Sarcopenic obesity in older adults: aetiology, epidemiology and treatment strategies

In the paper

“Leptin upregulates the pro-inflammatory cytokines IL-6 and TNF, which results in a reduction in the anabolic actions of insulinlike growth factor 1 (IGF1)61.”

What the sources say

• Disputed

  The section “The Anabolic Effects of Leptin on Skeletal Muscle” (page unavailable) says leptin treatment increases IGF-1 and that IGF-1 likely mediates leptin’s anabolic effects—the opposite of the claimed reduction. The passages found do not describe leptin upregulating IL-6 or TNF. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [61] Hamrick, M. W. Role of the cytokine-like hormone leptin in muscle-bone crosstalk with aging. J. Bone Metab. 24, 1–8 (2017). sourceExperimental — accuracy not yet measured

In the paper

“Peak oxygen consumption is potentially inversely related to frailty129,130, suggesting that improvements in VO2 max following aerobic training counteract frailty131,132.”

What the sources say

• ?Not checked — no full text of the sourcecites [129] Moayedi, Y. et al. The prognostic significance of frailty compared to peak oxygen consumption and B-type natriuretic peptide in patients with advanced heart failure. Clin. Transplant. https://doi.org/10.1111/ctr.13158 (2018). source
• Disputed

  The Results (Effect of endurance training; page unavailable) report that cardiopulmonary peak VO₂ did not change after training, contrary to the attributed improvement. Post-exercise muscle oxygen consumption increased, but that is a different measure. The paper does not assess frailty or whether a change in VO₂ max counteracts it. (LLM, conf=0.83)

  Checked by a reasoning model — may be wrong.

  cites [130] Jones, S. et al. Assessment of exercise capacity and oxygen consumption using a 6 min stepper test in older adults. Front. Physiol. 8, 408 (2017). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [131] Binder, E. F. et al. Effects of exercise training on frailty in community-dwelling older adults: results of a randomized, controlled trial. J. Am. Geriatr. Soc. 50, 1921–1928 (2002). This is a randomized controlled trial demonstrating that intensive exercise training can improve measures of physical function. source
• Supported

  The Results (page not available) report lower VO₂ peak in the frail groups than in the nonfrail group, supporting the potential inverse relationship cited to this paper. The aerobic-training inference has separate citations in the citing sentence and is not attributed to this source. (LLM, conf=0.90)

  cites [132] Villareal, D. T., Banks, M., Siener, C., Sinacore, D. R. & Klein, S. Physical frailty and body composition in obese elderly men and women. Obes. Res. 12, 913–920 (2004). source

In the paper

“Obesity is inversely related to BMD and fractures313 but might increase the fracture risk through bone quality314,315 or frailty132,316 independent of BMD.”

What the sources say

• Disputed

  The Discussion (page not provided) says BMD is positively correlated with BMI and that many obese individuals have higher BMD—the opposite of an inverse relationship. It does support an inverse association between obesity and hip-fracture risk in adults, but not the claimed inverse association with BMD. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [313] Tang, X. et al. Obesity and risk of hip fracture in adults: a meta-analysis of prospective cohort studies. PLoS ONE 8, e55077 (2013). sourceExperimental — accuracy not yet measured

In the paper

“In vitro trials demonstrate that myostatin inhibitors increase muscle mass and strength446, suppress irisin, downregulate inflammatory cytokines and improve insulin resistance447.”

What the sources say

• ?Not checked — no full text of the sourcecites [446] Camporez, J. P. et al. Anti-myostatin antibody increases muscle mass and strength and improves insulin sensitivity in old mice. Proc. Natl Acad. Sci. USA 113, 2212–2217 (2016). This study evaluates a treatment consisting of anti-myostatin antibody administration for 4 weeks, showing improved muscle mass and strength in young and old mice. source
• Disputed

  The Results section, “Myostatin inhibition increases irisin expression” (page unavailable), reports increased irisin after myostatin knockdown in cultured muscle cells—the opposite of the claimed suppression. The Discussion (page unavailable) supports reduced inflammation and improved insulin resistance after myostatin inhibition, but reports the insulin-resistance finding in high-fat-diet-fed mice, not as an in vitro trial. The muscle-mass and strength clause carries a different citation and is not judged here. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [447] Dong, J. et al. Inhibition of myostatin in mice improves insulin sensitivity via irisin-mediated cross talk between muscle and adipose tissues. Int. J. Obes. (Lond.) 40, 434–442 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Obesity activates macrophages, mast cells and T lymphocytes, promoting a low-level inflammation that results in the secretion of tumour necrosis factor (TNF), leptin and growth hormone (GH)57–59.”

What the sources say

• ?Not checked — no full text of the sourcecites [57] Schrager, M. A. et al. Sarcopenic obesity and inflammation in the InCHIANTI study. J. Appl. Physiol. (1985) 102, 919–925 (2007). This is an epidemiological study that shows that obesity directly affects inflammation and negatively affects muscle strength. source
• Partly supported

  The Introduction describes obesity as low-grade systemic inflammation and identifies TNF-α and leptin as adipose-tissue secretory products. It mentions macrophages and mast cells as possible contributors to inflammation, but does not establish their activation; the passages do not support the added claims about T lymphocytes or growth hormone. Page numbers were not available in our copy. (LLM, conf=0.88)

  cites [58] Forsythe, L. K., Wallace, J. M. & Livingstone, M. B. Obesity and inflammation: the effects of weight loss. Nutr. Res. Rev. 21, 117–133 (2008). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [59] Park, H. S., Park, J. Y. & Yu, R. Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. Diabetes Res. Clin. Pract. 69, 29–35 (2005). source

In the paper

“Elevated cytokine levels observed in hypogonadal states are associated with truncal obesity, which exacerbates the development of sarcopenia44,45.”

What the sources say

• Partly supported

  The section “Testosterone, muscle strength and mass” (page unavailable) reports that suppressing testosterone in young men increased adiposity and decreased muscle strength. It does not report elevated cytokines, specify truncal obesity, or establish that obesity exacerbates sarcopenia. (LLM, conf=0.78)

  cites [44] Kadi, F. Cellular and molecular mechanisms responsible for the action of testosterone on human skeletal muscle. A basis for illegal performance enhancement. Br. J. Pharmacol. 154, 522–528 (2008). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [45] Bondanelli, M. et al. Activation of the somatotropic axis by testosterone in adult men: evidence for a role of hypothalamic growth hormone-releasing hormone. Neuroendocrinology 77, 380–387 (2003). source

In the paper

“Obesity also induces leptin resistance, promoting reduced muscle fatty oxidation and ectopic fat deposition65,66.”

What the sources say

• Partly supported

  The paper’s discussion of age-related fat redistribution says fat can accumulate in muscle and other non-adipose tissues. It does not say that obesity induces leptin resistance or that leptin resistance reduces muscle fatty-acid oxidation and thereby causes ectopic fat deposition; the leptin-resistance mention found in our copy is a reference-list title about aging. (LLM, conf=0.84)

  cites [65] Cartwright, M. J., Tchkonia, T. & Kirkland, J. L. Aging in adipocytes: potential impact of inherent, depot-specific mechanisms. Exp. Gerontol. 42, 463–471 (2007). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [66] Shulman, G. I. Ectopic fat in insulin resistance, dyslipidemia, and cardiometabolic disease. N. Engl. J. Med. 371, 1131–1141 (2014). source

In the paper

“Exercise can affect hormonal balance, reduce oxidative stress, induce mitochondrial synthesis, alter immunological and motor function and improve muscle oxidative capacity92–95.”

What the sources say

• ?Not checked — no full text of the sourcecites [92] Joseph, A. M., Adhihetty, P. J. & Leeuwenburgh, C. Beneficial effects of exercise on age-related mitochondrial dysfunction and oxidative stress in skeletal muscle. J. Physiol. 594, 5105–5123 (2016). source
• ?Not checked — no full text of the sourcecites [93] Schubert, M. M., Sabapathy, S., Leveritt, M. & Desbrow, B. Acute exercise and hormones related to appetite regulation: a meta-analysis. Sports Med. 44, 387–403 (2014). source
• Partly supported

  The Discussion reports that low-intensity aerobic exercise reduced oxidative stress in spontaneously hypertensive rats. The Methods identify soleus citrate synthase activity as a marker of muscle oxidative activity, and the Results report higher activity in trained rats. The paper does not establish the claimed effects on hormonal balance, mitochondrial synthesis, or immunological and motor function. (LLM, conf=0.90)

  cites [94] Roque, F. R. et al. Aerobic exercise reduces oxidative stress and improves vascular changes of small mesenteric and coronary arteries in hypertension. Br. J. Pharmacol. 168, 686–703 (2013). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [95] Kumaraguru, U., Nandakumar, S., Chi, D., Stone, M. & Krishnaswamy, G. Resistance training and aerobic exercise alters immune function (87.25). J. Immunol. 184, 87.25 (2010). source

In the paper

“The regeneration potential of muscle is impaired, which might promote fibrosis, thereby promoting insulin resistance76–79, partially owing to impaired mitochondrial fatty acid oxidation and increased lipolysis76,80.”

