New Zealand blackcurrant (NZBC) is known to alter exercise-induced physiological and metabolic responses with chronic (i.e., 7 days) dosing. We examined the effects of acute intake of New Zealand blackcurrant (NZBC) extract on 4 h indoor cycling-induced physiological and metabolic responses in a male amateur Ironman athlete (age: 49 years; BMI: 24.3 kg·m-2; V˙O2max: 58.6 mL·kg-1·min-1; maximal aerobic power: 400 W; history: 14 Ironman events in 16 years) three weeks before competition. Indirect calorimetry was used and heart rate was recorded at 30 min intervals during 4 h indoor (~22.4 °C, relative humidity: ~55%) constant power (165 W) cycling on a Trek Bontrager connected to a Kickr smart trainer. Blood lactate and rating of perceived exertion (RPE) were taken at 60 min intervals. Study was a single-blind placebo-controlled study with capsules (4 × 105 mg anthocyanins) taken 2 h before starting the 4 h of cycling. Water was allowed ad libitum with personalised consumption of gels [a total of eight with three with caffeine (100 mg)], two bananas and 8 × electrolyte capsules (each 250 mg sodium and 125 mg potassium) at personalised time-points. With NZBC extract (CurraNZ), during 4 h of cycling (mean of 8 measurements), minute ventilation was 8% lower than placebo. In addition, there was no difference for oxygen uptake, with carbon dioxide production found to be 4% lower with NZBC extract. With the NZBC extract, the ventilatory equivalents were lower for oxygen and carbon dioxide by 5.5% and 3.7%; heart rate was lower by 10 beats·min-1; lactate was 40% different with lower lactate at 2, 3 and 4 h; RPE was lower at 2, 3 and 4 h; and carbohydrate oxidation was 11% lower. With NZBC extract, there was a trend for fat oxidation to be higher by 13% (p = 0.096), with the respiratory exchange ratio being lower by 0.02 units. Acute intake of New Zealand blackcurrant extract (420 mg anthocyanins) provided beneficial physiological and metabolic responses during 4 h of indoor constant power cycling in a male amateur Ironman athlete 3 weeks before a competition. Future work is required to address whether acute and chronic dosing strategies with New Zealand blackcurrant provide a nutritional ergogenic effect for Ironman athletes to enhance swimming, cycling and running performance.

This study explored the impact of varying energy availability (EA) on the 24-h interstitial fluid glucose concentration (IGC) in five elite male Japanese triathletes at a training camp. Measurements of IGC, energy and macronutrient intake, and exercise energy expenditure (EEE) through metabolic equivalents (METs) from training logs were conducted. Three subjects were evaluated over two 4-day periods, and two subjects over one 4-day period. Findings revealed significant correlations of daily mean nocturnal IGC with daily EA (r = 0.553, p = 0.001) and energy intake (EI) (r = 0.595, p < 0.001). However, no significant correlation was found between mean daily nocturnal IGC and EEE (r = -0.278, p = 0.124). Daytime IGC was ≥110 mg/dL for >50% of the time in all subjects, except on 1 day in one subject, and never fell <70 mg/dL. Therefore, daily EA may influence nocturnal IGC in elite male triathletes, although high daytime IGC levels were maintained without hypoglycemia.

In oxidative phosphorylation, respiratory complex I serves as an entry point in the electron transport chain for electrons generated in catabolic processes in the form of NADH. An ancestral version of the complex, lacking the NADH-oxidising module, is encoded in a significant number of bacterial genomes. Amongst them is Desulfitobacterium hafniense, a strict anaerobe capable of conserving energy via organohalide respiration. This study investigates the role of the complex I-like enzyme in D. hafniense energy metabolism using rotenone as a specific complex I inhibitor under different growth conditions. The investigation revealed that the complex I-like enzyme was essential for growth with lactate and pyruvate but not in conditions involving H2 as an electron donor. In addition, a previously published proteomic dataset of strain DCB-2 was analysed to reveal the predominance of the complex under different growth conditions and to identify potential redox partners. This approach revealed seven candidates with expression patterns similar to Nuo homologues, suggesting the use of diverse electron sources. Based on these results, we propose a model where the complex I-like enzyme serves as an electron entry point into the respiratory chain for substrates delivering electrons within the cytoplasm, such as lactate or pyruvate, with ferredoxins shuttling electrons to the complex.

