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Cited by 131Mitochondrial Function and PathologyCardiovascular and exercise physiologyAdipose Tissue and Metabolism

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The impact of exercise on mitochondrial dynamics and the role of Drp1 in exercise performance and training adaptations in skeletal muscle

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Moore, Timothy M., Zhou, Zhenqi, Cohn, Whitaker, Norheim, Frode, Lin, Amanda J., Kalajian, Nareg, Strumwasser, Alexander R., Cory, Kevin, Whitney, Kate, Ho, Theodore, Ho, Timothy, Lee, Joseph L., Rucker, Daniel H., Shirihai, Orian, van der Bliek, Alexander M., Whitelegge, Julian P., Seldin, Marcus M., Lusis, Aldons J., Lee, Sindre, Drevon, Christian A., Mahata, Sushil K., Turcotte, Lorraine P., Hevener, Andrea L.·2019·Molecular Metabolism
DOI 10.1016/j.molmet.2018.11.012PMC PMC6407367
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Abstract

Objective Mitochondria are organelles primarily responsible for energy production, and recent evidence indicates that alterations in size, shape, location, and quantity occur in response to fluctuations in energy supply and demand. We tested the impact of acute and chronic exercise on mitochondrial dynamics signaling and determined the impact of the mitochondrial fission regulator Dynamin related protein (Drp)1 on exercise performance and muscle adaptations to training. Methods Wildtype and muscle-specific Drp1 heterozygote (mDrp1 +/− ) mice, as well as dysglycemic (DG) and healthy normoglycemic men (control) performed acute and chronic exercise. The Hybrid Mouse Diversity Panel, including 100 murine strains of recombinant inbred mice , was used to identify muscle Dnm1L (encodes Drp1)-gene relationships. Results Endurance exercise impacted all aspects of the mitochondrial life cycle , i.e. fission-fusion, biogenesis, and mitophagy . Dnm1L gene expression and Drp1 Ser616 phosphorylation were markedly increased by acute exercise and declined to baseline during post-exercise recovery. Dnm1L expression was strongly associated with transcripts known to regulate mitochondrial metabolism and adaptations to exercise. Exercise increased the expression of DNM1L in skeletal muscle of healthy control and DG subjects, despite a 15% ↓( P = 0.01) in muscle DNM1L expression in DG at baseline. To interrogate the role of Dnm1L further, we exercise trained male mDrp1 +/− mice and found that Drp1 deficiency reduced muscle endurance and running performance, and altered muscle adaptations in response to exercise training. Conclusion Our findings highlight the importance of mitochondrial dynamics, specifically Drp1 signaling, in the regulation of exercise performance and adaptations to endurance exercise training.

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Figure 1 Schematic depicting exercise protocols for humans and mice. (A) Acute and chronic cyclying exercise was performed by healthy normoglycemic (control) and Dysglycemic (DG) men, age 40–65 years (N = 13/group). (B) Wildtype mice were studied during acute (EX45, EX90, EX90 + 3 h Rest) and chronic exercise (TRN, TRN + EX90) experiments 1–3. Exercise training (TRN) was achieved using voluntary running wheels for 30 days. Muscle was harvested 30 h after the last bout of exercise. An additional cohort of TRN mice performed an acute bout of moderate intensity treadmill running (TRN + EX90). (C) A panel of recombinant inbred strains of mice (84 strains of male and female mice, N = 4 mice/strain and a 15-strain subset of female mice, N = 4 mice/strain), the UCLA HMDP, were studied to determine the relationship between sex and Dnm1L expression and Dnm1L gene–gene relationships. (D) Muscle-specific Drp1 heterozygous (mDrp1+/−) mice were studied at rest and following EX90 and TRN.