What the sources say

• ?Not checked — no full text of the sourcecites [76] Kalinkovich, A. & Livshits, G. Sarcopenic obesity or obese sarcopenia: a cross talk between age-associated adipose tissue and skeletal muscle inflammation as a main mechanism of the pathogenesis. Ageing Res. Rev. 35, 200–221 (2017). source
• ?Not checked — no full text of the sourcecites [77] Kob, R. et al. Sarcopenic obesity: molecular clues to a better understanding of its pathogenesis? Biogerontology 16, 15–29 (2015). source
• ?Not checked — no full text of the sourcecites [78] Stinkens, R., Goossens, G. H., Jocken, J. W. & Blaak, E. E. Targeting fatty acid metabolism to improve glucose metabolism. Obes. Rev. 16, 715–757 (2015). source
• Partly supported

  The ‘Mitochondria, lipids, and insulin resistance’ section discusses impaired fat oxidation as one proposed contributor to skeletal-muscle insulin resistance, while noting that this explanation is debated. The ‘Concluding remarks’ link excessive lipolysis to insulin resistance. Neither section connects impaired muscle regeneration or fibrosis to those mechanisms; page numbers are not available in our copy. (LLM, conf=0.88)

  cites [79] Aon, M. A., Bhatt, N. & Cortassa, S. C. Mitochondrial and cellular mechanisms for managing lipid excess. Front. Physiol. 5, 282 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [80] Bruce, C. R. et al. Muscle oxidative capacity is a better predictor of insulin sensitivity than lipid status. J. Clin. Endocrinol. Metab. 88, 5444–5451 (2003). source

In the paper

“Elevated TNF directly inhibits adiponectin63, arresting muscle protein synthesis and mitochondrial processes64.”

What the sources say

• ?Could not verify

  Citation 63 is attached to the assertion that elevated TNF directly inhibits adiponectin; the muscle-process assertion has a separate citation. The Results section describes adiponectin inhibiting TNFα-induced inflammation in endothelial cells, but the passages found when searching for TNF suppression of adiponectin do not address whether TNF directly inhibits adiponectin. No page number is available in our copy. (LLM, conf=0.74)

  cites [63] Wang, Y. et al. Adiponectin inhibits tumor necrosis factor-alpha-induced vascular inflammatory response via caveolin-mediated ceramidase recruitment and activation. Circ. Res. 114, 792–805 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [64] Lang, C. H., Frost, R. A., Nairn, A. C., MacLean, D. A. & Vary, T. C. TNF-alpha impairs heart and skeletal muscle protein synthesis by altering translation initiation. Am. J. Physiol. Endocrinol. Metab. 282, E336–E347 (2002). source

In the paper

“While muscle cells can regenerate through satellite mesenchymal progenitor cells, their numbers decline with age, which contributes to reduced muscle function88,89.”

What the sources say

• Partly supported

  The Introduction describes satellite cells as myogenic progenitors essential for skeletal-muscle repair and reports an age-associated decline in their numbers. It says this decline *may* contribute to muscle deterioration, rather than establishing that it does; it also calls the cells myogenic, not mesenchymal. (LLM, conf=0.88)

  cites [88] Shefer, G., Rauner, G., Stuelsatz, P., Benayahu, D. & Yablonka-Reuveni, Z. Moderate-intensity treadmill running promotes expansion of the satellite cell pool in young and old mice. FEBS J. 280, 4063–4073 (2013). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction (page unavailable) says satellite cells are muscle progenitor cells involved in skeletal-muscle repair and growth, and that their dysfunction could contribute to sarcopenia. The Discussion (page unavailable) reports delayed proliferation of precursor cells from old rats, but our copy does not establish that satellite-cell numbers decline with age or that a decline in numbers causes reduced muscle function. (LLM, conf=0.87)

  cites [89] Zwetsloot, K. A., Childs, T. E., Gilpin, L. T. & Booth, F. W. Non-passaged muscle precursor cells from 32-month old rat skeletal muscle have delayed proliferation and differentiation. Cell Prolif. 46, 45–57 (2013). sourceExperimental — accuracy not yet measured

In the paper

“Increased muscle protein synthesis with exercise sensitizes muscle insulin action and promotes anabolism96–100.”

What the sources say

• ?Not checked — no full text of the sourcecites [96] Carraro, F., Stuart, C. A., Hartl, W. H., Rosenblatt, J. & Wolfe, R. R. Effect of exercise and recovery on muscle protein synthesis in human subjects. Am. J. Physiol. 259, E470–E476 (1990). source
• Partly supported

  The Results (Muscle protein synthesis; page not provided) report an approximately 40% post-exercise increase in muscle protein synthesis in the control group, and the Discussion links post-exercise synthesis to muscle protein anabolism. The paper does not show that increased protein synthesis sensitizes muscle insulin action; its insulin discussion concerns blood insulin concentrations, not insulin sensitivity. (LLM, conf=0.88)

  cites [97] Drummond, M. J. et al. Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis. J. Physiol. 587, 1535–1546 (2009). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [98] Fujita, S. et al. Aerobic exercise overcomes the age-related insulin resistance of muscle protein metabolism by improving endothelial function and Akt/mammalian target of rapamycin signaling. Diabetes 56, 1615–1622 (2007). source
• ?Not checked — no full text of the sourcecites [99] Levenhagen, D. K. et al. Postexercise nutrient intake timing in humans is critical to recovery of leg glucose and protein homeostasis. Am. J. Physiol. Endocrinol. Metab. 280, E982–E993 (2001). source
• ?Not checked — no full text of the sourcecites [100] Sheffield-Moore, M. et al. Postexercise protein metabolism in older and younger men following moderate-intensity aerobic exercise. Am. J. Physiol. Endocrinol. Metab. 287, E513–E522 (2004). source

In the paper

“Potential mechanisms explaining these changes include age-related reductions in protea some activity, deficiencies in ubiquitylation and autophagy and impairments in removing degraded proteins and end products82–84.”

What the sources say

• Partly supported

  The Results section, “Autophagy Declines during Aging” (page unavailable), reports reduced autophagy markers in aged mice and elderly sedentary people. The Discussion (page unavailable) says autophagy clears damaged proteins and organelles and that its failure contributes to aging. The paper does not establish the claimed age-related reduction in proteasome activity or deficiency in ubiquitylation. (LLM, conf=0.88)

  cites [82] Carnio, S. et al. Autophagy impairment in muscle induces neuromuscular junction degeneration and precocious aging. Cell Rep. 8, 1509–1521 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [83] Marcell, T. J. Sarcopenia: causes, consequences, and preventions. J. Gerontol. A Biol. Sci. Med. Sci. 58, M911–M916 (2003). source
• Partly supported

  The Introduction (page unavailable) links declining autophagy with accumulation of damaged cellular components, and the Discussion (page unavailable) says age-impaired quality-control pathways may allow damaged proteins to accumulate. However, the Introduction explicitly says it is unclear whether proteasome activity increases or decreases with age in skeletal muscle, and the copy does not establish a specific age-related deficiency in ubiquitylation. (LLM, conf=0.86)

  cites [84] Wohlgemuth, S. E., Seo, A. Y., Marzetti, E., Lees, H. A. & Leeuwenburgh, C. Skeletal muscle autophagy and apoptosis during aging: effects of calorie restriction and life-long exercise. Exp. Gerontol. 45, 138–148 (2010). sourceExperimental — accuracy not yet measured

In the paper

“The synthesis of mitochondria in myocytes is upregulated to meet the demands associated with an increase in capillary density, which in turn leads to increased oxygen extraction and metabolism122 through the induction of calcium and metabolic signalling pathways such as those involving 5’-AMP-activated serine/threonine-protein kinase (AMPK) and sirtuins123.”

What the sources say

• ?Not checked — no full text of the sourcecites [122] Marzetti, E. et al. Modulation of age-induced apoptotic signaling and cellular remodeling by exercise and calorie restriction in skeletal muscle. Free Radic. Biol. Med. 44, 160–168 (2008). source
• Partly supported

  The passages labelled Abstract (page unavailable) link AMPK and SIRT1 activity to mitochondrial gene expression and oxygen consumption in myotubes and skeletal muscle. They do not establish calcium signalling or say that increased capillary density drives mitochondrial synthesis; the paper measures cellular oxygen consumption, not oxygen extraction associated with capillary density. (LLM, conf=0.85)

  cites [123] Canto, C. et al. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity. Nature 458, 1056–1060 (2009). sourceExperimental — accuracy not yet measured

In the paper

“This lipotoxicity impairs muscle fibre contractility and interferes with muscle protein synthesis, exacerbating sarcopenia82–84.”

What the sources say

• Partly supported

  The Discussion reports that oxidative stress impairs acto-myosin function and muscle force, supporting the contractility component. The Results section ‘Autophagy Declines during Aging’ says age-related muscle loss is believed to involve reduced protein synthesis, but our copy does not link either effect to lipotoxicity or show that lipotoxicity exacerbates sarcopenia. No page numbers are available in our copy. (LLM, conf=0.78)

  cites [82] Carnio, S. et al. Autophagy impairment in muscle induces neuromuscular junction degeneration and precocious aging. Cell Rep. 8, 1509–1521 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [83] Marcell, T. J. Sarcopenia: causes, consequences, and preventions. J. Gerontol. A Biol. Sci. Med. Sci. 58, M911–M916 (2003). source
• ?Could not verify

  The Introduction links muscle loss to an imbalance between protein synthesis and degradation, while the Discussion reports lipid-peroxidation markers in aged rat muscle. Neither passage says that lipotoxicity impairs fibre contractility or interferes with protein synthesis. Searches for lipotoxicity, intramuscular fat, and those proposed effects found no passage addressing that causal claim; page numbers were unavailable. (LLM, conf=0.76)

  cites [84] Wohlgemuth, S. E., Seo, A. Y., Marzetti, E., Lees, H. A. & Leeuwenburgh, C. Skeletal muscle autophagy and apoptosis during aging: effects of calorie restriction and life-long exercise. Exp. Gerontol. 45, 138–148 (2010). sourceExperimental — accuracy not yet measured

In the paper

“Myocyte apoptosis can be abrogated by physical activity125,126, while mechanisms of cellular quality control, including autophagy, mitophagy and mitochondriogenesis127, contribute to the development of sarcopenic obesity and could be potential targets for therapy.”

