Table 4.
Summary of studies on the effects of green tea and EGCG on skeletal muscle health.
| First Author, Year, Citation | Experimental Design and Treatments | Effects of Green Tea or EGCG |
|---|---|---|
| Cellular Studies | ||
| Babu, 2017, [95] |
Model: C2C12 skeletal muscle cells Treatment: Pretreated with or without GTE (20, 40, and 80 μg/mL) for 2 h followed by with or without citrinin treatment (0, 25, 50, 75, and 100 μM) for 24 h |
Compared to citrinin the treated without GTE group, the citrinin-treated GTE group showed: ↑ Cell viability dose-dependently ↓ Citrinin-induced LDH release ↑ Myotube integrity and cell morphology ↓ ROS 3-fold at 80 μg/mL ↓ Citrinin-induced antioxidant enzyme activity |
| Dorchies, 2009, [94] |
Model: Primary culture muscle cells from an mdx mouse model treated with H2O2 Treatment: Control (no EGCG) or EGCG (10 mg/mL) for 48 h |
Compared to the control group, the EGCG group showed: ↑ Glutathione content ↑ Cell survival ↑ 67LR (a receptor for EGCG) |
| Hong, 2020, [137] |
Model: C2C12 skeletal muscle cells with or without 100 μM of H2O2 for 48 h Treatment: Control (no EGCG), GTE or tannase-converted GTE (1, 5, 10, 15, and 20 μg/mL) for 24 h |
Compared to the control group, the H2O2-treated tannase-converted GTE group showed: ↑ Myotube density and fusion ↑ mRNA expression of myogenin, Myf5, MyoD ↑ FOXO1 and FOXO3 transcription levels ↓ Oxidative-stress-induced ↓ AMPK |
| Kim, 2017, [139] |
Model: Satellite cells isolated from 8-week-old C57BL/6 mice Treatment: Control (no EGCG) and EGCG (10 μM) for 72 h |
Compared to the control group, the EGCG group showed: ↑ MHC (myogenic factor) ↑ TAZ localization TAZ knockdown inhibits EGCG-induced myogenic differentiation |
| Kim, 2017, [138] |
Model: C2C12 myoblasts Treatment: Control (no EGCG) and EGCG (10 μM) for 24 h |
Compared to the control group, the EGCG group showed: ↑ MHC content ↑ Myogenin and muscle creatine kinase gene expression ↑ Number of multinucleated cells |
| Mirza, 2014, [121] |
Model: C2C12 skeletal muscle cells with or without starvation media and TNF-α Treatment: Control (no EGCG) or EGCG (10–150 μM) for 24 h |
Compared to the control group, the EGCG group showed: ↓ Protein degradation at 10 μM ↑ Protein degradation at >10 μM ↑ pAkt and pFoxO3a expression at >10 μM ↔ pAkt and pFoxO3a expression at 10 μM |
| Mirza, 2016, [144] |
Model: C2C12 skeletal muscle cells treated with or without PIF (4.2 nM) or TNF-α (25 ng/mL) Treatment: Control (no EGCG) and EGCG (10 μM) for 24 h |
Compared to the control group, the protein-degradation-induced EGCG group showed: ↓ PIF- or TNF-α-induced protein degradation ↔ Protein synthesis rates |
| Wang, 2016, [93] |
Model: C2C12 skeletal muscle cells Treatment: Control (no EGCG) or EGCG (0, 5, 25, and 50 μM) with or without H2O2 (300μM) for 48 h |
Compared to the control group, the EGCG group (at 25 μM) showed: ↓ SDH ↑ CAT and GSH-Px activity ↓ PGC-1α and NRF-1 protein content ↓ Intracellular ROS levels Compared to the EGCG group, the EGCG and H2O2 groups showed: ↑ p-AMPKα/AMPKα ↑ MyHC 1 |
| Animal Studies | ||
| Alway, 2014, [143] |
Model: Brown Norway inbred aged (34 months) rats Treatment: Fed a control diet (no GTE) or GTE (50 mg/kg) for 7 days prior and throughout. Rats either received 14 days hindlimb suspension or 14 days hindlimb suspension and 14 days ambulation |
Compared to the control group, the GTE with ambulation group showed: ↑ Activation of myogenic progenitor cells ↑ Muscle fiber area ↓ Bax and FADD |
| Alway, 2015, [140] |
