bims-ensmum 2026-08-30 papers

Med Sci Sports Exerc. 2026 Aug 27.

Photobiomodulation Does Not Increase Mitochondrial Respiration in Skeletal Muscle or Skin Tissue in Humans.

Thorben Aussieker, Heather L Petrick, Lisa M E Kuin, Jeremias Kaiser, Cas J Fuchs, Esther Kornips, Kostas Tsintzas, Scott Cooper, Sandra Lammers, Stephan Praet, Tim Snijders, Luc J C van Loon.

PURPOSE: Low-level laser therapy, also referred to as photobiomodulation (PBM), is rapidly gaining popularity as a non-invasive treatment for various conditions and as a means to enhance health and performance. PBM has been proposed to directly increase mitochondrial activity in skin and skeletal muscle and activate various molecular signalling pathways. However, evidence for the proposed properties of PBM in vivo in humans is lacking.
METHODS: In a within-participant study design, 12 healthy men and women (6/6 m/f; age: 25±6 y; BMI: 23.3±2.2kg/m2) received PBM on a randomized leg, while the other leg received sham-treatment (no light emitted, CON). Three cycles of PBM or sham-treatment were performed for 5 min 16 sec each (5.6 kJ light energy/cycle for PBM). Skin temperature was measured before and after treatment. After treatment, skin and muscle samples were collected from both legs. Mitochondrial respiration was measured in permeabilized muscle fibers and minced skin tissue using an Oroboros Oxygraph-O2k. Muscle metabolic gene expression was assessed using custom made microfluidic cards.
RESULTS: Skin temperature increased only in the PBM treated leg (+8.0±1.4 °C; P<0.001). No differences were observed between the PBM and CON treated legs in maximal complex I+II-linked respiration in skin (2.7±0.8 vs 2.6±0.7 pmol/sec/mg wet weight, respectively; P=0.66) or muscle (474±114 vs 467±81 pmol/sec/mg dry weight, respectively; P=0.71). Furthermore, no differences were observed in muscle mitochondrial ADP sensitivity (apparent ADP half-time: 1310±180 vs 1229±240 µM ADP, respectively; P=0.14). Of the 91 genes, expression between legs differed for 3 genes only.
CONCLUSIONS: A single session of photobiomodulation does not increase mitochondrial respiration in skin or underlying muscle tissue and does not modulate muscle gene expression ex vivo in humans.

Keywords: LOW-LEVEL LASER THERAPY (LLLT); MITOCHONDRIA; MUSCLE; PHOTOTHERAPY; SKIN

DOI: https://doi.org/10.1249/MSS.0000000000004120

J Physiol. 2026 Aug 24.

Musculoskeletal and physiological responses to vortex wave stimulation in older adults.

Alexander Waddell, Marie Korzepa, Archie E Belfield, Ben Fry, Rickson C Mesquita, David Smith, Jonathan Quinlan, Leigh Breen.

Reductions in musculoskeletal mass and function can occur with ageing and disuse. While resistance exercise training is known to minimise these detriments, it is not always feasible. Vortex wave stimulation (VWS) may mitigate skeletal muscle decline in such scenarios. The aim of the present study was to explore the acute physiological and metabolic effects of VWS in healthy older adults. Fourteen participants consumed deuterium oxide (D2O) stable oral isotope tracer for 7 days. Serial skeletal muscle biopsies were obtained to measure integrated rates of myofibrillar (iMyoPS) and sarcoplasmic (iSarcPS) muscle protein synthesis and regulatory signalling over ∼48 h before (habitual) and after two consecutive-day bouts of VWS. Myoelectrical activity and muscle oxygenation during VWS, and pre-post changes in peripheral blood flow and concentrations of inflammatory and bone turnover markers were also measured. There was an increase in iMyoPS (0.23% day-1, P = 0.025), but not iSarcPS (0.07% day-1, P = 0.582) above habitual rates following VWS. There was no difference in the expression of anabolic signalling proteins, nor peripheral blood flow following VWS. Myoelectrical activity increased during VWS (9.47 µV, P = 0.010), while muscle oxygenation decreased at the gastrocnemius (P = 0.001) and quadriceps (P = 0.017). There was a reduction in P1NP (8.27 µg L-1) and lactate (0.84 mmol L-1) concentration post-VWS (both P < 0.001), while there was no difference in other biomarkers. This is the first study to demonstrate that VWS elicits acute physiological responses congruent with musculoskeletal adaptive remodelling, which warrants further exploration. KEY POINTS: Resistance exercise is known to mitigate skeletal muscle atrophy associated with ageing and/or disuse but is not always feasible. We investigated, for the first time, the effects of a novel mechanical stimulus - vortex wave stimulation (VWS) - on integrated rates of myofibrillar and sarcoplasmic muscle protein synthesis, alongside other musculoskeletal and physiological outcomes, in healthy older adults. We demonstrated that VWS elevated myofibrillar, but not sarcoplasmic muscle protein synthesis compared to baseline, while increasing myoelectrical activity and reducing muscle oxygen saturation, lactate and bone turnover markers. These findings suggest VWS elicits acute physiological responses congruent with musculoskeletal adaptive remodelling.

