bims-kimdis 2023-09-03 papers

bims-kimdis

Biomed News

on Ketones, inflammation and mitochondria in disease

Issue of 2023‒09‒03
fourteen papers selected by
Matías Javier Monsalves Álvarez

β-hydroxybutyrate impairs bovine oocyte maturation via pyruvate dehydrogenase (PDH) associated energy metabolism abnormality.
Effects of Dietary Intake of Medium-chain Triacylglycerols on Energy Restriction-induced Weight Control and Loss of Skeletal Muscle in Rats.
NLRP3 inflammasome activation promotes liver inflammation and fibrosis in experimental biliary atresia.
Resistance Exercise Training Rescues Mitochondrial Dysfunction in Skeletal Muscle of Patients with Myotonic Dystrophy Type 1.
Crosstalk between NLRP3 inflammasome and calpain in Alzheimer's disease.
Preserved respiratory chain capacity and physiology in mice with profoundly reduced levels of mitochondrial respirasomes.
Ageing of skeletal muscle extracellular matrix and mitochondria: finding a potential link.
Impact of aerobic fitness status, menstrual cycle phase, and oral contraceptive use on exercise substrate oxidation and metabolic flexibility in females.
Insights of mitochondrial involvement in alcoholic fatty liver disease.
Determination of Poly(3-hydroxybutyrate) Content in Cyanobacterium Synechocystis sp. PCC 6803 Using Acid Hydrolysis Followed by High-performance Liquid Chromatography.
The regulatory effect of intermittent fasting on inflammasome activation in health and disease.
Low skeletal muscle mass and liver fibrosis in children with cerebral palsy.
Sodium Butyrate Induced Neural Stem/Progenitor Cell Death in an Experimental Model of Japanese Encephalitis.
Use of NIRS to explore skeletal muscle oxygenation during different training sessions in professional boxing.

Front Pharmacol. 2023 ;14 1243243

β-hydroxybutyrate impairs bovine oocyte maturation via pyruvate dehydrogenase (PDH) associated energy metabolism abnormality.

Kai-Yan Zhang, Jing Guo, Cheng-Lin Zhan, Chong-Shan Yuan, Chang-Guo Min, Zhi-Qiang Li, Hong-Yu Liu, Jun Wang, Jing Zhao, Wen-Fa Lu, Xin Ma.

  Background: Ketosis is one of the most frequent and costly metabolic disorders in high-producing dairy cows, and negatively associated with the health and reproductive performance of bovine. Ketosis is mainly caused by the accumulation of ketone body β-hydroxybutyric acid and its diagnosis is based on β-hydroxybutyrate (βHB) concentration in blood. Methods: In this study, we investigated the effects of βHB on bovine oocyte maturation in the concentration of subclinical (1.2 mM) βHB and clinical (3.6 mM). Results: The results showed βHB disrupted bovine oocyte maturation and development capacity. Further analysis showed that βHB induced oxidative stress and mitochondrial dysfunction, as indicated by the increased level of reactive oxygen species (ROS), disrupted mitochondrial structure and distribution, and depolarized membrane potential. Furthermore, oxidative stress triggered early apoptosis, as shown by the enhanced levels of Caspase-3 and Annexin-V. Moreover, 3.6 mM βHB induced the disruption of the pyruvate dehydrogenase (PDH) activity, showing with the decrease of the global acetylation modification and the increase of the abnormal spindle rate. Conclusion: Our study showed that βHB in subclinical/clinical concentration had toxic effects on mitochondrial function and PDH activity, which might affect energy metabolism and epigenetic modification of bovine oocytes and embryos.

Keywords:  PDH; acetylation modification; bovine reproductive performance; oocyte maturation; β-hydroxybutyrate (βHB)

DOI:  https://doi.org/10.3389/fphar.2023.1243243
J Oleo Sci. 2023 ;72(9): 849-858

Effects of Dietary Intake of Medium-chain Triacylglycerols on Energy Restriction-induced Weight Control and Loss of Skeletal Muscle in Rats.

