Baseline subcellular lipid droplet distributions in arm (m. triceps brachii) and leg (m. vastus lateralis) muscle fibres (n = 20 observations) A, subcellular lipid droplet volume fractions. * P < 0.0001 main limb effect in intermyofibrillar and subsarcolemmal regions; †P = 0.0002 main fibre type effect in intermyofibrillar region. B, subcellular lipid droplet size in diameter. * P < 0.001 main limb effect in type 2 fibres; †P = 0.007 main fibre type effect in leg muscle. C, subcellular lipid droplet numbers. * P < 0.0001 main limb effect in intermyofibrillar and subsarcolemmal regions; †P < 0.0001 main fibre type effect in intermyofibrillar region. Bars and lines represent medians with interquartile range (A and C), or means with 95% confidence intervals (B).

Baseline subcellular lipid droplet distributions in arm (m. triceps brachii) and leg (m. vastus lateralis) muscle fibres (n = 20 observations) A, subcellular lipid droplet volume fractions. * P < 0.0001 main limb effect in intermyofibrillar and subsarcolemmal regions; †P = 0.0002 main fibre type effect in intermyofibrillar region. B, subcellular lipid droplet size in diameter. * P < 0.001 main limb effect in type 2 fibres; †P = 0.007 main fibre type effect in leg muscle. C, subcellular lipid droplet numbers. * P < 0.0001 main limb effect in intermyofibrillar and subsarcolemmal regions; †P < 0.0001 main fibre type effect in intermyofibrillar region. Bars and lines represent medians with interquartile range (A and C), or means with 95% confidence intervals (B).

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Key points: Although lipid droplets in skeletal muscle are an important energy source during endurance exercise, our understanding of lipid metabolism in this context remains incomplete. Using transmission electron microscopy, two distinct subcellular pools of lipid droplets can be observed in skeletal muscle - one beneath the sarcolemma and the o...

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... fraction. The baseline lipid droplet volume fraction, size and density in the different locations are shown in Fig. 2, with the absolute values of the lipid droplet volume fractions shown in Table 1. The intermyofibrillar and total lipid droplet volume fractions were 4-fold higher in leg than in arm muscles, and the subsarcolemmal lipid droplet volume fraction was 6-fold higher in leg than in arm muscles (P < 0.0001). Furthermore, the inter- ...
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... droplet size. At baseline, there was no difference in lipid droplet size between the intermyofibrillar and sub- sarcolemmal regions (Fig. 2B). However, in type 2 muscle fibres, lipid droplet diameter was found to be 24% larger in the legs than in the arms (P < 0.001), while in type 1 muscle fibres, lipid droplet diameter tended to be 12% larger in the legs than in the arms (P = 0.05). Furthermore, lipid droplet diameter was 8% larger in type 2 than in type 1 fibres (P = ...
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... droplet numbers. Intermyofibrillar and sub- sarcolemmal lipid droplet numbers were found to be 59-60% higher in leg than in arm muscles (P < 0.001) (Fig. 2C). Comparing fibre types in upper and lower limbs, intermyofibrillar lipid droplet numbers were observed to be 68% higher in type 1 than in type 2 fibres (P < 0.0001), while there was no difference between subsarcolemmal lipid droplet numbers (P = ...

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... ATHL showed more lipidmitochondrial contact sites than OVWE, as reported for myocytes of active and athletic populations (55), along with greater fatty acidoxidative capacity. Higher exercise-induced utilization of intramyocellular lipids may therefore protect against DAG-induced insulin resistance in physically active individuals (42,56,57). Both longitudinal training studies (58) as well as cross-sectional studies (59) also indicate a shift toward type I fibers or a more oxidative phenotype after endurance training. ...
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The athlete’s paradox states that intramyocellular triglyceride accumulation associates with insulin resistance in sedentary but not in endurance-trained humans. Underlying mechanisms and the role of muscle lipid distribution and composition on glucose metabolism remain unclear. We compared highly trained athletes (ATHL) with sedentary normal weight (LEAN) and overweight-to-obese (OVWE) male and female individuals. This observational study found that ATHL show higher insulin sensitivity, muscle mitochondrial content, and capacity, but lower activation of novel protein kinase C (nPKC) isoforms, despite higher diacylglycerol concentrations. Notably, sedentary but insulin sensitive OVWE feature lower plasma membrane-to-mitochondria sn -1,2-diacylglycerol ratios. In ATHL, calpain-2, which cleaves nPKC, negatively associates with PKCε activation and positively with insulin sensitivity along with higher GLUT4 and hexokinase II content. These findings contribute to explaining the athletes’ paradox by demonstrating lower nPKC activation, increased calpain, and mitochondrial partitioning of bioactive diacylglycerols, the latter further identifying an obesity subtype with increased insulin sensitivity (NCT03314714).
