Mediation of the Acute Stress Response by the Skeleton

Berger, Julian; Singh, Parminder; Khrimian, Lori; Morgan, Donald A.; Chowdhury, Subrata; Arteaga‐Solis, Emilio; Horváth, Tamas L.; Domingos, Ana I.; Marsland, Anna L.; Yadav, Vijay K.; Rahmouni, Kamal; Gao, Xiao‐Bing; Karsenty, Gérard

doi:10.1016/j.cmet.2019.08.012

Cited by 126 publications

(125 citation statements)

References 78 publications

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“…Together, these 2 studies propose a new perspective on how exercise capacity is regulated by distinguishing between muscle mass and muscle function and by identifying bone via the hormone osteocalcin as a focal regulator of exercise capacity. They also provide credence to the recently proposed notion that bone might have evolved as a tool to escape danger (27).…”

Section: Methodssupporting

confidence: 66%

Muscle-derived interleukin 6 increases exercise capacity by signaling in osteoblasts

Chowdhury¹,

Schulz²,

Palmisano³

et al. 2020

Journal of Clinical Investigation

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Section: Methodssupporting

confidence: 66%

Muscle-derived interleukin 6 increases exercise capacity by signaling in osteoblasts

Chowdhury¹,

Schulz²,

Palmisano³

et al. 2020

Journal of Clinical Investigation

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“…According to the hypothesis of Berger et al [104], bones evolved ontogenetically to enhance the ability to escape danger in the wild. In line with this theory, they showed in animals and humans that stressors induce a rapid outflow of circulating osteocalcin, which is necessary to develop an ASR.…”

Section: Doms and Ontogenesismentioning

confidence: 99%

“…In line with this theory, they showed in animals and humans that stressors induce a rapid outflow of circulating osteocalcin, which is necessary to develop an ASR. Osteocalcin inhibits the activity of post-synaptic parasympathetic neurons in order to let the sympathetic tone become full blown [104]. Our theory of superposition of compression with cognitive demand-induced acute axonopathy entails that strenuous or unaccustomed eccentric exercise induced SNS activity could be an essential underlying factor at DOMS initiation with likely ASR involvement, so the possible role of osteocalcin in cross-talking should be investigated.…”

Section: Doms and Ontogenesismentioning

confidence: 99%

Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage

2020

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According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy could coincide with microinjury of the surrounding tissues and is enhanced by immune-mediated inflammation. DOMS is masked by sympathetic nervous system activity at initiation, but once it subsides, a safety mode comes into play to prevent further injury. DOMS becomes manifest when the microinjured non-nociceptive sensory fibers of the muscle spindle stop inhibiting the effects of the microinjured, hyperexcited nociceptive sensory fibers, therefore providing the ‘open gate’ in the dorsal horn to hyperalgesia. Reactive oxygen species and nitric oxide play a cross-talking role in the parallel, interlinked degeneration–regeneration mechanisms of these injured tissues. We propose that the mitochondrial electron transport chain generated free radical involvement in the acute compression axonopathy. ‘Closed gate exercises’ could be of nonpharmacological therapeutic importance, because they reduce neuropathic pain in addition to having an anti-inflammatory effect. Finally, DOMS could have an important ontogenetical role by not just enhancing ability to escape danger to survive in the wild, but also triggering muscle growth.

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“…Recent and growing evidence suggests that states of the body are determinants and mediators of mental states (e.g. Berger et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Perfect Timing: Mobile Brain/Body Imaging scaffolds the 4E-cognition research program (published version)

Parada¹,

Rossi²

2020

Preprint

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Recent technological advancements encompassed under the Mobile Brain/Body Imaging (MoBI) framework, have produced exciting new experimental results linking mind, brain, and behavior. The main goal of the MoBI approach is to model brain and body dynamics during every-day, natural, real-life situations. However, even though considerable advances have been made in both hardware and software, technical and analytical conditions are not yet optimal. The MoBI approach is based on attaching synchronized, small, and lightweight neurobehavioral sensors to and around participants during behaviorally-measured structured, semi-structured, and unstructured settings. These sensors have yet to become fully unobtrusive or transparent. Even though a considerable technical and analytical gap still exists, acquisition of brain/body dynamics during real-world situations as well as in virtual, modified, and/or extended laboratory settings has been -in many cases- successful. Nevertheless, even if the technical/analytical gap is breached, novel hypotheses, measures, and experimental paradigms are needed in order to tackle MoBI’s ultimate goal: to model and understand cognition, behavior, and experience as it emerges and unfolds unto and from the world. Such a goal is not completely novel or unique to the MoBI framework; it is at the core of a long-standing scientific and philosophical challenge. The present work starts by briefly reviewing the historical origins of complexity in order to identify three “waves and ripples of complexity” derived from naturalist accounts to the historical brain/body problem. We furthermore argue for a current 4th wave. Finally, we offer the reader what we consider to be the main objective for the MoBI+4E framework in its quest for understanding the functional role of brain/body/world couplings in the emergence of cognition.

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Mediation of the Acute Stress Response by the Skeleton

Cited by 126 publications

References 78 publications

Muscle-derived interleukin 6 increases exercise capacity by signaling in osteoblasts

Muscle-derived interleukin 6 increases exercise capacity by signaling in osteoblasts

Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage

Perfect Timing: Mobile Brain/Body Imaging scaffolds the 4E-cognition research program (published version)

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