What the sources say

• Partly supported

  The Introduction links declining cellular quality control to age-related muscle loss and describes the importance of removing damaged mitochondria and generating new ones. The Discussion suggests that improved cellular quality control may benefit muscle function after weight loss and exercise. But the Abstract explicitly says it remains undetermined whether impaired cellular quality control contributes to sarcopenia; the paper does not establish that these mechanisms cause sarcopenic obesity or identify all three as therapeutic targets. No page numbers are available in our copy. (LLM, conf=0.88)

  cites [127] Wohlgemuth, S. E. et al. An exploratory analysis of the effects of a weight loss plus exercise program on cellular quality control mechanisms in older overweight women. Rejuvenation Res. 14, 315–324 (2011). sourceExperimental — accuracy not yet measured

In the paper

“The FNIH suggested testing for low lean mass using DXA (defined using appendicular lean mass) and reduced muscle function using handgrip strength.”

What the sources say

• Supported

  The Methods (Measures; page unavailable) define appendicular lean mass as the sum of arm and leg lean mass and describe its measurement using DXA in the main study datasets. The Results (Table 3; page unavailable) recommend BMI-adjusted appendicular lean mass for low lean mass and handgrip-strength cutpoints for weakness. The paper notes that two contributing datasets used other body-composition methods. (LLM, conf=0.92)

  cites [182] Studenski, S. A. et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J. Gerontol. A Biol. Sci. Med. Sci. 69, 547–558 (2014). This report details recommendations from the Foundation of the National Institutes on Health Sarcopenia Project, which aggregated multiple cohorts of older adults and created cut-off points to permit identification of low muscle mass and low muscle strength. source

In the paper

“Investigators assigned participants to partake in varying intensities of resistance exercises. The investigators reported no alterations in concentrations of leptin, but participants had intensity-dependent changes in adiponectin139,145 — high-intensity resistance training led to an increase in the concentrations of adiponectin for 24 hours after exercise in inactive adults who were overweight139.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [139] Fatouros, I. G. et al. Intensity of resistance exercise determines adipokine and resting energy expenditure responses in overweight elderly individuals. Diabetes Care 32, 2161–2167 (2009). source
• ?Not checked — no full text of the sourcecites [145] Fatouros, I. G. et al. Leptin and adiponectin responses in overweight inactive elderly following resistance training and detraining are intensity related. J. Clin. Endocrinol. Metab. 90, 5970–5977 (2005). source

In the paper

“Dual-energy X-ray absorptiometry (DXA) is recommended for the assessment of appendicular lean mass in the diagnosis of sarcopenia156 owing to its affordability, availability and diagnostic accuracy157.”

What the sources say

• Supported

  The citation to this paper (156) supports the recommendation to use DXA, not the subsequent rationale cited to 157. In the Assessment techniques section, the paper calls DXA the preferred alternative for research and clinical use, and Table 5 lists DXA measurements of appendicular lean mass for diagnosing sarcopenia. Page numbers are not provided in the supplied passages. (LLM, conf=0.91)

  cites [156] Cruz-Jentoft, A. J. et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 39, 412–423 (2010). source
• ?Not checked — no full text of the sourcecites [157] Kendler, D. L. et al. The Official Positions of the International Society for Clinical Densitometry: indications of use and reporting of DXA for body composition. J. Clin. Densitom. 16, 496–507 (2013). source

In the paper

“The Foundation for the National Institutes of Health (FNIH) Sarcopenia Project182 suggested a causal, indirect relationship between muscle mass and function in their definition of sarcopenia.”

What the sources say

• Supported

  The passage labeled Abstract > Conclusions describes an indirect pathway: some adults have functional limitations because they are weak, and are weak in part because they have low muscle mass. The Discussion says the project links lean mass to weakness and weakness to mobility impairment. The paper cautions that this is not a direct, strong causal pathway for everyone. (LLM, conf=0.87)

  cites [182] Studenski, S. A. et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J. Gerontol. A Biol. Sci. Med. Sci. 69, 547–558 (2014). This report details recommendations from the Foundation of the National Institutes on Health Sarcopenia Project, which aggregated multiple cohorts of older adults and created cut-off points to permit identification of low muscle mass and low muscle strength. source

In the paper

“Resistance training seems to be more efficient in reducing leptin levels than aerobic training alone146, though conflicting evidence exists147.”

What the sources say

• Supported

  The Discussion reports that resistance or strength training produced greater leptin suppression than aerobic training for the same amount of fat loss. The Results (Additional analyses) likewise report a steeper relationship between fat loss and leptin reduction for resistance or mixed training than for aerobic training. The separate statement about conflicting evidence is attached to citation 147, not this source. (LLM, conf=0.92)

  cites [146] Rostas, I. et al. In middle-aged and old obese patients, training intervention reduces leptin level: a meta-analysis. PLoS ONE 12, e0182801 (2017). source
• ?Not checked — no full text of the sourcecites [147] Nikseresht, M., Sadeghifard, N., Agha-Alinejad, H. & Ebrahim, K. Inflammatory markers and adipocytokine responses to exercise training and detraining in men who are obese. J. Strength Cond. Res. 28, 3399–3410 (2014). source

In the paper

“Following a 12-week diet–exercise intervention in male and female frail adults with obesity aged 69 ± 1 years, investigators reported reduced skeletal muscle levels of mRNA for TLR4, IL6 and TNF, increased mechano growth factor mRNA and increased fat-free mass in the exercise group, and these results were independent of weight loss133.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [133] Lambert, C. P., Wright, N. R., Finck, B. N. & Villareal, D. T. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese elderly persons. J. Appl. Physiol. (1985) 105, 473–478 (2008). sourceExperimental — accuracy not yet measured

In the paper

“Expression of skeletal muscle TNF, IL-1β and nitric oxide synthase, inducible in patients with heart failure was reduced following aerobic training, suggesting that aerobic exercise has anti-inflammatory effects135.”

What the sources say

• Supported

  The Discussion reports that six months of aerobic endurance training reduced skeletal-muscle TNF-alpha, IL-1-beta, and iNOS expression in patients with stable chronic heart failure. It explicitly describes these as local anti-inflammatory effects. (LLM, conf=0.95)

  cites [135] Gielen, S. et al. Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure. J. Am. Coll. Cardiol. 42, 861–868 (2003). source

In the paper

“Assessments of lean mass are highly reproducible and can be used for clinical monitoring, while a detailed assessment of visceral fat is not as accurate150,161–163.”

What the sources say

• ?Not checked — no full text of the sourcecites [150] Woodrow, G. Body composition analysis techniques in the aged adult: indications and limitations. Curr. Opin. Clin. Nutr. Metab. Care 12, 8–14 (2009). source
• ?Not checked — no full text of the sourcecites [161] Park, Y. W., Heymsfield, S. B. & Gallagher, D. Are dual-energy X-ray absorptiometry regional estimates associated with visceral adipose tissue mass? Int. J. Obes. Relat. Metab. Disord. 26, 978–983 (2002). source
• Partly supported

  The Abstract (page unavailable) says DXA measures body composition with high precision, which broadly supports the lean-mass reproducibility claim, but the paper does not establish its use for clinical monitoring. The Discussion (page unavailable) reports strong agreement between DXA and CT visceral-fat measurements, rather than finding detailed visceral-fat assessment less accurate. (LLM, conf=0.82)

  cites [162] Kaul, S. et al. Dual-energy X-ray absorptiometry for quantification of visceral fat. Obesity 20, 1313–1318 (2012). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page unavailable) says DXA cannot measure visceral fat directly and that modelling it introduces estimation errors. It does not establish that lean-mass assessments are highly reproducible or suitable for clinical monitoring, or compare their accuracy with visceral-fat assessments. The study also reports that DXA visceral-fat measurements performed comparably to clinical CT. (LLM, conf=0.82)

  cites [163] Micklesfield, L. K., Goedecke, J. H., Punyanitya, M., Wilson, K. E. & Kelly, T. L. Dual-energy X-ray performs as well as clinical computed tomography for the measurement of visceral fat. Obesity 20, 1109–1114 (2012). sourceExperimental — accuracy not yet measured

In the paper

“The European Working Group for the Study of Sarcopenia (EWGSOP)156 identified sarcopenia cut-off points and tools for its measurement. They recognized the lack of diagnostic criteria for sarcopenia but integrated low muscle mass and function (strength or performance) in their terminology, believing that the relationship between these two measures is not linear nor bidirectional73,156,181.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [156] Cruz-Jentoft, A. J. et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 39, 412–423 (2010). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [73] Goodpaster, B. H. et al. The loss of skeletal muscle strength, mass, and quality in older adults: the health, aging and body composition study. J. Gerontol. A Biol. Sci. Med. Sci. 61, 1059–1064 (2006). This study shows that loss of strength with ageing is much more rapid than the concomitant loss of muscle mass, suggesting a decline in muscle quality. source
• ?Not checked — no full text of the sourcecites [181] Janssen, I., Baumgartner, R. N., Ross, R., Rosenberg, I. H. & Roubenoff, R. Skeletal muscle cutpoints associated with elevated physical disability risk in older men and women. Am. J. Epidemiol. 159, 413–421 (2004). source

In the paper

“EWGSOP recommended that muscle mass is assessed by DXA or bioelectrical impedance, using mathematical thresholds and formulas presented in their consensus document.”