BACKGROUND: It is unclear whether variation in thyroid stimulating hormone (TSH) levels within the reference range affect energy expenditure and clinical symptoms and even within the normal range of TSH levels, resting energy expenditure may alter. The aim of the present study was to determine whether treated hypothyroid subjects and healthy subjects with a low-normal TSH range (0.3-2.3 mIU/L) have better clinical outcomes and increased energy expenditure than those with a high-normal TSH range (2.3-4.3 mIU/L).
METHODS: This was a case-control study of 160 overweight/obese women with TSH levels across the reference range of 0.3-4.3 mU/l. Subjects were paired in four groups: healthy subjects with low-normal target TSH (n = 40), healthy subjects with high-normal target TSH (n = 40), subjects with treated hypothyroidism with low-normal target TSH (n = 40), and subjects with treated hypothyroidism with high-normal target TSH (n = 40). Resting energy expenditure (RMR), dietary intake, body composition, physical activity, and biochemical markers were assessed.
RESULTS: Subjects with low-normal (≤2.3 mU/L) and high-normal (>2.3 mU/L) TSH levels did not differ in terms of RMR, serum T3 levels, and clinical symptoms except fatigue (P = 0.013). However, serum fT4 levels were found to be significantly different between the study groups (P = 0.002). Serum fT4 concentration was the highest in subjects with treated hypothyroidism with low-normal target TSH.
CONCLUSIONS: Variation in serum TSH levels within the reference range did not significantly affect REE and clinical symptoms except fatigue in healthy and women with hypothyroidism.

In glucose transporter 1 deficiency syndrome (Glut1DS), glucose transport into brain is reduced due to impaired Glut1 function in endothelial cells at the blood-brain barrier. This can lead to shortages of glucose in brain and is thought to contribute to seizures. Ketogenic diets are the first-line treatment and, among many beneficial effects, provide auxiliary fuel in the form of ketone bodies that are largely metabolized by neurons. However, Glut1 is also the main glucose transporter in astrocytes. Here, we review data indicating that glucose shortage may also impact astrocytes in addition to neurons and discuss the expected negative biochemical consequences of compromised astrocytic glucose transport for neurons. Based on these effects, auxiliary fuels are needed for both cell types and adding medium chain triglycerides (MCTs) to ketogenic diets is a biochemically superior treatment for Glut1DS compared to classical ketogenic diets. MCTs provide medium chain fatty acids (MCFAs), which are largely metabolized by astrocytes and not neurons. MCFAs supply energy and contribute carbons for glutamine and γ-aminobutyric acid synthesis, and decanoic acid can also block α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid glutamate receptors. MCTs do not compete with metabolism of ketone bodies mostly occurring in neurons. Triheptanoin, an anaplerotic but also gluconeogenic uneven MCT, may be another potential addition to ketogenic diets, although maintenance of \"ketosis\" can be difficult. Gene therapy has also targeted both endothelial cells and astrocytes. Other approaches to increase fuel delivery to the brain currently investigated include exchange of Glut1DS erythrocytes with healthy cells, infusion of lactate, and pharmacological improvement of glucose transport. In conclusion, although it remains difficult to assess impaired astrocytic energy metabolism in vivo, astrocytic energy needs are most likely not met by ketogenic diets in Glut1DS. Thus, we propose prospective studies including monitoring of blood MCFA levels to find optimal doses for add-on MCT to ketogenic diets and assessing of short- and long-term outcomes.

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disorder. The most devastating variant is bulbar-onset ALS, which portends a median survival of 24 months from the onset of symptoms. Abundant evidence indicates that neuron metabolism and mitochondrial function are impaired in ALS. Metabolic strategies, particularly fasting and ketogenic diet protocols, alter neuron metabolism and mitochondria function in a manner that may mitigate the symptoms of this disorder. We report the case of a 64-year-old man with a 21-month history of progressive, deteriorating bulbar-onset ALS, with an associated pseudobulbar affect, who implemented a time-restricted ketogenic diet (TRKD) for 18 months. During this time, he improved in ALS-related function (7% improvement from baseline), forced expiratory volume (17% improvement), forced vital capacity (13% improvement), depression (normalized), stress levels (normalized), and quality of life (19% improvement), particularly fatigue (23% improvement). His swallowing impairment and neurocognitive status remained stable. Declines were measured in physical function, maximal inspiratory pressure, and maximal expiratory pressure. Weight loss was attenuated and no significant adverse effects occurred. This case study represents the first documented occurrence of a patient with ALS managed with either a fasting or ketogenic diet protocol, co-administered as a TRKD. We measured improved or stabilized ALS-related function, forced expiratory volume, forced vital capacity, swallowing, neurocognitive status, mood, and quality of life. Measurable declines were restricted to physical function, maximal inspiratory pressure, and maximal expiratory pressure. Now over 45 months since symptom onset, our patient remains functionally independent and dedicated to his TRKD.

The Tour Divide (TD) is a 4385 km ultra-endurance bicycle race that follows the continental divide from Canada to Mexico. In this case study, we performed a comprehensive molecular and physiological profile before and after the completion of the TD. Assessments were performed 35 days before the start (Pre-TD) and ∼36 h after the finish (Post-TD). Total energy expenditure was assessed during the first 9 days by doubly labelled water (2 H2 18 O), abdominal and leg tissue volumes via MRI, and graded exercise tests to quantify fitness and substrate preference. Vastus lateralis muscle biopsies were taken to measure mitochondrial function via respirometry, and vascular function was assessed using Doppler ultrasound. The 47-year-old male subject took 16 days 7 h 45 min to complete the route. He rode an average of 16.8 h/day. Neither maximal O2 uptake nor maximal power output changed pre- to post-TD. Measurement of total energy expenditure and dietary recall records suggested maintenance of energy balance, which was supported by the lack of change in body weight. The subject lost both appendicular and trunk fat mass and gained leg lean mass pre- to post-TD. Skeletal muscle mitochondrial and vascular endothelial function decreased pre- to post-TD. Overall, exercise performance was maintained despite reductions in muscle mitochondrial and vascular endothelial function post-TD, suggesting a metabolic reserve in our highly trained athlete.

