Dataset Information

Scaling of adult human bone and skeletal muscle mass to height in the US population.

ABSTRACT: OBJECTIVES:The scaling of structural components to body size is well studied in mammals, although comparable human observations in a large and diverse sample are lacking. The current study aimed to fill this gap by examining the scaling relationships between total body (TB) and regional bone and skeletal muscle (SM) mass with body size, as defined by stature, in a nationally representative sample of the US population. METHODS:Subjects were 17,126 non-Hispanic (NH) white, NH black, and Mexican American men and women, aged ?18?years, evaluated in the National Health and Nutrition Examination Survey who had TB and regional bone mineral (BMin) and lean soft tissue (LST) mass measured by dual-energy X-ray absorptiometry. BMin and appendicular LST served as surrogate bone and SM mass measures, respectively. The allometric model, BMin or LST = ?(height)? , in a logarithmic form was used to generate scaling exponents. RESULTS:The findings were similar across all gender and race groups: body mass scaled to height with powers of ~2.0 (mean ??±?SE, 1.94?±?0.08-2.29?±?0.09) while TB and appendicular BMin and appendicular LST scaled to height with consistently larger powers than those for body mass (eg, all P?

SUBMITTER: Heymsfield SB

PROVIDER: S-EPMC6634976 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Scaling of adult human bone and skeletal muscle mass to height in the US population.

Heymsfield Steven B SB Hwaung Phoenix P Ferreyro-Bravo Fernando F Heo Moonseong M Thomas Diana M DM Schuna John M JM

American journal of human biology : the official journal of the Human Biology Council 20190514 4

<h4>Objectives</h4>The scaling of structural components to body size is well studied in mammals, although comparable human observations in a large and diverse sample are lacking. The current study aimed to fill this gap by examining the scaling relationships between total body (TB) and regional bone and skeletal muscle (SM) mass with body size, as defined by stature, in a nationally representative sample of the US population.<h4>Methods</h4>Subjects were 17,126 non-Hispanic (NH) white, NH black, ...[more]

PMID: 31087593

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Project description:BackgroundMitochondrial oxidative phosphorylation (OxPhos) is a critical regulator of skeletal muscle mass and function. Although muscle atrophy due to mitochondrial dysfunction is closely associated with bone loss, the biological characteristics of the relationship between muscle and bone remain obscure. We showed that muscle atrophy caused by skeletal muscle-specific CR6-interacting factor 1 knockout (MKO) modulates the bone marrow (BM) inflammatory response, leading to low bone mass.MethodsMKO mice with lower muscle OxPhos were fed a normal chow or high-fat diet and then evaluated for muscle mass and function, and bone mineral density. Immunophenotyping of BM immune cells was also performed. BM transcriptomic analysis was used to identify key factors regulating bone mass in MKO mice. To determine the effects of BM-derived CXCL12 (C-X-C motif chemokine ligand 12) on regulation of bone homeostasis, a variety of BM niche-resident cells were treated with recombinant CXCL12. Vastus lateralis muscle and BM immune cell samples from 14 patients with hip fracture were investigated to examine the association between muscle function and BM inflammation.ResultsMKO mice exhibited significant reductions in both muscle mass and expression of OxPhos subunits but increased transcription of mitochondrial stress response-related genes in the extensor digitorum longus (P < 0.01). MKO mice showed a decline in grip strength and a higher drop rate in the wire hanging test (P < 0.01). Micro-computed tomography and von Kossa staining revealed that MKO mice developed a low mass phenotype in cortical and trabecular bone (P < 0.01). Transcriptomic analysis of the BM revealed that mitochondrial stress responses in skeletal muscles induce an inflammatory response and adipogenesis in the BM and that the CXCL12-CXCR4 (C-X-C chemokine receptor 4) axis is important for T-cell homing to the BM. Antagonism of CXCR4 attenuated BM inflammation and increased bone mass in MKO mice. In humans, patients with low body mass index (BMI = 17.2 ± 0.42 kg/m2 ) harboured a larger population of proinflammatory and cytotoxic senescent T-cells in the BMI (P < 0.05) and showed reduced expression of OxPhos subunits in the vastus lateralis, compared with controls with a normal BMI (23.7 ± 0.88 kg/m2 ) (P < 0.01).ConclusionsDefects in muscle mitochondrial OxPhos promote BM inflammation in mice, leading to decreased bone mass. Muscle mitochondrial dysfunction is linked to BM inflammatory cytokine secretion via the CXCL12-CXCR4 signalling axis, which is critical for inducing low bone mass.

Dataset Information

Scaling of adult human bone and skeletal muscle mass to height in the US population.

Publications

Scaling of adult human bone and skeletal muscle mass to height in the US population.

Similar Datasets

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