Tissue damage is regarded as an unwanted medical condition to be avoided. However, introducing tolerable tissue damages has been used as a therapeutic intervention in traditional and complementary medicine to cure discomfort and illness. Eccentric exercise is known to cause significant necrosis and insulin resistance of skeletal muscle. The purpose of this study was to determine the magnitude of muscle damage and blood glucose responses during an oral glucose tolerance test (OGTT) after eccentric training in 21 young participants. They were challenged by 5 times of 100-meter downhill sprinting and 20 times of squats training at 30 pounds weight load for 3 days, which resulted in a wide spectrum of muscle creatine kinase (CK) surges in plasma, 48 h after the last bout of exercise. Participants were then divided into two groups according the magnitude of CK increases (low CK: +48% ± 0.3; high CK: +137% ± 0.5, P < 0.05). Both groups show comparable decreases in blood glucose levels in OGTT, suggesting that this muscle-damaging exercise does not appear to decrease but rather improve glycemic control in men. Conclusion: The result of the study rejects the hypothesis that eccentric exercise decreases glucose tolerance. Improved glucose tolerance with CK increase implicates a beneficial effect of replacing metabolically weaker muscle fibers by eccentric exercise in Darwinian natural selection fashion.
Body mass index (BMI) is positively associated with survival in heart failure (HF) patients with reduced ejection fraction (HFrEF). However, emerging evidence shows that this benefit may not exist in diabetic patients with HFrEF. As this relationship has not been investigated in Asian patients, the aim of this study was to examine the association between obesity and outcomes in HrEFF patients with and without diabetes mellitus (DM), and discuss the potential underlying mechanisms.
The analysis included 900 patients with acute decompensated HF from the Taiwan Society of Cardiology-Heart Failure with Reduced Ejection Fraction Registry, of whom 408 had DM (45%). The association between BMI and all-cause mortality was examined using multivariate Cox proportional hazards regression after adjusting for covariates and Kaplan–Meier survival analysis. Echocardiography parameters were also analyzed in patients with different BMI and DM status.
After adjusting for confounding factors, BMI was a significant independent predictive factor for all-cause mortality in the non-diabetic patients (hazard ratio [HR], 0.88; 95% confidence interval [CI], 0.81–0.95) and in Kaplan–Meier survival analysis (log-rank test,
P
= .034). For diabetic patients, BMI was not a significant predictive factor for all-cause mortality (HR, 0.96; 95% CI, 0.90–1.02) and in Kaplan–Meier survival analysis (log-rank test
P
= .169). Both DM (47.8 vs 45.4 mm,
P
= .014) and higher BMI (48.6 vs 44.9 mm,
P
< .001) are independently associated with higher left atrial size. Patients with a higher BMI had a lower proportion of severe mitral regurgitation (10.0% vs 14.1%,
P
< .001).
In non-diabetic patients with HFrEF, BMI was a significant predictor of survival. However, in diabetic patients with HF, BMI was not a significant predictor of survival. Diastolic dysfunction in patients with DM and obesity may have played a role in this finding.
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