Exercise Training and Insulin Resistance: A Current Review
Open accessAbstract
There is a general perception that increased physical activity will improve glucose homeostasis in all individuals. While this is an attractive concept, this conclusion may be overly simplistic and even misleading. The topic was reviewed extensively over 30 years ago and it was concluded that acute exercise enhances glucose uptake. However, in some cases the chronic influence of interventions utilizing exercise may have little effect on glucose metabolism. Moreover, insulin resistance often returns to near baseline levels within a couple of days following cessation of the exercise bout; leaving the overall effectiveness of the intervention in question. Since improving glucose homeostasis should be the focal endpoint of any intervention designed to mitigate the overwhelming degree of insulin resistance in individuals at risk for metabolic disease, it is essential to evaluate the key components of a successful approach.
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Sedentary behavior promotes low-grade chronic inflammation.
“with sedentary behavior promoting low-grade chronic inflammation”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
The Introduction links excess fat and insulin-resistance-related changes to chronic inflammation, and the Exercise-Induced Weight Loss section reports reduced inflammatory markers after exercise. Neither passage establishes that sedentary behavior itself promotes low-grade chronic inflammation; the Introduction mentions sedentary people in connection with insulin resistance, not as the stated cause of inflammation. Page numbers are unavailable in our copy. (LLM, conf=0.79)
Experimental — accuracy not yet measuredAdipokines secreted by adipose tissue during physical activity modulate energy metabolism in a context-dependent manner.
“Adipokines, such as leptin, adiponectin, resistin, chemerin, and pro-inflammatory cytokines (e.g., TNF-α, IL-6), secreted by adipose tissue during physical activity modulate energy metabolism in a context-dependent manner”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
The Exercise-Induced Weight Loss section reports that aerobic training increased adiponectin alongside improved lipid profiles and reduced insulin resistance; the Introduction links fat accumulation to the release of pro-inflammatory cytokines. The review does not establish that the listed adipokines are secreted during physical activity or that they modulate energy metabolism in the claimed context-dependent manner. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRegular exercise supports metabolic flexibility.
“whereas regular exercise reduces adipose tissue mass, promotes its browning, induces an anti-inflammatory profile, and supports metabolic flexibility”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
Regular exercise induces an anti-inflammatory profile.
“whereas regular exercise reduces adipose tissue mass, promotes its browning, induces an anti-inflammatory profile, and supports metabolic flexibility”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
Regular exercise reduces adipose tissue mass.
“whereas regular exercise reduces adipose tissue mass, promotes its browning, induces an anti-inflammatory profile, and supports metabolic flexibility”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
Aging is associated with a progressive decline in metabolic flexibility due to reduced mitochondrial function, chronic low-grade inflammation, and hormonal alterations.
“Importantly, aging is also associated with a progressive decline in metabolic flexibility, due to reduced mitochondrial function, chronic low-grade inflammation, and hormonal alterations”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
The Introduction says insulin resistance is common in older adults and links inflammation to fat accumulation and insulin resistance, but it does not describe a progressive age-related decline in metabolic flexibility. Searches for metabolic flexibility and for aging-related mitochondrial, inflammatory, and hormonal changes found no passage establishing the claimed decline or its proposed causes. (LLM, conf=0.72)
Experimental — accuracy not yet measuredRegular exercise promotes adipose tissue browning.
“whereas regular exercise reduces adipose tissue mass, promotes its browning, induces an anti-inflammatory profile, and supports metabolic flexibility”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [75]
The ‘Importance of Regional Body Composition > Exercise alone without weight loss’ section reports reductions in abdominal and subcutaneous fat after exercise, but does not address adipose tissue browning. Searches for browning, brown adipose tissue, and beige adipocytes found no passage supporting that specific claim in our copy; no page numbers were provided. (LLM, conf=0.72)
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References 50 · Cited by 76
Research works printed but not linked: 5
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- [23]Johnson NA Sachinwalla T Walton DW Smith K Armstrong A Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss Hepatology 2009 50 1105 1112 19637289
- [24]Whyte LJ Gill JM Cathcart AJ Effect of 2 weeks of sprint interval training on health-related outcomes in sedentary overweight/obese men Metabolism 2010 59 1421 1428 20153487
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- Authors
- Keshel, T. E.
- Affiliations
- University of Alaska Fairbanks (US)
- Corresponding author
- Keshel, Tyler E
- Venue
- Journal of Obesity & Weight Loss Therapy
- Publisher
- OMICS Publishing Group
- Published
- 2015
- Volume
- s5
- Issue
- Suppl 5
- ISSN
- 2165-7904 (ISSN-L)
- PMC
- PMC4625541
- OpenAlex
- W2111405129
- Cited by
- 76
- References
- 50
- Citations by year
- 2025: 9 · 2024: 10 · 2023: 4 · 2022: 13 · 2021: 11 · 2020: 10 · 2019: 4 · 2018: 8 · 2017: 4 · 2016: 3
- FWCI
- 3.68
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Journal of Obesity & Weight loss Therapy (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by)
- Funders
- American Heart Association
- National Institutes of Health
- National Institute on Aging
- National Institute of General Medical Sciences (P30GM103325)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK064716)
- Topics
- Health Sciences › Medicine › Physiology › Physical Activity and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- exercise training, insulin resistance, glucose homeostasis, glucose uptake, acute exercise, metabolic disease risk
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