Keywords: human physiology; sarcopenia; skeletal muscle

DOI: https://doi.org/10.1113/JP291437

Nat Commun. 2026 07 28. pii: 9125. [Epub ahead of print]17(1):

Skeletal muscle properties in long COVID and ME/CFS differ from those induced by bed rest.

Braeden T Charlton, Anouk Slaghekke, Brent Appelman, Moritz Eggelbusch, Jelle Y Huijts, Wendy Noort, Paul W Hendrickse, Frank W Bloemers, Jelle J Posthuma, Paul van Amstel, Richie P Goulding, Hans Degens, Richard T Jaspers, Michèle van Vugt, Rob C I Wüst.

Patients with long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suffer from post-exertional malaise. The accompanying physical inactivity may contribute to a lower aerobic capacity and may explain skeletal muscle adaptations in these patients. Here, we compare whole-body exercise responses and skeletal muscle adaptations after strict 60-day bed rest in healthy people with those in long COVID and ME/CFS patients, and healthy age- and sex-matched controls. Bed rest alters respiratory and cardiovascular responses to maximal exercise, which are dissimilar in patients. Bed rest causes muscle atrophy without altering fiber type. Both patient groups have more glycolytic fibers, and ME/CFS patients display type I-specific atrophy. Only after bed rest is oxidative phosphorylation capacity associated with maximal oxygen uptake. As skeletal muscle characteristics differ between patients and healthy individuals after bed rest, physical inactivity cannot solely explain the lower exercise capacity and skeletal muscle adaptations in long COVID and ME/CFS patients.

DOI: https://doi.org/10.1038/s41467-026-75725-y

Am J Clin Nutr. 2026 Aug 25. pii: S0002-9165(26)00301-1. [Epub ahead of print] 101492

Lactose and Sucrose Each Stimulate Hepatic De Novo Lipogenesis: A Randomised Crossover Trial.

Steven Carter, Bruno Spellanzon, Elspeth Johnson, Francoise Koumanov, Kaitlyn M J H Dennis, Coco A Taylor Start, Louise Bradshaw, Alfonso Moreno-Cabañas, Lucy H Merrell, Emma E Vincent, Benedita Deslandes, Jennifer L Maher, Matthew J Neville, James A Betts, Dylan Thompson, Leanne Hodson, Javier T Gonzalez.

