Abstract
Although physical training has been shown to improve bone mass, the time of day to exercise for optimal bone growth remains uncertain. Here we show that engaging in physical activity during the early active phase, as opposed to the subsequent active or rest phase, results in a more substantial increase in bone length of male and female mice. Transcriptomic and metabolomic methodologies identify that exercise during the early active phase significantly upregulates genes associated with bone development and metabolism. Notably, oxidative phosphorylation-related genes show a rhythmic expression in the chondrification centre, with a peak at the early active phase, when more rhythmic genes in bone metabolism are expressed and bone growth is synergistically promoted by affecting oxidative phosphorylation, which is confirmed by subsequent pharmacological investigations. Finally, we construct a signalling network to predict the impact of exercise on bone growth. Collectively, our research sheds light on the intricacies of human exercise physiology, offering valuable implications for interventions.
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Data availability
Transcriptome raw data of this study have been deposited in the Genome Sequence Archive53 in the National Genomics Data Center54, China National Center for Bioinformation/Beijing Institute of Genomics, Chinese Academy of Sciences, and will be publicly available under accession code CRA015794 on 08 April 2026. Source data are provided with this paper.
References
Jacobi, L. & Cash, T. F. In pursuit of the perfect appearance: discrepancies among self-ideal percepts of multiple physical attributes. J. Appl. Social Psychol. 24, 379–396 (1994).
McCormack, S. E. et al. Association between linear growth and bone accrual in a diverse cohort of children and adolescents. JAMA Pediatr. 171, e171769 (2017).
Alves, J. G. B. & Alves, G. V. Effects of physical activity on children’s growth. J. Pediatr. 95, 72–78 (2019).
Karlsson, M. K. & Rosengren, B. E. Exercise and peak bone mass. Curr. Osteoporos. Rep. 18, 285–290 (2020).
Bouillon, R. et al. Skeletal and extraskeletal actions of vitamin D: current evidence and outstanding questions. Endocr. Rev. 40, 1109–1151 (2019).
Tong, X. et al. The effect of exercise on the prevention of osteoporosis and bone angiogenesis. BioMed. Res. Int. 2019, 8171897 (2019).
Gabriel, B. M. & Zierath, J. R. Circadian rhythms and exercise - re-setting the clock in metabolic disease. Nat. Rev. Endocrinol. 15, 197–206 (2019).
Arciero, P. J. et al. Morning exercise reduces abdominal fat and blood pressure in women; evening exercise increases muscular performance in women and lowers blood pressure in men. Front. Physiol. 13, 893783 (2022).
Casanova-Vallve, N. et al. Daily running enhances molecular and physiological circadian rhythms in skeletal muscle. Mol. Metab. 61, 101504 (2022).
Savikj, M. et al. Afternoon exercise is more efficacious than morning exercise at improving blood glucose levels in individuals with type 2 diabetes: a randomised crossover trial. Diabetologia 62, 233–237 (2019).
Schumacher, L. M., Thomas, J. G., Raynor, H. A., Rhodes, R. E. & Bond, D. S. Consistent morning exercise may be beneficial for individuals with obesity. Exerc. Sport Sci. Rev. 48, 201–208 (2020).
Kronenberg, H. M. Developmental regulation of the growth plate. Nature 423, 332–336 (2003).
Hollander, J. M. & Zeng, L. The emerging role of glucose metabolism in cartilage development. Curr. Osteoporos. Rep. 17, 59–69 (2019).
Stegen, S. et al. HIF-1α metabolically controls collagen synthesis and modification in chondrocytes. Nature 565, 511–515 (2019).
Zheng, L., Zhang, Z., Sheng, P. & Mobasheri, A. The role of metabolism in chondrocyte dysfunction and the progression of osteoarthritis. Ageing Res. Rev. 66, 101249 (2021).
Sato, S. et al. Time of exercise specifies the impact on muscle metabolic pathways and systemic energy homeostasis. Cell Metab. 30, 92–110 (2019).
Fan, W. & Evans, R. M. Exercise mimetics: impact on health and performance. Cell Metab. 25, 242–247 (2017).
Cantó, C. et al. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity. Nature 458, 1056–1060 (2009).
Yu, S. et al. Circadian rhythm modulates endochondral bone formation via MTR1/AMPKβ1/BMAL1 signaling axis. Cell Death Differ. 29, 874–887 (2022).
van der Lee, R. et al. Transcriptome analysis of complex I-deficient patients reveals distinct expression programs for subunits and assembly factors of the oxidative phosphorylation system. BMC Genomics 16, 691 (2015).