... This increase could be attributed to a reduction in lipolysis, physical inactivity, an increase in dietary fat intake, or a combination of these factors. Prior research has shown decreases in total IMCL content and IMF IMCL cell fraction following metabolic stress from exhaustive exercise (Badin et al., 2013;Koh et al., 2017). Paradoxically, exercise typically elicits an anaerobic response in PAD patients due to ischemia within the leg muscles, potentially dampening the overall lipolysis occurring within this tissue and contributing to IMCL growth. ...
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Peripheral artery disease (PAD) is an atherosclerotic condition that impairs blood flow to the lower extremities, resulting in myopathy in affected skeletal muscles. Improving our understanding of PAD and developing novel treatment strategies necessitates a comprehensive examination of cellular structural alterations that occur in the muscles with disease progression. Here we aimed to employ electron microscopy to quantify skeletal muscle ultrastructural alterations responsible for the myopathy of PAD. Fifty-two participants (22 controls, 10 PAD Stage II, and 20 PAD Stage IV) were enrolled. Gastrocnemius biopsies were obtained to determine mitochondrial respiration and oxidative stress. Skeletal muscle sarcomere, mitochondria, lipid droplets, and sarcoplasm were assessed using transmission electron microscopy and focused ion beam scanning electron microscopy. Controls and PAD Stage II patients underwent walking performance tests: 6-minute walking test, 4-minute walking velocity, and maximum graded treadmill test. We identified several prominent ultrastructural modifications in PAD gastrocnemius, including reduced sarcomere dimensions, alterations in mitochondria number and localization, myofibrillar disorientation, changes in lipid droplets, and modifications in mitochondria-lipid droplet contact area. These changes correlated with impaired mitochondrial respiration and increased ROS production. We observed progressive deterioration in mitochondrial parameters across PAD stages. Stage II PAD showed impaired mitochondrial function and structure, while stage IV exhibited further deterioration, more pronounced structural alterations, and a decrease in mitochondrial content. The walking performance of Stage II PAD patients was significantly reduced. Our findings suggest that pathological mitochondria play a key role in the skeletal muscle dysfunction of PAD patients and represent an important target for therapeutic interventions aimed at improving clinical and functional outcomes in this patient population. Our data indicate that treatments should be implemented early and may include therapies designed to preserve and enhance mitochondrial biogenesis and respiration, optimize mitochondrial-lipid droplet interactions, or mitigate oxidative stress.
... This discrepancy may be because of sampling errors associated with small sample sizes in individual studies and/or the methodologic variability among studies, such as the following: 1) the difference in HFD total fat content, 2) HFD duration, and/ or 3) the measurement techniques used to quantify IMCL content. Transmission electron microscopy [10] and immunofluorescence microscopy can determine fiber-type-specific IMCL content in muscle biopsies [11]. Biochemical estimates of IMCL from mixed muscle biopsy samples do not reveal fiber-type-specific IMCL content and are potentially confounded by extramyocellular lipid [12], contributing to a large variability in the measurement of IMCL content across serial muscle biopsies [13]. ...
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Fatty acids are stored within the muscle as intramyocellular lipids (IMCL). Some, but not all, studies indicate that following a high-fat diet (HFD), IMCL may accumulate and affect insulin sensitivity. This systematic review and meta-analysis aimed to quantify the effects of an HFD on IMCL. It also explored the potential modifying effects of HFD fat content and duration, IMCL measurement technique, physical activity status, and the associations of IMCL with insulin sensitivity. Five databases were systematically searched for studies that examined the effect of ≥3 d of HFD (>35% daily energy intake from fat) on IMCL content in healthy individuals. Meta-regressions were used to investigate associations of the HFD total fat content, duration, physical activity status, IMCL measurement technique, and insulin sensitivity with IMCL responses. Changes in IMCL content and insulin sensitivity (assessed by hyperinsulinemic-euglycemic clamp) are presented as standardized mean difference (SMD) using a random effects model with 95% confidence intervals (95% CIs). Nineteen studies were included in the systematic review and 16 in the meta-analysis. IMCL content increased following HFD (SMD = 0.63; 95% CI: 0.31, 0.94, P = 0.001). IMCL accumulation was not influenced by total fat content (P = 0.832) or duration (P = 0.844) of HFD, physical activity status (P = 0.192), or by the IMCL measurement technique (P > 0.05). Insulin sensitivity decreased following HFD (SMD = –0.34; 95% CI: –0.52, –0.16; P = 0.003), but this was not related to the increase in IMCL content following HFD (P = 0.233). Consumption of an HFD (>35% daily energy intake from fat) for ≥3 d significantly increases IMCL content in healthy individuals regardless of HFD total fat content and duration of physical activity status. All IMCL measurement techniques detected the increased IMCL content following HFD. The dissociation between changes in IMCL and insulin sensitivity suggests that other factors may drive HFD-induced impairments in insulin sensitivity in healthy individuals. This trial was registered at PROSPERO as CRD42021257984.