BACKGROUND: Fructose-containing sugars can exaggerate postprandial lipaemia and stimulate hepatic de novo lipogenesis (DNL) relative to glucose-based carbohydrates. Despite being consumed by most of the global population, the effects of galactose-containing sugars on hepatic DNL are currently unknown.
OBJECTIVE: To assess the effects of lactose ingestion on lipaemia and DNL.
METHODS: Twenty-four adults without obesity (12 male and 12 female) completed three laboratory visits in a randomised, crossover design (33±14-day washout; mean±SD). During laboratory visits, participants consumed beverages containing 50g fat with 100g of carbohydrate. The control carbohydrate was a glucose polymer (maltodextrin), the experimental carbohydrate was galactose-containing carbohydrate (lactose) and the active comparator was fructose-containing carbohydrate (sucrose). Hepatic DNL was assessed by the 2H2O method and [U-13C]-palmitate was added to the test drink to trace the fate of the ingested fat. Blood and breath samples were taken to determine plasma metabolite and hormone concentrations, in addition to plasma and breath 2H and 13C enrichments. Summary statistics were analysed by one-way ANOVA, and time series data by two-way (time x treatment) ANOVA or linear mixed models when data were missing.
RESULTS: The plasma triacylglycerol iAUC (mean±SD) in response to maltodextrin was 0.85±1.13mmol·L-1·360 min and peak hepatic DNL was 11±3%. Following lactose ingestion, plasma triacylglycerol iAUC increased to 1.63±1.47mmol·L-1·360 min (p<0.001 versus maltodextrin), and hepatic DNL increased to 22±4% (p<0.001 versus maltodextrin), to a degree statistically indistinguishable from following sucrose ingestion [1.50±1.58mmol/L-1·360 min (p=0.41 versus lactose); and 23±4% (p=0.54 versus lactose)]. Contributions of dietary fat to VLDL- and Chylomicron-TG-palmitate were both higher following ingestion of lactose versus maltodextrin (both p<0.05), and were statistiscally indistinguishable following lactose ingestion versus sucrose (both p>0.05).
CONCLUSIONS: Lactose ingestion stimulates hepatic DNL by a magnitude that is not statistically different from fructose. This challenges the prevailing view that galactose-containing sugars are metabolically equivalent to glucose-based carbohydrates.
CLINICAL TRIALS REGISTRATION: NCT04924530 (https://clinicaltrials.gov/study/NCT04924530).

Keywords: Sugars; fructose; galactose; glucose; lipids; metabolism

DOI: https://doi.org/10.1016/j.ajcnut.2026.101492

Exp Physiol. 2026 Aug 24.

Multi-omics identifies promoter methylation and gene expression changes associated with human skeletal muscle atrophy.

Jamie-Lee M Thompson, Thomas M Doering, Boris P Budiono, Kristen L Mackenzie-Shalders, Kevin J Ashton, Paul J Dunn, Vernon G Coffey.

Skeletal muscle atrophy is a secondary complication in the aetiology of injury and chronic disease. Identifying mechanisms that control muscle mass is necessary to characterise atrophy and develop prevention strategies. We aimed to integrate transcriptomic and epigenomic data to identify key regulatory pathways controlled by promoter DNA methylation during muscle unloading. Twenty-one healthy men (20-40 years) completed a 4-week standardised exercise programme prior to a 14-day knee brace immobilisation with dietary control. Skeletal muscle mass and strength were assessed before and after immobilisation and biopsies were collected (m. vastus lateralis) before, at 3 days, and at completion at 14 days. RNA and DNA were isolated and analysed using Illumina RNA sequencing and DNA methylation 850K EPIC BeadChips. The 14-day immobilisation decreased muscle mass (∼9%; P < 0.0001) and strength (∼16%; P < 0.0001). At 3 days, most biological processes (BPs) were upregulated/hypomethylated (157 gene sets); upregulated BPs included cell signalling and protein ubiquitination and downregulated BPs included metabolism. After 14 days, BPs were predominantly downregulated/hypermethylated, including translation and ribosome biogenesis. Across both time points, HDAC4, GADD45A and CHRNA1 emerged as methylation-regulated candidate mediators of atrophy. HDAC4 and GADD45A showed strong correlations primarily at day 3, and CHRNA1 remained significant at both time points, extending prior observations in animals to human skeletal muscle. We have characterised changes in gene expression related to hypo- and hyper-methylation during muscle unloading in humans. These data extend our understanding of the regulatory processes that occur during skeletal muscle atrophy that, at the individual gene level, may be useful in developing strategies for reducing muscle wasting.

Keywords: genetics; unloading; wasting

DOI: https://doi.org/10.1113/EP093999