Mountain Ultramarathon Induces Early Increases of Muscle Damage, Inflammation, and Risk for Acute Renal Injury.

Purpose: This study aimed to investigate changes in muscle damage during the course of a 217-km mountain ultramarathon (MUM). In an integrative perspective, inflammatory response and renal function were also studied. Methods: Six male ultra-runners were tested four times: pre-race, at 84 km, at 177 km, and immediately after the race. Blood samples were analyzed for serum muscle enzymes, acute-phase protein, cortisol, and renal function biomarkers. Results: Serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) increased significantly throughout the race (P < 0.001, P < 0.001; P = 0.002, respectively), and effect size (ES) denoted a large magnitude of muscle damage. These enzymes increased from pre-race (132 ± 18, 371 ± 66, and 28 ± 3 U/L, respectively) to 84 km (30, 1.8, and 3.9-fold, respectively); further increased from 84 to 177 km (4.6, 2.9, and 6.1-fold, respectively), followed by a stable phase until the finish line. Regarding the inflammatory response, significant differences were found for C-reactive protein (CRP) (P < 0.001) and cortisol (P < 0.001). CRP increased from pre-race (0.9 ± 0.3 mg/L) to 177 km (243-fold), cortisol increased from pre-race (257 ± 30 mmol/L) to the 84 km (2.9-fold), and both remained augmented until the finish line. Significant changes were observed for creatinine (P = 0.03), urea (P = 0.001), and glomerular filtration rate (GFR) (P < 0.001), and ES confirmed a moderate magnitude of changes in renal function biomarkers. Creatinine and urea increased, and GFR decreased from pre-race (1.00 ± 0.03 mg/dL, 33 ± 6 mg/dL, and 89 ± 5 ml/min/1.73 m2, respectively) to 84 km (1.3, 3.5, and 0.7-fold, respectively), followed by a plateau phase until the finish line. Conclusion: This study shows evidence that muscle damage biomarkers presented early peak levels and they were followed by a plateau phase during the last segment of a 217-km MUM. The acute-phase response had a similar change of muscle damage. In addition, our data showed that our volunteers meet the risk criteria for acute kidney injury from 84 km until they finished the race, without demonstrating any clinical symptomatology.

Is lactate production related to muscular fatigue? A pedagogical proposition using empirical facts.

The cause-effect relationship between lactic acid, acidosis, and muscle fatigue has been established in the literature. However, current experiments contradict this premise. Here, we describe an experiment developed by first-year university students planned to answer the following questions: 1) Which metabolic pathways of energy metabolism are responsible for meeting the high ATP demand during high-intensity intermittent exercise? 2) Which metabolic pathways are active during the pause, and how do they influence phosphocreatine synthesis? and 3) Is lactate production related to muscular fatigue? Along with these questions, students received a list of materials available for the experiment. In the classroom, they proposed two protocols of eight 30-m sprints at maximum speed, one protocol with pauses of 120 s and the other protocol with pauses of 20 s between sprints. Their performances were analyzed through the velocity registered by photocells. Blood lactate was analyzed before the first sprint and after the eighth sprint. Blood uric acid was analyzed before exercise and 15 and 60 min after exercises. When discussing the data, students concluded that phosphocreatine restoration is time dependent, and this fact influenced the steady level of performance in the protocol with pauses of 120 s compared with the performance decrease noted in the protocol with pauses of 20 s. As the blood lactate levels showed similar absolute increases after both exercises, the students concluded that lactate production is not related to the performance decrement. This activity allows students to integrate the understanding of muscular energy pathways and to reconsider a controversial concept with facts that challenge the universality of the hypothesis relating lactate production to muscular fatigue.

Understanding the glycemic index and glycemic load and their practical applications.

We have introduced the study of synthesis pathways using two experiments: 1-the determination of the glycemic index (GI) of some foods and the effects of fiber and fat on the GI; 2-the determination of blood glucose levels after the ingestion of meals with high and low glycemic loads (GL). After a practice assembly, when the foods and meals that were eaten by the students were tallied, the students were divided into groups. At the next class, three members of each group, who had fasted for 8 hr, ingested 50 g of carbohydrate in food or a meal. After ingestion, the blood glucose was measured with a portable device every 30 min for a period of 2 hr. Discussion of the data obtained in experiment 1 allowed the students to understand the mechanism of action of insulin and to understand how the GI, as presented in the literature, is determined. The students also concluded that the addition of fiber to food reduces the glycemic response even with high GI foods, and these results could be a useful strategy for diet prescription. Discussion of experiment 2 allowed the students to understand that the amount of food intake is a determining factor for the glycemic response and subsequent release of insulin. These experimental observations allowed the students to transfer theoretical knowledge to their daily lives very easily. The students approved the classes and felt encouraged to study the synthesis pathways and metabolic integration in the fed state.