Troy, K. L., Mancuso, M. E., Butler, T. A. & Johnson, J. E. Exercise early and often: effects of physical activity and exercise on women’s bone health. Int. J. Environ. Res. Public Health 15, 878 (2018).
Bass, J. & Takahashi, J. S. Circadian integration of metabolism and energetics. Science 330, 1349–1354 (2010).
Tan, V. P. et al. Influence of physical activity on bone strength in children and adolescents: a systematic review and narrative synthesis. J. Bone Miner. Res. 29, 2161–2181 (2014).
Yu, S. et al. Circadian BMAL1 regulates mandibular condyle development by hedgehog pathway. Cell Prolif. 53, e12727 (2020).
Sato, S. et al. Atlas of exercise metabolism reveals time-dependent signatures of metabolic homeostasis. Cell Metab. 34, 329–345 (2022).
Schroeder, A. M. et al. Voluntary scheduled exercise alters diurnal rhythms of behaviour, physiology and gene expression in wild-type and vasoactive intestinal peptide-deficient mice. J. Physiol. 590, 6213–6226 (2012).
Qi, Z., Liu, W. & Lu, J. The mechanisms underlying the beneficial effects of exercise on bone remodeling: roles of bone-derived cytokines and microRNAs. Prog. Biophys. Mol. Biol. 122, 131–139 (2016).
Herrmann, M. et al. Interactions between muscle and bone-where physics meets biology. Biomolecules 10, 432 (2020).
Kirk, B., Feehan, J., Lombardi, G. & Duque, G. Muscle, bone, and fat crosstalk: the biological role of myokines, osteokines, and adipokines. Curr. Osteoporos. Rep. 18, 388–400 (2020).
Deymier, A. C., Deymier, P. A., Latypov, M. & Muralidharan, K. Effect of stress on the dissolution/crystallization of apatite in aqueous solution: a thermochemical equilibrium study. Philos. Trans. A Math. Phys. Eng. Sci. 381, 20220242 (2023).
Li, X. et al. Stimulation of Piezo1 by mechanical signals promotes bone anabolism. eLife 8, e49631 (2019).
Pomerants, T., Tillmann, V., Karelson, K., Jürimäe, J. & Jürimäe, T. Impact of acute exercise on bone turnover and growth hormone/insulin-like growth factor axis in boys. J. Sports Med. Phys. Fit. 48, 266–271 (2008).
Hughes, J. M., Guerriere, K. I., Popp, K. L., Castellani, C. M. & Pasiakos, S. M. Exercise for optimizing bone health after hormone-induced increases in bone stiffness. Front. Endocrinol. 14, 1219454 (2023).
Scott, A., Khan, K. M., Duronio, V. & Hart, D. A. Mechanotransduction in human bone: in vitro cellular physiology that underpins bone changes with exercise. Sports Med. 38, 139–160 (2008).
Lee, S. Y., Abel, E. D. & Long, F. Glucose metabolism induced by Bmp signaling is essential for murine skeletal development. Nat. Commun. 9, 4831 (2018).
Hollander, J. M. et al. A critical bioenergetic switch is regulated by IGF2 during murine cartilage development. Commun. Biol. 5, 1230 (2022).
Rajpurohit, R., Mansfield, K., Ohyama, K., Ewert, D. & Shapiro, I. M. Chondrocyte death is linked to development of a mitochondrial membrane permeability transition in the growth plate. J. Cell. Physiol. 179, 287–296 (1999).
Tourmente, M., Varea-Sánchez, M. & Roldan, E. R. S. Faster and more efficient swimming: energy consumption of murine spermatozoa under sperm competition. Biol. Reprod. 100, 420–428 (2019).
Jin, L. et al. FGF21-Sirtuin 3 axis confers the protective effects of exercise against diabetic cardiomyopathy by governing mitochondrial integrity. Circulation 146, 1537–1557 (2022).
Wang, B. et al. The mitochondrial Ahi1/GR participates the regulation on mtDNA copy numbers and brain ATP levels and modulates depressive behaviors in mice. Cell Commun. Signal. 21, 21 (2023).
Li, J., King, N. C. & Sinoway, L. I. Interstitial ATP and norepinephrine concentrations in active muscle. Circulation 111, 2748–2751 (2005).
Hargreaves, M. & Spriet, L. L. Skeletal muscle energy metabolism during exercise. Nat. Metab. 2, 817–828 (2020).