This study documented seasonal levels of microplastics (MPs) and biomarkers (condition index, neurotoxicity, energy, oxidative stress) in mussels (Mytilus galloprovincialis), and water physico-chemical parameters in the Douro estuary (NE Atlantic coast), and estimated the human risk of MP intake (HRI) through mussels. Mussel stress was determined through the Integrated Biomarker Response (IBR). HRI was estimated from mussel MP concentrations and consumer habits. MPs were mainly micro-fibres (72 %) with varied chemical composition. Seasonal MP means (±SEM) in mussels ranged from 0.111 ± 0.044 (spring) to 0.312 ± 0.092 MPs/g (summer). Seasonal variations of mussel stress (IBR: 1.4 spring to 9.7 summer) and MP concentrations were not related. MeO-BDEs, PBDEs, temperature, salinity and other factors likely contributed to mussel stress variation. HRI ranged from 2438 to 2650 MPs/year. Compared to the literature, MP contamination in mussels is low, as well as the human risk of MP intake through their consumption.

UNASSIGNED: Autologous myoblast patch (AMP) transplantation has resulted in good clinical outcomes for end-stage ischaemic cardiomyopathy, but the mechanisms behind them are unclear. Herein, we report the relationship between mitochondrial function and coronary flow reserve (CFR) before and after AMP transplantation.
UNASSIGNED: The patient was a 73-year-old man who underwent coronary artery bypass grafting (CABG). At that time, the left ventricular ejection fraction (LVEF) was 53%, but it declined to 25% after 6 years. He was diagnosed with ischaemic cardiomyopathy (ICM). Coronary flow reserve in NH3-positron emission tomography (NH3-PET) was impaired to 1.69. In Tc-99m MIBI scintigraphy, the washout rate (WR) was 17%, suggestive of impaired mitochondrial function. He was not a candidate for heart transplantation, and we performed AMP transplantation 6 years after CABG. One year after AMP transplantation, LVEF, CFR, and Tc-99m MIBI WR improved to 36%, 2.07, and 7%, respectively. The Tc-99m MIBI WR improved especially in the anterolateral region, and the CFR increased in almost all segments.
UNASSIGNED: In this case, AMP transplantation for ICM improved cardiac function, CFR, and mitochondrial function. The mitochondrial transfer from the transplanted myoblasts to the damaged myocardium may have contributed to the mitochondrial function improvement. This probably induced myocardial energy metabolism recovery and decreased oxygen demand. AMP transplantation also has the potential to improve microvascular dysfunction, due to angiogenesis induction. These effects can lead to improved prognoses of ICM after AMP transplantation, highlighting its potential to cure refractory heart failure.

Long-distance \"thru-hiking\" has extraordinary physical demands and has become increasingly popular. This report describes a man (55 y) who thru-hiked the Pacific Crest Trail in 2021 and was at risk of developing the relative energy deficiency in sport (RED-S) syndrome. Hiking distance was 3767 km over 128 d. Eighty-eight days (69%) were full days of hiking, covering 38±8 km/d (mean±SD) in 7.9±1.6 h/d. Exercise energy expenditure above rest (heart rate vs indirect calorimetry regression method) was 2834±1518 kcal/d, total energy expenditure was 5702±1323 kcal/d, and energy intake was 4141 kcal/d. Body mass decreased by 9%, and fat mass (dual-energy X-ray absorptiometry) decreased by 46%. Energy availability (energy intake minus exercise energy expenditure) was 19.3 kcal/d/kg fat-free mass, indicating low energy availability (defined as <30 kcal/d/kg). Dual-energy X-ray absorptiometry-measured spine bone mineral density (BMD) decreased by 8.6%, with little to no decrease in total hip (-1.0%) and femoral neck (-1.5%) BMD. Total cholesterol, low-density lipoprotein cholesterol, and triglycerides increased by 24, 39, and 57%, respectively. Within 8 mo after the hike, BMD and serum lipids nearly or fully returned to baseline. No changes in high-density lipoprotein cholesterol, glycemia, or blood pressure were observed. According to guidelines, these observations are consistent with a moderate risk of RED-S, and a medical evaluation and treatment plan are advisable in order to avoid clinical manifestations (eg, stress fractures, anemia, psychological disturbances). To minimize RED-S risk, it may be prudent for thru-hikers to optimize energy availability by moderating daily hiking distances and/or increasing food intake.