PMC:4719559 / 21743-22971 JSONTXT

{"project":"TEST0","denotations":[{"id":"26793301-157-163-73110","span":{"begin":157,"end":159},"obj":"[\"2228848\"]"},{"id":"26793301-180-186-73111","span":{"begin":517,"end":519},"obj":"[\"4263680\"]"},{"id":"26793301-233-239-73112","span":{"begin":755,"end":757},"obj":"[\"16239250\"]"},{"id":"26793301-193-199-73113","span":{"begin":953,"end":955},"obj":"[\"11985533\", \"15856066\", \"15528398\"]"}],"text":"Immediately at the onset of exercise, central command modulates the level of sympathetic and parasympathetic efferent activity to the vasculature and heart [11]. The magnitude of control is largely influenced by the individual’s perceived effort during actual or attempted exercise, independent of absolute workload or force production. For example, increasing or decreasing central command at a given muscle tension during static exercise results in a corresponding increase or decrease in cardiovascular responses [28]. Although the exact location of integration of these signals is unknown, it appears to include regions of the insular and anterior cingulate cortexes that interact with thalamic and brainstem structures of cardiovascular integration [29]. Nutrient signaling within the hypothalamus and dorsal vagal complex that controls appetite and sympathetic outflow may modulate the influence of central command through shared neural pathways [30–32]. The blunted neural and cardiovascular responses during handgrip in this study are consistent with, but do not prove, a reduction in central command output. More mechanistic studies are needed to determine whether and how caloric restriction modulates central command."}

{"project":"MyTest","denotations":[{"id":"26793301-2228848-30256729","span":{"begin":157,"end":159},"obj":"2228848"},{"id":"26793301-4263680-30256730","span":{"begin":517,"end":519},"obj":"4263680"},{"id":"26793301-16239250-30256731","span":{"begin":755,"end":757},"obj":"16239250"},{"id":"26793301-11985533-30256732","span":{"begin":953,"end":955},"obj":"11985533"},{"id":"26793301-15856066-30256732","span":{"begin":953,"end":955},"obj":"15856066"},{"id":"26793301-15528398-30256732","span":{"begin":953,"end":955},"obj":"15528398"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Immediately at the onset of exercise, central command modulates the level of sympathetic and parasympathetic efferent activity to the vasculature and heart [11]. The magnitude of control is largely influenced by the individual’s perceived effort during actual or attempted exercise, independent of absolute workload or force production. For example, increasing or decreasing central command at a given muscle tension during static exercise results in a corresponding increase or decrease in cardiovascular responses [28]. Although the exact location of integration of these signals is unknown, it appears to include regions of the insular and anterior cingulate cortexes that interact with thalamic and brainstem structures of cardiovascular integration [29]. Nutrient signaling within the hypothalamus and dorsal vagal complex that controls appetite and sympathetic outflow may modulate the influence of central command through shared neural pathways [30–32]. The blunted neural and cardiovascular responses during handgrip in this study are consistent with, but do not prove, a reduction in central command output. More mechanistic studies are needed to determine whether and how caloric restriction modulates central command."}

{"project":"0_colil","denotations":[{"id":"26793301-2228848-73110","span":{"begin":157,"end":159},"obj":"2228848"},{"id":"26793301-4263680-73111","span":{"begin":517,"end":519},"obj":"4263680"},{"id":"26793301-16239250-73112","span":{"begin":755,"end":757},"obj":"16239250"},{"id":"26793301-11985533-73113","span":{"begin":953,"end":955},"obj":"11985533"},{"id":"26793301-15528398-73113","span":{"begin":953,"end":955},"obj":"15528398"},{"id":"26793301-15856066-73113","span":{"begin":953,"end":955},"obj":"15856066"}],"text":"Immediately at the onset of exercise, central command modulates the level of sympathetic and parasympathetic efferent activity to the vasculature and heart [11]. The magnitude of control is largely influenced by the individual’s perceived effort during actual or attempted exercise, independent of absolute workload or force production. For example, increasing or decreasing central command at a given muscle tension during static exercise results in a corresponding increase or decrease in cardiovascular responses [28]. Although the exact location of integration of these signals is unknown, it appears to include regions of the insular and anterior cingulate cortexes that interact with thalamic and brainstem structures of cardiovascular integration [29]. Nutrient signaling within the hypothalamus and dorsal vagal complex that controls appetite and sympathetic outflow may modulate the influence of central command through shared neural pathways [30–32]. The blunted neural and cardiovascular responses during handgrip in this study are consistent with, but do not prove, a reduction in central command output. More mechanistic studies are needed to determine whether and how caloric restriction modulates central command."}

{"project":"2_test","denotations":[{"id":"26793301-2228848-30256729","span":{"begin":157,"end":159},"obj":"2228848"},{"id":"26793301-4263680-30256730","span":{"begin":517,"end":519},"obj":"4263680"},{"id":"26793301-16239250-30256731","span":{"begin":755,"end":757},"obj":"16239250"},{"id":"26793301-11985533-30256732","span":{"begin":953,"end":955},"obj":"11985533"},{"id":"26793301-15856066-30256732","span":{"begin":953,"end":955},"obj":"15856066"},{"id":"26793301-15528398-30256732","span":{"begin":953,"end":955},"obj":"15528398"}],"text":"Immediately at the onset of exercise, central command modulates the level of sympathetic and parasympathetic efferent activity to the vasculature and heart [11]. The magnitude of control is largely influenced by the individual’s perceived effort during actual or attempted exercise, independent of absolute workload or force production. For example, increasing or decreasing central command at a given muscle tension during static exercise results in a corresponding increase or decrease in cardiovascular responses [28]. Although the exact location of integration of these signals is unknown, it appears to include regions of the insular and anterior cingulate cortexes that interact with thalamic and brainstem structures of cardiovascular integration [29]. Nutrient signaling within the hypothalamus and dorsal vagal complex that controls appetite and sympathetic outflow may modulate the influence of central command through shared neural pathways [30–32]. The blunted neural and cardiovascular responses during handgrip in this study are consistent with, but do not prove, a reduction in central command output. More mechanistic studies are needed to determine whether and how caloric restriction modulates central command."}