Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences.

Extreme or unaccustomed eccentric exercise can cause exercise-induced muscle damage, characterized by structural changes involving sarcomere, cytoskeletal, and membrane damage, with an increased permeability of sarcolemma for proteins. From a functional point of view, disrupted force transmission, altered calcium homeostasis, disruption of excitation-contraction coupling, as well as metabolic changes bring about loss of strength. Importantly, the trauma also invokes an inflammatory response and clinically presents itself by swelling, decreased range of motion, increased passive tension, soreness, and a transient decrease in insulin sensitivity. While being damaging and influencing heavily the ability to perform repeated bouts of exercise, changes produced by exercise-induced muscle damage seem to play a crucial role in myofibrillar adaptation. Additionally, eccentric exercise yields greater hypertrophy than isometric or concentric contractions and requires less in terms of metabolic energy and cardiovascular stress, making it especially suitable for the elderly and people with chronic diseases. This review focuses on our current knowledge of the mechanisms underlying exercise-induced muscle damage, their dependence on genetic background, as well as their consequences at the structural, functional, metabolic, and clinical level. A comprehensive understanding of these is a prerequisite for proper inclusion of eccentric training in health promotion, rehabilitation, and performance enhancement.

Development of a screening tool using electronic health records for undiagnosed Type 2 diabetes mellitus and impaired fasting glucose detection in the Slovenian population.

AIM: To develop and validate a simplified screening test for undiagnosed Type 2 diabetes mellitus and impaired fasting glucose for the Slovenian population (SloRisk) to be used in the general population. METHODS: Data on 11 391 people were collected from the electronic health records of comprehensive medical examinations in five Slovenian healthcare centres. Fasting plasma glucose as well as information related to the Finnish Diabetes Risk Score questionnaire, FINDRISC, were collected for 2073 people to build predictive models. Bootstrapping-based evaluation was used to estimate the area under the receiver-operating characteristic curve performance metric of two proposed logistic regression models as well as the Finnish Diabetes Risk Score model both at recommended and at alternative cut-off values. RESULTS: The final model contained five questions for undiagnosed Type 2 diabetes prediction and achieved an area under the receiver-operating characteristic curve of 0.851 (95% CI 0.850-0.853). The impaired fasting glucose prediction model included six questions and achieved an area under the receiver-operating characteristic curve of 0.840 (95% CI 0.839-0.840). There were four questions that were included in both models (age, sex, waist circumference and blood sugar history), with physical activity selected only for undiagnosed Type 2 diabetes and questions on family history and hypertension drug use selected only for the impaired fasting glucose prediction model. CONCLUSIONS: This study proposes two simplified models based on FINDRISC questions for screening of undiagnosed Type 2 diabetes and impaired fasting glucose in the Slovenian population. A significant improvement in performance was achieved compared with the original FINDRISC questionnaire. Both models include waist circumference instead of BMI.