What the sources say

• Supported

  The Assessment techniques section recommends DXA for research and clinical use and describes BIA as a portable alternative. Tables 4 and 5 list both methods for muscle-mass assessment and give indices, formulas, and cut-off points; the supplied passages do not specify page numbers. (LLM, conf=0.92)

  cites [156] Cruz-Jentoft, A. J. et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 39, 412–423 (2010). source

In the paper

“Resistance exercise increases the number and size of fast twitching muscle fibres (IIA and IIX), which improve glucose metabolism in muscle and muscle protein synthesis102,103,137–139.”

What the sources say

• ?Not checked — no full text of the sourcecites [102] Yarasheski, K. E., Zachwieja, J. J. & Bier, D. M. Acute effects of resistance exercise on muscle protein synthesis rate in young and elderly men and women. Am. J. Physiol. 265, E210–E214 (1993). source
• ?Not checked — no full text of the sourcecites [103] Yarasheski, K. E. et al. Resistance exercise training increases mixed muscle protein synthesis rate in frail women and men >/=76 yr old. Am. J. Physiol. 277, E118–E125 (1999). source
• ?Not checked — no full text of the sourcecites [137] Andersen, L. L. et al. Changes in the human muscle force-velocity relationship in response to resistance training and subsequent detraining. J. Appl. Physiol. (1985) 99, 87–94 (2005). source
• ?Not checked — no full text of the sourcecites [138] Englund, D. A., Sharp, R. L., Selsby, J. T., Ganesan, S. S. & Franke, W. D. Resistance training performed at distinct angular velocities elicits velocity-specific alterations in muscle strength and mobility status in older adults. Exp. Gerontol. 91, 51–56 (2017). source
• Partly supported

  The Conclusions (page not available in our copy) say chronic resistance exercise can add muscle mass and that muscle protein turnover may remain elevated after heavy exercise. They do not identify increases in the number or size of type IIA or IIX fibres, or say that such changes improve muscle glucose metabolism and protein synthesis. The study examined acute responses in overweight older adults, not those fibre changes. (LLM, conf=0.84)

  cites [139] Fatouros, I. G. et al. Intensity of resistance exercise determines adipokine and resting energy expenditure responses in overweight elderly individuals. Diabetes Care 32, 2161–2167 (2009). sourceExperimental — accuracy not yet measured

In the paper

“The International Working Group for the Study of Sarcopenia (IWGS) provided a consensus definition for sarcopenia180 as the combination of low whole-body or appendicular lean mass and poor physical functioning (gait speed ≤1 m/s).”

What the sources say

• Partly supported

  The Current Consensus Definition section defines sarcopenia using low whole-body or appendicular fat-free mass combined with poor physical functioning. It specifies gait speed of less than 1.0 m/s, however, whereas the citing sentence says ≤1 m/s; the paper's threshold does not include exactly 1.0 m/s. No page number is available in our copy. (LLM, conf=0.86)

  cites [180] Fielding, R. A. et al. Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J. Am. Med. Dir. Assoc. 12, 249–256 (2011). This is a consensus statement from the International Working Group on Sarcopenia that presents evidence and a definition for the identification of sarcopenia. sourceExperimental — accuracy not yet measured

In the paper

“A study into the effects of aerobic activity in patients who had recovered from breast cancer reported that individuals who were randomized to the aerobic exercise group demonstrated reductions in insulin and leptin and increases in the adiponectin:leptin ratio but no significant changes in adiponectin compared with participants in the usual activity group148.”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [148] Friedenreich, C. M. et al. Changes in insulin resistance indicators, IGFs, and adipokines in a year-long trial of aerobic exercise in postmenopausal women. Endocr. Relat. Cancer 18, 357–369 (2011). sourceExperimental — accuracy not yet measured

In the paper

“Further validation of bioelectrical impedance results is needed in individuals aged ≥80 years, as they are at increased risk of sarcopenic obesity177,178.”

What the sources say

• Partly supported

  The Results report that sarcopenic obesity prevalence increased with age, supporting the concern about older individuals. The Methods say body composition was measured with DEXA, and the Discussion mentions bioelectrical impedance only as an approach used elsewhere; neither section calls for further validation of its results in people aged ≥80 years. Page numbers are unavailable in our copy. (LLM, conf=0.86)

  cites [177] Batsis, J. A., Mackenzie, T. A., Lopez-Jimenez, F. & Bartels, S. J. Sarcopenia, sarcopenic obesity, and functional impairments in older adults: National Health and Nutrition Examination Surveys 1999–2004. Nutr. Res. 35, 1031–1039 (2015). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [178] Batsis, J. A. et al. Variation in the prevalence of sarcopenia and sarcopenic obesity in older adults associated with different research definitions: dual-energy X-ray absorptiometry data from the National Health and Nutrition Examination Survey 1999–2004. J. Am. Geriatr. Soc. 61, 974–980 (2013). This study applies multiple definitions of sarcopenic obesity on a cohort of American adults and emphasizes the varied prevalences of this disorder. source

In the paper

“Furthermore, a 12-week aerobic and resistance programme increased serum levels of ghrelin and adiponectin by 47% and 55%, respectively, and reduced circulating levels of CD14+ and CD16+ inflammatory monocytes, adding additional evidence to the anti-inflammatory effects of exercise136.”

What the sources say

• Supported

  The paper reports that 12 weeks of combined aerobic and resistance training increased ghrelin and adiponectin by 47% and 55%, respectively (opening summary). The Discussion reports a concomitant reduction in circulating CD14+CD16+ inflammatory monocytes and presents the findings as evidence relevant to exercise’s anti-inflammatory effects. Page numbers are not available in the supplied passages. (LLM, conf=0.91)

  cites [136] Markofski, M. M. et al. Exercise training modifies ghrelin and adiponectin concentrations and is related to inflammation in older adults. J. Gerontol. A Biol. Sci. Med. Sci. 69, 675–681 (2014). source

In the paper

“This algorithm was meant for clinical application using gait speed (<0.8 m/s) before muscle mass or strength measurement.”

What the sources say

• Partly supported

  The ‘Sarcopenia screening and assessment’ section says the EWGSOP algorithm was intended for clinical practice and begins with gait-speed measurement, supporting the stated sequence. But that section gives a risk cut-off of >0.8 m/s, not <0.8 m/s. The ‘Assessment techniques’ table lists <0.8 m/s as a gait-speed cut-off without explicitly tying it to the algorithm. (LLM, conf=0.84)

  cites [156] Cruz-Jentoft, A. J. et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 39, 412–423 (2010). sourceExperimental — accuracy not yet measured

In the paper

“The rates of sarcopenic obesity increased with age, reaching 48.0% and 27.5% in females and males, respectively, in those aged over 80 years198.”

What the sources say

• Supported

  Table 3 in the Results reports that low lean mass with obesity increased across age groups in both sexes. In the 80+ group, prevalence was 48.0% for females and 27.5% for males. (LLM, conf=0.95)

  cites [198] Batsis, J. A., Mackenzie, T. A., Emeny, R. T., Lopez-Jimenez, F. & Bartels, S. J. Low lean mass with and without obesity, and mortality: results from the 1999–2004 National Health and Nutrition Examination Survey. J. Gerontol. A Biol. Sci. Med. Sci. 72, 1445–1451 (2017). This report details the definition of low lean mass determined by the Foundation of the National Institutes of Health, as well as the adverse association between low lean mass and mortality. source

In the paper

“FNIH deliberately avoided the term sarcopenia to differentiate between qualitative (strength) and quantitative (mass) components.”

What the sources say

• Supported

  In the passage labelled Abstract > Conclusions (no page number available), the authors say they decided to avoid the term “sarcopenia” because its meaning was confused, using “low lean mass” and “weakness” instead. That supports the claim that FNIH deliberately used separate terms for mass and strength. (LLM, conf=0.91)

  cites [182] Studenski, S. A. et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J. Gerontol. A Biol. Sci. Med. Sci. 69, 547–558 (2014). This report details recommendations from the Foundation of the National Institutes on Health Sarcopenia Project, which aggregated multiple cohorts of older adults and created cut-off points to permit identification of low muscle mass and low muscle strength. source

In the paper

“FNIH stated that sex-specific cut-off points could be adjusted for BMI.”

What the sources say

• Supported

  The Results (Table 3) give separate cutoffs for men and women using BMI-adjusted appendicular lean mass, and also list BMI-adjusted grip-strength cutoffs as an alternative. This supports the statement that FNIH presented sex-specific cutoffs adjusted for BMI. (LLM, conf=0.93)

  cites [182] Studenski, S. A. et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J. Gerontol. A Biol. Sci. Med. Sci. 69, 547–558 (2014). This report details recommendations from the Foundation of the National Institutes on Health Sarcopenia Project, which aggregated multiple cohorts of older adults and created cut-off points to permit identification of low muscle mass and low muscle strength. source

In the paper

“Investigators from the Cardiovascular Health Study used low grip strength and high waist circumference to define low muscle strength and obesity. Rates approached 11.1%201, while data from FNIH classified 4.1% of men and 14.0% of women as having sarcopenic obesity using high BMI and low grip strength as measures of obesity and low muscle strength, respectively202.”

What the sources say

• Supported

  The Measurements section says waist circumference and grip strength were used to classify participants. The Results (Subject Characteristics) report that 11.1% were sarcopenic-obese under the obesity-by-muscle-strength classification; the Discussion specifies high waist circumference and low hand-grip strength. (LLM, conf=0.92)

  cites [201] Stephen, W. C. & Janssen, I. Sarcopenic-obesity and cardiovascular disease risk in the elderly. J. Nutr. Health Aging 13, 460–466 (2009). source

In the paper

“The separate criteria for muscle mass and strength implied the need to target interventions for individuals with low mass or low strength.”