... Effects of acute exercise bout on IMCL content is not conclusive. Consistent with our results, several previous studies reported no change, whereas a decrease in IMCL has also been reported (Schrauwen-Hinderling et al. 2003a;Koh et al. 2017). Exercise induces lipolysis at a rate that exceeds the oxidation of FFA, resulting in elevated plasma FFA levels, mainly from the adipose tissues (Schrauwen-Hinderling et al. 2003b). ...
... There is very little information available on effects of acute endurance exercise on lipid droplet morphology. Koopman et al. (2006) reported a decrease in lipid droplet size after resistance exercise and Koh et al. (2017) reported no change in the lipid droplet size after 52-63 minutes of skiing in athletes. Smaller lipid droplets have been associated with better insulin sensitivity, improved aerobic fitness, increased mitochondrial size, increased oxidative enzyme activity and whole-body lipid oxidation (Covington et al. 2017;He et al. 2004). ...
... This study was limited to only males, as with the previous similar studies on lipid droplet morphological effect of acute exercise (Koopman et al. 2006;Koh et al. 2017;Strauss et al. 2020). Since there is sex based differences in lipid deposition and substrate utilization (Devries 2016), future studies should be expanded to both genders. ...
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Purpose Smaller lipid droplet morphology and GLUT 4 protein expression have been associated with greater muscle oxidative capacity and glucose uptake, respectively. The main purpose of this study was to determine the effect of an acute long-duration exercise bout on skeletal muscle lipid droplet morphology, GLUT4, perilipin 3, and perilipin 5 expressions. Methods Twenty healthy men (age 24.0 ± 1.0 years, BMI 23.6 ± 0.4 kg/m²) were recruited for the study. The participants were subjected to an acute bout of exercise on a cycle ergometer at 50% VO2max until they reached a total energy expenditure of 650 kcal. The study was conducted after an overnight fast. Vastus lateralis muscle biopsies were obtained before and immediately after exercise for immunohistochemical analysis to determine lipid, perilipin 3, perilipin 5, and GLUT4 protein contents while GLUT 4 mRNA was quantified using RT-qPCR. Results Lipid droplet size decreased whereas total intramyocellular lipid content tended to reduce (p = 0.07) after an acute bout of endurance exercise. The density of smaller lipid droplets in the peripheral sarcoplasmic region significantly increased (0.584 ± 0.04 to 0.638 ± 0.08 AU; p = 0.01) while larger lipid droplets significantly decreased (p < 0.05). GLUT4 mRNA tended to increase (p = 0.05). There were no significant changes in GLUT 4, perilipin 3, and perilipin 5 protein levels. Conclusion The study demonstrates that exercise may impact metabolism by enhancing the quantity of smaller lipid droplets over larger lipid droplets.
... Human type II fibres are hence enriched with creatine phosphate (CrP) and glycogen energy depots 75 and contain higher levels of adenylate kinase 21 , glycogenolysis and glycolysis metabolic machinery 14,21 . Conversely, type I fibres are more abundant in peroxisomes 14 , mitochondria 14,21,76,77 and intramyocellular lipids (IMCLs) [76][77][78] , consistent with their slower ATP turnover 74 (Supplementary Fig. 1b). ...
... Glycogen granules are nonuniformly distributed between intramyofibrillar, intermyofibrillar and subsarcolemmal pools 35,267,268 . Alternatively, intramyocellular lipids are stored in lipid droplets (LDs) found predominantly at central (intermyofibrillar) but also peripheral (subsarcolemmal) regions within healthy muscle fibres 76,78 . During submaximal 54 and longer-duration high-intensity interval 55 exercise most ATP in muscle is regenerated by mitochondrial oxidative phosphorylation (OXPHOS) (see the section 'Acute exercise muscle metabolism') ( Fig. 2). ...
