Aims
Green tea extract (GTE) can exert antiobesity and anti‐inflammatory effects. Our study determined whether the benefits of GTE are summative with exercise‐induced changes in anthropometric indices, and the levels of inflammatory cytokines, adiponectin and irisin in inactive overweight women.
Methods
Thirty overweight female participants were randomized to 3 groups: endurance training + placebo (ET + P); endurance training + GTE (ET + GTE); and Control (no exercise) + placebo (Control, n = 10). The exercise intervention consisted of an 8‐week endurance‐training programme of 3 sessions per week (aerobics, aerobic circuit training, and fast walking or jogging at a moderate intensity of 40–59% of the heart rate reserve). The dose of GTE used was 500 mg/day in the form of a green tea capsule.
Results
Body weight, body mass index, waist to hip ratio and body fat percentage were decreased in both ET + P and ET + GTE interventions (P < .001 for both interventions). The reduction of anthropometric values in the ET + GTE group was significantly higher than ET + P interventions (P < .001). Both exercise interventions also significantly (P < .001) increased adiponectin (ET + GTE = 5.28 mg/mL [95% confidence interval {CI}, 4.48 to 6.08] and ET + P = 3.34 mg/mL [95% CI, 2.76 to 3.92]) and decreased high‐sensitivity C‐reactive protein (hs‐CRP; ET + GTE = −0.95 mg/L [95% CI, −1.15 to −0.75] and ET + P = −0.35 mg/L [95% CI, −0.46 to −0.24]). Changes in adiponectin and hs‐CRP were greater (P < .05) in ET + GTE compared to ET + P. There were no significant differences in irisin, interleukin‐6 or tumour necrosis factor‐α between the 3 groups (P > .05).
Conclusions
GTE improves exercise‐induced body composition by further decreasing exercise‐induced changes in weight, body mass index, waist to hip ratio and body fat percentage. The combination of GTE and exercise also produced greater changes in anti‐inflammatory (increases in adiponectin) and metabolic (decreases in hs‐CRP) markers than exercise alone.
We performed a systematic review and dose–response meta-analysis of observational studies assessing the association between UPF consumption and adult mortality risk. A systematic search was conducted using ISI Web of Science, PubMed/MEDLINE, and Scopus electronic databases from inception to August 2021. Data were extracted from seven cohort studies (totaling 207,291 adults from four countries). Using a random-effects model, hazard ratios (HR) of pooled outcomes were estimated. Our results showed that UPF consumption was related to an enhanced risk of all-cause mortality (HR = 1.21; 95% CI: 1.13, 1.30; I2 = 21.9%; p < 0.001), cardiovascular diseases (CVDs)-cause mortality (HR = 1.50; 95% CI: 1.37, 1.63; I2 = 0.0%; p < 0.001), and heart-cause mortality (HR = 1.66; 95% CI: 1.50, 1.85; I2 = 0.0%; p = 0.022), but not cancer-cause mortality. Furthermore, our findings revealed that each 10% increase in UPF consumption in daily calorie intake was associated with a 15% higher risk of all-cause mortality (OR = 1.15; 95% CI: 1.09, 1.21; I2 = 0.0%; p < 0.001). The dose–response analysis revealed a positive linear association between UPF consumption and all-cause mortality (Pnonlinearity = 0.879, Pdose–response = p < 0.001), CVDs-cause mortality (Pnonlinearity = 0.868, Pdose–response = p < 0.001), and heart-cause mortality (Pnonlinearity = 0.774, Pdose–response = p < 0.001). It seems that higher consumption of UPF is significantly associated with an enhanced risk of adult mortality. Despite this, further experimental studies are necessary to draw a more definite conclusion.
Purpose: Due to the mechanistic role of myostatin and follistatin in modulating muscle mass, shifts in the 3 follistatin to myostatin ratio (F: M) may help explain changes in muscular size in response to resistance training 4 (RT). The present study examined whether differential responses in follistatin and myostatin occur based on the 5 amount of active musculature in a RT program in middle-aged men. 6 Methods: Forty middle-aged men (age= 46.5±3.1 years) were randomly assigned to one of 4 groups, upper-body 7 RT (UB; n=10), lower-body RT (LB; n=10), combined RT (UB+LB; n=10) or control (C; n=10). The training 8 protocol consisted of 3 exercise sessions per week for 8 weeks. Blood samples were obtained at baseline and 48 9 hours after the final session of the training program. 10 Results: Muscle mass significantly increased (p˂0.05) following UB= 0.76 ± 0.46 kg, LB= 0.90 ± 0.29 kg, 11 UB+LB= 1.38 ± 0.70 kg, compared to no changes after control. Serum follistatin increased in the LB= 0.24 ± 0.06 12 ng.mL-1 , UB= 0.27 ± 0.17 ng.mL-1 , UB+LB= 0.50 ± 0.18 ng.mL-1 , while serum myostatin decreased in the LB=-13 0.11 ± 0.08 ng.mL-1 and UB+LB=-0.34 ± 0.23 ng.mL-1 , but not UB= 0.07 ± 0.16 ng.mL-1. Further, change in 14 concentration following training was larger between UB+LB and either LB or UB alone for both follistatin and 15 myostatin. 16 Conclusions: Both UB and LB increase muscle mass and alter the F: M ratio, however the change in these 17 endocrine markers is approximately twice as large if UB and LB is combined. The endocrine response to RT of 18 myostatin and follistatin may depend on the volume of muscle mass activated during training.
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