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Prolonged passive heat treatment (PHT) has been suggested to trigger skeletal muscle adaptations that may improve muscle maintenance in older individuals. To assess the effects of PHT on skeletal muscle tissue capillarization, perfusion capacity, protein synthesis rates, hypertrophy and leg strength, 14 older adults (9 males, 5 females; 73 ± 6 years) underwent 8 weeks of PHT (infrared sauna: 3× per week, 45 min at ∼60°C). Before and after PHT we collected muscle biopsies to assess skeletal muscle capillarization and fibre cross‐sectional area (CSA). Basal and postprandial muscle tissue perfusion kinetics and protein synthesis rates were assessed using contrast‐enhanced ultrasound and primed continuous l‐[ring‐13C6]phenylalanine infusions, respectively. One‐repetition maximum (1RM) leg strength and vastus lateralis muscle CSA were assessed. Type I and type II muscle fibre capillarization strongly increased following PHT (capillary‐to‐fibre perimeter exchange index: +31 ± 18 and +33 ± 30%, respectively; P < 0.001). No changes were observed in basal (0.24 ± 0.27 vs. 0.18 ± 0.11 AU; P = 0.266) or postprandial (0.20 ± 0.12 vs. 0.18 ± 0.14 AU; P = 0.717) microvascular blood flow following PHT. Basal (0.048 ± 0.014 vs. 0.051 ± 0.019%/h; P = 0.630) and postprandial (0.041 ± 0.012 vs. 0.051 ± 0.024%/h; P = 0.199) muscle protein synthesis rates did not change in response to prolonged PHT. Furthermore, no changes in vastus lateralis muscle CSA (15.3 ± 4.6 vs. 15.2 ± 4.6 cm2; P = 0.768) or 1RM leg strength (46 ± 12 vs. 47 ± 12 kg; P = 0.087) were observed over time. In conclusion, prolonged PHT increases muscle tissue capillarization but this does not improve muscle microvascular blood flow or increase muscle protein synthesis rates in healthy, older adults. Prolonged PHT does not induce skeletal muscle hypertrophy or increase leg strength in healthy, older adults. Key points: Repeated exposure to heat has been suggested to trigger skeletal muscle adaptive responses.We investigated the effect of 8 weeks of whole‐body passive heat treatment (PHT; infrared sauna: 3× per week for 45 min at ∼60°C) on skeletal muscle tissue capillarization, perfusion capacity, basal, and postprandial muscle protein synthesis rates, muscle (fibre) hypertrophy, and leg strength in healthy, older adults.Prolonged PHT increases muscle tissue capillarization, but this does not improve muscle microvascular blood flow or increase muscle protein synthesis rates.Despite increases in muscle tissue capillarization, prolonged PHT does not suffice to induce skeletal muscle hypertrophy or increase leg strength in healthy, older adults. [ABSTRACT FROM AUTHOR]

Endothelium-dependent vasodilation can be tested using a variety of shear stress paradigms, some of which may involve the production of reactive oxygen species. The purpose of this study was to compare different methods for assessing endothelial function and their specific involvement of reactive oxygen species and influence of aerobic training status. Twenty-nine (10 F) young and healthy participants (VO2max: 34–74 mL·kg−1·min−1) consumed either an antioxidant cocktail (AOC; vitamin C, vitamin E, α-lipoic acid) or placebo (PLA) on each of two randomized visits. Endothelial function was measured via three different brachial artery flow-mediated dilation (FMD) tests: reactive hyperemia (RH-FMD: 5 min cuff occlusion and release), sustained shear (SS-FMD: 6 min rhythmic handgrip), and progressive sustained shear (P-SS-FMD: three intensities of 3 min of rhythmic handgrip). Baseline artery diameter decreased (all tests: 3.8 ± 0.5 to 3.7 ± 0.6 mm, p = 0.004), and shear rate stimulus increased (during RH-FMD test, p = 0.021; during SS-FMD test, p = 0.36; during P-SS-FMD test, p = 0.046) following antioxidant consumption. However, there was no difference in FMD following AOC consumption (RH-FMD, PLA: 8.1 ± 2.6%, AOC: 8.2 ± 3.5%, p = 0.92; SS-FMD, PLA: 6.9 ± 3.9%, AOC: 7.8 ± 5.2%, p = 0.15) or FMD per shear rate slope (P-SS-FMD: PLA: 0.0039 ± 0.0035 mm·s−1, AOC: 0.0032 ± 0.0017 mm·s−1, p = 0.28) and this was not influenced by training status/fitness (all p > 0.60). Allometric scaling did not alter these outcomes (all p > 0.40). Reactive oxygen species may not be integral to endothelium-dependent vasodilation tested using reactive, sustained, or progressive shear protocols in young males and females, regardless of fitness level. [ABSTRACT FROM AUTHOR]

