Preventive measures for the critical postexercise period in sickle cell trait and disease

Abstract

The immediate post-exercise/physical activity period is critical for sickle cell trait (SCT) carriers and disease (SCD) patients. Indeed, exercise-related blood acidosis known to trigger the cascade: HbS deoxygenation and polymerization, and subsequently red blood cells sickling, aggravates during the initial post-exercise period. This deterioration lies on the conjunction of two facts: First, blood lactate and H+ concentrations continue to increase during several minutes after exercise completion, aggravating blood acidosis. Second, blood lactate concentrations remain elevated and pH altered for 20-45 minutes in case of inactivity after intense exercise, keeping acid/base balance disturbed for a long period post-exercise. Therefore, the risk of complications (including vaso-occlusive crises and even sudden deaths) persists and even worsens several minutes after intensive exercise completion in SCT carriers or SCD patients. Light physical activity following intense exercise (namely active recovery) may, by accelerating lactate removal and acid/base balance restoration, be of paramount importance in that context. Scientific evidences suggest that a light exercise below or at maximum to the first lactate threshold would constitute an appropriate strategy.

Cardiac diastolic maladaptation is associated with the severity of exercise intolerance in sickle cell anemia patients

“…The indexed arteriovenous oxygen difference or O 2 extraction (AV-O 2 Δ in mL O 2 /L blood/m 2 of body surface area) was calculated as the ratio of to cardiac index (CI) obtained from and echocardiography data recorded at each level of effort 23 . Preventive measures for the critical post-exercise period were applied and consisted in 2 min of active recovery followed by at least 8 min of passive recovery, including rehydration 5 . Patients were clinically monitored for 1 h following the procedure.…”

“…Poor physical capacities are common in patients homozygous for HbS—also called sickle cell anemia (SCA)—as a result of anemia and multiple pulmonary, cardiac, endothelial, muscle, and metabolic dysfunctions 2 . For these patients, elevated pulmonary arterial pressure, diastolic dysfunction, impaired oxygen transport and delivery 3 and early blood lactate accumulation 4 , 5 translate into poor adaptation to physical activities. During an exercise of increasing intensity, significant activation of glycogenolysis and glycolysis leads to muscle lactate production, accumulation and subsequently to an increase in blood concentrations 6 , 7 .…”