Trial reportSports medicine (Auckland, N.Z.)2025
Phosphoproteomics Uncovers Exercise Intensity-Specific Skeletal Muscle Signaling Networks Underlying High-Intensity Interval Training in Healthy Male Participants.
Trial report in Sports medicine (Auckland, N.Z.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Multi‑omics approaches to decipher the molecular mechanisms of exercise‑mediated bone protection: From mechanistic insights to personalized exercise prescription (Review).Molecular medicine reports · 2026Review
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Lactate as a metabolic-epigenetic signal linking high-intensity interval training (HIIT) to miRNA-Centered remodeling of the skeletal muscle methylome and transcriptome.Redox biology · 2025Article
- Twenty years of progress in human exercise metabolism research.Nature reviews. Endocrinology · 2025Article
- Vigorous But Not Moderate Physical Activity Is Associated With Reduced Cardiovascular Disease Risk In Young Hispanic Men.The American journal of cardiology · 2025Article
- Aerobic and resistance exercise-regulated phosphoproteome and acetylproteome modifications in human skeletal muscle.Nature communications · 2025Article
- Kinase-phosphatase balance in exercise adaptation: phosphorylation programs, PTM crosstalk, and actionable gaps.Frontiers in sports and active living · 2025Review
- Mechanism of exercise-derived circulating exosomes as a target for sarcopenia management.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundIn response to exercise, protein kinases and signaling networks are engaged to blunt homeostatic threats generated by acute contraction-induced increases in skeletal muscle energy and oxygen demand, as well as serving roles in the adaptive response to chronic exercise training to blunt future disruptions to homeostasis. High-intensity interval training (HIIT) is a time-efficient exercise modality that induces superior or similar health-promoting skeletal muscle and whole-body adaptations compared with prolonged, moderate-intensity continuous training (MICT). However, the skeletal muscle signaling pathways underlying HIIT's exercise intensity-specific adaptive responses are unknown.
objectiveWe mapped human muscle kinases, substrates, and signaling pathways activated/deactivated by an acute bout of HIIT versus work-matched MICT.
methodsIn a randomized crossover trial design (Australian New Zealand Clinical Trials Registry number ACTRN12619000819123; prospectively registered 6 June 2019), ten healthy male participants (age 25.4 ± 3.2 years; BMI 23.5 ± 1.6 kg/m
resultsBioinformatic analyses uncovered exercise intensity-specific signaling networks, including > 1000 differentially phosphorylated sites (± 1.5-fold change; adjusted P < 0.05; ≥ 3 participants) after 5 min and 10 min HIIT and/or MICT relative to rest. After 5 and 10 min, 92 and 348 sites were differentially phosphorylated by HIIT, respectively, versus MICT. Plasma lactate concentrations throughout HIIT were higher than MICT (P < 0.05), and correlation analyses identified > 3000 phosphosites significantly correlated with lactate (q < 0.05) including top functional phosphosites underlying metabolic regulation.
conclusionsCollectively, this first global map of the work-matched HIIT versus MICT signaling networks has revealed rapid exercise intensity-specific regulation of kinases, substrates, and pathways in human skeletal muscle that may contribute to HIIT's skeletal muscle adaptations and health-promoting effects. Preprint: The preprint version of this work is available on medRxiv, https://doi.org/10:1101/2024.07.11.24310302 .
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