Figure 1 Schematic depicting exercise protocols for humans and mice. (A) Acute and chronic cyclying exercise was performed by healthy normoglycemic (control) and Dysglycemic (DG) men, age 40–65 years (N = 13/group). (B) Wildtype mice were studied during acute (EX45, EX90, EX90 + 3 h Rest) and chronic exercise (TRN, TRN + EX90) experiments 1–3. Exercise training (TRN) was achieved using voluntary running wheels for 30 days. Muscle was harvested 30 h after the last bout of exercise. An additional cohort of TRN mice performed an acute bout of moderate intensity treadmill running (TRN + EX90). (C) A panel of recombinant inbred strains of mice (84 strains of male and female mice, N = 4 mice/strain and a 15-strain subset of female mice, N = 4 mice/strain), the UCLA HMDP, were studied to determine the relationship between sex and Dnm1L expression and Dnm1L gene–gene relationships. (D) Muscle-specific Drp1 heterozygous (mDrp1+/−) mice were studied at rest and following EX90 and TRN.CC BY-NC-ND · PubMed Central
Figure 2 A single session of moderate intensity exercise increases pro-fission phosphorylation of Drp1 in a time dependent manner and alters the mitochondrial proteome. (A) Quadriceps mRNA expression (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED, EX45, EX90, and EX90+3 h Rest (N = 6/group; one-way ANOVA with Tukey post hoc analysis). (B–E) Immunoblot densitometry of quadriceps protein and phospho-protein abundance of mitochondrial fission, fusion, and autophagy signaling, in SED (open bars), EX45 (light gray bars), EX90 (dark gray bars), and EX90+3 h Rest (closed black bars) for C57BL/6J (N = 6/group; additional representative immunoblots presented in Supplemental Figure 1; one-way ANOVA with Tukey's post hoc analysis). Muscle Drp1Ser616 phosphorylation in (A) male and female C57BL/6J (N = 6 mice/time point), and (C) female A/J, BALB/CJ, and C3H/HeJ mice (N = 6 mice/group). (F) Transmission electron micrograph (TEM) images of mouse soleus muscle from SED and EX90 groups. (G) Frequency of mitochondrial area (nm2) determined from the TEMs obtained from SED and EX90 muscle (494 mitochondria visualized/group; Kolmogorov–Smirnov test for cumulative distribution comparison, P = 0.52). (H) Mitochondrial proteomics of gastrocnemius muscle represented in a volcano plot for EX90 vs. SED groups. Dashed line indicates significance threshold and blue dots indicate significance SED vs. EX90 (two-tailed unpaired t-test with Bonferroni correction). (I) Mitochondrial proteomics pathway analysis. (J) Mitochondrial proteomics functional annotation of significantly impacted protein clusters. Data are means ± SEM (N = 6/group). *, P < 0.05 vs. SED.
Figure 2 A single session of moderate intensity exercise increases pro-fission phosphorylation of Drp1 in a time dependent manner and alters the mitochondrial proteome. (A) Quadriceps mRNA expression (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED, EX45, EX90, and EX90+3 h Rest (N = 6/group; one-way ANOVA with Tukey post hoc analysis). (B–E) Immunoblot densitometry of quadriceps protein and phospho-protein abundance of mitochondrial fission, fusion, and autophagy signaling, in SED (open bars), EX45 (light gray bars), EX90 (dark gray bars), and EX90+3 h Rest (closed black bars) for C57BL/6J (N = 6/group; additional representative immunoblots presented in Supplemental Figure 1; one-way ANOVA with Tukey's post hoc analysis). Muscle Drp1Ser616 phosphorylation in (A) male and female C57BL/6J (N = 6 mice/time point), and (C) female A/J, BALB/CJ, and C3H/HeJ mice (N = 6 mice/group). (F) Transmission electron micrograph (TEM) images of mouse soleus muscle from SED and EX90 groups. (G) Frequency of mitochondrial area (nm2) determined from the TEMs obtained from SED and EX90 muscle (494 mitochondria visualized/group; Kolmogorov–Smirnov test for cumulative distribution comparison, P = 0.52). (H) Mitochondrial proteomics of gastrocnemius muscle represented in a volcano plot for EX90 vs. SED groups. Dashed line indicates significance threshold and blue dots indicate significance SED vs. EX90 (two-tailed unpaired t-test with Bonferroni correction). (I) Mitochondrial proteomics pathway analysis. (J) Mitochondrial proteomics functional annotation of significantly impacted protein clusters. Data are means ± SEM (N = 6/group). *, P < 0.05 vs. SED.CC BY-NC-ND · PubMed Central
Figure 3 Chronic exercise training increases pro-fusion phosphorylation of Drp1 in post-exercise recovery period (Experiment 2). (A) Body and tissue weights (quadriceps, gastrocnemius, gonadal WAT, inguinal WAT, and heart) in SED and TRN female mice (N = 6/group; two-way repeated measures ANOVA with Tukey post hoc analysis for left panel and; two-tailed unpaired t-test for right panel). (B) Quadriceps mRNA abundance (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED vs. TRN (N = 6/group; two-tailed unpaired t-test). Muscles were harvested from TRN mice 30 h following the cessation of exercise including a 6 h fast. (C–E) Immunoblot densitometry of quadriceps protein and phospho-protein abundance representing mitochondrial fission, fusion, and autophagy signaling, in SED (open bars) and TRN (closed bars) mice (N = 6/group) (representative immunoblots presented in Supplemental Figure 1). (F) Mitochondrial proteomics determined by mass spectrometry analysis of gastrocnemius muscle and presented as a volcano plot (dashed line indicates significance threshold; blue dots indicate significance, N = 4/group; two-tailed unpaired t-test with Bonferroni correction). (G) Mitochondrial proteomics pathway analysis (two-tailed unpaired t-test), and (H) mitochondrial functional annotation of significantly impacted protein clusters. Data are means ± SEM. *, P < 0.05 vs. SED.
