The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Steven L. Britton - One of the best experts 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, 2020Co-Authors: Sira Karvinen, Steven L. Britton, Haihui Zhuang, Xiaobo Zhang, Xiaowei Ojanen, Timo Tormakangas, Vidya Velagapudi, Markku Alen, Lauren M Koch, Heikki KainulainenAbstract: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, 2019Co-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 ThyfaultAbstract:: 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, 2017Co-Authors: Henry J Thompson, Lauren G. Koch, Steven L. Britton, Elizabeth S. Neil, Lee W. Jones, John N McginleyAbstract: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, 2017Co-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 BurgessAbstract: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.
-
High Aerobic Capacity Mitigates Changes in the Plasma Metabolomic Profile Associated with Aging.
Journal of Proteome Research, 2016Co-Authors: Oluyemi S. Falegan, Lauren G. Koch, Steven L. Britton, Hans J. Vogel, Dustin S. Hittel, Russ. T. Hepple, Jane ShearerAbstract:Advancing age is associated with declines in maximal oxygen consumption. Declines in Aerobic Capacity not only contribute to the aging process but also are an independent risk factor for morbidity, cardiovascular disease, and all-cause mortality. Although statistically convincing, the relationships between Aerobic Capacity, aging, and disease risk remain largely unresolved. To this end, we employed sensitive, system-based metabolomics approach to determine whether enhanced Aerobic Capacity could mitigate some of the changes seen in the plasma metabolomic profile associated with aging. Metabolomic profiles of plasma samples obtained from young (13 month) and old (26 month) rats bred for low (LCR) or high (HCR) running Capacity using proton nuclear magnetic resonance spectroscopy (1H NMR) were examined. Results demonstrated strong profile separation in old and low Aerobic Capacity rats, whereas young and high Aerobic Capacity rat models were less predictive. Significantly differential metabolites between th...
Tim Takken - One of the best experts 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, 2012Co-Authors: Tjerk Munsterman, Tim Takken, Harriët WittinkAbstract: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, 2010Co-Authors: Olaf Verschuren, Tim TakkenAbstract: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, 2008Co-Authors: Raoul H H Engelbert, Martine Plantinga, Frank R Van Genderen, Marijke Van Den Berg, Paul J M Helders, Tim TakkenAbstract: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 - One of the best experts on this subject based on the ideXlab platform.
-
intrinsic high Aerobic Capacity in male rats protects against diet induced insulin resistance
Endocrinology, 2019Co-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 ThyfaultAbstract:: 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, 2017Co-Authors: Henry J Thompson, Lauren G. Koch, Steven L. Britton, Elizabeth S. Neil, Lee W. Jones, John N McginleyAbstract: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, 2017Co-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 BurgessAbstract: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.
-
High Aerobic Capacity Mitigates Changes in the Plasma Metabolomic Profile Associated with Aging.
Journal of Proteome Research, 2016Co-Authors: Oluyemi S. Falegan, Lauren G. Koch, Steven L. Britton, Hans J. Vogel, Dustin S. Hittel, Russ. T. Hepple, Jane ShearerAbstract:Advancing age is associated with declines in maximal oxygen consumption. Declines in Aerobic Capacity not only contribute to the aging process but also are an independent risk factor for morbidity, cardiovascular disease, and all-cause mortality. Although statistically convincing, the relationships between Aerobic Capacity, aging, and disease risk remain largely unresolved. To this end, we employed sensitive, system-based metabolomics approach to determine whether enhanced Aerobic Capacity could mitigate some of the changes seen in the plasma metabolomic profile associated with aging. Metabolomic profiles of plasma samples obtained from young (13 month) and old (26 month) rats bred for low (LCR) or high (HCR) running Capacity using proton nuclear magnetic resonance spectroscopy (1H NMR) were examined. Results demonstrated strong profile separation in old and low Aerobic Capacity rats, whereas young and high Aerobic Capacity rat models were less predictive. Significantly differential metabolites between th...
-
Role of intrinsic Aerobic Capacity and ventilator-induced diaphragm dysfunction
Journal of Applied Physiology, 2015Co-Authors: Kurt J. Sollanek, Lauren G. Koch, Steven L. Britton, Ashley J. Smuder, Michael P. Wiggs, Aaron B. Morton, Scott K. PowersAbstract:Prolonged mechanical ventilation (MV) leads to rapid diaphragmatic atrophy and contractile dysfunction, which is collectively termed “ventilator-induced diaphragm dysfunction” (VIDD). Interestingly, endurance exercise training prior to MV has been shown to protect against VIDD. Further, recent evidence reveals that sedentary animals selectively bred to possess a high Aerobic Capacity possess a similar skeletal muscle phenotype to muscles from endurance trained animals. Therefore, we tested the hypothesis that animals with a high intrinsic Aerobic Capacity would naturally be afforded protection against VIDD. To this end, animals were selectively bred over 33 generations to create two divergent strains, differing in Aerobic Capacity: high-Capacity runners (HCR) and low-Capacity runners (LCR). Both groups of animals were subjected to 12 h of MV and compared with nonventilated control animals within the same strains. As expected, contrasted to LCR animals, the diaphragm muscle from the HCR animals contained higher levels of oxidative enzymes (e.g., citrate synthase) and antioxidant enzymes (e.g., superoxide dismutase and catalase). Nonetheless, compared with nonventilated controls, prolonged MV resulted in significant diaphragmatic atrophy and impaired diaphragm contractile function in both the HCR and LCR animals, and the magnitude of VIDD did not differ between strains. In conclusion, these data demonstrate that possession of a high intrinsic Aerobic Capacity alone does not afford protection against VIDD. Importantly, these results suggest that endurance exercise training differentially alters the diaphragm phenotype to resist VIDD. Interestingly, levels of heat shock protein 72 did not differ between strains, thus potentially representing an important area of difference between animals with intrinsically high Aerobic Capacity and exercise-trained animals.
