We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.
TIRI is a feasible noncontact technology to monitor airflow during polysomnography. In its current methodologic incarnation, it demonstrates a high degree of chance-corrected agreement with the oronasal thermistor in the detection of apnea and hypopneas but demonstrates a lesser degree of chance-corrected agreement with Pn. Further overnight validation studies must be performed to evaluate its potential in clinical sleep medicine.
After bolus and continuous enteral feeding of the same protein, different digestion and absorption kinetics and anabolic responses are observed. Establishing which mode of feeding has the highest anabolic potential in patients with chronic obstructive pulmonary disease (COPD) may aid in the prevention of muscle wasting, but an important confounding factor is the duration of assessments after bolus feeding. We hypothesized that the anabolic response to bolus and continuous feeding in COPD patients is comparable when methodological issues are addressed. Twenty-one older adults (12 patients with stage II-IV COPD and 9 healthy controls) were studied after intake of a fast-absorbing hydrolyzed casein protein-carbohydrate mixture either as a single bolus or as small sips (crossover design). Whole body protein synthesis (PS), breakdown (PB), net PS (PS - PB) protein efficiency (netPSPE), net protein balance (phenylalanine (PHE) intake - PHE hydroxylation) protein efficiency (netBalPE), and splanchnic PHE extraction (SPE) were assessed using stable isotope tracer methodology. Bolus feeding assessments were done at 90, 95, and 99% of the calculated duration of the anabolic response. At 99%, netBalPE was higher for sip feeding than bolus feeding in both groups (<0.0001). Nevertheless, bolus feeding was associated with a lower SPE (<0.0001) and higher netPSPE (<0.0001). At 90% compared with 99%, PS and netBalPE after bolus feeding was significantly overestimated. In conclusion, several factors complicate a comparison of the anabolic capacity of bolus and continuous feeding in acute studies, including the critical role of SPE calculation and assumptions, and the duration of postprandial assessments after bolus feeding.
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