Impaired heart function can develop in individuals with diabetes in the absence of coronary artery disease or hypertension, suggesting mechanisms beyond hypertension/increased afterload contribute to diabetic cardiomyopathy. Identifying therapeutic approaches that improve glycemia and prevent cardiovascular disease are clearly required for clinical management of diabetes-related comorbidities. Since intestinal bacteria are important for metabolism of nitrate, we examined whether dietary nitrate and fecal microbial transplantation (FMT) from nitrate-fed mice could prevent high-fat diet (HFD)–induced cardiac abnormalities. Male C57Bl/6N mice were fed a low-fat diet (LFD), HFD, or HFD+Nitrate (4 mmol/L sodium nitrate) for 8 weeks. HFD-fed mice presented with pathological left ventricle (LV) hypertrophy, reduced stroke volume, and increased end-diastolic pressure, in association with increased myocardial fibrosis, glucose intolerance, adipose inflammation, serum lipids, LV mitochondrial reactive oxygen species (ROS), and gut dysbiosis. In contrast, dietary nitrate attenuated these detriments. In HFD-fed mice, FMT from HFD+Nitrate donors did not influence serum nitrate, blood pressure, adipose inflammation, or myocardial fibrosis. However, microbiota from HFD+Nitrate mice decreased serum lipids, LV ROS, and similar to FMT from LFD donors, prevented glucose intolerance and cardiac morphology changes. Therefore, the cardioprotective effects of nitrate are not dependent on reducing blood pressure, but rather mitigating gut dysbiosis, highlighting a nitrate-gut-heart axis. Article Highlights: Identifying therapeutic approaches that prevent cardiometabolic diseases are clearly important, and nitrate represents one such potential compound given its multifactorial metabolic effects. We aimed to determine whether nitrate could prevent high-fat diet (HFD)–induced cardiac abnormalities and whether this was dependent on the gut microbiome. Dietary nitrate attenuated HFD-induced pathological changes in cardiac remodelling, left ventricle reactive oxygen species, adipose inflammation, lipid homeostasis, glucose intolerance, and gut dysbiosis. Fecal microbial transplantation from nitrate-fed mice also prevented serum dyslipidemia, left ventricle reactive oxygen species, glucose intolerance, and cardiac dysfunction. Therefore, the cardioprotective effects of nitrate are related to mitigating gut dysbiosis, highlighting a nitrate-gut-heart axis. [ABSTRACT FROM AUTHOR]

Supplemental digital content is available in the text. Purpose: Sprint interval training (SIT) has gained popularity as a time-effective alternative to moderate-intensity endurance training (END). However, whether SIT is equally effective for decreasing cardiometabolic risk factors remains debatable, as many beneficial effects of exercise are thought to be transient, and unlike END, SIT is not recommended daily. Therefore, in line with current exercise recommendations, we examined the ability of SIT and END to improve cardiometabolic health in overweight/obese males. Methods: Twenty-three participants were randomized to perform 6 wk of constant workload SIT (3 d·wk−1, 4–6 × 30 s ~170% W peak, 2 min recovery, n = 12) or END (5 d·wk−1, 30–40 min, ~60% W peak, n = 11) on cycle ergometers. Aerobic capacity (V˙O2peak), body composition, blood pressure (BP), arterial stiffness, endothelial function, glucose and lipid tolerance, and free-living glycemic regulation were assessed pre- and posttraining. Results: Both END and SIT increased V˙O2peak (END ~15%, SIT ~5%) and glucose tolerance (~20%). However, only END decreased diastolic BP, abdominal fat, and improved postprandial lipid tolerance, representing improvements in cardiovascular risk factors that did not occur