Li, E. et al. BMAL1 regulates mitochondrial fission and mitophagy through mitochondrial protein BNIP3 and is critical in the development of dilated cardiomyopathy. Protein Cell 11, 661–679 (2020).
Wan, M. C. et al. Upregulation of mitochondrial dynamics is responsible for osteogenic differentiation of mesenchymal stem cells cultured on self-mineralized collagen membranes. Acta Biomater. 136, 137–146 (2021).
Wang, J. et al. Disrupting circadian rhythm via the PER1-HK2 axis reverses trastuzumab resistance in gastric cancer. Cancer Res. 82, 1503–1517 (2022).
Anderson, G. & Reiter, R. J. Melatonin: roles in influenza, COVID-19, and other viral infections. Rev. Med. Virol. 30, e2109 (2020).
Zilber, S. et al. Mouse femoral intramedullary injection model: technique and microCT scan validation. J. Biomed. Mater. Res. B Appl. Biomater. 84, 286–290 (2008).
Wang, Z. X. et al. Aged bone matrix-derived extracellular vesicles as a messenger for calcification paradox. Nat. Commun. 13, 1453 (2022).
Welz, P. S. et al. BMAL1-driven tissue clocks respond independently to light to maintain homeostasis. Cell 177, 1436–1447 (2019).
Kumar, L. & E Futschik, M. Mfuzz: a software package for soft clustering of microarray data. Bioinformation 2, 5–7 (2007).
Stegen, S., Moermans, K., Stockmans, I., Thienpont, B. & Carmeliet, G. The serine synthesis pathway drives osteoclast differentiation through epigenetic regulation of NFATc1 expression. Nat. Metab. 6, 141–152 (2024).
Chen, G. et al. Developmental growth plate cartilage formation suppressed by artificial light at night via inhibiting BMAL1-driven collagen hydroxylation. Cell Death Differ. 30, 1503–1516 (2023).
Chen, T. et al. The genome sequence archive family: Toward explosive data growth and diverse data types. Genomics Proteomics Bioinformatics 19, 578–583 (2021).
CNCB-NGDC Members and Partners. Database resources of the National Genomics Data Center, China National Center for Bioinformation in 2024. Nucleic Acids Res. 52, D18–D32 (2024).
Acknowledgements
This research was supported by the National Natural Science Foundation of China (U23A20443, 31725011 and 82030070 to L.C. and 82100960 to S.Y.) and the National Key Research and Development Program of China (2021YFC2400404 to L.C.).
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Concept and design, S.Y. and L.C.; experimentation, S.Y., X.L., G.C., J.Y. and W.Z.; acquisition, analysis or interpretation of data, S.Y., Q.T., X.L., G.C., M.X., J.Y., Y.Y., W.Z., J.W. and L.Z.; drafting of the manuscript, S.Y. and Q.T.; critical revision of the manuscript for important intellectual content, L.C., L.Z. and Y.H.; supervision, L.C.; funding acquisition, L.C. and S.Y. All authors reviewed the manuscript.
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Extended data
Extended Data Fig. 1 Exercise during the Early Active Phase Can Robustly Expedite Bone Growth.
a, b, Food intake (a) and body weight (b) of sedentary (Sed) and exercise (Exe) mice (n = 12, Sed, Exe at ZT1, ZT5, and ZT 13 mice; n = 8, Exe at ZT9 mice; n = 11, Exe at ZT17 mice; n = 10, Exe at ZT21 mice; Data were presented as mean ± SD and analyzed using one-way ANOVA with Tukey multiple comparisons test). c, Images of calcein double labeling of the femoral diaphyseal cortical bones of Sed and Exe mice. Scale bar, 100 μm. d, e, Quantification of mineralization apposition rate (MAR) and bone formation rate (BFR) of the femoral metaphyseal cortical bones (n = 3 biologically independent experiments, Data were presented as mean ± SD and analyzed using one-way ANOVA with Tukey multiple comparisons test).
Extended Data Fig. 2 Exercise during the Early Active Phase Can Robustly Expedite Bone Growth in Female mice.