Model: Fischer 344 brown Norway aged (34 months) rats Treatment: Fed control (no GTE) or GTE (50 mg/kg) for 7 days prior and throughout. Rats either received 14 days hindlimb suspension or 14 days hindlimb suspension and 14 days ambulation |
Compared to the control group or GTE with suspension group, the GTE with suspension and ambulation group showed: ↓ Suspension-induced muscle mass loss, cross-sectional area, and tetanic force ↔ Muscle mass and force during ambulation ↑ Number of nuclei adjacent to basal lamina (SC proliferation) ↑ Number of nuclei inside sarcolemma (SC differentiation) ↓ Protein carbonyl levels |
| Bhattacharya, 2015, [142] |
Model: Young adult male BALB/c mice Treatment: Fed a control diet (no EGCG) or EGCG (250 mg/kg/d) for 39 days and given access to a running wheel |
Compared to the control group, the EGCG group showed: ↑ Lean body mass (trend) |
| Buetler, 2002, [99] |
Model: Mdx mouse treated with or without tert-butylhydroperoxide Treatment: Fed standard diet supplemented with or without 0.01% and 0.05% (by wt) GTE for 4 weeks |
Compared to the control group, the GTE group showed: ↓ Necrosis in the fast-twitch muscle elongator digitorum longus ↓ Oxidative stress induced by tert-butylhydroperoxide treatment |
| Call, 2008, [132] |
Model: C57BL/6J mice treated with a high-fat diet Treatment: Fed a control diet (no GTE) or GTE (0.5%, 45% EGCG) and endurance exercised (voluntary wheel running) for 3 weeks |
Compared to the control group, the GTE group showed: ↑ Total distance running (128%) ↑ Citrate synthase activity ↓ Serum creatine kinase |
| Cao, 2007, [110] |
Model: Male Wistar Rat Treatment: Rats were fed a high-fructose diet (induced insulin resistance and oxidative stress) and green tea solid extract (EGCG 12.75%) (1 or 2 g/kg) diet for 6 weeks |
Compared to the control (high-fat alone), the GTE group showed: ↑ mRNA expression of anti-inflammatory tristetraproline family in liver and muscle ↓ mRNA expression of proinflammatory genes in liver and muscle |
| Chen, 2020, [145] |
Model: Male BALB/c mice Treatment: Fed a control diet (no GTE) or GTE (0.2 g/kg) and/or endurance exercised (treadmill running) for 8 weeks Model: C2C12 skeletal muscle cells Treatment: Pretreated with or without (control group) GTE (0.01%) and then exposed to ammonium chloride (5 mM) |
Compared to the control group, the GTE with exercise group showed: ↑ Endurance capacity and urea-cycle-related gene expression Compared to the control group, the GTE group showed: ↓ Hyperammonemia-induced reduced mitochondrial respiration |
| Dorchies, 2006, [98] |
Model: Mdx mice Treatment: Fed a standard diet with or without 0.25% GTE (EGCG, 0.1%) for 5 weeks |
Compared to the control group, the GTE group showed: ↑ Phasic and tetanic tensions almost to matched control values ↑ Residual force by 30–50% |
| Evans, 2010, [114] |
Model: Mdx mice Treatment: Fed a control diet (no GTE), 0.25%, or 0.5% GTE (EGCG >45%) for 21 days |
Compared to the control group, the GTE group showed: ↓ Serum creatine kinase ↑ Area of normal fiber morphology ↓ Area of regenerating fibers ↓ NF-κB staining in regenerating muscle fibers |
| Haramizu, 2013, [112] |
Model: Male ICR mice Treatment: Fed a control diet (no GTE) or GTE (0.5%) for 3 weeks. Mice were then downhill running exercised (induce muscle damage) |
Compared to the control group, the GTE group showed: ↓ Muscle-damage-induced reduction in voluntary wheel-running activity, tetanic force ↓ Muscle-damage-induced reduction in plasma creatine phosphokinase levels ↓ TNF-α, IL-1β, MCP-1 |