... Intramyocellular lipids (IMCLs) are stored in the hydrophobic core of lipid droplet ellipsoids 77 at peripheral (subsarcolemmal, SS LD ) and central (intermyofibrillar, IMF LD ) regions within fibres [76][77][78]268 . Women may have ~43% more individual lipid droplets in muscle, contributing to a greater (~84%) density of total IMCLs than in men 334 . ...
Article
Viewing metabolism through the lens of exercise biology has proven an accessible and practical strategy to gain new insights into local and systemic metabolic regulation. Recent methodological developments have advanced understanding of the central role of skeletal muscle in many exercise-associated health benefits and have uncovered the molecular underpinnings driving adaptive responses to training regimens. In this Review, we provide a contemporary view of the metabolic flexibility and functional plasticity of skeletal muscle in response to exercise. First, we provide background on the macrostructure and ultrastructure of skeletal muscle fibres, highlighting the current understanding of sarcomeric networks and mitochondrial subpopulations. Next, we discuss acute exercise skeletal muscle metabolism and the signalling, transcriptional and epigenetic regulation of adaptations to exercise training. We address knowledge gaps throughout and propose future directions for the field. This Review contextualizes recent research of skeletal muscle exercise metabolism, framing further advances and translation into practice.
... Studies have consistently reported decreased intramuscular lipids during an acute exercise bout in healthy young, lean untrained and physically trained individuals. This has been demonstrated using diverse methods, including transmission electron microscopy (TEM) (Staron et al., 1989;Devries et al., 2007;Chee et al., 2016;Koh et al., 2017), light microscopy De Bock et al., 2007;Stellingwerff et al., 2007;Shepherd et al., 2012Shepherd et al., , 2013Jevons et al., 2020;Daemen et al., 2021;Fell et al., 2021), stable isotope tracers (Romijn et al., 1993;Romijn et al., 2000;Bergman et al., 2018) and 1 H-magnetic resonance spectroscopy (Krssak et al., 2000;Brechtel et al., 2001;Decombaz et al., 2001;Schrauwen-Hinderling, van Loon et al., 2003;White et al., 2003;Zehnder et al., 2005;De Bock et al., 2007;Vermathen et al., 2012;Egger et al., 2013;Bucher et al., 2014). However, metabolically compromised (i.e. ...
... Indeed, using the TEM method, LDs are observed in two distinct subcellular compartments of skeletal muscle fibres, specifically the intermyofibrillar and subsarcolemmal regions (Sengers et al., 1976). Interestingly, acute exercise decreases the LD content in the intermyofibrillar more than in the subsarcolemmal space in lean young individuals (Chee et al., 2016) and endurance-trained athletes (Koh et al., 2017;Jevons et al., 2020). Contrary to these groups, obese patients with type 2 diabetes store an increased number of enlarged LDs, specifically in the subsarcolemmal space as evaluated with TEM (Nielsen et al., 2010;Daemen et al., 2018;Koh et al., 2018;de Almeida et al., 2023). ...
... Healthy young lean untrained (Decombaz et al., 2001;Shepherd et al., 2012Shepherd et al., , 2013Daemen et al., 2021), moderately active (White et al., 2003;De Bock et al., 2007;Devries et al., 2007;Egger et al., 2013;Bucher et al., 2014;Chee et al., 2016) and endurance-trained athletes (Staron et al., 1989;Romijn et al., 1993;Krssak et al., 2000;Romijn et al., 2000;Brechtel et al., 2001;Decombaz et al., 2001;Schrauwen-Hinderling, van Loon et al., 2003;van Loon et al., 2003;Zehnder et al., 2005;Stellingwerff et al., 2007;Vermathen et al., 2012;Koh et al., 2017;Bergman et al., 2018;Jevons et al., 2020;Fell et al., 2021), but not metabolically compromised (Chee et al., 2016;Bergman et al., 2018) or elderly lean individuals (Chee et al., 2016), reduce intramuscular LDs during acute exercise. Given the differences in methodology and exercise prescriptions in the previous studies, we confirm these results by demonstrating no net reduction in intramuscular LDs in middle-aged patients with type 2 diabetes nor glucose-tolerant lean and obese controls. ...