a, Scheme of exercise applied in this study. The female mice were subjected to treadmill running following a 5-day per week acclimatization protocol at ZT1, ZT5, ZT9, ZT13, ZT17, and ZT21, respectively. b, Three-dimensional visualization of femora from micro-CT images of sedentary and exercise mice at ZT1, ZT5, ZT9, ZT13, ZT17, and ZT21. The red boxes indicate the levels of cartilaginous osteogenesis tissues. c, Micro-CT analysis of the total length, bone volume / total volume (BV/TV), and trabecular thickness (Tb.Th) of femora (n = 5). d, Representative images of S-O staining of the distal femora in sedentary and exercise mice. Scale bar, 50 μm. e–h, The height of proliferation zone (PZ), hypertrophic zone (HZ), and chondrocyte number per column in the PZ and HZ of growth plate cartilages (n = 3 biologically independent experiments). i, j, EdU staining analysis of proliferating cells in PZ from the growth plate cartilages. Arrowheads indicate EdU+ cells (n = 3). Scale bar, 50 μm. It is the growth plate cartilages between the white lines. k, Images of calcein double labeling of the femoral metaphyseal cancellous bones of sedentary and exercise mice. Scale bar, 100 μm. l, Quantification of mineralization apposition rate (MAR) of the femoral metaphyseal cancellous bones (n = 3 biologically independent experiments). The white line is the calcein deposit of the first injection, and the red line is the second injection. c, e-h, j, l, Data were presented as mean ± SD and analyzed using one-way ANOVA with the Tukey multiple comparisons test.
Extended Data Fig. 3 Exercise at ZT13 in Synergy with Intrinsic Bone Metabolic Rhythms Activates the Expression of Bone Growth-Related Genes.
a, Heatmaps displaying rhythmic transcripts before and after exercise during the rest phase (ZT1, ZT5) or active phase (ZT13, ZT17, ZT21). b, GO analysis of rhythmic transcripts both in Sed and Exe. Numbers within the charts indicate number of transcripts identified within each biological pathway. c, Heatmaps displaying rhythmic transcripts before and after exercise in bone development (left), metabolic process (middle) and glucose metabolic process (right) after exercise during the early active phase (ZT13).
Extended Data Fig. 4 Exercise at ZT13 Enhances the Association between OXPHOS and Bone Growth.
a, KEGG analysis of the top 30 pathways after exercise at the early active phase. b, The network of the DEGs among top enriched pathway. c, d, Radar plots representing the DEGs related to glycolysis and oxidative phosphorylation after exercise at the early rest phase (c) and early active phase (d). e, f, Sankey diagram for glycolysis (e) and oxidative phosphorylation (f)- ossification interaction after exercise at the active phase (ZT13, ZT17, ZT21) and early rest phase (ZT1).
Extended Data Fig. 5 Oxidative Phosphorylation Is Markedly Activated by Exercise during the Early Active Phase.
a, b, Heatmap of representational DEGs related to oxidative phosphorylation (a) and glycolysis (b). c, d, qRT-PCR analysis of the mRNA levels of Atp6v0c1, Cox11, Ndufv3, Ldha, Pfkp, and Adh7 at indicated time. Differential rhythmicity analysis performed with the 1-component cosinor analysis. The false discovery rate (FDR) method was applied for adjustment, adjusted P values correspond to the statistical significance of amplitude changes in Exe versus Sed mice at the early rest and active phase (n = 4 biologically independent experiments, Data were presented as mean ± SD). e, f, Western blot analysis of the levels of ATP6V0D1 and PFKP in the femoral metaphysis tissue from Sed and Exe mice during the early rest versus active phase (n = 3 biologically independent experiments, Data were presented as mean ± SD and analyzed using two-way ANOVA with Tukey multiple comparisons test). g, Immunofluorescence of PFKP in the growth plate cartilages after exercise during the early rest versus active phase. Scale bar, 50 μm. One technical replicate of three biological replicates for each group.
Extended Data Fig. 6 Physical Activity during the Active Phase Stimulates Bone Growth through the Process of Oxidative Phosphorylation.
a, The schematic shows mice injected with oxidative phosphorylation inhibitor (oligomycinA, Selleckchem, 15 mg/kg/d, intraperitoneal injection) or equal solvent 60 minutes before exercise. b, Representative images of micro-CT reconstruction of femora from Sed and Exe mice with or without oxidative phosphorylation inhibitor injection. c, Micro-CT analysis of the total femora length, BV/TV, Tb.Th, and Tb.N of Sed and Exe mice injected oxidative phosphorylation inhibitor or equal solvent (n = 5 biologically independent experiments). d, e, Representative images of S-O staining of the distal femora in Sed and Exe mice injected with oxidative phosphorylation inhibitor or equal solvent (n = 3 biologically independent experiments). Scale bar, 50 μm. f, g, EdU staining of proliferating cells in PZ from the growth plate cartilages in Sed and Exe mice injected oxidative phosphorylation inhibitor or equal solvent. Arrowheads indicate EdU+ cells (n = 3 biologically independent experiments). Scale bar, 50 μm. c, e, g, Data were presented as mean ± SD and analyzed using two-way ANOVA with the Tukey multiple comparisons test.