| Hong, 2020, [104] |
Model: Male ICR aged mice (24 months) Treatment: Fed a control diet, epicatechin (2 mg/kg), or tannase-converted GTE (20 or 40 mg/kg) diet |
Compared to the control group, the tannase-converted GTE group or epicatechin group showed: ↑ Lean mass at 40 mg/kg for the tannase-converted GTE group ↑ MyoD, myogenin for both groups ↓ Myostatin for both groups ↑ S6K, follistatin at 40 mg/kg for the tannase-converted GTE group ↑ SOD, CAT for both groups ↓ FoxO3a, ↑ mTOR at 40 mg/kg for the tannase-converted GTE group ↓ MuRF-1 and atrogin-1 for the tannase-converted GTE group |
| Kumaran, 2008, [100] |
Model: Male albino Wistar aged (34 months) rats Treatment: Fed a control diet (no EGCG) or EGCG (100 mg/kg/d) for 30 days |
Compared to the control group, the EGCG group showed: ↓ Lipid peroxidation and protein carbonyl content |
| Meador, 2015, [127] |
Model: Sprague–Dawley aged (20 months) rats Treatment: Fed a control diet (no EGCG) or EGCG (200 mg/kg) for 8 weeks |
Compared to the control group, the EGCG group showed: ↑ Muscle mass, cross-sectional area ↑ IL-15, IGF-1 |
| Murase, 2005, [130] |
Model: BALB/c mice Treatment: Fed a control diet (no GTE) or GTE (0.2–0.5%) for 10 weeks and then endurance exercised (swimming until exhaustion) |
Compared to the control group, the GTE group showed: ↑ Swimming times to exhaustion (8–24%) ↑ β-oxidation activity, fat oxidation, and plasma free fatty acid concentration ↓ Respiratory quotient and plasma lactate concentration ↑ Fatty acid translocase/CD36 mRNA expression |
| Murase, 2006, [131] |
Model: BALB/c mice Treatment: Exercised with or without GTE (0.2–0.5%) for 10 weeks and then endurance exercised (treadmill running until exhaustion) |
Compared to the control (exercise only) group, the GTE group showed: ↑ Running times to exhaustion 30% ↓ Respiratory exchange ratio, malonyl-CoA content, and plasma lactate concentration ↑ β-oxidation activity, muscle glycogen content, and plasma free fatty acid concentration |
| Murase, 2008, [129] |
Model: Senescence-accelerated prone mice Treatment: Fed a control diet (no GTE) or GTE (0.35%, EGCG 41%) for 10 weeks and/or endurance exercised (treadmill running) |
Compared to the control group, the GTE group showed: Maintained endurance capacity ↓ Oxidative stress Compared to the control group, the GTE with the exercise group showed: ↑ Oxygen consumption, fatty acid β-oxidation, mitochondria-related mRNA expression |
| Nakae, 2008, [97] |
Model: Mdx mice Treatment: Fed vehicle (control group) or EGCG (180 mg/kg/d) for 5 weeks |
Compared to the control group, the EGCG group showed: ↓ Development of dystrophic muscle lesions |
| Onishi, 2018, [141] |
Model: Senescence-accelerated mouse prone-8 Treatment: Fed a control diet, an HFD diet, or HFD with 0.5% GTEs (71.68% EGCG) (GTE group) diet for 4 months |
Compared to the HFD group, the GTE group showed: ↑ Muscle mass ↑ Akt and S6K phosphorylation |
| Ota, 2011, [101] |
Model: BALB/c mice Treatment: Fed a control diet (no GTE) or a diet containing 0.5% GTE (81% catechins) for 14 days, and then mice were subjected to continuous tail suspension for 10 days |
Compared to the control group, the GTE group showed: ↓ Unloading induced muscle tetanic force loss ↑ Total antioxidant potential ↓ Carbonylated protein levels |
| Sae-Tan, 2014, [128] |
Model: C57bl/6J mice treated with a high-fat diet Treatment: Fed control (high-fat) diet or 0.32% EGCG for 16 weeks |
Compared to the GTE without exercise group, the GTE with exercise group showed: ↓ Body mass and visceral fat ↑ PGC-1α, Cytb, CO III (mitochondrial metabolism enzymes) |