Yuma Yokota, Ayumi Fukazawa, Yudai Nonaka, Takuya Karasawa, Michiyo Kimura, Shin Terada.

  Dietary intake of medium-chain triacylglycerols (MCTs) is known to alleviate obesity. MCTs have also been suggested to beneficially influence protein metabolism. This study evaluated the effects of dietary intake of MCTs on energy restriction-induced weight control and loss of skeletal muscle. Rats were divided into the following groups: 1) AL-LCT group that received the AIN-93G-based control diet containing long-chain triacylglycerols (LCTs) ad libitum, 2) ER-LCT group fed the control diet with 30% energy restriction, and 3) ER-MCT group fed a diet containing MCTs with 30% energy restriction. After the 4-wk dietary treatment, both energy-restricted groups had significantly lower body weight than the AL-LCT group and rats in the ER-MCT group were significantly lighter than those in the ER-LCT group. In contrast, the extent of energy restriction-induced loss of skeletal muscle was not significantly different between the two energy-restricted groups, resulting in an increase in muscle mass relative to body weight in the ER-MCT group. Despite maintaining the lower body weight, dietary intake of MCTs did not further influence signaling pathways involved in protein synthesis or breakdown. These results suggest that intake of MCTs could be a valuable dietary intervention to maintain a lower body weight and increase relative muscle mass without negative effects on skeletal muscle protein metabolism.

Keywords:  energy restriction; medium-chain triacylglycerols; rat; skeletal muscle; weight control

DOI:  https://doi.org/10.5650/jos.ess23061
Dig Liver Dis. 2023 Aug 25. pii: S1590-8658(23)00847-2. [Epub ahead of print]

NLRP3 inflammasome activation promotes liver inflammation and fibrosis in experimental biliary atresia.

Junfeng Wang, Min Du, Lingdu Meng, Shiwei He, Ye Zhu, Yifan Yang, Xue Ren, Yanlei Huang, Song Sun, Rui Dong, Shan Zheng, Gong Chen.

  BACKGROUND: Biliary atresia (BA) is characterized by a progressive fibroinflammatory cholangiopathy in early infants with unknown etiology. Although innate immune disorder is involved in its mechanism, role of NLRP3 inflammasome in BA remains largely undefined.AIM: To explore the role of NLRP3 inflammasome in BA.
METHODS: The expressions of NLRP3 inflammasome-related genes were determined in BA patients. Role of NLRP3 inflammasome was evaluated using MCC950 in experimental BA. Furthermore, gadolinium chloride, a macrophage scavenger, was applied to validate the inflammasome's cellular localization. Finally, the effects of NLRP3 inflammasome activation on liver fibrosis were explored in vivo and vitro in experimental BA.
RESULTS: The components of NLRP3 inflammasome were up-regulated in BA patients. Inflammasome-related genes showed positively correlated with liver inflammation and fibrosis in BA patients. In experimental BA, inflammasome-related genes were up-regulated, and their expressions were inhibited by MCC950, which promoted mice growth, protected liver function, alleviated obstructive jaundice, inhibited liver inflammation, and reduced serum IL-1β level. NLRP3 inflammasome was expressed in macrophages, and macrophage elimination exerted the same protective roles as MCC950 did in BA. Additionally, NLRP3 inflammasome activation promoted liver fibrosis in experimental BA.
CONCLUSIONS: NLRP3 inflammasome activation in macrophages promoted liver inflammation and fibrosis in experimental BA.

Keywords:  Biliary atresia; Liver fibrosis; Liver inflammation; NLRP3 inflammasome

DOI:  https://doi.org/10.1016/j.dld.2023.08.039
J Neuromuscul Dis. 2023 Aug 25.

Resistance Exercise Training Rescues Mitochondrial Dysfunction in Skeletal Muscle of Patients with Myotonic Dystrophy Type 1.

