1.Introduction The field of exercise science is experiencing a renaissance,with recent research illuminating the molecular,cellular,and systemic effects of physical activity.This is largely due to the now unequivocal ...1.Introduction The field of exercise science is experiencing a renaissance,with recent research illuminating the molecular,cellular,and systemic effects of physical activity.This is largely due to the now unequivocal evidence that a lack of physical activity,not only has direct effects on the prevalence of non-contagious diseases(NCDs)but has profound additive effects of other risk factors for NCD such as obesity and hypertension.1 The articles in this special topic of Journal of Sport and Health Science(JSHS)are dedicated to research on Exercise biochemistry&metabolism.展开更多
Background Obesity is a risk factor for developing cardiometabolic disease.Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality.This study examined the effec...Background Obesity is a risk factor for developing cardiometabolic disease.Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality.This study examined the effect of high-fat feeding on cardiac morphology and mitochondrial function,alongside the mitigating effects of voluntary exercise training.Methods Six-week-old male C57Bl/6 J mice commenced a high fat diet(HFD)or chow diet and were randomized to receive locked(sedentary)or unlocked(voluntary exercise training(VET))running wheels at 10 weeks of age.Mice were monitored until 30 weeks of age and euthanized for collection of tissues.Magnetic resonance imaging was performed to assess body composition,and echocardiography was performed to assess cardiac function.Results Compared with chow-fed animals,the HFD increased body weight and adiposity and decreased cardiolipins(CL)in the heart,which are required for maintaining adequate mitochondrial respiration.Importantly,VET reversed these effects and induced physiological cardiac hypertrophy.Cardiac mitochondrial respiratory chain analysis revealed decreased complexes II and IV activity following high fat feeding,while VET enhanced complex I activity,emphasizing the cardioprotective effect of exercise training in obesity.Conclusion This study uncovers mechanisms by which obesity and exercise impact cardiac mitochondrial health and suggests the mitochondria is a therapeutic target in obesity-related cardiovascular diseases.展开更多
Purpose:Regular exercise can reduce incidence and progression of breast cancer,but the mechanisms for such effects are not fully understood.The purpose of this study was to examine the mechanisms behind the protective...Purpose:Regular exercise can reduce incidence and progression of breast cancer,but the mechanisms for such effects are not fully understood.The purpose of this study was to examine the mechanisms behind the protective effects of exercise.Methods:We used a variety of rodent and human experimental model systems to determine whether exercise training can reduce tumor burden in breast cancer and to identify mechanism associated with any exercise training effects on tumor burden.Results:We show that voluntary wheel running slows tumor development in the mammary specific polyomavirus middle T antigen overexpression(MMTV-PyMT)mouse model of breast cancer but only when mice are not housed alone.We identify the proteoglycan decorin as a contraction-induced secretory factor that systemically increases in patients with breast cancer immediately following exercise.Moreover,high expression of decorin in tumors is associated with improved prognosis in patients,while treatment of breast cancer cells in vitro with decorin reduces cell proliferation.Notwithstanding,when we overexpressed decorin in murine muscle or injected recombinant decorin systemically into mouse models of breast cancer,elevated plasma decorin concentrations did not result in higher tumor decorin levels and tumor burden was not improved.Conclusion:Exercise training is anti-tumorigenic in a mouse model of luminal breast cancer,but the effect is abrogated by social isolation.The proteoglycan decorin is an exercise-induced secretory protein,and tumor decorin levels are positively associated with improved prognosis in patients.The hypothesis that elevated plasma decorin is a mechanism by which exercise training improves breast cancer progression in humans is not,however,supported by our pre-clinical data since elevated circulating decorin did not increase tumor decorin levels in these models.展开更多
Obesity has been linked to a range of pathologies,including dementia.In contrast,regular physical activity is associated with the prevention or reduced progression of neurodegeneration.Specifically,physical activity c...Obesity has been linked to a range of pathologies,including dementia.In contrast,regular physical activity is associated with the prevention or reduced progression of neurodegeneration.Specifically,physical activity can improve memory and spatial cognition,reduce age-related cognitive decline,and preserve brain volume,but the mechanisms are not fully understood.Accordingly,we investigated whether any detrimental effects of high-fat diet(HFD)-induced obesity on cognition,motor behavior,adult hippocampal neurogenesis,and brain-derived neurotrophic factor(BDNF)could be mitigated by voluntary exercise training in male C57Bl/6 mice.HFD-induced impairment of motor function was not reversed by exercise.Importantly,voluntary wheel running improved long-term memory and increased hippocampal neurogenesis,suggesting that regular physical activity may prevent cognitive decline in obesity.展开更多
文摘1.Introduction The field of exercise science is experiencing a renaissance,with recent research illuminating the molecular,cellular,and systemic effects of physical activity.This is largely due to the now unequivocal evidence that a lack of physical activity,not only has direct effects on the prevalence of non-contagious diseases(NCDs)but has profound additive effects of other risk factors for NCD such as obesity and hypertension.1 The articles in this special topic of Journal of Sport and Health Science(JSHS)are dedicated to research on Exercise biochemistry&metabolism.