| Serrano, 2013, [124] |
Model: Male C57BL6 mice Treatment: Fed a control diet or tea beverage (EGCG 37.8%) for 3 months |
Compared to the control group, the EGCG group showed: ↓ Oxidative damage ↑ AMP-activated protein kinase α levels ↓ UCP-2 and UCP-4 ↑ Porin ↓ Mitochondrial DNA to nuclear DNA ratio |
| Shen, 2012, [102] |
Model: Female Sprague–Dawley rats Treatment: Fed a high-fat diet for 4 months and then fed with or without GTE (0.5%) for additional 4 months |
Compared to the control (high-fat without GTE) group, the GTE group showed: ↑ Glutathione peroxidase (reduces ROS) |
| Takahashi, 2017, [45] |
Model: Brown Norway inbred aged (34 months) rats Treatment: Fed a control diet (no EGCG) or EGCG (50 mg/kg). Rats either received 14 days hindlimb suspension or 14 days hindlimb suspension and 14 days ambulation |
Compared to the control group, the EGCG without ambulation group showed: ↑ ATG16L2, SNCA, TM9SF1, Pink1, PIM-2 gene expression ↑ ATG12, ↓ Beclin-1 protein content Compared to the control group, the EGCG group with ambulation showed: ↓ Beclin1 and LC3-II/I protein content |
| Wang, 2015, [103] |
Model: Male Kunming mice Treatment: Intraperitoneally injected daily vehicle (control group) or EGCG at the dose of 55, 75, 100, and 200 mg/kg for 5 consecutive days |
Compared to the control group, the EGCG group showed: ↓ SOD, catalase, glutathione peroxidase at 75 mg/kg ↔ Endogenous antioxidant activity Hepatotoxicity triggered at 200 mg/kg |
| Wang (2011), [113] |
Model: Male C57BL/6 mice Treatment: Mice were injected with LLC cells (induced LLC tumor) and then fed EGCG (0.2 mg/mouse/d, prevention or 0.6, treatment mg/mouse/d) for 12 days |
Compared to the control group, the EGCG group showed: ↓ Leukocyte infiltration ↓ NF-κB, and MuRF1, MAFbx (E3-ligases) ↓ Tumor volume and mass |
| Zhang (2020), [111] |
Model: C57BL/6J mice Treatment:Mice were fed with HFD for 10 weeks to induce obesity. Obese mice were fed with continuous HFD, HFD with GTE (EGCG 12.5%), HFD with Ex, and HFD with both GTE and Ex for 8 weeks |
Compared to the control group, the GTE + EX showed: ↓ blood glucose, serum total cholesterol, triglyceride, insulin, and alanine aminotransferase activity GTE, GTE + EX, EX ↓ proinflammatory gene expression GTE, GTE + EX ↑ IkBα (NF-κB inhibitor) activity GTE + EX ↑ glucose transport genes mRNA |
| Human Studies | ||
| Hadi, 2017, [105] |
Model: Men (n = 18; 20.94 ± 1.43 years) soccer players Treatment: Supplemented with or without (placebo group) GTE (450 mg/d) for 6 weeks Exercise: Maintained the same exercise schedule throughout the study |
Compared to the placebo group, the GTE group showed: ↓ MDA levels |
| Jowko, 2015, [106] |
Model: Male (n = 16; 21.6 ± 1.5 years) sprinters Treatment: Supplemented with or without (placebo group) GTE (980 mg/d) for 4 weeks Exercise: Repeated cycle sprint test |
Compared to the placebo group, the GTE group showed: ↓ MDA and SOD levels ↑ Total antioxidant capacity |
| Panza, 2008, [107] |
Model: Weight-trained men (n = 14; 19–30 years) Treatment: Supplement with water (placebo) or with GTE (200 mL) 3 times per day for 8 days. Exercise: Resistance exercise (Ex) protocol consisted of a warm-up followed by 4 sets of 10, 8, 6, and 4 repetitions, with 75%, 80%, 85%, and 90% of 1-RM, respectively |
Compared to the placebo group, the GTE group showed: ↓ LH, aspartate aminotransferase, and uric acid ↑ GSH-Px ↓ Ex-induced increase in CK and xanthine oxidase |
| Silva, 2018, [109] |