What the sources say

• Partly supported

  The Conclusions distinguish weakness from low muscle mass and suggest that people whose low mass contributes to weakness may benefit from muscle-mass interventions, while people weak for other reasons may need different interventions. The Discussion proposes trials for people with varying degrees of weakness and low lean mass. It does not establish a need to target interventions at everyone with low mass or low strength; it says low mass alone is not consistently associated with adverse outcomes. (LLM, conf=0.85)

  cites [182] Studenski, S. A. et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J. Gerontol. A Biol. Sci. Med. Sci. 69, 547–558 (2014). This report details recommendations from the Foundation of the National Institutes on Health Sarcopenia Project, which aggregated multiple cohorts of older adults and created cut-off points to permit identification of low muscle mass and low muscle strength. sourceExperimental — accuracy not yet measured

In the paper

“In one study, BMI correctly classified 41.0% of men and 45.1% of women as being obese and waist circumference correctly classified 64.2% of men and 81.0% ofwomen as being obese194.”

What the sources say

• Partly supported

  The Abstract Results report that BMI ≥30 kg/m² correctly classified 41.0% of obese men and 45.1% of obese women. The Results say Table 2B assesses waist circumference, but the passages available in our copy do not give the claimed 64.2% and 81.0% figures, so that part is not verified. (LLM, conf=0.83)

  cites [194] Batsis, J. A. et al. Diagnostic accuracy of body mass index to identify obesity in older adults: NHANES 1999–2004. Int. J. Obes. (Lond.) 40, 761–767 (2016). This study emphasizes the challenges of using BMI as a marker for obesity. BMI has a poor sensitivity in ascertaining body fat-defined obesity that worsens with age. sourceExperimental — accuracy not yet measured

In the paper

“Obesity is defined as an unhealthy excess body fat that increases the risk of medical illness and mortality186.”

What the sources say

• Supported

  The “Definition of Obesity” section directly defines obesity as an unhealthy excess of body fat that increases the risk of medical illness and premature mortality. The citing sentence closely paraphrases that definition. (LLM, conf=0.95)

  cites [186] Villareal, D. T. et al. Obesity in older adults: technical review and position statement of the American Society for Nutrition and NAASO, The Obesity Society. Am. J. Clin. Nutr. 82, 923–934 (2005). This study highlights current guidelines for the management of older adults with obesity. source

In the paper

“Aerobic exercise improves cardiorespiratory fitness and has beneficial effects on mortality276–278.”

What the sources say

• Supported

  The Abstract’s Methods and Results report that exercise significantly increased cardiorespiratory fitness. The Conclusions also report better survival after exercise interventions in secondary-prevention studies; mortality was not an outcome measured by this meta-analysis. (LLM, conf=0.87)

  cites [276] Lin, X. et al. Effects of exercise training on cardiorespiratory fitness and biomarkers of cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials. J. Am. Heart Assoc. 4, e002014 (2015). source
• ?Not checked — no full text of the sourcecites [277] Hwang, C. L., Wu, Y. T. & Chou, C. H. Effect of aerobic interval training on exercise capacity and metabolic risk factors in people with cardiometabolic disorders: a meta-analysis. J. Cardiopulm. Rehabil. Prev. 31, 378–385 (2011). source
• ?Not checked — no full text of the sourcecites [278] Sui, X. M. et al. Cardiorespiratory fitness and adiposity as mortality predictors in older adults. JAMA 298, 2507–2516 (2007). source

In the paper

“intentional weight loss in older adults improves morbidity and physical function186”

What the sources say

• Partly supported

  The Physical function and quality of life section reports improved physical function in obese older adults when moderate weight loss was combined with exercise. The Medical complications section reports improvements in obesity-related metabolic abnormalities, but says most studies of these effects were conducted in middle-aged adults; it does not establish improved morbidity in older adults. The claim also omits the exercise component of the physical-function finding. (LLM, conf=0.86)

  cites [186] Villareal, D. T. et al. Obesity in older adults: technical review and position statement of the American Society for Nutrition and NAASO, The Obesity Society. Am. J. Clin. Nutr. 82, 923–934 (2005). This study highlights current guidelines for the management of older adults with obesity. sourceExperimental — accuracy not yet measured

In the paper

“chronic calorie restriction does not seem to reduce muscle protein synthesis, but it might increase it105,255”

What the sources say

• ?Could not verify

  The Methods (Experimental protocol; page unavailable) say participants were counseled to maintain a weight-maintaining diet, not to restrict calories. The Results (Muscle protein synthesis rate; page unavailable) report increased synthesis after exercise training. The copy therefore does not address whether chronic calorie restriction reduces or increases muscle protein synthesis; I searched for calorie restriction, energy restriction, and weight loss. (LLM, conf=0.76)

  cites [105] Villareal, D. T., Smith, G. I., Sinacore, D. R., Shah, K. & Mittendorfer, B. Regular multicomponent exercise increases physical fitness and muscle protein anabolism in frail, obese, older adults. Obesity (Silver Spring) 19, 312–318 (2011). This study demonstrates that a multicomponent exercise programme consisting of strength, endurance, flexibility and balance increases the basal rate of muscle protein synthesis without affecting the magnitude of the muscle protein anabolic response to feeding. sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (Muscle protein synthesis; page unavailable) report that postabsorptive and total muscle protein synthesis increased after weight loss, while postprandial synthesis did not change. But the Discussion says measurements were made after energy balance was restored, not during calorie restriction, and that the study could not separate the effects of restriction from weight loss. The broader claim about chronic calorie restriction therefore goes beyond this finding in older women. (LLM, conf=0.86)

  cites [255] Campbell, W. W. et al. Resistance training preserves fat-free mass without impacting changes in protein metabolism after weight loss in older women. Obesity (Silver Spring) 17, 1332–1339 (2009). sourceExperimental — accuracy not yet measured

In the paper

“Distributing protein intake throughout the day259 or pulse feeding at main meals260 could be beneficial for the stimulation of muscle protein synthesis in patients with sarcopenic obesity.”

What the sources say

• Partly supported

  The “Protein intake pattern” section says pulse feeding may improve feeding-induced protein synthesis in older adults. The “Sarcopenic obesity and protein intake” section recommends increased protein intake for sarcopenic obesity, but does not specifically recommend pulse feeding or establish its benefit for protein synthesis in those patients. Page numbers were not available in our copy. (LLM, conf=0.86)

  cites [259] Deutz, N. E. et al. Protein intake and exercise for optimal muscle function with aging: recommendations from the ESPEN Expert Group. Clin. Nutr. 33, 929–936 (2014). These are the European Society for Clinical Nutrition and Metabolism workshop recommendations on protein requirements in elderly individuals. sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [260] Bouillanne, O. et al. Impact of protein pulse feeding on lean mass in malnourished and at-risk hospitalized elderly patients: a randomized controlled trial. Clin. Nutr. 32, 186–192 (2013). source

In the paper

“The findings demonstrated increases in physical performance test scores (higher score equals higher level of function), more so in the combined aerobic and resistance exercise group (27.9 to 33.4 points (21% increase)) than in the aerobic (29.3 to 33.2 points (14% increase)) or resistance group (28.8 to 32.7 points (14% increase)) alone.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [247] Villareal, D. T. et al. Aerobic or resistance exercise, or both in dieting obese older adults. N. Engl. J. Med. 376, 1943–1955 (2017). This is a randomized trial of older adults with obesity and frailty demonstrating that weight loss coupled with both aerobic and resistance activities is associated with improved physical function. source

In the paper

“patients in the intervention group regained appendicular lean mass during the second year and that weight loss was 5.2 kg less in the intervention group than in participants in the control group, whose weight did not markedly change after the second year310”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [310] Gallagher, D. et al. Changes in skeletal muscle and organ size after a weight-loss intervention in overweight and obese type 2 diabetic patients. Am. J. Clin. Nutr. 105, 78–84 (2017). source

In the paper

“Adipose tissue has been shown to be inversely associated with bone material strength and positively associated with cortical porosity, indicating an adverse effect of adipose tissue on bone microstructure317.”

What the sources say

• Partly supported

  The Results report that local tibial adipose tissue was inversely correlated with bone material strength index and positively correlated with cortical porosity in older women. The Discussion describes an adverse effect on cortical bone microstructure as possible, whereas the citing sentence presents it without that qualification and does not specify the studied population. (LLM, conf=0.85)

  cites [317] Sundh, D. et al. A high amount of local adipose tissue is associated with high cortical porosity and low bone material strength in older women. J. Bone Miner. Res. 31, 749–757 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Although the LIFE study is considered a standard for physical activity in older adults282, we acknowledge its lack of evidence in sarcopenic obesity and the lack of power in this pilot trial.”

What the sources say

• Supported

  The citation is attached to the identification of the LIFE study as a physical-activity study in older adults. The Abstract’s Design, Setting, and Participants section describes a randomized trial of 1,635 sedentary adults aged 70–89. The statements about sarcopenic obesity and the citing authors’ pilot trial are not attributed to this citation. (LLM, conf=0.88)

  cites [282] Pahor, M. et al. Effect of structured physical activity on prevention of major mobility disability in older adults: the LIFE study randomized clinical trial. JAMA 311, 2387–2396 (2014). This study reports on a gold standard, structured, long-term physical activity intervention, consisting of 3–4 times of aerobic, resistance and flexibility training per week, that demonstrates improvements in mobility disability over a 2.6-year follow-up. source

In the paper

“Weight loss in younger adults (age 45–65 years) led to loss of lean mass after calorie restriction (4% reduction in lean mass; P < 0.0001), which was partially lessened by augmentation with aerobic activity (2% reduction in lean mass in participants who had augmented weight loss with aerobic activity; P = 0.05)311.”