Valeria Di Leo, Conor Lawless, Marie-Pier Roussel, Tiago B Gomes, Gráinne S Gorman, Oliver M Russell, Helen A L Tuppen, Elise Duchesne, Amy E Vincent.

  BACKGROUND: Myotonic dystrophy type 1 (DM1) is a dominant autosomal neuromuscular disorder caused by the inheritance of a CTG triplet repeat expansion in the Dystrophia Myotonica Protein Kinase (DMPK) gene. At present, no cure currently exists for DM1 disease.OBJECTIVE: This study investigates the effects of 12-week resistance exercise training on mitochondrial oxidative phosphorylation in skeletal muscle in a cohort of DM1 patients (n = 11, men) in comparison to control muscle with normal oxidative phosphorylation.
METHODS: Immunofluorescence was used to assess protein levels of key respiratory chain subunits of complex I (CI) and complex IV (CIV), and markers of mitochondrial mass and cell membrane in individual myofibres sampled from muscle biopsies. Using control's skeletal muscle fibers population, we classified each patient's fibers as having normal, low or high levels of CI and CIV and compared the proportions of fibers before and after exercise training. The significance of changes observed between pre- and post-exercise within patients was estimated using a permutation test.
RESULTS: At baseline, DM1 patients present with significantly decreased mitochondrial mass, and isolated or combined CI and CIV deficiency. After resistance exercise training, in most patients a significant increase in mitochondrial mass was observed, and all patients showed a significant increase in CI and/or CIV protein levels. Moreover, improvements in mitochondrial mass were correlated with the one-repetition maximum strength evaluation.
CONCLUSIONS: Remarkably, 12-week resistance exercise training is sufficient to partially rescue mitochondrial dysfunction in DM1 patients, suggesting that the response to exercise is in part be due to changes in mitochondria.

Keywords:  Myotonic dystrophy type 1; mitochondrial dysfunction; myotonic dystrophy type 1 therapy; oxidative phosphorylation deficiency; resistance exercise training; skeletal muscle; strength training

DOI:  https://doi.org/10.3233/JND-230099
Eur J Neurosci. 2023 Aug 31.

Crosstalk between NLRP3 inflammasome and calpain in Alzheimer's disease.

Rumaiza Mamsa, Kedar S Prabhavalkar, Lokesh Kumar Bhatt.

  Amyloid plaques are considered to be the pathological hallmark of Alzheimer's disease (AD). Neuroinflammation further aggravates the pathogenesis of Alzheimer's disease. Calpains and NOD-like receptor protein-3 (NLRP3) inflammasomes are involved in the neuroinflammatory pathway and affect the progression of Alzheimer's disease. Hyperactivation of calpains is responsible for the activation of NLRP3 inflammasome, thereby affecting each other's molecular mechanism and causing astrogliosis, microgliosis, and neuronal dysfunction. Further, calpain hyperactivation is also associated with calcium homeostasis that acts as one of the triggers in the activation of NLRP3 inflammasome. Calpain activity is required for the maturation of interleukin-1β, a key mediator of neuroinflammatory responses. The membrane potential/calcium/calpain/caspase-1 axis acts as an unconventional regulator of inflammasomes. The complex crosstalk between NLRP3 inflammasome and calpain leads to a series of events. Targeting the molecular mechanism associated with calpain-NLRP3 inflammasome activation and regulation can be a therapeutic and prophylactic perspective towards Alzheimer's disease. This review discusses calpains and NLRP3 inflammasome crosstalk in the pathogenesis of AD.

Keywords:  Alzheimer's disease; NLRP3 inflammasome; amyloid-beta; calpain; neuroinflammation

DOI:  https://doi.org/10.1111/ejn.16139
Cell Metab. 2023 Aug 22. pii: S1550-4131(23)00289-9. [Epub ahead of print]

Preserved respiratory chain capacity and physiology in mice with profoundly reduced levels of mitochondrial respirasomes.

