bims-ensmum Biomed News
on Exercise and nutrition in skeletal muscle metabolism
Issue of 2026–10–11
five papers selected by
Rachel M. Handy, University of Guelph and Universiteit Mastricht



  1. Med Sci Sports Exerc. 2026 Oct 07.
       PURPOSE: To investigate the effects of ingesting 60 versus 100 g CHO·h⁻¹ during prolonged cycling on durability, substrate oxidation, and muscle glycogen utilization in endurance athletes.
    METHODS: Fifteen trained male cyclists and triathletes completed a 15-min time trial (15-min TT) in a fresh state and following two prolonged intermittent cycling (PIC) protocols. After consuming a CHO-enriched diet for 24 hours, participants cycled for 240 min at 60 % of their fresh 15-min TT mean power output (MPO₁₅min), interspersed with high-intensity intervals. In a randomized, double-blind, crossover design, participants consumed either 60 g CHO·h⁻¹ (CHO60) or 100 g CHO·h⁻¹ (CHO100) through beverages and gels in a 1:0.8 glucose:fructose ratio. Muscle biopsies were obtained from m. vastus lateralis before and after the PIC protocols to assess glycogen content.
    RESULTS: 15-min TT performance was impaired after the PIC protocol in both conditions but with a greater reduction in CHO60 compared with CHO100 (-9.3 ± -2.0% vs -6.4 ± -1.7%, P= 0.025). Accordingly, MPO₁₅ was 9 W higher in CHO100 than CHO60 (P = 0.028). Muscle glycogen content decreased substantially during exercise, with similar glycogen availability after the PIC protocols between conditions (CHO60: 192 ± 99 mmol · kg -1 DW; CHO100: 209 ± 111 mmol · kg -1 DW, P = 0.56). Whole-body CHO oxidation was better preserved during the PIC protocol in CHO100 (CHO60: 2.6 ± 0.6 g·min -1 to 1.9 ± 0.4 g·min -1, CHO100: 2.6 ± 0.4 g·min -1 to 2.3 ± 0.5 g·min -1, condition x time; P = 0.047), whereas blood glucose concentrations remained stable in both conditions (CHO60: 5.6 ± 1.0 mmol·L -1 to 5.7 ± 0.9 mmol·L -1, CHO100: 6.0 ± 0.9 mmol·L -1 to 6.1 ± 0.9 mmol·L -1, effect of time; P = 0.43).
    CONCLUSIONS: Consuming 100 versus 60 g CHO·h⁻¹ during prolonged intermittent cycling improved durability without altering muscle glycogen utilization.
    Keywords:  CARBOHYDRATE METABOLISM; FATIGUE RESISTANCE; NUTRITION; RESILIENCE
    DOI:  https://doi.org/10.1249/MSS.0000000000004180
  2. Med Sci Sports Exerc. 2026 Oct 07.
       PURPOSE: Given recent controversy surrounding the optimal CHO intake during exercise, we assessed the effects of CHO ingestion at rates of 10, 90, 120 and 150 g.h -1 on substrate metabolism and exercise capacity.
    METHODS: Eight trained males cycled for 3 hours, followed by an exercise capacity test (150% lactate threshold). Participants completed an initial familiarization comprising 10 g.h -1 (maltodextrin) with subsequent trials randomized (90, 120 and 150 g.h -1: 1:0.8 ratio of maltodextrin to fructose drinks enriched with [U 13-C] glucose-fructose).
    RESULTS: Mean exogenous CHO oxidation increased in a dose dependent manner where 150 > 120 > 90 g.h -1 (1.62 ± 0.45; 1.48 ± 0.44; 1.23 ± 0.35 g.min -1, respectively, all P<0.05), though substantial variation was observed within trials (range of 0.3, 0.6 and 0.9 g.min -1 for 90, 120 and 150 g.h -1, respectively). Whole-body CHO oxidation did not differ (P=0.97) between 150 and 120 g.h -1 (both trials = 2.6 ± 0.3 g.min -1), with both trials greater than 90 and 10 g.h -1 (2.3 ± 0.5; 1.7 ± 0.7 g.min -1, respectively). Blood glucose was lower in 10 g.h -1 (3.8 ± 0.2, P<0.01) versus 90, 120 and 150 g.h -1 (4.6 ± 0.2, 4.6 ± 0.1, 4.8 ± 0.2 mmol.L -1; P>0.05 between higher doses). Total exercise duration was lower in 10 g.h -1 (2:41:28 ± 0:24:47 h:min:secs,) versus 90 (3:04:59 ± 0:01:52), 120 (3:05:24 ± 0:03:28, both P<0.05) and 150 g.h -1 (3:00:39 ± 0:07:00, P=0.06), with no differences (P>0.05) between higher rates. Optimal exercise capacity was achieved with 107 g.h -1 (95 % CI: 92-122 g.h -1).
    CONCLUSIONS: Data demonstrate 150 g.h -1 does not increase whole-body CHO oxidation versus 120 g.h -1, though variations in ergogenic dose and exogenous CHO oxidation rates support CHO personalization.
    Keywords:  FRUCTOSE; MALTODEXTRIN; METABOLISM; STABLE ISOTOPES
    DOI:  https://doi.org/10.1249/MSS.0000000000004176
  3. Eur J Appl Physiol. 2026 Oct 03.
       PURPOSE: Acute nitrate-rich beetroot juice (BRJ) supplementation has been shown to improve aspects of endurance exercise performance. These effects may, in part, be due to nitric oxide-mediated effects on skeletal muscle contractility and mitochondrial function. However, no studies have investigated the effects of chronic BRJ supplementation with resistance training (RT) on molecular markers of mitochondrial adaptation and redox state within the skeletal muscle of older adults. Likewise, whether supplementation affects functional outcomes in this population is unresolved.