What the sources say

• Supported

  The Methods identify participants as sedentary adults aged 45–65. The Abstract Results report that lower-extremity lean mass fell about 4% with calorie restriction (p<0.0001) and about 2% with calorie restriction plus exercise (p=0.05). The percentages refer specifically to lower-extremity lean mass, rather than whole-body lean mass. (LLM, conf=0.94)

  cites [311] Weiss, E. P., Jordan, R. C., Frese, E. M., Albert, S. G. & Villareal, D. T. Effects of weight loss on lean mass, strength, bone, and aerobic capacity. Med. Sci. Sports Exerc. 49, 206–217 (2017). source

In the paper

“A combined treatment of diet and exercise improved physical function in frail older men with obesity aged ≥65 years for 1 year, despite resulting in a reduction in oestradiol levels and only a modest increase in testosterone levels299.”

What the sources say

• Supported

  The Methods specify men aged ≥65 years with obesity and frailty in a 52-week study. The Results report improved physical performance in the diet–exercise group over one year, alongside decreased estradiol and a modest increase in testosterone. (LLM, conf=0.94)

  cites [299] Armamento-Villareal, R., Aguirre, L. E., Qualls, C. & Villareal, D. T. Effect of lifestyle intervention on the hormonal profile of frail, obese older men. J. Nutr. Health Aging 20, 334–340 (2016). source

In the paper

“levels of adiponectin increased in individuals with overweight or obesity compared with controls (diet resulted in 9.5% increase in adiponectin (P < 0.001), and diet and exercise resulted in a 6.6% increase in adiponectin (P < 0.001)). Furthermore, levels of leptin in individuals with obesity or overweight decreased by 27.1% in the diet group and 40.1% in the diet and exercise group302.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [302] Abbenhardt, C. et al. Effects of individual and combined dietary weight loss and exercise interventions in postmenopausal women on adiponectin and leptin levels. J. Intern. Med. 274, 163–175 (2013). sourceExperimental — accuracy not yet measured

In the paper

“2 days of high-resistance concentric exercise with one bout of low-resistance exercise increased muscle expression of pro-inflammatory cytokine receptors, maximized muscle mass and total lean mass and improved knee extension283”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [283] Stec, M. J. et al. Randomized, four-arm, dose-response clinical trial to optimize resistance exercise training for older adults with age-related muscle atrophy. Exp. Gerontol. 99, 98–109 (2017). sourceExperimental — accuracy not yet measured

In the paper

“Energy restriction with a hypocaloric diet with or without exercise results in the loss of approximately one-quarter of lean mass per unit weight, which could worsen sarcopenia and osteopenia154.”

What the sources say

• Partly supported

  The Introduction describes fat-free-mass loss during hypocaloric dieting as a clinical risk, and the Conclusions identify one-quarter of weight loss as fat-free mass as an approximation, not a fixed result. The “With Diet” section reports that adding exercise can reduce fat-free-mass losses. The copy does not specifically link these losses to worsening osteopenia. (LLM, conf=0.87)

  cites [154] Heymsfield, S. B., Gonzalez, M. C., Shen, W., Redman, L. & Thomas, D. Weight loss composition is one-fourth fat-free mass: a critical review and critique of this widely cited rule. Obes. Rev. 15, 310–321 (2014). sourceExperimental — accuracy not yet measured

In the paper

“individuals in the physical activity group had reductions in IL-8 but no differences in other inflammatory markers303”

What the sources say

• Partly supported

  The Abstract Results report that IL-8 was the only biomarker affected in the main analysis, with a 9.9% lower adjusted level in the physical-activity group at 12 months. But they also report reduced IL-15 in participants with high baseline IL-15, and say neither association remained significant after accounting for multiple comparisons. The claim omits those qualifications. (LLM, conf=0.86)

  cites [303] Beavers, K. M. et al. Long-term physical activity and inflammatory biomarkers in older adults. Med. Sci. Sports Exerc. 42, 2189–2196 (2010). sourceExperimental — accuracy not yet measured

In the paper

“A 12-week aerobic exercise regime in combination with a low glycaemic index diet or high glycaemic index diet resulted in reductions in leptin levels in two groups of participants who had elevated levels of adiponectin, suggesting that the reductions in leptin were a result of exercise training and independent of dietary glycaemic index304.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [304] Kelly, K. R. et al. Lifestyle-induced decrease in fat mass improves adiponectin secretion in obese adults. Med. Sci. Sports Exerc. 46, 920–926 (2014). source

In the paper

“Whole-body vibration therapy was as efficient as a fitness programme at increasing knee extension and lower leg muscle mass in non-institutionalized men aged 60–80 years old372 and improved quality of life and functional measures373.”

What the sources say

• ?Not checked — no full text of the sourcecites [372] Bogaerts, A. et al. Impact of whole-body vibration training versus fitness training on muscle strength and muscle mass in older men: a 1-year randomized controlled trial. J. Gerontol. A Biol. Sci. Med. Sci. 62, 630–635 (2007). source
• Supported

  Citation 373 is attached to the claim that whole-body vibration improved quality of life and functional measures, not to the preceding comparison with a fitness programme. The Discussion reports a significant increase in the quality-of-life index and significant improvements in physical fitness after the 12-week intervention. (LLM, conf=0.92)

  cites [373] Chang, S. F., Lin, P. C., Yang, R. S. & Yang, R. J. The preliminary effect of whole-body vibration intervention on improving the skeletal muscle mass index, physical fitness, and quality of life among older people with sarcopenia. BMC Geriatr. 18, 17 (2018). source

In the paper

“Widespread availability of DXA even in low-resource areas344 permits this evaluation.”

What the sources say

• Partly supported

  The Results report that 75.4% of rural Medicare beneficiaries lived within five miles of a DXA provider, supporting availability in many rural US areas. But the paper does not establish availability in low-resource areas as such; its Discussion also notes that rural access is more vulnerable to provider closures. The cited paper studies access to DXA testing, not its use to evaluate muscle mass. (LLM, conf=0.84)

  cites [344] Curtis, J. R. et al. The geographic availability and associated utilization of dual-energy X-ray absorptiometry (DXA) testing among older persons in the United States. Osteoporos. Int. 20, 1553–1561 (2009). sourceExperimental — accuracy not yet measured

In the paper

“Hengting Chen and colleagues370 identified 10 randomized trials of whole-body vibration therapy showing its usefulness in younger adults (difference (d) = 0.35 (95% CI 0.05–0.64; P = 0.02)), but this usefulness was not seen in older adults (d = −0.04 (95% CI −0.28 to 0.21; P = 0.78)).”

What the sources say

• Partly supported

  The Abstract (Results) identifies 10 randomized trials, and the Results (Main analysis) report the quoted effect sizes and confidence intervals: a significant improvement in young adults but not in older adults. The measured outcome was muscle or lean mass, however, so the unqualified claim that therapy was generally “useful” extends beyond what the review established. The quoted P = 0.78 for older adults does not appear in the available Results passage. (LLM, conf=0.82)

  cites [370] Chen, H., Ma, J., Lu, B. & Ma, X. L. The effect of whole-body vibration training on lean mass: a PRISMA-compliant meta-analysis. Medicine (Baltimore) 96, e8390 (2017). sourceExperimental — accuracy not yet measured

In the paper

“The introduction in 2016 of an International Classification of Diseases 10 code for sarcopenia (M62.84) will permit clinical recognition and promote its diagnosis, classification and drug development339,340.”

What the sources say

• Supported

  The Abstract says sarcopenia received ICD-10-CM code M62.84 in September 2016, marking its recognition as a disease entity. It also predicts greater physician interest in diagnosis, more diagnostic tools, and accelerated drug development; the code supplies the classification described in the claim. (LLM, conf=0.91)

  cites [339] Anker, S. D., Morley, J. E. & von Haehling, S. Welcome to the ICD-10 code for sarcopenia. J. Cachexia Sarcopenia Muscle 7, 512–514 (2016). sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Data and Results sections discuss obesity, smoking and disability in forecasts of healthy life expectancy, not sarcopenia coding. Searches for sarcopenia, M62.84, ICD-10 and related diagnostic terms found no passage addressing the claimed effects of the code’s introduction. (LLM, conf=0.76)

  cites [340] Cao, B. Future healthy life expectancy among older adults in the US: a forecast based on cohort smoking and obesity history. Popul. Health Metr. 14, 23 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Levels of osteocalcin were increased in the diet-only group (36 ± 11.6%), yet its levels were no different than baseline in individuals on diet coupled with exercise;”

What the sources say

• Supported

  Section 3.2 (Results) reports that serum undercarboxylated osteocalcin increased by 36.0 ± 11.6% at 12 months in the diet-only group and did not change in the diet-plus-exercise group. The quoted percentage refers specifically to undercarboxylated osteocalcin, rather than total osteocalcin. (LLM, conf=0.94)

  cites [320] Colleluori, G., Napoli, N., Phadnis, U., Armamento-Villareal, R. & Villareal, D. T. Effect of weight loss, exercise, or both on undercarboxylated osteocalcin and insulin secretion in frail, obese older adults. Oxid. Med. Cell. Longev. 2017, 4807046 (2017). source

In the paper

“The review included heterogeneous studies using different methodologies, training and vibration characteristics.”