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Intramuscular lipid droplets (LDs) and mitochondria are essential organelles in cellular communication and metabolism, supporting local energy demands during muscle contractions. While insulin resistance impacts cellular functions and systems within the skeletal muscle, it remains unclear whether the interaction of LDs and mitochondria is affected by exercise and the role of obesity and type 2 diabetes. By employing transmission electron microscopy (TEM), we aimed to investigate the effects of 1 h of ergometry cycling on LD morphology, subcellular distribution and mitochondrial contact in skeletal muscle fibres of patients with type 2 diabetes and glucose‐tolerant lean and obese controls, matched for equal exercise intensities. Exercise did not change LD volumetric density, numerical density, profile size or subcellular distribution. However, evaluated as the magnitude of inter‐organelle contact, exercise increased the contact between LDs and mitochondria with no differences between the three groups. This effect was most profound in the subsarcolemmal space of type 1 muscle fibres, and here the absolute contact length increased on average from ∼275 to ∼420 nm. Furthermore, the absolute contact length before exercise (ranging from ∼140 to ∼430 nm) was positively associated with the fat oxidation rate during exercise. In conclusion, we showed that acute exercise did not mediate changes in the LD volume fractions, numbers or size but increased the contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. These data suggest that the increased LD–mitochondria contact with exercise is not disturbed in obesity or type 2 diabetes. image Key points Type 2 diabetes is associated with altered interactivity between lipid droplets (LDs) and mitochondria in the skeletal muscle. Physical contact between the surface of LDs and the surrounding mitochondrial network is considered favourable for fat oxidation. We show that 1 h of acute exercise increases the length of contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. This contact length between LDs and mitochondria is not associated with a net decrease in the LD volumetric density after the acute exercise. However, it correlates with the fat oxidation rate during exercise. Our data establish that exercise mediates contact between LDs and the mitochondrial network and that this effect is not impaired in individuals with type 2 diabetes or obesity.
... Additionally, there are a number of metabolic differences between these upper and lower body muscle groups, particularly related to fat utilization. Specifically, compared to legs, arm muscles have been reported to display lower fat oxidation capacity [51], lower 3-hydroxy-acyl-CoAdehydrogenase (HAD) activity (necessary for fatty acid oxidation) [39], lower intramyocellular lipid (IMCL) content [52], and higher exercise-induced lactate release [53]. While these factors are not directly related to fat-free mass, they highlight some considerable differences in upper and lower body skeletal muscle metabolism, which could have implications for the effects of vitamin D status on muscle size in the upper and lower extremities. ...
Article
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Vitamin D insufficiency is a global health concern and low vitamin D status is regularly associated with reduced muscle mass and sarcopenia in observational research. Recent research using Mendelian randomization (MR) has highlighted the potentially causal positive effect of serum vitamin D (25(OH)D) on total, trunk and upper body appendicular fat-free mass (FFM). However, no such effect was found in lower body FFM, a result that mirrors the outcomes of some vitamin D intervention studies. Here we review the current literature on vitamin D, muscle mass and strength and discuss some potential mechanisms for the differing effects of vitamin D on upper and lower body FFM. In particular, differences in distribution of the vitamin D receptor as well as androgen receptors, in the upper and lower body musculature, will be discussed.
... During moderate-intensity exercise in healthy individuals, IMTG-derived fatty acids contribute 50% to total fat oxidation, with the remaining 50% attributable to plasma FA (van Loon et al. 2001). Serial muscle biopsies combined with microscopy-based analyses enable net changes in IMTG content to be determined and using this approach it is now known that IMTG utilisation preferentially occurs in type I fibres from IMTG-containing LDs (van Loon et al. 2003a;Shepherd et al. 2013), which are located in the IMF region (Koh et al. 2017;Jevons et al. 2020). Moreover, in healthy individuals IMTG utilisation and FA oxidation during exercise is closely related to pre-exercise IMTG content (Shepherd et al. 2013) whereby those with greatest IMTG stores have the greatest IMTG utilisation. ...