Ulrik Wisloff - One of the best experts on this subject based on the ideXlab platform.
-
Aerobic Capacity dependent differences in cardiac gene expression
Physiological Genomics, 2008Co-Authors: Mette Langaas, Lauren G. Koch, Steven L. Britton, Morten A Hoydal, Ole J Kemi, Garrett Heinrich, Sonia M Najjar, Oyvind Ellingsen, Ulrik WisloffAbstract:Aerobic Capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn Aerobic Capacity and cardiac gene expression we examined genome-wide gene expression in hearts of rats artificially selected for high and low running Capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in human, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in these animals. Left ventricle gene expression of both sedentary and exercise-trained HCR and LCR was characterized by microarray and gene ontology analysis. Out of 28,000 screened genes, 1,540 were differentially expressed between sedentary HCR and LCR. Only one gene was found differentially expressed by exercise training, but this gene had unknown name and function. Sedentary HCR expressed higher amounts of genes involved in lipid metabolism, whereas sedentary LCR expressed higher amounts of the genes involved in glucose metabolism. This suggests a switch in cardiac energy substrate utilization from normal mitochondrial fatty acid β-oxidation in HCR to carbohydrate metabolism in LCR, an event that often occurs in diseased hearts. LCR were also associated with pathological growth signaling and cellular stress. Hypoxic conditions seemed to be a common source for several of these observations, triggering hypoxia-induced alterations of transcription. In conclusion, inborn high vs. low Aerobic Capacity was associated with differences in cardiac energy substrate, growth signaling, and cellular stress.
-
cardiovascular risk factors emerge after artificial selection for low Aerobic Capacity
Science, 2005Co-Authors: Ulrik Wisloff, Lauren G. Koch, Sonia M Najjar, Oyvind Ellingsen, Per Magnus Haram, Steven J Swoap, Qusai Y Alshare, Mats A Fernstrom, Khadijeh Rezaei, Steven L. BrittonAbstract:In humans, the strong statistical association between fitness and survival suggests a link between impaired oxygen metabolism and disease. We hypothesized that artificial selection of rats based on low and high intrinsic exercise Capacity would yield models that also contrast for disease risk. After 11 generations, rats with low Aerobic Capacity scored high on cardiovascular risk factors that constitute the metabolic syndrome. The decrease in Aerobic Capacity was associated with decreases in the amounts of transcription factors required for mitochondrial biogenesis and in the amounts of oxidative enzymes in skeletal muscle. Impairment of mitochondrial function may link reduced fitness to cardiovascular and metabolic disease.
Els Chm Van Den Ende - One of the best experts on this subject based on the ideXlab platform.
-
dynamic exercise programs Aerobic Capacity and or muscle strength training in patients with rheumatoid arthritis
Cochrane Database of Systematic Reviews, 2009Co-Authors: Emalie J Hurkmans, Florus Van Der Giesen, Thea Vliet P M Vlieland, Jan W Schoones, Els Chm Van Den EndeAbstract:Background An up-to-date overview of the effectiveness and safety of dynamic exercise therapy (exercise therapy with a sufficient intensity, duration, and frequency to establish improvement in Aerobic Capacity and/or muscle strength) is lacking. Objectives To assess the effectiveness and safety of short-term ( three months) dynamic exercise therapy programs (Aerobic Capacity and/or muscle strength training), either land or water-based, for people with RA. To do this we updated a previous Cochrane review (van den Ende 1998) and made categories for the different forms of dynamic exercise programs. Search methods A literature search (to December 2008) within various databases was performed in order to identify randomised controlled trials (RCTs). Selection criteria RCTs that included an exercise program fulfilling the following criteria were selected: a) frequency at least twice weekly for > 20 minutes; b) duration > 6 weeks; c) Aerobic exercise intensity > 55% of the maximum heart rate and/or muscle strengthening exercises starting at 30% to 50% of one repetition maximum; and d) performed under supervision. Moreover, the RCT included one or more of the following outcome measures: functional ability, Aerobic Capacity, muscle strength, pain, disease activity or radiological damage. Data collection and analysis Two review authors independently selected eligible studies, rated the methodological quality, and extracted data. A qualitative analysis (best-evidence synthesis) was performed and, where appropriate, a quantitative data analysis (pooled effect sizes). Main results In total, eight studies were included in this updated review (two additional studies). Four of the eight studies fulfilled at least 8/10 methodological criteria. In this updated review four different dynamic exercise programs were found: (1) short-term, land-based Aerobic Capacity training, which results show moderate evidence for a positive effect on Aerobic Capacity (pooled effect size 0.99 (95% CI 0.29 to 1.68). (2) short-term, land-based Aerobic Capacity and muscle strength training, which results show moderate evidence for a positive effect on Aerobic Capacity and muscle strength (pooled effect size 0.47 (95% CI 0.01 to 0.93). (3) short-term, water-based Aerobic Capacity training, which results show limited evidence for a positive effect on functional ability and Aerobic Capacity. (4) long-term, land-based Aerobic Capacity and muscle strength training, which results show moderate evidence for a positive effect on Aerobic Capacity and muscle strength. With respect to safety, no deleterious effects were found in any of the included studies. Authors' conclusions Based on the evidence, Aerobic Capacity training combined with muscle strength training is recommended as routine practice in patients with RA.