What the sources say

• Supported

  The Methods (Statistical methods; page unavailable) identify differences in control interventions, vibration frequency, magnitude, acceleration, dose, and lean-mass measurement as sources of clinical heterogeneity. The Inclusion and exclusion criteria also allowed varied training positions, vibration settings, and study durations, supporting the characterization of the included studies as heterogeneous. (LLM, conf=0.88)

  cites [370] Chen, H., Ma, J., Lu, B. & Ma, X. L. The effect of whole-body vibration training on lean mass: a PRISMA-compliant meta-analysis. Medicine (Baltimore) 96, e8390 (2017). source

In the paper

“Adverse events associated with testosterone supplementation include polycythemia420, possible cardiovascular events421, venous thromboembolism422 and prostatism423.”

What the sources say

• Supported

  Citation 420 is attached to “polycythemia,” not to the later adverse events, which have separate citations. The Abstract (Introduction) identifies polycythemia as a side effect of testosterone therapy, supporting the attributed claim. (LLM, conf=0.94)

  cites [420] Ohlander, S. J., Varghese, B. & Pastuszak, A. W. Erythrocytosis following testosterone therapy. Sex. Med. Rev. 6, 77–85 (2018). source
• ?Not checked — no full text of the sourcecites [421] Albert, S. G. & Morley, J. E. Testosterone therapy, association with age, initiation and mode of therapy with cardiovascular events: a systematic review. Clin. Endocrinol. (Oxf.) 85, 436–443 (2016). source
• Supported

  Citation 422 is attached specifically to venous thromboembolism, not the other listed adverse events. The Abstract reports that starting testosterone treatment was associated with increased venous thromboembolism risk, peaking within six months and declining thereafter (page not specified). (LLM, conf=0.93)

  cites [422] Martinez, C. et al. Testosterone treatment and risk of venous thromboembolism: population based case-control study. BMJ 355, i5968 (2016). source

In the paper

“Bariatric surgery leads to loss of fat mass394, alters gut hormones395 and can exacerbate weight loss-induced sarcopenia396–398 and osteoporosis399–402.”

What the sources say

• Partly supported

  This source is cited for the sarcopenia portion of the sentence, not the separately cited claims about fat mass, gut hormones, or osteoporosis. The Results and Conclusions (pages unavailable) report continued lean-tissue loss and reduced handgrip strength after Roux-en-Y gastric bypass in five women. They do not establish that bariatric surgery generally exacerbates diagnosed, weight-loss-induced sarcopenia. (LLM, conf=0.82)

  cites [394] Cole, A. J. et al. Long-term body composition changes in women following roux-en-Y gastric bypass surgery. JPEN J. Parenter. Enteral Nutr. 41, 583–591 (2017). sourceExperimental — accuracy not yet measured
• Supported

  This source supports the ‘alters gut hormones’ clause, to which its citation is attached. The Final conclusions report augmented GLP-1 secretion after Roux-en-Y gastric bypass surgery. The separately cited claims about fat mass, sarcopenia, and osteoporosis are not attributed to this source. (LLM, conf=0.92)

  cites [395] Anderwald, C. H. et al. Alterations in gastrointestinal, endocrine, and metabolic processes after bariatric Roux-en-Y gastric bypass surgery. Diabetes Care 35, 2580–2587 (2012). source
• ?Not checked — no full text of the sourcecites [396] Lyytinen, T., Liikavainio, T., Paakkonen, M., Gylling, H. & Arokoski, J. P. Physical function and properties of quadriceps femoris muscle after bariatric surgery and subsequent weight loss. J. Musculoskelet. Neuronal Interact. 13, 329–338 (2013).
• ?Not checked — no full text of the sourcecites [397] Thibault, R., Huber, O., Azagury, D. E. & Pichard, C. Twelve key nutritional issues in bariatric surgery. Clin. Nutr. 35, 12–17 (2016). source
• ?Not checked — no full text of the sourcecites [398] Vaurs, C. et al. Determinants of changes in muscle mass after bariatric surgery. Diabetes Metab. 41, 416–421 (2015). source

In the paper

“Over 56 weeks, testosterone-treated participants (mean age 53 years) had greater reductions in fat mass (mean between-group difference 2.9 kg; P = 0.04) and visceral fat (−2,678 mm2; P = 0.04) than controls.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [419] Ng Tang Fui, M. et al. Effects of testosterone treatment on body fat and lean mass in obese men on a hypocaloric diet: a randomised controlled trial. BMC Med. 14, 153 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Testosterone-treated participants also had greater lean mass regain during weight maintenance (mean between-group difference 3.4 kg; P = 0.002) following the very-low-energy diet, suggesting that weight loss was exclusively fat mass419.”

What the sources say

• Partly supported

  The Discussion reports greater lean-mass regain in testosterone-treated men after the very-low-energy diet. It says the 3.4 kg difference was measured at study end, not specifically as a between-group difference in regain during weight maintenance, and describes weight loss as 'almost exclusive' fat-mass loss rather than exclusively fat-mass loss. Page numbers are not available in the supplied passages. (LLM, conf=0.87)

  cites [419] Ng Tang Fui, M. et al. Effects of testosterone treatment on body fat and lean mass in obese men on a hypocaloric diet: a randomised controlled trial. BMC Med. 14, 153 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Conflicting data exist; in some studies, vitamin K antagonists demonstrate no differences in BMD or fracture rates461, while other data suggest lessening of steroid-induced BMD462 and sex-specific improvements in insulin sensitivity463.”

What the sources say

• ?Not checked — no full text of the sourcecites [461] Jamal, S. A., Browner, W. S., Bauer, D. C. & Cummings, S. R. Warfarin use and risk for osteoporosis in elderly women. Study of Osteoporotic Fractures Research Group. Ann. Intern. Med. 128, 829–832 (1998). source
• ?Not checked — no full text of the sourcecites [462] Yonemura, K., Kimura, M., Miyaji, T. & Hishida, A. Short-term effect of vitamin K administration on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis. Calcif. Tissue Int. 66, 123–128 (2000). source
• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [463] Yoshida, M. et al. Effect of vitamin K supplementation on insulin resistance in older men and women. Diabetes Care 31, 2092–2096 (2008). source

In the paper

“Early trials demonstrated a greater total lean mass of 1.3 kg (P < 0.001), better physical function as measured by reduced stair climb time (P = 0.013), a trend towards lower blood levels of glucose of 6.9 ± 2.5 mg/dl (P = 0.052) and lower insulin sensitivity (−27.5% versus 2.6%; P = 0.013) with 3 mg per day of GTx-024 (an orally bioavailable nonsteroidal SARM) than with placebo429.”

What the sources say

• Partly supported

  The Results report that 3 mg daily increased lean body mass by about 1.3 kg versus placebo (P < 0.001), and the paper reports improved Stair Climb Test performance (P = 0.013). But the Discussion says treatment decreased insulin resistance—a beneficial effect—not insulin sensitivity as the citing sentence claims. It also describes a significant reduction in fasting glucose rather than the claimed trend; the quoted glucose and percentage-change figures were not verified in the retrieved passages (page numbers unavailable). (LLM, conf=0.90)

  cites [429] Dalton, J. T. et al. The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women: results of a double-blind, placebo-controlled phase II trial. J. Cachexia Sarcopenia Muscle 2, 153–161 (2011). sourceExperimental — accuracy not yet measured

In the paper

“In mice, transplantation of satellite cells into damaged muscle leads to self-renewal and muscle regeneration466,467.”

What the sources say

• ?Not checked — no full text of the sourcecites [466] Collins, C. A. et al. Stem cell function, self-renewal, and behavioral heterogeneity of cells from the adult muscle satellite cell niche. Cell 122, 289–301 (2005). source
• Supported

  The paper reports that transplanted mouse muscle stem cells self-renewed and contributed to muscle fibres (Abstract). It also reports that, after injury, donor-derived cells expanded alongside evidence of muscle regeneration. In the described experiment, cells were transplanted into irradiated muscle before the additional notexin injury, a timing detail the paraphrase compresses. (LLM, conf=0.90)

  cites [467] Sacco, A., Doyonnas, R., Kraft, P., Vitorovic, S. & Blau, H. M. Self-renewal and expansion of single transplanted muscle stem cells. Nature 456, 502–506 (2008). source

In the paper

“Enobosarm, a non-steroidal SARM, successfully increased muscle mass and physical function in patients without cancer and in those with advanced lung, colorectal or breast cancer or lymphoma427–429.”

What the sources say

• Partly supported

  The “Novel Drug: Enobosarm” section reports improved lean body mass and physical function in people without cancer and in patients with the listed cancer types. It does not specify that the patients in the cancer study had advanced disease, so that qualifier is not supported by this copy. (LLM, conf=0.83)

  cites [427] Crawford, J. et al. Study design and rationale for the phase 3 clinical development program of enobosarm, a selective androgen receptor modulator, for the prevention and treatment of muscle wasting in cancer patients (POWER Trials). Curr. Oncol. Rep. 18, 37 (2016). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results and Discussion report increased lean body mass and stair-climb power with enobosarm in patients with cancer, including the non-small-cell lung and colorectal cancer groups. The Methods list breast cancer and lymphoma as eligible diagnoses, but the Discussion groups their outcomes under “other cancers” rather than demonstrating improvements for each separately. The paper also reports a previous study’s findings in people without cancer; that was not a population in this trial. (LLM, conf=0.82)

  cites [428] Dobs, A. S. et al. Effects of enobosarm on muscle wasting and physical function in patients with cancer: a double-blind, randomised controlled phase 2 trial. Lancet Oncol. 14, 335–345 (2013). sourceExperimental — accuracy not yet measured
• Partly supported

  The Patients and methods section says the participants were healthy volunteers without evidence of disease, and the Results report increased lean body mass and improved physical function. This paper does not report those outcomes in patients with advanced lung, colorectal or breast cancer, or lymphoma. (LLM, conf=0.90)

  cites [429] Dalton, J. T. et al. The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women: results of a double-blind, placebo-controlled phase II trial. J. Cachexia Sarcopenia Muscle 2, 153–161 (2011). sourceExperimental — accuracy not yet measured

In the paper

“One study464 reported that over 3 years vitamin K supplementation was not implicated in the age-related changes in skeletal muscle or adipose tissue mass in older community-dwelling adults.”