Extended Data Fig. 7 Physical Activity during the Active Phase Stimulates Bone Growth through the Process of Oxidative Phosphorylation.
a, Adenosine triphosphate (ATP) production of femur in Sed and Exe mice intraperitoneally injected oxidative phosphorylation inhibitor or equal solvent (n = 3 biologically independent experiments). b, The content of NAD+ and NADH, and the ratio of NAD + / NADH of femur in Sed and Exe mice injected oxidative phosphorylation inhibitor or equal solvent (n = 3 biologically independent experiments). c, d, Western blot analysis of the levels of ATP6V0D1, Cyclin D2, SOX9 and COL2α1 in the femoral metaphysis tissue from Sed and Exe mice injected oxidative phosphorylation inhibitor (oligomycin A) or equal solvent during the early rest versus active phase (n = 3 biologically independent experiments). e, f, Immunofluorescence of COL2α1 and ACAN in the growth plate cartilages after exercise during the early rest versus active phase with or without oxidative phosphorylation inhibitor injection. Scale bars, 50 μm. One technical replicate of three biological replicates for each group. a, b, d, Data were presented as mean ± SD and analyzed using two-way ANOVA with Tukey multiple comparisons test.
Extended Data Fig. 8 Stimulating Oxidative Phosphorylation Pharmacologically during the Early Active Phase Enhances Bone Growth.
a, ATP production of femur in Sed and Exe mice intraperitoneally injected oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). b, The content of NAD+ and NADH, and the ratio of NAD + / NADH of femur in Sed and Exe mice intraperitoneally injected oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). c, d, Western blot analysis of the levels of AMPKα1/α2, p-AMPKα1/α2, ATP6V0D1, COX IV, Cyclin D2, COL2α1 and ACAN in the femoral metaphysis tissue from Sed and Exe mice intraperitoneally injected oxidative phosphorylation activator or equal solvent (n = 6 biologically independent experiments). a, b, d, Data were presented as mean ± SD and analyzed using two-way ANOVA with Tukey multiple comparisons test.
Extended Data Fig. 9 Stimulating Oxidative Phosphorylation Pharmacologically during the Early Active Phase Enhances Bone Growth.
a, ATP production of femur in Sed and Exe mice intramedullary injected oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). b, The content of NAD+ and NADH, and the ratio of NAD + / NADH of femur in Sed and Exe mice intramedullary injected oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). c, d, Western blot analysis of the levels of AMPKα1/α2, p-AMPKα1/α2, ATP6V0D1, COX IV, Cyclin D2, COL2α1 and ACAN in the femoral metaphysis tissue from Sed and Exe mice intramedullary injected oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). a, b, d, Data were presented as mean ± SD and analyzed using two-way ANOVA with Tukey multiple comparisons test.
Extended Data Fig. 10 Stimulating Oxidative Phosphorylation Pharmacologically during the Early Active Phase Enhances Bone Growth.
a, Representative images of micro-CT reconstruction of femora from Sed and Exe mice with or without oxidative phosphorylation activator injection (AICAR, Selleckchem, 50 mg/kg/d, a total of 28 days, intramedullary injection). b, Micro-CT analysis of the total femora length, BV/TV, Tb.Th, and Tb.N of Sed and Exe mice intramedullary injected oxidative phosphorylation activator or equal solvent (n = 5 biologically independent experiments). c, d, Representative images of S-O staining of the distal femora in Sed and Exe mice intramedullary injected with oxidative phosphorylation activator or equal solvent (n = 3 biologically independent experiments). Scale bar, 50 μm. e, f, EdU staining of proliferating cells in PZ from the growth plate cartilages in Sed and Exe mice intramedullary injected oxidative phosphorylation activator or equal solvent. Arrowheads indicate EdU+ cells (n = 3 biologically independent experiments). Scale bar, 50 μm. g, h, Immunofluorescence of COL2α1 and ACAN in the growth plate cartilages after exercise at the early rest versus active phase with or without oxidative phosphorylation activator intramedullary injection. Scale bars, 50 μm. b, d, f, Data were presented as mean ± SD and analyzed using two-way ANOVA with the Tukey multiple comparisons test.
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Yu, S., Tang, Q., Lu, X. et al. Time of exercise differentially impacts bone growth in mice. Nat Metab 6, 1036–1052 (2024). https://doi.org/10.1038/s42255-024-01057-0
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DOI: https://doi.org/10.1038/s42255-024-01057-0
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