Dusanka Milenkovic, Jelena Misic, Johannes F Hevler, Thibaut Molinié, Injae Chung, Ilian Atanassov, Xinping Li, Roberta Filograna, Andrea Mesaros, Arnaud Mourier, Albert J R Heck, Judy Hirst, Nils-Göran Larsson.

  The mammalian respiratory chain complexes I, III2, and IV (CI, CIII2, and CIV) are critical for cellular bioenergetics and form a stable assembly, the respirasome (CI-CIII2-CIV), that is biochemically and structurally well documented. The role of the respirasome in bioenergetics and the regulation of metabolism is subject to intense debate and is difficult to study because the individual respiratory chain complexes coexist together with high levels of respirasomes. To critically investigate the in vivo role of the respirasome, we generated homozygous knockin mice that have normal levels of respiratory chain complexes but profoundly decreased levels of respirasomes. Surprisingly, the mutant mice are healthy, with preserved respiratory chain capacity and normal exercise performance. Our findings show that high levels of respirasomes are dispensable for maintaining bioenergetics and physiology in mice but raise questions about their alternate functions, such as those relating to the regulation of protein stability and prevention of age-associated protein aggregation.

Keywords:  OXPHOS; mitochondria; mitochondrial respirasomes; supercomplexes

DOI:  https://doi.org/10.1016/j.cmet.2023.07.015
Ann Med. 2023 ;55(2): 2240707

Ageing of skeletal muscle extracellular matrix and mitochondria: finding a potential link.

Lubing Cai, Luze Shi, Zhen Peng, Yaying Sun, Jiwu Chen.

  Aim: To discuss the progress of extracellular matrix (ECM) characteristics, mitochondrial homeostasis, and their potential crosstalk in the pathogenesis of sarcopenia, a geriatric syndrome characterized by a generalized and progressive reduction in muscle mass, strength, and physical performance.Methods: This review focuses on the anatomy and physiology of skeletal muscle, alterations of ECM and mitochondria during ageing, and the role of the interplay between ECM and mitochondria in the pathogenesis of sarcopenia.Results: Emerging evidence points to a clear interplay between mitochondria and ECM in various tissues and organs. Under the ageing process, the ECM undergoes changes in composition and physical properties that may mediate mitochondrial changes via the systematic metabolism, ROS, SPARC pathway, and AMPK/PGC-1α signalling, which in turn exacerbate muscle degeneration. However, the precise effects of such crosstalk on the pathobiology of ageing, particularly in skeletal muscle, have not yet been fully understood.Conclusion: The changes in skeletal muscle ECM and mitochondria are partially responsible for the worsened muscle function during the ageing process. A deeper understanding of their alterations and interactions in sarcopenic patients can help prevent sarcopenia and improve its prognoses.

Keywords:  Ageing; extracellular matrix; mitochondria; reactive oxygen species; sarcopenia

DOI:  https://doi.org/10.1080/07853890.2023.2240707
Appl Physiol Nutr Metab. 2023 Sep 01.

Impact of aerobic fitness status, menstrual cycle phase, and oral contraceptive use on exercise substrate oxidation and metabolic flexibility in females.

Alyssa A Olenick, Regis C Pearson, Nathan T Jenkins.

