The effect of unilateral and bilateral strength training on the bilateral deficit and lean tissue mass in post-menopausal women

2006 ◽  
Vol 97 (3) ◽  
pp. 253-260 ◽  
Author(s):  
Cora L. Janzen ◽  
Philip D. Chilibeck ◽  
K. Shawn Davison
Author(s):  
Stephen M. Cornish ◽  
Darren G. Candow ◽  
Nathan T. Jantz ◽  
Philip D. Chilibeck ◽  
Jonathan P. Little ◽  
...  

Purpose:The authors examined the combined effects of conjugated linoleic acid (CLA), creatine (C), and whey protein (P) supplementation during strength training.Methods:Sixty-nine participants (52 men, 17 women; M ± SD age 22.5 ± 2.5 yr) were randomly assigned (double-blind) to 1 of 3 groups: CCP (6 g/d CLA + 9 g/d C + 36 g/d P; n = 22), CP (C + P + placebo oil; n = 25), or P (P + placebo oil; n = 22) during 5 wk of strength training (4–5 sets, 6–12 repetitions, 6 d/wk). Measurements were taken for body composition (air-displacement plethysmography), muscle thickness (ultrasound) of the flexors and extensors of the elbow and knee, 1-repetitionmaximum (1-RM) strength (leg press and bench press), urinary markers of bone resorption (N-telopeptides, NTx), myofibrillar protein catabolism (3-methylhistidine; 3-MH), oxidative stress (8-isoprostanes), and kidney function (microalbumin) before and after training.Results:Contrast analyses indicated that the CCP group had a greater increase in bench-press (16.2% ± 11.3% vs. 9.7% ± 17.0%; p < .05) and legpress (13.1% ± 9.9% vs. 7.7% ± 14.2%; p < .05) strength and lean-tissue mass (2.4% ± 2.8% vs. 1.3% ± 4.1%; p < .05) than the other groups combined. All groups increased muscle thickness over time (p < .05). The relative change in 3-MH (CCP –4.7% ± 70.2%, CP –0.4% ± 81.4%, P 20.3% ± 75.2%) was less in the groups receiving creatine (p < .05), with the difference for NTx also close to significance (p = .055; CCP–3.4% ± 66.6%, CP–3.9% ± 64.9%, P 26.0% ± 63.8%). There were no changes in oxidative stress or kidney function.Conclusion:Combining C, CLA, and P was beneficial for increasing strength and lean-tissue mass during heavy resistance training.


Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1912
Author(s):  
Scott C. Forbes ◽  
Darren G. Candow ◽  
Sergej M. Ostojic ◽  
Michael D. Roberts ◽  
Philip D. Chilibeck

Creatine supplementation in conjunction with resistance training (RT) augments gains in lean tissue mass and strength in aging adults; however, there is a large amount of heterogeneity between individual studies that may be related to creatine ingestion strategies. Therefore, the purpose of this review was to (1) perform updated meta-analyses comparing creatine vs. placebo (independent of dosage and frequency of ingestion) during a resistance training program on measures of lean tissue mass and strength, (2) perform meta-analyses examining the effects of different creatine dosing strategies (lower: ≤5 g/day and higher: >5 g/day), with and without a creatine-loading phase (≥20 g/day for 5–7 days), and (3) perform meta-analyses determining whether creatine supplementation only on resistance training days influences measures of lean tissue mass and strength. Overall, creatine (independent of dosing strategy) augments lean tissue mass and strength increase from RT vs. placebo. Subanalyses showed that creatine-loading followed by lower-dose creatine (≤5 g/day) increased chest press strength vs. placebo. Higher-dose creatine (>5 g/day), with and without a creatine-loading phase, produced significant gains in leg press strength vs. placebo. However, when studies involving a creatine-loading phase were excluded from the analyses, creatine had no greater effect on chest press or leg press strength vs. placebo. Finally, creatine supplementation only on resistance training days significantly increased measures of lean tissue mass and strength vs. placebo.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Da Young Lee ◽  
Zhe Jiao ◽  
Andrew Antolic ◽  
Daiana Weiss ◽  
M. Neale Weitzmann ◽  
...  

Background: Cachexia is wasting of normal body tissue and occurs in chronic medical diseases. It is a common complication of heart failure (HF) that is associated with very high mortality. Growth differentiation factor 15 (GDF15) regulates food intake and can cause cancer cachexia. GDF15 is a sensitive biomarker in humans, though its biologic function in HF is unknown. This study investigated the role of GDF15 in HF. Methods: We utilized a genetic mouse model of dilated cardiomyopathy (DCM) caused by a mutation in the phospholamban gene (PLN R9C ). PLN R9C mice have dysregulated cardiac calcium handling (a common feature of nearly all forms of HF) and develop progressive DCM that leads to HF and premature death. Q-PCR and ELISA were performed to assess expression, tissue distribution and circulating levels of GDF15 in PLN R9C and age-matched wild type (WT) mice. A double transgenic mouse was created by crossing our DCM model with a constitutive Gdf15 knock-out (KO). Using this novel model, we quantified food intake, and assessed fat and lean tissue mass by tissue weight at necropsy and by dual-energy X-ray absorptiometry (DXA). Cardiac function was assessed using echocardiography, and histochemistry performed to quantify cardiac fibrosis. Survival was assessed by Kaplan-Meier. Results: GDF15 mRNA (43-fold; p<0.01) and protein (54-fold; p<0.01) were increased in LV tissue, and circulating GDF15 was elevated (8.3-fold; p=0.03) in PLN R9C mice. Gdf15 was expressed at low levels and was not increased in other organs in PLN R9C mice. PLN R9C mice developed cachexia (reduced fat and lean mass by tissue weight, reduced fat mass by DXA vs. WT; p<0.01 for all) and consumed less food (p<0.01 vs. WT). Gdf15 KO in PLN R9C preserved fat and lean tissue mass and resulted in higher food intake (p≤0.01 for all). Gdf15 KO had no effect on cardiac structure or function by echocardiography and PLN R9C / Gdf15 KO mice displayed only a small reduction in cardiac fibrosis relative to PLN R9C mice (3%; p<0.01). Despite this, Gdf15 KO prolonged survival in PLN R9C (29±3 vs. 25±3 weeks; p<0.01). Conclusions: GDF15 is a novel cardiac hormone produced in HF that triggers anorexia and cachexia in HF by an extra-cardiac mechanism.


2013 ◽  
Vol 25 (4) ◽  
pp. 1297-1304 ◽  
Author(s):  
S. A. Jackowski ◽  
J. L. Lanovaz ◽  
C. Van Oort ◽  
A. D. G. Baxter-Jones

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