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Key points: Muscle glycogen and intramuscular triglycerides (IMTG, stored in lipid droplets) are important energy substrates during prolonged exercise.Exercise‐induced changes in lipid droplet (LD) morphology (i.e. LD size and number) have not yet been studied under nutritional conditions typically adopted by elite endurance athletes, that is, after carbohydrate (CHO) loading and CHO feeding during exercise.We report for the first time that exercise reduces IMTG content in both central and peripheral regions of type I and IIa fibres, reflective of decreased LD number in both fibre types whereas reductions in LD size were exclusive to type I fibres.Additionally, CHO feeding does not alter subcellular IMTG utilisation, LD morphology or muscle glycogen utilisation in type I or IIa/II fibres.In the absence of alterations to muscle fuel selection, CHO feeding does not attenuate cell signalling pathways with regulatory roles in mitochondrial biogenesis. We examined the effects of carbohydrate (CHO) feeding on lipid droplet (LD) morphology, muscle glycogen utilisation and exercise‐induced skeletal muscle cell signalling. After a 36 h CHO loading protocol and pre‐exercise meal (12 and 2 g kg–1, respectively), eight trained males ingested 0, 45 or 90 g CHO h–1 during 180 min cycling at lactate threshold followed by an exercise capacity test (150% lactate threshold). Muscle biopsies were obtained pre‐ and post‐completion of submaximal exercise. Exercise decreased (P < 0.01) glycogen concentration to comparable levels (∼700 to 250 mmol kg–1 DW), though utilisation was greater in type I (∼40%) versus type II fibres (∼10%) (P < 0.01). LD content decreased in type I (∼50%) and type IIa fibres (∼30%) (P < 0.01), with greater utilisation in type I fibres (P < 0.01). CHO feeding did not affect glycogen or IMTG utilisation in type I or II fibres (all P > 0.05). Exercise decreased LD number within central and peripheral regions of both type I and IIa fibres, though reduced LD size was exclusive to type I fibres. Exercise induced (all P < 0.05) comparable AMPKThr172 (∼4‐fold), p53Ser15 (∼2‐fold) and CaMKIIThr268 phosphorylation (∼2‐fold) with no effects of CHO feeding (all P > 0.05). CHO increased exercise capacity where 90 g h–1 (233 ± 133 s) > 45 g h–1 (156 ± 66 s; P = 0.06) > 0 g h–1 (108 ± 54 s; P = 0.03). In conditions of high pre‐exercise CHO availability, we conclude CHO feeding does not influence exercise‐induced changes in LD morphology, glycogen utilisation or cell signalling pathways with regulatory roles in mitochondrial biogenesis. Key points: Muscle glycogen and intramuscular triglycerides (IMTG, stored in lipid droplets) are important energy substrates during prolonged exercise.Exercise‐induced changes in lipid droplet (LD) morphology (i.e. LD size and number) have not yet been studied under nutritional conditions typically adopted by elite endurance athletes, that is, after carbohydrate (CHO) loading and CHO feeding during exercise.We report for the first time that exercise reduces IMTG content in both central and peripheral regions of type I and IIa fibres, reflective of decreased LD number in both fibre types whereas reductions in LD size were exclusive to type I fibres.Additionally, CHO feeding does not alter subcellular IMTG utilisation, LD morphology or muscle glycogen utilisation in type I or IIa/II fibres.In the absence of alterations to muscle fuel selection, CHO feeding does not attenuate cell signalling pathways with regulatory roles in mitochondrial biogenesis. [ABSTRACT FROM AUTHOR]

Key points: Reduced carbohydrate (CHO) availability before and after exercise may augment endurance training‐induced adaptations of human skeletal muscle, as mediated via modulation of cell signalling pathways.However, it is not known whether such responses are mediated by CHO restriction, energy restriction or a combination of both.In recovery from a twice per day training protocol where muscle glycogen concentration is maintained within 200–350 mmol kg−1 dry weight (dw), we demonstrate that acute post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate potent cell signalling pathways that regulate hallmark adaptations associated with endurance training.In contrast, consuming CHO before, during and after an acute training session attenuated markers of bone resorption, effects that are independent of energy availability.Whilst the enhanced muscle adaptations associated with CHO restriction may be regulated by absolute muscle glycogen concentration, the acute within‐day fluctuations in CHO availability inherent to twice per day training may have chronic implications for bone turnover. We examined the effects of post‐exercise carbohydrate (CHO) and energy availability (EA) on potent skeletal muscle cell signalling pathways (regulating mitochondrial biogenesis and lipid metabolism) and indicators of bone metabolism. In a repeated measures