    METHODS: In the current study, 27 older adults (56 ± 7 years old, 85.9 ± 20.6 kg, 36.1 ± 8.3% body fat) were block-randomized to consume either a nitrate-depleted (Placebo) or nitrate-rich (~ 13 mmol) BRJ daily and complete 12 weeks of supervised total body RT (2 days per week). Vastus lateralis (VL) biopsies and measurements of leg extensor peak force, strength-endurance, and fatigue were obtained prior to training and ~72 h following the last training bout.
    RESULTS: In all participants, RT increased VL citrate synthase activity (i.e., mitochondrial content), certain proteins indicative of mitochondrial biogenesis and dynamics, and most leg extensor performance variables. However, BRJ supplementation did not confer additional benefits with any of the outcomes.
    CONCLUSIONS: RT in middle-aged and older adults dynamically alters muscle mitochondrial markers and knee extensor performance variables, albeit increased dietary BRJ consumption does not confer additional benefits.
    Keywords:  Mitochondria; Nitrate supplementation; Older adults; Redox state; Resistance training; Skeletal muscle
    DOI:  https://doi.org/10.1007/s00421-026-06460-x
  4. Am J Physiol Cell Physiol. 2026 Oct 05.
      Exercise induces diverse adaptations in skeletal muscle, and extracellular matrix remodeling plays a key role in these adaptations. Capillaries, which are essential for transporting oxygen and other molecules to maintain skeletal muscle function, are crucial for exercise adaptation. Perlecan, a heparan sulfate proteoglycan and a major basement membrane molecule in skeletal muscle, has been implicated in capillary formation and maintenance. However, its role in exercise adaptation remains unclear. Herein, we used male mice lacking perlecan expression outside of cartilage (Hspg2-/--Tg) as well as Hspg2 wild-type transgenic control mice to examine the regulatory relationship between perlecan and PGC-1α isoforms, which are key mediators of exercise-induced metabolic and angiogenic responses. Following acute treadmill exercise, Hspg2-/--Tg mice showed a significant increase in the mRNA expression of alternative promoter-driven PGC-1α isoforms (ex1b and ex1b') 3 h after exercise, whereas proximal promoter-driven isoforms showed little response. This isoform-specific response was accompanied by enhanced expression of angiogenesis-related genes, including Vegfa, Angpt1, Angpt2, and Hif1a, which peaked 3 h after exercise in perlecan-deficient muscle. In parallel with these transcriptional changes, immunofluorescent analysis revealed significantly higher baseline capillary density in Hspg2-/--Tg quadriceps muscle, a difference that became even more pronounced after 2 wk of exercise training. These findings demonstrate that perlecan deficiency enhances baseline vascular remodeling features and the angiogenic transcriptional response to exercise, suggesting that the composition of the basement membrane extracellular matrix critically regulates exercise-induced PGC-1α isoform expression and muscle-vascular crosstalk during skeletal muscle adaptation.
    Keywords:  acute exercise; extracellular matrix; perlecan; skeletal muscle; vascular adaptation
    DOI:  https://doi.org/10.1152/ajpcell.00956.2025
  5. Med Sci Sports Exerc. 2026 Oct 07.
       INTRODUCTION: Repeated sprint training in hypoxia (RSH) or with blood flow restriction (RS-BFR) are known to enhance the repeated-sprint ability. However, studies directly comparing their underlying molecular mechanisms are scarce.
    METHODS: Here we used a comprehensive approach combining pre- and post-intervention testing including sprint performance tests, neuromuscular assessments, skeletal muscle biopsies for protein levels quantification, and blood samples for systemic metabolites analyses to characterize the specific adaptations induced by RSH and RS-BFR. Recreationally active men performed 9 sessions of RSH (FiO₂ ~0.136; n=9) or RS-BFR (45% arterial occlusion; n=8).
    RESULTS: Both RSH and RS-BFR similarly improved exercise performance without significant changes in knee extensor maximal voluntary contraction force. Both training modalities reduced the levels of oxidative phosphorylation proteins while increasing markers of mitochondrial dynamics and mitochondrial translation proteins. Glycolytic remodelling was evident in both groups, with increased levels of the glucose transporter 4 and phosphofructokinase proteins, accompanied by marked upregulation of the S100A13-Akt signalling. Unbiased muscle proteomics and plasma metabolomics also revealed common and more specific signatures. Both RSH and RS-BFR increased plasma levels of intermediates metabolites of lipid metabolism. RSH specifically upregulated cytoplasmic translation pathways in muscle and increased the kynurenate/kynurenine ratio in plasma, whereas RS-BFR was characterized by an upregulation of immune and inflammatory pathways both in muscle and plasma.
    CONCLUSIONS: In summary, 3-week of RS-BFR elicits performance adaptations comparable to RSH, supported by largely shared muscular and systemic metabolic adaptations. The specific characteristics of the adaptations induced by each method, however, are particularly interesting and could influence the outcome of regular training.
    Keywords:  EXERCISE; GLYCOLYSIS; METABOLOMICS; MITOCHONDRIA; PERFORMANCE; PROTEOMICS
    DOI:  https://doi.org/10.1249/MSS.0000000000004179