基金MAF is supported by an NHMRC Investigator Grant(APP1194141)Research in his laboratory was supported by project grants from the NHMRC(APP1042465,APP1041760,and APP1156511).
文摘Background Obesity is a risk factor for developing cardiometabolic disease.Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality.This study examined the effect of high-fat feeding on cardiac morphology and mitochondrial function,alongside the mitigating effects of voluntary exercise training.Methods Six-week-old male C57Bl/6 J mice commenced a high fat diet(HFD)or chow diet and were randomized to receive locked(sedentary)or unlocked(voluntary exercise training(VET))running wheels at 10 weeks of age.Mice were monitored until 30 weeks of age and euthanized for collection of tissues.Magnetic resonance imaging was performed to assess body composition,and echocardiography was performed to assess cardiac function.Results Compared with chow-fed animals,the HFD increased body weight and adiposity and decreased cardiolipins(CL)in the heart,which are required for maintaining adequate mitochondrial respiration.Importantly,VET reversed these effects and induced physiological cardiac hypertrophy.Cardiac mitochondrial respiratory chain analysis revealed decreased complexes II and IV activity following high fat feeding,while VET enhanced complex I activity,emphasizing the cardioprotective effect of exercise training in obesity.Conclusion This study uncovers mechanisms by which obesity and exercise impact cardiac mitochondrial health and suggests the mitochondria is a therapeutic target in obesity-related cardiovascular diseases.
基金supported by an NHMRC Investigator Grant (APP1194141)supported by project grants from the NHMRC (APP1042465, APP1041760, and APP1156511)。
文摘Purpose:Regular exercise can reduce incidence and progression of breast cancer,but the mechanisms for such effects are not fully understood.The purpose of this study was to examine the mechanisms behind the protective effects of exercise.Methods:We used a variety of rodent and human experimental model systems to determine whether exercise training can reduce tumor burden in breast cancer and to identify mechanism associated with any exercise training effects on tumor burden.Results:We show that voluntary wheel running slows tumor development in the mammary specific polyomavirus middle T antigen overexpression(MMTV-PyMT)mouse model of breast cancer but only when mice are not housed alone.We identify the proteoglycan decorin as a contraction-induced secretory factor that systemically increases in patients with breast cancer immediately following exercise.Moreover,high expression of decorin in tumors is associated with improved prognosis in patients,while treatment of breast cancer cells in vitro with decorin reduces cell proliferation.Notwithstanding,when we overexpressed decorin in murine muscle or injected recombinant decorin systemically into mouse models of breast cancer,elevated plasma decorin concentrations did not result in higher tumor decorin levels and tumor burden was not improved.Conclusion:Exercise training is anti-tumorigenic in a mouse model of luminal breast cancer,but the effect is abrogated by social isolation.The proteoglycan decorin is an exercise-induced secretory protein,and tumor decorin levels are positively associated with improved prognosis in patients.The hypothesis that elevated plasma decorin is a mechanism by which exercise training improves breast cancer progression in humans is not,however,supported by our pre-clinical data since elevated circulating decorin did not increase tumor decorin levels in these models.
基金supported by an NHMRC Investigator Grant(APP1194141)supported by project grants from the NHMRC(APP1042465,APP1041760,and APP1156511).
文摘Obesity has been linked to a range of pathologies,including dementia.In contrast,regular physical activity is associated with the prevention or reduced progression of neurodegeneration.Specifically,physical activity can improve memory and spatial cognition,reduce age-related cognitive decline,and preserve brain volume,but the mechanisms are not fully understood.Accordingly,we investigated whether any detrimental effects of high-fat diet(HFD)-induced obesity on cognition,motor behavior,adult hippocampal neurogenesis,and brain-derived neurotrophic factor(BDNF)could be mitigated by voluntary exercise training in male C57Bl/6 mice.HFD-induced impairment of motor function was not reversed by exercise.Importantly,voluntary wheel running improved long-term memory and increased hippocampal neurogenesis,suggesting that regular physical activity may prevent cognitive decline in obesity.