The influence of menstrual cycle phase and fitness status on metabolism during high-intensity interval exercise (HIIE) was assessed. Twenty-five females (24.4(3.6) yr) were categorized by normal menstrual cycle (n = 14) vs. oral contraceptive use (n = 11) and by aerobic fitness, high fit females (HFF: n = 13) vs. low fit females (LFF: n = 12). HIIE was four sets of four repetitions with 3 min rest between intervals on a cycle ergometer at a power output halfway between the ventilatory threshold and V̇O2peak and performed during follicular (FOL: day 2-7 or inactive pills) and luteal phases (LUT: day ~21 or 3rd week of active pills). Substrate oxidation was assessed via indirect calorimetry, blood lactate via finger stick, and recovery skeletal muscle oxidative metabolism (mV̇O2) via continuous-wave near-infrared spectroscopy. HFF oxidized more fat (g•kg-1) during the full session (FOL: p = 0.050, LUT: p = 0.001), high intervals (FOL: p = 0.048, LUT: p = 0.001), low intervals (FOL: p = 0.032, LUT: p = 0.024) and LUT recovery (p = 0.033). Carbohydrate oxidation area under the curve was greater in HFF during FOL (FOL: p = 0.049, LUT: p = 0.124). Blood lactate was lower in LFF in FOL (p ≤ 0.05) but not LUT. Metabolic flexibility (Δ fat oxidation g•kg-1•min-1) was greater in HFF than LFF during intervals 2-3 in FOL and 1-4 in LUT (p ≤ 0.05). Fitness status more positively influences exercise metabolic flexibility during HIIE than cycle phase or OC use.

DOI: https://doi.org/10.1139/apnm-2023-0101
J Cell Physiol. 2023 Aug 29.

Insights of mitochondrial involvement in alcoholic fatty liver disease.

Nithyananthan Subramaiyam.

  Alcoholic liver disease (ALD) is a global concern affecting most of the population and leading to the development of end-stage liver disease. Metabolic alterations due to increased alcohol consumption surge the hepatic accumulation of lipids and develop into a severe form of alcoholic steatohepatitis (ASH), depending on age and the consumption rate. The mitochondria in the hepatocyte actively regulate metabolic homeostasis and are disrupted in ALD pathogenesis. The increased NADH upon ethanol metabolism inhibits the mitochondrial oxidation of fatty acids, alters oxidative phosphorylation, and favors de novo lipogenesis. The higher mitochondrial respiration in early ALD increases free radical generation, whereas mitochondrial respiration is uncoupled in chronic ALD, affecting the cellular energy status. The defective glutathione importer due to excessive cholesterol loading and low adenosine triphosphate accounts for additional oxidative stress leading to hepatocyte apoptosis. The defective mitochondrial transcription machinery and sirtuins function in ALD affect mitochondrial function and biogenesis. The metabolites of ethanol metabolism epigenetically alter the gene expression profile of hepatic cell populations by modulating the promoters and sirtuins, aiding hepatic fibrosis and inflammation. The defect in mitophagy increases the accumulation of megamitochondria in hepatocytes and attracts immune cells by releasing mitochondrial damage-associated molecular patterns to initiate hepatic inflammation and ASH progression. Thus, maintaining mitochondrial lipid homeostasis and antioxidant capacity pharmacologically could provide a better outcome for ALD management.

Keywords:  alcoholic liver disease; mitochondrial biogenesis; mitochondrial damage; mitochondrial damage-associated molecular patterns; mitochondrial quality control; oxidative stress

DOI:  https://doi.org/10.1002/jcp.31100
Bio Protoc. 2023 Aug 20. 13(16): e4790

Determination of Poly(3-hydroxybutyrate) Content in Cyanobacterium Synechocystis sp. PCC 6803 Using Acid Hydrolysis Followed by High-performance Liquid Chromatography.

Janine Kaewbai-Ngam, Aran Incharoensakdi, Tanakarn Monshupanee.

  Various photoautotrophic cyanobacteria accumulate intracellular poly(3-hydroxybutyrate) (PHB) granules. This protocol can be used for determining the PHB contents of the cells as % PHB weight per dry cell weight using acid hydrolysis followed by high-performance liquid chromatography (HPLC). This HPLC analysis is rapid, with a running time of approximately 5 min per sample. The technique can accurately determine PHB concentrations in the range of 2-1,000 μg/mL PHB. However, this technique is not applicable for determining the contents of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) in cyanobacteria.

