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 Heat shock proteins(HSPs)are key molecular chaperones that help maintain protein homeostasis by stabilizing or removing damaged proteins during cellular stress.Aging weakens these stress–response systems,d...Background Heat shock proteins(HSPs)are key molecular chaperones that help maintain protein homeostasis by stabilizing or removing damaged proteins during cellular stress.Aging weakens these stress–response systems,disrupting proteostasis and increasing vulnerability to sarcopenia.High-intensity training(HIT)can counteract these declines by activating protective pathways such as the HSP response.HSPs are highly responsive to stress,examining their regulation during aging is important,as altered HSP activity is linked to the progressive loss of muscle mass.Methods This study investigated the abundance and phosphorylation of HSPs in skeletal muscle from healthy,active young and older adults(n=7 per group),assessed at baseline and again in the older group following 12 weeks of HIT.Using calibrated Western blotting on both whole-muscle homogenates and pooled single muscle fibres,we quantified HSP content and phosphorylation to determine how aging and exercise influence stress–responsive protein regulation at both the tissue and cellular levels.Results In whole muscle homogenates,HSPs(HSP72,HSP27,andαB-crystallin)did not differ between young and older adults,while higher phosphorylation of small HSPs(sHSPs):phospho-HSP27 at Serine15(pHSP27 Ser15)and phospho-αB-crystallin at Serine59(pαB-crystallin Ser59)(∼1.8-fold and∼2.9-fold,respectively)were found in muscle from older adults,indicating higher cellular stress associated with aging.A 12-week HIT intervention in older adults reduced homogenate pHSP27 Ser15 and pαB-crystallin Ser59 abundances to similar levels found in young adults.Total HSPs typically displayed a distinct fiber-type profile in both age groups,with more in type I compared to type II fibers,distinguished by the presence of myosin heavy chain I(MHCI)or MHCII.Phosphorylation at pHSP27 Ser15 and pαB-crystallin Ser59 was not different between type I and type II fibers.The HIT in older adults decreased total and phosphorylated sHSPs in both type I and type II fibers but increased HSP72 in type I fibers.Conclusion HIT has the potential to mitigate age-related cellular stress and modulate protein expression patterns in aging skeletal muscle and,perhaps,has the potential to delay age-related muscle decline,thereby improving muscle health in older adults.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.
文摘Background Heat shock proteins(HSPs)are key molecular chaperones that help maintain protein homeostasis by stabilizing or removing damaged proteins during cellular stress.Aging weakens these stress–response systems,disrupting proteostasis and increasing vulnerability to sarcopenia.High-intensity training(HIT)can counteract these declines by activating protective pathways such as the HSP response.HSPs are highly responsive to stress,examining their regulation during aging is important,as altered HSP activity is linked to the progressive loss of muscle mass.Methods This study investigated the abundance and phosphorylation of HSPs in skeletal muscle from healthy,active young and older adults(n=7 per group),assessed at baseline and again in the older group following 12 weeks of HIT.Using calibrated Western blotting on both whole-muscle homogenates and pooled single muscle fibres,we quantified HSP content and phosphorylation to determine how aging and exercise influence stress–responsive protein regulation at both the tissue and cellular levels.Results In whole muscle homogenates,HSPs(HSP72,HSP27,andαB-crystallin)did not differ between young and older adults,while higher phosphorylation of small HSPs(sHSPs):phospho-HSP27 at Serine15(pHSP27 Ser15)and phospho-αB-crystallin at Serine59(pαB-crystallin Ser59)(∼1.8-fold and∼2.9-fold,respectively)were found in muscle from older adults,indicating higher cellular stress associated with aging.A 12-week HIT intervention in older adults reduced homogenate pHSP27 Ser15 and pαB-crystallin Ser59 abundances to similar levels found in young adults.Total HSPs typically displayed a distinct fiber-type profile in both age groups,with more in type I compared to type II fibers,distinguished by the presence of myosin heavy chain I(MHCI)or MHCII.Phosphorylation at pHSP27 Ser15 and pαB-crystallin Ser59 was not different between type I and type II fibers.The HIT in older adults decreased total and phosphorylated sHSPs in both type I and type II fibers but increased HSP72 in type I fibers.Conclusion HIT has the potential to mitigate age-related cellular stress and modulate protein expression patterns in aging skeletal muscle and,perhaps,has the potential to delay age-related muscle decline,thereby improving muscle health in older adults.
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.
