Low‐intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults

Liepinsh, Edgars; Makarova, Elina; Plakane, Līga; Konrāde, Ilze; Liepins, Kaspars; Videja, Melita; Sevostjanovs, Eduards; Grı̄nberga, Solveiga; Makrecka-Kūka, Marina; Dambrova, Maija

doi:10.14814/phy2.14489

Cited by 23 publications

(27 citation statements)

References 45 publications

(52 reference statements)

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“…There are also findings that people with a single nucleotide polymorphism in the NDUFB6 gene encoding a subunit of mitochondrial complex I do not respond to exercise by improving insulin sensitivity and glucose homeostasis [ 76 ], which is direct evidence that mitochondria are critical for exercise benefits in diabetes. Low-intensity exercises in healthy volunteers with a sedentary lifestyle increased PBMCs ROUTINE respiration, LEAK and OXPHOS with fatty acid substrates-dependent respiration by 31%, 65%, and 76%, respectively [ 77 ]. In addition, during 60 min of low-intensity exercise, a 2-fold higher lipolysis rate was observed, and 57% more fat was metabolized than during the incremental-load exercise [ 77 ].…”

Section: Interventions Targeting Mitochondria In Diabetesmentioning

confidence: 99%

“…Low-intensity exercises in healthy volunteers with a sedentary lifestyle increased PBMCs ROUTINE respiration, LEAK and OXPHOS with fatty acid substrates-dependent respiration by 31%, 65%, and 76%, respectively [ 77 ]. In addition, during 60 min of low-intensity exercise, a 2-fold higher lipolysis rate was observed, and 57% more fat was metabolized than during the incremental-load exercise [ 77 ]. High intensity interval training increased electron transfer (ET) capacity (respiration in the presence of uncoupler) in muscle of T2D patients and controls, irrespective of IR [ 78 ].…”

Section: Interventions Targeting Mitochondria In Diabetesmentioning

confidence: 99%

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Targeting Mitochondria in Diabetes

Jakovljevic

Pavlović

Jotić

et al. 2021

IJMS

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Type 2 diabetes (T2D), one of the most prevalent noncommunicable diseases, is often preceded by insulin resistance (IR), which underlies the inability of tissues to respond to insulin and leads to disturbed metabolic homeostasis. Mitochondria, as a central player in the cellular energy metabolism, are involved in the mechanisms of IR and T2D. Mitochondrial function is affected by insulin resistance in different tissues, among which skeletal muscle and liver have the highest impact on whole-body glucose homeostasis. This review focuses on human studies that assess mitochondrial function in liver, muscle and blood cells in the context of T2D. Furthermore, different interventions targeting mitochondria in IR and T2D are listed, with a selection of studies using respirometry as a measure of mitochondrial function, for better data comparison. Altogether, mitochondrial respiratory capacity appears to be a metabolic indicator since it decreases as the disease progresses but increases after lifestyle (exercise) and pharmacological interventions, together with the improvement in metabolic health. Finally, novel therapeutics developed to target mitochondria have potential for a more integrative therapeutic approach, treating both causative and secondary defects of diabetes.

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Section: Interventions Targeting Mitochondria In Diabetesmentioning

confidence: 99%

Section: Interventions Targeting Mitochondria In Diabetesmentioning

confidence: 99%

Targeting Mitochondria in Diabetes

Jakovljevic

Pavlović

Jotić

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…Unsurprisingly, whole-body prolonged exercises resulted in post-exercise increases in FAO products, and decreases in plasma triacylglycerol esters and phospholipids have been observed in athletes [ 96 , 97 ]. Most recently, a study also showed low-intensity exercise was able to improve mitochondrial oxidative bioenergetics and increased FAO in peripheral blood mononuclear cells (PBMCs) in sedentary individuals [ 98 ].…”

Section: Exercise As a Regulator Of Immunometabolismmentioning

confidence: 99%

Impact of Exercise on Immunometabolism in Multiple Sclerosis

Afzal

Dowling

McCoy

2020

JCM

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Multiple Sclerosis (MS) is a chronic, autoimmune condition characterized by demyelinating lesions and axonal degradation. Even though the cause of MS is heterogeneous, it is known that peripheral immune invasion in the central nervous system (CNS) drives pathology at least in the most common form of MS, relapse-remitting MS (RRMS). The more progressive forms’ mechanisms of action remain more elusive yet an innate immune dysfunction combined with neurodegeneration are likely drivers. Recently, increasing studies have focused on the influence of metabolism in regulating immune cell function. In this regard, exercise has long been known to regulate metabolism, and has emerged as a promising therapy for management of autoimmune disorders. Hence, in this review, we inspect the role of key immunometabolic pathways specifically dysregulated in MS and highlight potential therapeutic benefits of exercise in modulating those pathways to harness an anti-inflammatory state. Finally, we touch upon current challenges and future directions for the field of exercise and immunometabolism in MS.

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“…Irisin has also been found to favourably alter genes in adipocytes that are affected by the SARS-CoV-2 [ 19 ] and to modulate macrophage reactive oxygen species (ROS), displaying anti-oxidant and anti-inflammatory properties [ 20 ]. Critically, exercise can enhance mitochondrial function and capacity in peripheral blood mononuclear cells (PBMCs) [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Nunn

Guy²,

Brysch

et al. 2020

Immun Ageing

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Infection with SARs-COV-2 displays increasing fatality with age and underlying co-morbidity, in particular, with markers of the metabolic syndrome and diabetes, which seems to be associated with a “cytokine storm” and an altered immune response. This suggests that a key contributory factor could be immunosenescence that is both age-related and lifestyle-induced. As the immune system itself is heavily reliant on mitochondrial function, then maintaining a healthy mitochondrial system may play a key role in resisting the virus, both directly, and indirectly by ensuring a good vaccine response. Furthermore, as viruses in general, and quite possibly this new virus, have also evolved to modulate immunometabolism and thus mitochondrial function to ensure their replication, this could further stress cellular bioenergetics. Unlike most sedentary modern humans, one of the natural hosts for the virus, the bat, has to “exercise” regularly to find food, which continually provides a powerful adaptive stimulus to maintain functional muscle and mitochondria. In effect the bat is exposed to regular hormetic stimuli, which could provide clues on how to resist this virus. In this paper we review the data that might support the idea that mitochondrial health, induced by a healthy lifestyle, could be a key factor in resisting the virus, and for those people who are perhaps not in optimal health, treatments that could support mitochondrial function might be pivotal to their long-term recovery.

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Low‐intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 23 publications

References 45 publications

Targeting Mitochondria in Diabetes

Targeting Mitochondria in Diabetes

Impact of Exercise on Immunometabolism in Multiple Sclerosis

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

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