What the sources say

• Supported

  The Methods describe a three-year trial in community-dwelling adults aged 60–80. The Results report no difference between vitamin K and control groups in three-year changes in appendicular lean mass or total fat mass in either women or men; the Discussion draws the same conclusion. (LLM, conf=0.93)

  cites [464] Shea, M. K., Dawson-Hughes, B., Gundberg, C. M. & Booth, S. L. Reducing undercarboxylated osteocalcin with vitamin k supplementation does not promote lean tissue loss or fat gain over 3 years in older women and men: a randomized controlled trial. J. Bone Miner. Res. 32, 243–249 (2017). source

In the paper

“Adiponectin is negatively correlated with age and obesity and counters the effects of leptin.”

In the paper

“A major subset of adults over the age of 65 is now classified as having sarcopenic obesity, a high-risk geriatric syndrome predominantly observed in an ageing population that is at risk of synergistic complications from both sarcopenia and obesity.”

In the paper

“All such secretory changes lead to insulin resistance, which is increased by muscle catabolism60, promoting gain in fat mass and a loss of muscle mass57.”

What the sources say

• ?Not checked — no full text of the sourcecites [60] Zamboni, M., Mazzali, G., Fantin, F., Rossi, A. & Di Francesco, V. Sarcopenic obesity: a new category of obesity in the elderly. Nutr. Metab. Cardiovasc. Dis. 18, 388–395 (2008). source
• ?Not checked — no full text of the sourcecites [57] Schrager, M. A. et al. Sarcopenic obesity and inflammation in the InCHIANTI study. J. Appl. Physiol. (1985) 102, 919–925 (2007). This is an epidemiological study that shows that obesity directly affects inflammation and negatively affects muscle strength. source

In the paper

“Ageing stimulates the infiltration of fat into muscle72,73, which might negatively affect sarcopenia74, as described below, and obesity promotes the deposition of fat in the liver, heart, pancreas and skeletal muscle (FIG. 1).”

What the sources say

• ?Not checked — no full text of the sourcecites [72] Gallagher, D. et al. Healthy percentage body fat ranges: an approach for developing guidelines based on body mass index. Am. J. Clin. Nutr. 72, 694–701 (2000). This study includes ethnically heterogeneous study populations, which allow the development of prediction formulas for healthy percentage body fat. source
• ?Not checked — no full text of the sourcecites [73] Goodpaster, B. H. et al. The loss of skeletal muscle strength, mass, and quality in older adults: the health, aging and body composition study. J. Gerontol. A Biol. Sci. Med. Sci. 61, 1059–1064 (2006). This study shows that loss of strength with ageing is much more rapid than the concomitant loss of muscle mass, suggesting a decline in muscle quality. source
• ?Not checked — no full text of the sourcecites [74] Visser, M. et al. Muscle mass, muscle strength, and muscle fat infiltration as predictors of incident mobility limitations in well-functioning older persons. J. Gerontol. A Biol. Sci. Med. Sci. 60, 324–333 (2005). This study shows that in sarcopenic obesity reflected by low cross-sectional thigh muscle area, greater fat infiltration into muscle is associated with mobility loss. source

In the paper

“Myostatin can be upregulated in skeletal muscle, inhibiting muscle genesis90.”

What the sources say

• ?Not checked — no full text of the sourcecites [90] Sakuma, K. et al. The adaptive responses in several mediators linked with hypertrophy and atrophy of skeletal muscle after lower limb unloading in humans. Acta Physiol. (Oxf.) 197, 151–159 (2009). source

In the paper

“A reduction in the number of mitochondria and elevated production of reactive oxygen species occur in muscle following the deposition of intramyocellular lipids. This process can impair muscle function and might reduce the oxidative capacity of muscle81.”

What the sources say

• ?Not checked — no full text of the sourcecites [81] Kohara, K. Sarcopenic obesity in aging population: current status and future directions for research. Endocrine 45, 15–25 (2014). source

In the paper

“The deposition of intramyocellular lipids promotes lipotoxicity and inflammation and induces dedifferentiation of mesenchymal adipocyte-like progenitor cells that express fatty tissue genes75.”

What the sources say

• ?Not checked — no full text of the sourcecites [75] Sepe, A., Tchkonia, T., Thomou, T., Zamboni, M. & Kirkland, J. L. Aging and regional differences in fat cell progenitors — a mini-review. Gerontology 57, 66–75 (2011). source

In the paper

“This finding could be due to skeletal muscle preferentially depositing fat for a source of energy as opposed to glucose86,87.”

What the sources say

• ?Not checked — no full text of the sourcecites [86] Kusminski, C. M., Shetty, S., Orci, L., Unger, R. H. & Scherer, P. E. Diabetes and apoptosis: lipotoxicity. Apoptosis 14, 1484–1495 (2009). source
• ?Not checked — no full text of the sourcecites [87] Nilsson, M. I. et al. Abnormal protein turnover and anabolic resistance to exercise in sarcopenic obesity. FASEB J. 27, 3905–3916 (2013). source

In the paper

“Aerobic activity can improve the oxidative capacity of muscle by counteracting the negative effect of intra- myocellular lipids and accelerating lipolysis, which results in an increase in capillary density121.”

What the sources say

• ?Not checked — no full text of the sourcecites [121] Suetta, C. et al. Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse. J. Appl. Physiol. (1985) 97, 1954–1961 (2004). source

In the paper

“These mediators stimulate mitochondrial production, which promotes improved fatty acid metabolism124.”

What the sources say

• ?Not checked — no full text of the sourcecites [124] Marzetti, E. et al. Physical activity and exercise as countermeasures to physical frailty and sarcopenia. Aging Clin. Exp. Res. 29, 35–42 (2017). This study provides an overview of the interplay between physical activity, exercise and sarcopenia. source

In the paper

“Reduced cytokine production can lead to improved glucose metabolism, insulin sensitivity and muscle protein synthesis, which might dampen the progression of sarcopenic obesity.”

In the paper

“One study reported an increase in intramyo cellular lipid deposition after young, healthy men and women aged 19–28 years were exposed to 30 days of leg disuse, which resulted in lower extremity muscle mass loss85.”

What the sources say

• ?Not checked — no full text of the sourcecites [85] Manini, T. M. et al. Reduced physical activity increases intermuscular adipose tissue in healthy young adults. Am. J. Clin. Nutr. 85, 377–384 (2007). source

In the paper

“Circulating inflammatory biomarkers, including IL-6, C-reactive protein and TNF, are downregulated by aerobic exercise and strength training, although the relationship is less clear with combined aerobic and resistance activities114–118.”

What the sources say

• ?Not checked — no full text of the sourcecites [114] Bruunsgaard, H., Bjerregaard, E., Schroll, M. & Pedersen, B. K. Muscle strength after resistance training is inversely correlated with baseline levels of soluble tumor necrosis factor receptors in the oldest old. J. Am. Geriatr. Soc. 52, 237–241 (2004). source
• ?Not checked — no full text of the sourcecites [115] Kohut, M. L. et al. Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of beta-blockers, BMI, and psychosocial factors in older adults. Brain Behav. Immun. 20, 201–209 (2006). source
• ?Not checked — no full text of the sourcecites [116] Forti, L. N. et al. Strength training reduces circulating interleukin-6 but not brain-derived neurotrophic factor in community-dwelling elderly individuals. Age (Dordr.) 36, 9704 (2014). source
• ?Not checked — no full text of the sourcecites [117] Beyer, I., Mets, T. & Bautmans, I. Chronic low-grade inflammation and age-related sarcopenia. Curr. Opin. Clin. Nutr. Metab. Care 15, 12–22 (2012). source
• ?Not checked — no full text of the sourcecites [118] Woods, J. A., Wilund, K. R., Martin, S. A. & Kistler, B. M. Exercise, inflammation and aging. Aging Dis. 3, 130–140 (2012).

In the paper

“The term sarcopenia is defined differently throughout the literature (TABLE 1), leading to confusion in the medical community and preventing any inter-study comparisons.”

In the paper

“Cut-off points might not capture such determinants, particularly when levels of fat mass are high, which questions the utility of bioelectrical impedance for the assessment of body composition by professional societies169 who recommend adjustment to population-specific, age-appropriate equations169,176.”

What the sources say

• ?Not checked — no full text of the sourcecites [169] Kyle, U. G. et al. Bioelectrical impedance analysis-part II: utilization in clinical practice. Clin. Nutr. 23, 1430–1453 (2004). This study demonstrates the application of bioelectrical impedance equations in clinical practice, as advocated by ESPEN. source
• ?Not checked — no full text of the sourcecites [176] Kyle, U. G. et al. Bioelectrical impedance analysis —part I: review of principles and methods. Clin. Nutr. 23, 1226–1243 (2004). source