after SIT. Although SIT, but not END, increased endothelial function, arterial stiffness was not altered in either group. Indices of free-living glycemic regulation were improved after END and trended toward an improvement after SIT (P = 0.06–0.09). However, glycemic control was better on exercise compared with rest days, highlighting the importance of exercise frequency. Furthermore, in an exploratory nature, favorable individual responses (V˙O2peak, BP, glucose tolerance, lipidemia, and body fat) were more prevalent after END than low-frequency SIT. Conclusion: As only high-frequency END improved BP and lipid tolerance, free-living glycemic regulation was better on days that participants exercised, and favorable individual responses were consistent after END, high-frequency END may favorably improve cardiometabolic health. [ABSTRACT FROM AUTHOR]

Key points: We determined if bed rest increased mitochondrially derived reactive oxygen species and cellular redox stress, contributing to the induction of insulin resistance.Bed rest decreased maximal and submaximal ADP‐stimulated mitochondrial respiration.Bed rest did not alter mitochondrial H2O2 emission in the presence of ADP concentrations indicative of resting muscle, the ratio of H2O2 emission to mitochondrial O2 consumption or markers of oxidative stressThe present data suggest strongly that mitochondrial H2O2 does not contribute to bed rest‐induced insulin resistance Mitochondrial H2O2 has been causally linked to diet‐induced insulin resistance, although it remains unclear if muscle disuse similarly increases mitochondrial H2O2. Therefore, we investigated the potential that an increase in skeletal muscle mitochondrial H2O2 emission, potentially as a result of decreased ADP sensitivity, contributes to cellular redox stress and the induction of insulin resistance during short‐term bed rest in 20 healthy males. Bed rest led to a decline in glucose infusion rate during a hyperinsulinaemic‐euglycaemic clamp (−42 ± 2%; P < 0.001), and in permeabilized skeletal muscle fibres it decreased OXPHOS protein content (−16 ± 8%) and mitochondrial respiration across a range of ADP concentrations (−13 ± 5%). While bed rest tended to increase maximal mitochondrial H2O2 emission rates (P = 0.053), H2O2 emission in the presence of ADP concentrations indicative of resting muscle, the ratio of H2O2 emission to mitochondrial O2 consumption, and markers of oxidative stress were not altered following bed rest. Altogether, while bed rest impairs mitochondrial ADP‐stimulated respiration, an increase in mitochondrial H2O2 emission does not contribute to the induction of insulin resistance following short‐term bed rest. Key points: We determined if bed rest increased mitochondrially derived reactive oxygen species and cellular redox stress, contributing to the induction of insulin resistance.Bed rest decreased maximal and submaximal ADP‐stimulated mitochondrial respiration.Bed rest did not alter mitochondrial H2O2 emission in the presence of ADP concentrations indicative of resting muscle, the ratio of H2O2 emission to mitochondrial O2 consumption or markers of oxidative stressThe present data suggest strongly that mitochondrial H2O2 does not contribute to bed rest‐induced insulin resistance [ABSTRACT FROM AUTHOR]

Key points: Blood flow restricted resistance exercise (BFR‐RE) is capable of inducing comparable adaptations to traditional resistance exercise (RE), despite a lower total exercise volume.It has been suggested that an increase in reactive oxygen species (ROS) production may be involved in this response; however, oxygen partial pressure (PO2) is reduced during BFR‐RE, and the influence of PO2 on mitochondrial redox balance remains poorly understood.In human skeletal muscle tissue, we demonstrate that both maximal and submaximal mitochondrial ROS emission rates are acutely decreased 2 h following BFR‐RE, but not RE, occurring along with a reduction in tissue oxygenation during BFR‐RE.We further suggest that PO2 is involved in this response because an in vitro analysis revealed that reducing PO2 dramatically decreased