Figure 3 Chronic exercise training increases pro-fusion phosphorylation of Drp1 in post-exercise recovery period (Experiment 2). (A) Body and tissue weights (quadriceps, gastrocnemius, gonadal WAT, inguinal WAT, and heart) in SED and TRN female mice (N = 6/group; two-way repeated measures ANOVA with Tukey post hoc analysis for left panel and; two-tailed unpaired t-test for right panel). (B) Quadriceps mRNA abundance (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED vs. TRN (N = 6/group; two-tailed unpaired t-test). Muscles were harvested from TRN mice 30 h following the cessation of exercise including a 6 h fast. (C–E) Immunoblot densitometry of quadriceps protein and phospho-protein abundance representing mitochondrial fission, fusion, and autophagy signaling, in SED (open bars) and TRN (closed bars) mice (N = 6/group) (representative immunoblots presented in Supplemental Figure 1). (F) Mitochondrial proteomics determined by mass spectrometry analysis of gastrocnemius muscle and presented as a volcano plot (dashed line indicates significance threshold; blue dots indicate significance, N = 4/group; two-tailed unpaired t-test with Bonferroni correction). (G) Mitochondrial proteomics pathway analysis (two-tailed unpaired t-test), and (H) mitochondrial functional annotation of significantly impacted protein clusters. Data are means ± SEM. *, P < 0.05 vs. SED.CC BY-NC-ND · PubMed Central
Figure 4 Drp1 pro-fission signaling is increased during acute exercise in muscle from trained female mice. (A) Quadriceps mRNA abundance (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED, EX90, and TRN + EX90 (N = 6/group; one-way ANOVA with Tukey post hoc analysis). Muscles were harvested from both EX90 groups immediately following the cessation of exercise. (B–D) Quadriceps protein and phospho-protein representing mitochondrial fission, fusion, and autophagy signaling, in SED (open bars), EX90 (gray bars), and TRN + EX90 (black bars) (N = 6/group; representative immunoblots presented in Figures. 4B and S1; one-way ANOVA with Tukey post hoc analysis). Data are means ± SEM (N = 6/group). *, P < 0.05 vs. SED.
