerobic Capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic Aerobic Capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative Capacity, gene expression profile, and transcriptional adaptations to an HFD.

  • Inherent Aerobic Capacity-dependent differences in breast carcinogenesis
    Carcinogenesis, 2017
    Co-Authors: Henry J Thompson, Lee W. Jones, Lauren G. Koch, Steven L. Britton, Elizabeth S. Neil, John N Mcginley

    Abstract:

    Although regular physical activity is associated with improvement in Aerobic Capacity and lower breast cancer risk, there are heritable sets of traits that affect improvement in Aerobic Capacity in response to physical activity. Although Aerobic Capacity segregates risk for a number of chronic diseases, the effect of the heritable component on cancer risk has not been evaluated. Therefore, we investigated breast carcinogenesis in rodent models of heritable fitness in the absence of induced physical activity. Female offspring of N:NIH rats selectively bred for low (LIAC) or high (HIAC) inherent Aerobic Capacity were injected intraperitoneally with 1-methyl-1-nitrosurea (70 mg/kg body wt). At study termination 33 weeks post-carcinogen, cancer incidence (14.0 versus 47.3%; P < 0.001) and multiplicity (0.18 versus 0.85 cancers per rat; P < 0.0001) were significantly decreased in HIAC versus LIAC rats, respectively. HIAC had smaller visceral and subcutaneous body fat depots than LIAC and activity of two proteins that regulated the mammalian target of rapamycin, protein kinase B (Akt), and adenosine monophosphate-activated protein kinase were suppressed and activated, respectively, in HIAC. Although many factors distinguish between HIAC and LIAC, it appears that the protective effect of HIAC against breast carcinogenesis is mediated, at least in part, via alterations in core metabolic signaling pathways deregulated in the majority of human breast cancers.

  • Aerobic Capacity mediates susceptibility for the transition from steatosis to steatohepatitis
    The Journal of Physiology, 2017
    Co-Authors: Matthew E Morris, Lauren G. Koch, Steven L. Britton, Colin S Mccoin, Julie Allen, Michelle L Gastecki, Justin A Fletcher, Xiaorong Fu, Wen Xing Ding, Shawn C Burgess

    Abstract:

    KEY POINTS: Low intrinsic Aerobic Capacity is associated with increased all-cause and liver-related mortality in humans. Low intrinsic Aerobic Capacity in the low Capacity runner (LCR) rat increases susceptibility to acute and chronic high-fat/high-sucrose diet-induced steatosis, without observed increases in liver inflammation. Addition of excess cholesterol to a high-fat/high-sucrose diet produced greater steatosis in LCR and high Capacity runner (HCR) rats. However, the LCR rat demonstrated greater susceptibility to increased liver inflammatory and apoptotic markers compared to the HCR rat. The progressive non-alcoholic fatty liver disease observed in the LCR rats following western diet feeding was associated with further declines in liver fatty acid oxidation and mitochondrial respiratory Capacity compared to HCR rats. ABSTRACT: Low Aerobic Capacity increases risk for non-alcoholic fatty liver disease and liver-related disease mortality, but mechanisms mediating these effects remain unknown. We recently reported that rats bred for low Aerobic Capacity (low Capacity runner; LCR) displayed susceptibility to high fat diet-induced steatosis in association with reduced hepatic mitochondrial fatty acid oxidation (FAO) and respiratory Capacity compared to high Aerobic Capacity (high Capacity runner; HCR) rats. Here we tested the impact of Aerobic Capacity on susceptibility for progressive liver disease following a 16-week ‘western diet’ (WD) high in fat (45% kcal), cholesterol (1% w/w) and sucrose (15% kcal). Unlike previously with a diet high in fat and sucrose alone, the inclusion of cholesterol in the WD induced hepatomegaly and steatosis in both HCR and LCR rats, while producing greater cholesterol ester accumulation in LCR compared to HCR rats. Importantly, WD-fed low-fitness LCR rats displayed greater inflammatory cell infiltration, serum alanine transaminase, expression of hepatic inflammatory markers (F4/80, MCP-1, TLR4, TLR2 and IL-1β) and effector caspase (caspase 3 and 7) activation compared to HCR rats. Further, LCR rats had greater WD-induced decreases in complete FAO and mitochondrial respiratory Capacity. Intrinsic Aerobic Capacity had no impact on WD-induced hepatic steatosis; however, rats bred for low Aerobic Capacity developed greater hepatic inflammation, which was associated with reduced hepatic mitochondrial FAO and respiratory Capacity and increased accumulation of cholesterol esters. These results confirm epidemiological reports that Aerobic Capacity impacts progression of liver disease and suggest that these effects are mediated through alterations in hepatic mitochondrial function.