design, nine males completed a morning (AM) and afternoon (PM) high‐intensity interval (HIT) (8 × 5 min at 85% V̇O2 peak) running protocol (interspersed by 3.5 h) under dietary conditions of (1) high CHO availability (HCHO: CHO ∼12 g kg−1, EA∼ 60 kcal kg−1 fat free mass (FFM)), (2) reduced CHO but high fat availability (LCHF: CHO ∼3 (−1, EA∼ 60 kcal kg−1 FFM) or (3), reduced CHO and reduced energy availability (LCAL: CHO ∼3 g kg−1, EA∼ 20 kcal kg−1 FFM). Muscle glycogen was reduced to ∼200 mmol kg−1 dw in all trials immediately post PM HIT (P < 0.01) and remained lower at 17 h (171, 194 and 316 mmol kg−1 dw) post PM HIT in LCHF and LCAL (P < 0.001) compared to HCHO. Exercise induced comparable p38MAPK phosphorylation (P < 0.05) immediately post PM HIT and similar mRNA expression (all P < 0.05) of PGC‐1α, p53 and CPT1 mRNA in HCHO, LCHF and LCAL. Post‐exercise circulating βCTX was lower in HCHO (P < 0.05) compared to LCHF and LCAL whereas exercise‐induced increases in IL‐6 were larger in LCAL (P < 0.05) compared to LCHF and HCHO. In conditions where glycogen concentration is maintained within 200–350 mmol kg−1 dw, we conclude post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate cell signalling pathways that regulate hallmark adaptations associated with endurance training. In contrast, consuming CHO before, during and after HIT running attenuates bone resorption, effects that are independent of energy availability and circulating IL‐6. Key points: Reduced carbohydrate (CHO) availability before and after exercise may augment endurance training‐induced adaptations of human skeletal muscle, as mediated via modulation of cell signalling pathways.However, it is not known whether such responses are mediated by CHO restriction, energy restriction or a combination of both.In recovery from a twice per day training protocol where muscle glycogen concentration is maintained within 200–350 mmol kg−1 dry weight (dw), we demonstrate that acute post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate potent cell signalling pathways that regulate hallmark adaptations associated with endurance training.In contrast, consuming CHO before, during and after an acute training session attenuated markers of bone resorption, effects that are independent of energy availability.Whilst the enhanced muscle adaptations associated with CHO restriction may be regulated by absolute muscle glycogen concentration, the acute within‐day fluctuations in CHO availability inherent to twice per day training may have chronic implications for bone turnover. [ABSTRACT FROM AUTHOR]

Key points: Obesity and sedentary behaviour are associated with capillary rarefaction and impaired muscle microvascular vasoreactivity, due to reduced nitric oxide bioavailability.Low‐volume high‐intensity interval training (HIT) is a time‐efficient alternative to traditional moderate‐intensity continuous training (MICT), but its effect on the muscle microvasculature has not been studied.The applicability of current laboratory‐ and gym‐based HIT protocols for obese individuals with low fitness and mobility has been disputed by public health experts, who cite the strenuous nature and complex protocols as major barriers. Therefore, we developed a virtually supervised HIT protocol targeting this group that can be performed at home without equipment (Home‐HIT).This study is the first to show that 12 weeks of virtually supervised Home‐HIT in obese individuals with elevated cardiovascular disease risk leads to similar increases in capillarisation and eNOS/NAD(P)Hoxidase protein ratio within the muscle microvascular endothelium as virtually supervised home‐based MICT and laboratory‐based HIT, while reducing many of the major barriers to exercise. This study investigated the effect of a novel virtually supervised home‐based high‐intensity interval training (HIT) (Home‐HIT) intervention in obese individuals with elevated cardiovascular disease (CVD) risk on capillarisation and muscle microvascular eNOS/NAD(P)Hoxidase ratio. Thirty‐two adults with elevated CVD risk (age 36 ± 10 years; body mass index 34.3 ± 5 kg m−2; V̇O2 peak 24.6 ± 5.7 ml kg min−1), completed one of three 12‐week training programmes: Home‐HIT (n = 9), laboratory‐based supervised HIT (Lab‐HIT; n = 10) or virtually supervised home‐based moderate‐intensity continuous training (Home‐MICT; n = 13). Muscle biopsies were taken before and after training to assess changes in vascular enzymes, capillarisation, mitochondrial density, intramuscular triglyceride content and GLUT4 protein expression using quantitative immunofluorescence microscopy. Training increased V̇O2 peak (P < 0.001), whole‐body insulin sensitivity (P = 0.033) and flow‐mediated dilatation (P < 0.001), while aortic pulse wave velocity decreased (P < 0.001) in all three groups. Immunofluorescence microscopy revealed comparable increases in total eNOS content in terminal arterioles and capillaries (P < 0.001) in the three