Abstract
Funding Acknowledgements
Type of funding sources: Public grant(s) – EU funding. Main funding source(s): European Commission, Region Guadeloupe
Background. Sickle cell trait (SCT) is an inherited red blood cell condition without medical consequence in most cases. However, its strong association with increased risk of exercise-induced sudden death (independent of pre-existing disease) or exertional collapse has been demonstrated in athletes, military recruits and firefighters. The mechanisms potentially leading to cardiac arrest during or after exercise in SCT have not been fully elucidated although contributing factors have been identified (the main one being rhabdomyolysis) or suspected. Warm environment (even without dehydration) can contribute to the occurrence of fatal events.
Purpose. The aims of this study were to 1) compare the biomarkers of myocardial and muscle injury response (and their determinants) to exercise in SCT carriers and controls performing a hard bout of exercise 2) identify the potential deleterious role of warmth during exercise and recovery in SCT and non-SCT.
Methods. Nine otherwise healthy 21 ± 3yo male students with SCT and 11 non-SCT (comparable in physical fitness, regular exercise participation and body mass index) were included. The volunteers performed in a randomized order 3 sessions: cycling exercise in a control (21°C) and warm (31°C) environment followed by recovery in a room at 21°C, and both exercise and recovery in a warm environment. The exercise was as follows: 18-min rectangular moderate intensity period + maximal incremental test + 3 30-s supramaximal sprints spaced with 20-s resting intervals. Recovery and hydration were planned between each exercise part. The ECG was monitored throughout exercise. Blood was sampled before and at the end of the exercise but also during the recovery including a meal up to 130-min after the end of exercise.
Results. No evidence of severe cardiac injury (ECG and biomarkers), rhabdomyolysis or occlusive events (clinical signs and biomarkers), infection (complete blood count), inflammation (biomarkers) or electrolyte imbalance (ionogram) was observed in the SCT carriers of this study: indices were comparable between SCT and non-SCT carriers, with normal exercise-related evolutions and normal recovery. Interestingly, some indices however converge towards a profile with lower complication risk in SCT.
The lactate concentrations tended to be lower in SCT than non-SCT during exercise (p = 0.062) and were significantly lower during the recovery in particular after exercising at 31°C but not at 21°C. The leukocytes count was lower in SCT than non-SCT (p = 0.043) and increased in a greater extent with exercise in the later (p = 0.041). The exercise-induced increase in cortisol and glucose concentrations observed in non-SCT did not occur in SCT carriers (interactions p and p = 0.040 and p = 0.033). Conclusions. Although these results do not evidence pathophysiological mechanisms, they feed the hypothesis of "storm" against which protective mechanisms could have developed and that may fail under particular conditions.
Exercise-induced death in sickle cell trait: role of aging, training, and deconditioning