mitochondrial ROS emissions and electron leak to ROS.Altogether, these data indicate that mitochondrial ROS emission rates are attenuated following BFR‐RE, and such a response is likely influenced by reductions in PO2. Low‐load blood flow restricted resistance exercise (BFR‐RE) training has been proposed to induce comparable adaptations to traditional resistance exercise (RE) training, however, the acute signalling events remain unknown. Although a suggested mechanism of BFR‐RE is an increase in reactive oxygen species (ROS) production, oxygen partial pressure (PO2) is reduced during BFR‐RE, and the influence of O2 tension on mitochondrial redox balance remains ambiguous. We therefore aimed to determine whether skeletal muscle mitochondrial bioenergetics were altered following an acute bout of BFR‐RE or RE, and to further examine the role of PO2 in this response. Accordingly, muscle biopsies were obtained from 10 males at rest and 2 h after performing three sets of single‐leg squats (RE or BFR‐RE) to failure at 30% one‐repetition maximum. We determined that mitochondrial respiratory capacity and ADP sensitivity were not altered in response to RE or BFR‐RE. Although maximal (succinate) and submaximal (non‐saturating ADP) mitochondrial ROS emission rates were unchanged following RE, BFR‐RE attenuated these responses by ∼30% compared to pre‐exercise, occurring along with a reduction in skeletal muscle tissue oxygenation during BFR‐RE (P < 0.01 vs. RE). In a separate cohort of participants, evaluation of mitochondrial bioenergetics in vitro revealed that mild O2 restriction (50 µm) dramatically attenuated maximal (∼4‐fold) and submaximal (∼50‐fold) mitochondrial ROS emission rates and the fraction of electron leak to ROS compared to room air (200 µm). Combined, these data demonstrate that mitochondrial ROS emissions are attenuated following BFR‐RE, a response which may be mediated by a reduction in skeletal muscle PO2. Key points: Blood flow restricted resistance exercise (BFR‐RE) is capable of inducing comparable adaptations to traditional resistance exercise (RE), despite a lower total exercise volume.It has been suggested that an increase in reactive oxygen species (ROS) production may be involved in this response; however, oxygen partial pressure (PO2) is reduced during BFR‐RE, and the influence of PO2 on mitochondrial redox balance remains poorly understood.In human skeletal muscle tissue, we demonstrate that both maximal and submaximal mitochondrial ROS emission rates are acutely decreased 2 h following BFR‐RE, but not RE, occurring along with a reduction in tissue oxygenation during BFR‐RE.We further suggest that PO2 is involved in this response because an in vitro analysis revealed that reducing PO2 dramatically decreased mitochondrial ROS emissions and electron leak to ROS.Altogether, these data indicate that mitochondrial ROS emission rates are attenuated following BFR‐RE, and such a response is likely influenced by reductions in PO2. [ABSTRACT FROM AUTHOR]

The movement of lipids across mitochondrial membranes represents a rate-limiting step in fatty acid oxidation within the heart. A key regulatory point in this process is flux through carnitine palmitoyltransferase-I (CPT-I), an enzyme located on the outer mitochondrial membrane. Malonyl-CoA (M-CoA) is a naturally occurring inhibitor of CPT-I; therefore, the abundance of M-CoA has long been considered a major regulator of fatty acid oxidation. A recent paper published in the Biochemical Journal by Altamimi et al. (Biochem. J. (2018) 475, 959–976) provides evidence for a novel mechanism to produce M-CoA. Specifically, these authors identified carnitine acetyltransferase within the cytosol and further show that flux in the reverse direction forms acetyl-CoA, which is the necessary substrate for the subsequent synthesis of M-CoA. The elegant study design and intriguing data presented by Altamimi et al. provide further insights into the reciprocal regulation of substrate selection within the heart, with implications for fuel utilization and the development of cardiac diseases. [ABSTRACT FROM AUTHOR]