Keywords:  Cyanobacteria; HPLC; Nitrogen deprivation; PHB; Poly(3-hydroxybutyrate); Synechocystis

DOI:  https://doi.org/10.21769/BioProtoc.4790
Nutr Rev. 2023 Aug 27. pii: nuad104. [Epub ahead of print]

The regulatory effect of intermittent fasting on inflammasome activation in health and disease.

Chenchen Wang, Zhiqin Liu, Jinpeng Cai, Xi Xu.

  Intermittent fasting (IF), one of the most popular diets, can regulate inflammation and promote health; however, the detailed molecular mechanisms are not fully understood. The present review aims to provide an overview of recent preclinical and clinical studies that have examined the effect of IF on inflammasome signaling, and to discuss the translational gap between preclinical and clinical studies. Three databases (PubMed, Web of Science, and Embase) were searched to identify all relevant preclinical and clinical studies up to October 30, 2022. A total of 1544 studies were identified through the database searches, and 29 preclinical and 10 clinical studies were included. Twenty-three of the 29 preclinical studies reported that IF treatment could reduce inflammasome activation in neurological diseases, metabolic and cardiovascular diseases, immune and inflammatory diseases, gastrointestinal diseases, and pulmonary diseases, and 7 of the 10 clinical studies demonstrated reduced inflammasome activation after IF intervention in both healthy and obese participants. Among various IF regimens, time-restricted eating seemed to be the most effective one in terms of inflammasome regulation, and the efficacy of IF might increase over time. This review highlights the regulatory effect of IF on inflammasome activation in health and disease. Future studies using different IF regimens, in various populations, are needed in order to evaluate its potential to be used alone or as an adjunct therapy in humans to improve health and counteract diseases.

Keywords:  clinical studies; inflammasome; intermittent fasting; preclinical studies

DOI:  https://doi.org/10.1093/nutrit/nuad104
Eur J Pediatr. 2023 Sep 01.

Low skeletal muscle mass and liver fibrosis in children with cerebral palsy.

Marie Mostue Naume, Marianne Hørby Jørgensen, Christina Engel Høi-Hansen, Maja Risager Nielsen, Alfred Peter Born, John Vissing, Lise Borgwardt, Dorte Marianne Rohde Stærk, Mette Cathrine Ørngreen.

  The purpose of the study was to conduct a nutritional and metabolic assessment of children with cerebral palsy, including an investigation of liver status, body composition, and bone mineral density. In this cross-sectional study we included 22 children with cerebral palsy. By using ultrasound, transient elastography, dual x-ray absorptiometry (DXA) scan, blood samples, anthropometric measurements, and a three-day diet registration, the nutritional and metabolic status was evaluated. Liver fibrosis and steatosis were found in four patients (18.2%), all with severe motor impairments, low skeletal muscle mass, and epilepsy. All patients with liver involvement had normal liver-related blood samples. Decreased bone mineral density was found in 26.3%, and 91.0% had low skeletal muscle mass. Fat mass and muscle mass were significantly lower in the patients with severe motor impairments compared to the patients with less severe motor impairments. Within the children classified as 'underweight' or 'normal' according to body mass index, body fat determined by DXA scan was normal or high in 50% of these patients.CONCLUSIONS: This study is the first to report liver fibrosis and steatosis in children with cerebral palsy. Possible causes of liver fibrosis and/or steatosis are altered body composition with low skeletal muscle mass, decreased mobility and medical drug intake. Further investigations of liver involvement and risk factors are needed.
WHAT IS KNOWN: • Children and adolescents with cerebral palsy are at risk of malnutrition and altered body composition, both of which can lead to fatty liver disease. • It is unknown whether children with cerebral palsy are at increased risk of metabolic disturbances such as fatty liver disease.
WHAT IS NEW: • Altered body composition and low skeletal muscle mass, regardless of ambulation is present in 91% of the children with cerebral palsy. • Liver fibrosis and/or steatosis were found in 18.2% of the patients. Possible causes are altered body composition, decreased mobility and medical drug intake.