Figure 4 Drp1 pro-fission signaling is increased during acute exercise in muscle from trained female mice. (A) Quadriceps mRNA abundance (presented in a heat map), representing mitochondrial fission, fusion, and autophagy signaling, in SED, EX90, and TRN + EX90 (N = 6/group; one-way ANOVA with Tukey post hoc analysis). Muscles were harvested from both EX90 groups immediately following the cessation of exercise. (B–D) Quadriceps protein and phospho-protein representing mitochondrial fission, fusion, and autophagy signaling, in SED (open bars), EX90 (gray bars), and TRN + EX90 (black bars) (N = 6/group; representative immunoblots presented in Figures. 4B and S1; one-way ANOVA with Tukey post hoc analysis). Data are means ± SEM (N = 6/group). *, P < 0.05 vs. SED.CC BY-NC-ND · PubMed Central
Figure 5 DNM1L gene expression and gene correlations in muscle from normoglycemic and dysglycemic men at rest and during exercise, and in 15 strains of recombinant inbred mice from the Hybrid Mouse Diversity Panel (HMDP). (A) Muscle DNM1L expression levels at basal and immediately following cycling training in N = 13 normoglycemic control and N = 13 dysglycemic (DG) men aged 40–65 years (two-way repeated measures ANOVA with Tukey's post hoc analysis). (B) Dnm1L muscle gene expression (presented as a dot plot) in a fifteen-strain subset (N = 4 mice/strain; two-tailed unpaired t-test) female HMDP mice, SED vs. TRN (normal chow fed mice 12 weeks of age). Muscles were harvested from TRN mice 30 h following the cessation of exercise (including a 6 h fast). (C) Dnm1L expression levels were elevated in female mouse muscle and showed greater variability over males. (D) Genes significantly correlated with Dnm1L expression (cut off criteria P < 0.0001; yield = 2483 genes significantly correlated including a high number of transcription factors) in skeletal muscle of male and female HMDP mice (12 weeks of age) fed a HF/HS diet for eight weeks (N = 84 strains/sex, 4 mice/strain). Muscles were harvested from HMDP mice following a 4–6 h fast. *, P < 0.05 vs. SED. #, P < 0.05 Pre-TRN vs. Post-TRN human muscle DNM1L expression.
Figure 5 DNM1L gene expression and gene correlations in muscle from normoglycemic and dysglycemic men at rest and during exercise, and in 15 strains of recombinant inbred mice from the Hybrid Mouse Diversity Panel (HMDP). (A) Muscle DNM1L expression levels at basal and immediately following cycling training in N = 13 normoglycemic control and N = 13 dysglycemic (DG) men aged 40–65 years (two-way repeated measures ANOVA with Tukey's post hoc analysis). (B) Dnm1L muscle gene expression (presented as a dot plot) in a fifteen-strain subset (N = 4 mice/strain; two-tailed unpaired t-test) female HMDP mice, SED vs. TRN (normal chow fed mice 12 weeks of age). Muscles were harvested from TRN mice 30 h following the cessation of exercise (including a 6 h fast). (C) Dnm1L expression levels were elevated in female mouse muscle and showed greater variability over males. (D) Genes significantly correlated with Dnm1L expression (cut off criteria P < 0.0001; yield = 2483 genes significantly correlated including a high number of transcription factors) in skeletal muscle of male and female HMDP mice (12 weeks of age) fed a HF/HS diet for eight weeks (N = 84 strains/sex, 4 mice/strain). Muscles were harvested from HMDP mice following a 4–6 h fast. *, P < 0.05 vs. SED. #, P < 0.05 Pre-TRN vs. Post-TRN human muscle DNM1L expression.CC BY-NC-ND · PubMed Central
Figure 6 Muscle-specific reduction in Drp1 reduces maximal running speed and muscle endurance capacity in female mice. (A–B) Immunoblots and densitometric analysis of skeletal and cardiac muscle Drp1 total protein in Control and mDrp1+/− mice (representative immunoblots N = 4 per genotype; densitometry N = 8; two-way unpaired t-test). (C) Maximum running speed (m/min), and (D) latency to fall (seconds; N = 3 with three independent trials/per animal) in SED Control (open bars) and mDrp1+/− (closed bars) mice (N = 7–9; two-tailed unpaired t-test). (E) Plasma lactate (mmol/l) and (F) muscle glycogen (mg/g) from quadriceps muscle of control (open bars) and mDrp1+/− (closed bars), SED vs. EX90 mice using repeated measures ANOVA and two-way ANOVA with Tukey's post hoc analysis respectively. (G–H) Quadriceps gene expression in Control (open bars) and mDrp1+/− (closed bars) mice after EX90 (two-tailed unpaired t-test). (I) Mitochondrial DNA copy number in quadriceps muscle of SED and EX90, Control (open bars) and mDrp1+/− (closed bars) mice (two-way ANOVA with Tukey post hoc analysis). (J–O) Inmmunoblots and densitometric analysis of protein and phospho-protein expression of select fission, fusion, and autophagy markers from quadriceps muscle of SED and EX90, Control (open bars) and mDrp1+/− (closed bars) mice (two-way ANOVA with Tukey's post hoc analysis). Data are means ± SEM. N = 6–8/group. *, P < 0.05 vs. control SED. #, P < 0.05 SED vs. EX90 for mDrp1+/−.