conditions. There was no change in eNOS ser1177 phosphorylation (arterioles P = 0.802; capillaries P = 0.311), but eNOS ser1177/eNOS content ratio decreased significantly following training in arterioles and capillaries (P < 0.001). Training decreased NOX2 content (arterioles P < 0.001; capillaries P < 0.001), but there was no change in p47phox content (arterioles P = 0.101; capillaries P = 0.345). All measures of capillarisation increased (P < 0.05). There were no between‐group differences. Despite having no direct supervision during exercise, virtually supervised Home‐HIT resulted in comparable structural and endothelial enzymatic changes in the skeletal muscle microvessels to the traditional training methods. We provide strong evidence that Home‐HIT is an effective novel strategy to remove barriers to exercise and improve health in an obese population at risk of CVD. Key points: Obesity and sedentary behaviour are associated with capillary rarefaction and impaired muscle microvascular vasoreactivity, due to reduced nitric oxide bioavailability.Low‐volume high‐intensity interval training (HIT) is a time‐efficient alternative to traditional moderate‐intensity continuous training (MICT), but its effect on the muscle microvasculature has not been studied.The applicability of current laboratory‐ and gym‐based HIT protocols for obese individuals with low fitness and mobility has been disputed by public health experts, who cite the strenuous nature and complex protocols as major barriers. Therefore, we developed a virtually supervised HIT protocol targeting this group that can be performed at home without equipment (Home‐HIT).This study is the first to show that 12 weeks of virtually supervised Home‐HIT in obese individuals with elevated cardiovascular disease risk leads to similar increases in capillarisation and eNOS/NAD(P)Hoxidase protein ratio within the muscle microvascular endothelium as virtually supervised home‐based MICT and laboratory‐based HIT, while reducing many of the major barriers to exercise. [ABSTRACT FROM AUTHOR]

Key points: Hormone‐sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) are the key enzymes involved in intramuscular triglyceride (IMTG) lipolysis. In isolated rat skeletal muscle, HSL translocates to IMTG‐containing lipid droplets (LDs) following electrical stimulation, but whether HSL translocation occurs in human skeletal muscle during moderate‐intensity exercise is currently unknown. Perilipin‐2 (PLIN2) and perilipin‐5 (PLIN5) proteins have been implicated in regulating IMTG lipolysis by interacting with HSL and ATGL in cell culture and rat skeletal muscle studies. This study investigated the hypothesis that HSL (but not ATGL) redistributes to LDs during moderate‐intensity exercise in human skeletal muscle, and whether the localisation of these lipases with LDs was affected by the presence of PLIN proteins on the LDs. HSL preferentially redistributed to PLIN5‐associated LDs whereas ATGL distribution was not altered with exercise; this is the first study to illustrate the pivotal step of HSL redistribution to PLIN5‐associated LDs following moderate‐intensity exercise in human skeletal muscle. Abstract: Hormone‐sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) control skeletal muscle lipolysis. ATGL is present on the surface of lipid droplets (LDs) containing intramuscular triglyceride (IMTG) in both the basal state and during exercise. HSL translocates to LD in ex vivo electrically stimulated rat skeletal muscle. Perilipin‐2‐ and perilipin‐5‐associated lipid droplets (PLIN2+ and PLIN5+ LDs) are preferentially depleted during exercise in humans, indicating that these PLINs may control muscle lipolysis. We aimed to test the hypothesis that in human skeletal muscle in vivo HSL (but not ATGL) is redistributed to PLIN2+ and PLIN5+ LDs during moderate‐intensity exercise. Muscle biopsies from 8 lean trained males (age 21 ± 1 years, BMI 22.6 ± 1.2 kg m−2 and V ̇ O 2 peak 48.2 ± 5.0 ml min−1 kg−1) were obtained before and immediately following 60 min of cycling exercise at ∼59% V ̇ O 2 peak . Cryosections were stained using antibodies targeting ATGL, HSL, PLIN2 and PLIN5. LDs were stained using BODIPY 493/503. Images were obtained using confocal immunofluorescence microscopy and object‐based colocalisation analyses were performed. Following exercise, HSL colocalisation to LDs increased (P < 0.05), and was significantly greater to PLIN5+ LDs (+53%) than to PLIN5− LDs (+34%) (P < 0.05), while the increases in HSL colocalisation to PLIN2+ LDs (+16%) and PLIN2− LDs (+28%) were not significantly different. Following exercise, the fraction of LDs colocalised with ATGL (0.53 ± 0.04) did not significantly change (P < 0.05) and was not affected by PLIN association to the LDs. This study presents the first evidence of exercise‐induced HSL redistribution to LDs in human skeletal muscle and identifies PLIN5 as a facilitator of this mechanism. [ABSTRACT FROM AUTHOR]