Keywords:  Altered body composition; Cerebral palsy; Liver fibrosis; Low skeletal muscle mass; Steatosis

DOI:  https://doi.org/10.1007/s00431-023-05177-9
Metab Brain Dis. 2023 Aug 31.

Sodium Butyrate Induced Neural Stem/Progenitor Cell Death in an Experimental Model of Japanese Encephalitis.

Anirudh Satheesan, Shivangi Sharma, Anirban Basu.

  The anti-inflammatory and neuroprotective effects of short chain fatty acid (SCFA) butyrate have been explored in a wide array of neurological pathologies. It is a 4-carbon SCFA produced from the fermentation of dietary fibers by the gut-microbiota. As evident from previous literature, butyrate plays a wide array of functions in CNS and interestingly enhances the differentiation potential of Neural stem/Progenitor Cells (NSPCs). Japanese encephalitis virus (JEV) is a well-known member of the Flaviviridae family and has been shown to alter neural stem cell pool of the brain, causing devastating consequences. In this study, we administered sodium butyrate (NaB) post JEV infection in BALB/c mouse model to examine any possible amelioration of the viral infection in NSPCs. In addition, ex vivo neurospheres and in vitro model of NSPCs were also used to study the effect of sodium butyrate in JEV infection. As an unprecedented finding, butyrate treated infected animals presented early onset of symptoms, as compared to their respective JEV infected groups. Alongside, we observed an increased viral load in NSPCs isolated from these animals as well as in cell culture models upon sodium butyrate treatment. Cytometric bead array analysis also revealed an increase in inflammatory cytokines, particularly, MCP-1 and IL-6. Further, increased expression of the key members of the canonical NF-κB pathway, viz-a-viz p-NF-κB, p-Iκ-Bα and p-IKK was observed. Overall, the increased inflammation and cell death caused early symptom progression in NaB-treated JEV infected animal model, which is contradictory to the well documented protective nature of NaB and therefore a better understanding of SCFA-based modulation of the gut-brain axis in viral infections is required.

Keywords:  Flaviviruses; Gut-Brain Axis; JEV; NSPCs; Neuro-immunomodulation; Sodium butyrate

DOI:  https://doi.org/10.1007/s11011-023-01279-3
Eur J Appl Physiol. 2023 Sep 01.

Use of NIRS to explore skeletal muscle oxygenation during different training sessions in professional boxing.

Andrew Usher, John Babraj.

  PURPOSE: The physiological examination of boxing has been limited to systemic response in amateur athletes. The demands of professional boxing have been overlooked, despite the different competition format. We sought to determine the physiological demands placed on skeletal muscle in professional boxing.METHODS: Ten male professional boxers (age 26 ± 5 years, height 177 ± 4 cm, weight 71 ± 6 kg) were recruited for this observational study. On different days, the athletes completed 6 × 3 min rounds of pad, bag or spar-based training with 1 min recovery between each round. Prior to each session, participants put on a heart rate monitor and near-infrared spectroscopy attached to the belly of the rectus femoris muscle to record heart rate and muscle oxygenation.
RESULTS: There were significantly less punches thrown in sparring compared to other training modalities (p < 0.001). Skeletal muscle oxygenation across training modalities consisted of a delay, fast desaturation and steady state. Across rounds there was a significant increase in time delay for desaturation (p = 0.016), rate of fast desaturation (p < 0.001) and duration of fast desaturation (p = 0.019). There was a significant difference in sparring for the heart rate where skeletal muscle oxygenation changes occurred compared to pads or bag sessions (p < 0.001).
CONCLUSION: The findings highlight differences in the skeletal muscle response to the different training modalities. Practitioners need to be aware of the muscular demands of each session to allow optimal adaptation across a training camp. Training needs to allow the skeletal muscle to achieve a new oxygenation steady state rapidly to promote efficient performance across rounds.

Keywords:  Desaturation; NIRS; Oxygenation; Recovery; Rectus femoris

DOI:  https://doi.org/10.1007/s00421-023-05305-1