Figure 6 Muscle-specific reduction in Drp1 reduces maximal running speed and muscle endurance capacity in female mice. (A–B) Immunoblots and densitometric analysis of skeletal and cardiac muscle Drp1 total protein in Control and mDrp1+/− mice (representative immunoblots N = 4 per genotype; densitometry N = 8; two-way unpaired t-test). (C) Maximum running speed (m/min), and (D) latency to fall (seconds; N = 3 with three independent trials/per animal) in SED Control (open bars) and mDrp1+/− (closed bars) mice (N = 7–9; two-tailed unpaired t-test). (E) Plasma lactate (mmol/l) and (F) muscle glycogen (mg/g) from quadriceps muscle of control (open bars) and mDrp1+/− (closed bars), SED vs. EX90 mice using repeated measures ANOVA and two-way ANOVA with Tukey's post hoc analysis respectively. (G–H) Quadriceps gene expression in Control (open bars) and mDrp1+/− (closed bars) mice after EX90 (two-tailed unpaired t-test). (I) Mitochondrial DNA copy number in quadriceps muscle of SED and EX90, Control (open bars) and mDrp1+/− (closed bars) mice (two-way ANOVA with Tukey post hoc analysis). (J–O) Inmmunoblots and densitometric analysis of protein and phospho-protein expression of select fission, fusion, and autophagy markers from quadriceps muscle of SED and EX90, Control (open bars) and mDrp1+/− (closed bars) mice (two-way ANOVA with Tukey's post hoc analysis). Data are means ± SEM. N = 6–8/group. *, P < 0.05 vs. control SED. #, P < 0.05 SED vs. EX90 for mDrp1+/−.CC BY-NC-ND · PubMed Central
Figure 7 Muscle-specific reduction in Drp1 alters response to exercise training (TRN). (A) Time to treadmill running exhaustion displayed in seconds and (B) cumulative distance run in kilometers for female Control (open bars) vs. mDrp1+/− (closed bars) mice (N = 7–9; two-tailed unpaired t-test). (C) Tissue weights in age-matched littermates of SED and TRN Control vs. mDrp1+/− (two-tailed unpaired t-test). (D) Body weights of Control vs. mDrp1+/−, pre- and post-exercise training (two-way repeated measures ANOVA with Tukey post hoc analysis). (E) Muscle fiber cross sectional area and (F) nuclei number/fiber from gastrocnemius muscle of SED (open bars) and TRN (closed bars) Control vs. mDrp1+/− (two-tailed unpaired t-test). (G–H) Cytochrome C oxidase staining in gastrocnemius muscle from TRN Control and mDrp1+/− animals (representative image for each genotype; COX + staining between the genotypes compared using two-tailed unpaired t-test). Data are means ± SEM (N = 7–9/group). *, P < 0.05, vs. Control. #, P < 0.05, from pre-training or SED mDrp1+/−. Φ, P < 0.05 vs. post-training or TRN Control. $, P < 0.05 main affect from pre-training.
Figure 7 Muscle-specific reduction in Drp1 alters response to exercise training (TRN). (A) Time to treadmill running exhaustion displayed in seconds and (B) cumulative distance run in kilometers for female Control (open bars) vs. mDrp1+/− (closed bars) mice (N = 7–9; two-tailed unpaired t-test). (C) Tissue weights in age-matched littermates of SED and TRN Control vs. mDrp1+/− (two-tailed unpaired t-test). (D) Body weights of Control vs. mDrp1+/−, pre- and post-exercise training (two-way repeated measures ANOVA with Tukey post hoc analysis). (E) Muscle fiber cross sectional area and (F) nuclei number/fiber from gastrocnemius muscle of SED (open bars) and TRN (closed bars) Control vs. mDrp1+/− (two-tailed unpaired t-test). (G–H) Cytochrome C oxidase staining in gastrocnemius muscle from TRN Control and mDrp1+/− animals (representative image for each genotype; COX + staining between the genotypes compared using two-tailed unpaired t-test). Data are means ± SEM (N = 7–9/group). *, P < 0.05, vs. Control. #, P < 0.05, from pre-training or SED mDrp1+/−. Φ, P < 0.05 vs. post-training or TRN Control. $, P < 0.05 main affect from pre-training.CC BY-NC-ND · PubMed Central
Figure 8 Alterations in gene and protein expression following chronic exercise training in female Control and mDrp1+/− animals. (A) Quadriceps gene expression expressed as fold-change for mDrp1+/− TRN relative to Control TRN animals (two-tailed unpaired t-test; normalized to 18S). (B) Mitochondrial DNA copy number in quadriceps muscle of female Control (open bars) and mDrp1+/− (closed bars) animals following TRN (two-tailed unpaired t-test). (C) Muscle protein expression in mDrp1+/− relative to Control following TRN (two-tailed unpaired t-test; representative immunoblots presented in Supplemental Figure 2). Muscles were harvested from TRN mice 30 h following the cessation of exercise including a 6 h fast. Data are means ± SEM. N = 7–9/group. *, P < 0.05 mDrp1+/− vs. Control.