Model: Untrained men (n = 20; 23 ± 5 years) Treatment: Supplemented with or without (placebo group) GTE (500 mg/d) for 15 days and exercised (induced DOMS in triceps sural) before and after supplementation Exercise: Calf raising exercise trial one (maximal voluntary repetitions) and trial two (75% of maximal repetitions with repeated sets until >50% maximal of maximal repetitions could be achieved) |
Compared to the placebo group, the GTE group showed: ↓ Creatine kinase |
| Townsend, 2018, [120] |
Model: Untrained men (n = 38; 18–35 years) Treatment: Supplemented with, without (control group), or with placebo, aqueous proprietary polyphenol blend (40% catechins, 3–8% EGCG) for 28 days. Then subjects completed acute low body resistance exercise protocol (induced muscle damage) Exercise: Squat (6 sets of 10 repetitions) and leg press, leg extension (4 sets of 10 repetitions) exercises all at 70% 1-RM |
Compared to the control group, the EGCG group showed: ↓ Muscle-damage-induced increase in Bcl-2, BAD |
| Tsai, 2017, [134] |
Model: Healthy men (n = 8; 22 ± 1 years) with regular recreational physical activities 3/week Treatment: Supplemented with or without (control group) GTE (500 mg/d) for 8 weeks and then performed cycling exercise Exercise: 60 min cycling exercise at 75% VO2max after a 5 min warm-up exercise (50 W), 24 h postsupplement |
Compared to the control group, the GTE group showed: ↑ Exercise-induced muscle GLUT4 protein content ↑ Fat oxidation energy reliance |
| Kuo 2015, [108] |
Model: Forty untrained men (age: 20 ± 1 years) Treatment: Assigned to placebo (control), GTE, endurance training (EX), or endurance training with GTE (GTE + EX). GTE groups orally took GTE (250 mg/day) for 4 weeks Exercise: 75% oxygen uptake reserve for three 20 min sessions per week |
Compared to the control group, the EX and GTE + EX groups showed: ↑ Exhaustive run time ↑ Maximal oxygen uptake ↓ Serum creatine kinase, MDA levels |
AMPK, 5’ AMP-activated protein kinase; ATG, autophagy-related protein; Akt, protein kinase B; BAD, Bcl-2 associated agonist of cell death; Bax, bcl-2-like protein 4; Bcl-2, B-cell lymphoma 2; CAT, catalase; CD36, cluster of differentiation 36; CO III, cytochrome c oxidase subunit III; Cytb, Cytochrome b; DOMS, delayed onset muscle soreness; EC, epicatechin; EGCG, epigallocatechin gallate; FADD, Fas-associated protein with death domain; FoxO, Forkhead box (Fox) O; GLUT4, glucose transporter type 4; GSH-Px, glutathione peroxidase; GTE, green tea extract; HFD, high-fat diet; HK, hexokinase; IGF-1, insulin-like growth factor 1; IL-15, interleukin-15; LC3, microtubule-associated protein 1A/1B-light chain 3; LDH, lactate dehydrogenase; 67LR, 67 laminin receptor; MDA, malondialdehyde; Mdx, Dystrophin-deficient mice; MHC, myosin heavy chain; mTOR, mammalian target of rapamycin; MuRF-1, muscle RING-finger protein-1; Myf5, myogenic factor 5; MyoD, myoblast determination protein 1; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NRF-1, nuclear respiratory factor 1; PGC-1α, Pparg coactivator 1 alpha; PIF, proteolysis-inducing factor; PIM-2, proviral Integrations of Moloney virus 2; Pink1, PTEN-induced kinase 1; PPAR-γ, peroxisome proliferator-activated receptor gamma; S6K, ribosomal protein S6 kinase beta-1; SDH, succinate dehydrogenase; SNCA, Synuclein Alpha; SOD, superoxide dismutase; TAZ, transcriptional coactivator with PDZ-binding motif; TM9SF1, transmembrane 9 superfamily member 1; TNF-α, tumor necrosis factor-alpha; UCP, uncoupling protein. ↑, increase; ↓, decrease; ↔, no change.