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Large intramuscular triglyceride (IMTG) stores in sedentary, obese individuals have been linked to insulin resistance, yet well-trained athletes exhibit high IMTG levels whilst maintaining insulin sensitivity. Contrary to previous assumptions, it is now known that IMTG content per se does not result in insulin resistance. Rather, insulin resistance is caused, at least in part, by the presence of high concentrations of harmful lipid metabolites, such as diacylglycerols and ceramides in muscle. Several mechanistic differences between obese sedentary individuals and their highly trained counterparts have been identified, which determine the differential capacity for IMTG synthesis and breakdown in these populations. In this review, we first describe the most up-to-date mechanisms by which a low IMTG turnover rate (both breakdown and synthesis) leads to the accumulation of lipid metabolites and results in skeletal muscle insulin resistance. We then explore current and potential exercise and nutritional strategies that target IMTG turnover in sedentary obese individuals, to improve insulin sensitivity. Overall, improving IMTG turnover should be an important component of successful interventions that aim to prevent the development of insulin resistance in the ever-expanding sedentary, overweight and obese populations. Novelty: A description of the most up-to-date mechanisms regulating turnover of the IMTG pool. An exploration of current and potential exercise/nutritional strategies to target and enhance IMTG turnover in obese individuals. Overall, highlights the importance of improving IMTG turnover to prevent the development of insulin resistance.
... It has recently been reported that~35% of isolated rat cortical astrocytes 24 h after the seeding (~6 × 10 4 cells/coverslip) contain multiple LDs with an average diameter of~450 nm (ranging between 0.2 and 1 µm; [37]), comparable with the measurements performed on hepatocytes [22,43], skeletal muscle [44,45], and tumor cell lines [46]. In contrast, adipocytes normally contain a single LD, occupying most of the cytoplasm and ranging up to 100 µm in diameter [47]. ...
Article
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In recent years, increasing evidence regarding the functional importance of lipid droplets (LDs), cytoplasmic storage organelles in the central nervous system (CNS), has emerged. Although not abundantly present in the CNS under normal conditions in adulthood, LDs accumulate in the CNS during development and aging, as well as in some neurologic disorders. LDs are actively involved in cellular lipid turnover and stress response. By regulating the storage of excess fatty acids, cholesterol, and ceramides in addition to their subsequent release in response to cell needs and/or environmental stressors, LDs are involved in energy production, in the synthesis of membranes and signaling molecules, and in the protection of cells against lipotoxicity and free radicals. Accumulation of LDs in the CNS appears predominantly in neuroglia (astrocytes, microglia, oligodendrocytes, ependymal cells), which provide trophic, metabolic, and immune support to neuronal networks. Here we review the most recent findings on the characteristics and functions of LDs in neuroglia, focusing on astrocytes, the key homeostasis-providing cells in the CNS. We discuss the molecular mechanisms affecting LD turnover in neuroglia under stress and how this may protect neural cell function. We also highlight the role (and potential contribution) of neuroglial LDs in aging and in neurologic disorders.
... There is growing interest in elucidating how contracting muscles use lipid droplets (LD) in order to sustain exercise metabolism and/or for unknown purposes. For instance, during high-volume, high-intensity exercise (i.e., 57 min and 11 mmol/L blood lactate), LD within myofibrils but not those LD located close to the sarcolemma are used [58]. This is surprising as this kind of exercise mostly relies on oxidative metabolism mainly through fatty acid and glucose oxidation [59]. ...
... Furthermore, during innate immune response, LD increase their size [62]. This may also reveal different effects of LDs within skeletal muscle fibers, for instance, type 2 fibers have lower LD density, but they seems to have higher size than those LD form type 1 fibers in the leg skeletal muscle [58]. Although the current evidence is scarce, it would be interesting to test whether exercise impacts innate immune function by altering LD-mitochondria contact. ...
Article
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The incidence and severity of metabolic diseases can be reduced by introducing healthy lifestyle habits including moderate exercise. A common observation in age-related metabolic diseases is an increment in systemic inflammation (the so-called inflammaging) where mitochondrial reactive oxygen species (ROS) production may have a key role. Exercise prevents these metabolic pathologies, at least in part, due to its ability to alter immunometabolism, e.g., reducing systemic inflammation and by improving immune cell metabolism. Here, we review how exercise regulates immunometabolism within contracting muscles. In fact, we discuss how circulating and resident macrophages alter their function due to mitochondrial signaling, and we propose how these effects can be triggered within skeletal muscle in response to exercise. Finally, we also describe how exercise-induced mitochondrial adaptations can help to fight against virus infection. Moreover, the fact that moderate exercise increases circulating immune cells must be taken into account by public health agencies, as it may help prevent virus spread. This is of interest in order to face not only acute respiratory-related coronavirus (SARS-CoV) responsible for the COVID-19 pandemic but also for future virus infection challenges.