Figure 8 Alterations in gene and protein expression following chronic exercise training in female Control and mDrp1+/− animals. (A) Quadriceps gene expression expressed as fold-change for mDrp1+/− TRN relative to Control TRN animals (two-tailed unpaired t-test; normalized to 18S). (B) Mitochondrial DNA copy number in quadriceps muscle of female Control (open bars) and mDrp1+/− (closed bars) animals following TRN (two-tailed unpaired t-test). (C) Muscle protein expression in mDrp1+/− relative to Control following TRN (two-tailed unpaired t-test; representative immunoblots presented in Supplemental Figure 2). Muscles were harvested from TRN mice 30 h following the cessation of exercise including a 6 h fast. Data are means ± SEM. N = 7–9/group. *, P < 0.05 mDrp1+/− vs. Control.CC BY-NC-ND · PubMed Central

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Authors
Moore, T. M., Zhou, Z., Cohn, W., Norheim, F., Lin, A. J., Kalajian, N., Strumwasser, A. R., Cory, K., Whitney, K., Ho, T., Ho, T., Lee, J. L., Rucker, D. H., Shirihai, O., van der Bliek, A. M., Whitelegge, J. P., Seldin, M. M., Lusis, A. J., Lee, S., Drevon, C. A., Mahata, S. K., Turcotte, L. P., & Hevener, A. L.
Affiliations
  • University of Southern California (US)
  • University of California, Los Angeles (US)
  • University of Oslo (NO)
  • University of California San Diego (US)
Corresponding author
Hevener, Andrea L.
ORCID
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2019-03
Volume
21
Pages
51-67
ISSN
2212-8778 (ISSN-L)
DOI
10.1016/j.molmet.2018.11.012
PMC
PMC6407367
OpenAlex
W2902937014
Cited by
131
References
79
Citations by year
2026: 16 · 2025: 20 · 2024: 14 · 2023: 17 · 2022: 17 · 2021: 16 · 2020: 22 · 2019: 9
FWCI
4.18
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Metabolism (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by)
  • NORA - Norwegian Open Research Archives (submittedVersion, cc-by-nc-nd)
Funders
  • Institute of Basic Medical Sciences
  • National Institute on Aging (5P30AG028748)
  • National Aeronautics and Space Administration
  • Norges Forskningsråd
  • American College of Sports Medicine
  • National Institutes of Health (P30DK063491, U24DK097748, F31DK108657, DK109724, 5T32HD007228)
  • U.S. Department of Veterans Affairs (NCT01803568, I01BX000323, HL28481, HL30568)
  • Seventh Framework Programme (289511)
  • Clinical and Translational Science Institute, University of California, Los Angeles (ULTR000124)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
mitochondrial dynamics, Drp1, mitochondrial fission, mitochondrial fusion, mitophagy, mitochondrial biogenesis, exercise training, endurance exercise, skeletal muscle, exercise performance, dysglycemia, Hybrid Mouse Diversity Panel, mitochondrial metabolism
MeSH terms
Physical Functional Performance, Adaptation, Physiological, Adult, Aged, Animals, Blood Glucose, Female, Humans, Male, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Microtubule-Associated Proteins, Middle Aged, Mitochondria, Phosphorylation, Physical Conditioning, Animal, Physical Endurance, Gene Deletion, Muscle, Skeletal, GTP Phosphohydrolases, Mitochondrial Proteins, Dynamins, Mice, Mitochondrial Dynamics

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