NCAA Division I American football players with sickle cell trait have altered hematological responses and hydration status.

Sickle cell trait (SCT) is a risk factor of collapse and sudden death in athletes. We conducted a longitudinal study to determine the hematological responses and hydration status in NCAA Division I American football players with SCT. The study took place over 2 years with 6 SCT and 6 position-matched controls (CON) in year 1; and 4 SCT and 4 CON in year 2. In year 2, three of the four SCT players were recruited and re-enrolled with new position-matched controls (total sample data = 10 SCT and 10 CON). Blood samples were taken at three visits: pre-camp, post-camp, and post-season to examine hemoglobin variants, complete blood counts, and chemistry panel 26. Hydration status was assessed by measuring body weight change, urine specific gravity, and urine and sweat electrolyte concentrations during the pre-season training camp. All SCT players were confirmed to have SCT (HbS = 37.9 ± 2.4%) and had greater red cell distribution width (RDW) compared to CON across all visits. Serum uric acid was higher in SCT (7.3 ± 1.0 mg/dL) compared to CON (6.1 ± 0.6 mg/dL; p = 0.001). Furthermore, serum creatine kinase levels were greater in SCT (1617.0 ± 1034.8 IU/L) at pre-camp compared to CON (1037.4 ± 602.8 IU/L; p = 0.03). SCT players exhibited lower pre- and post-practice urine electrolytes and urine specific gravity (SCT pre: 1.019 ± 0.005 vs. CON pre: 1.026 ± 0.008 p < 0.001; SCT post: 1.020 ± 0.005 vs. CON post: 1.030 ± 0.008 p < 0.01), whereas sweat sodium concentrations were higher in SCT players (55.4 ± 13.6 mmol/L) compared to CON (45.5 ± 10.6 mmol/L; p < 0.001). Given the evidence, greater uric acid and CPK levels in SCT players compared to CON may be an early indicator of altered kidney function and muscle damage, which could be added into NCAA guidelines for surveillance among SCT players. Consistent education and reinforcement of the importance of adequate fluid balance during exercise are critical for both SCT and CON players.

Free-living, continuous hypo-hydration, and cardiovascular response to exercise in a heated environment.

Chronic dehydration (DEH) and heat stress combined with poor cardiovascular (CV) health may influence physiological responses to exercise. We examined the effects of free-living induced hypo-hydration on physiological responses to exercise in a heated environment and whether resting CV health is related to these changes. Participants (N = 16, 20.6 ± 1.2 years) were randomized to 3 days of voluntary fluid restriction (DEH) or intake (hydration [HYD]) followed by an exercise bout. CV health was assessed by flow-mediated dilation (FMD), pulse wave analysis, and heart rate variability (HRV). HYD was assessed by weight, urine color, and specific gravity (USG). Exercise trials were conducted in a heated environment (30.3 ± 0.8°C, 27.4 ± 7.4% RH) on a cycle ergometer for 30 min. Heart rate (HR), weighted skin (Tsk ) and mean body temperature (Tb ) and skin blood flow (SBF) were assessed during exercise. Pre-exercise weight (P < 0.005), urine color, and USG (P < 0.001) were different in between trials. HR was greater in DEH (153 ± 26 bpm) versus HYD (144 ± 23 bpm, P = 0.02) after exercise. No group differences were found, but a time interaction P < 0.001) for all temperature responses and time-by-trial interaction for Tre (P < 0.01) and Tsk (P < 0.001) was observed. Greater changes in Tre (P = 0.02) and Tsk (P < 0.01) were associated with increased FMD. Free-living, continuous DEH alters weight, blood, and urine markers of HYD as well as HR response during exercise. Resting CV health was related to increased change in Tre and Tsk , suggesting CV health plays a role in the mechanism of heat dissipation when DEH even in college-age men and women.

Melanocortin receptor expression is associated with reduced CRP in response to resistance training.

The existing paradigm of exercise-induced decreases in chronic inflammation focuses on the expression of inflammatory receptors on systemic monocytes in response to exercise training, with the role of anti-inflammatory receptors largely ignored. Our recent preliminary studies indicate that the anti-inflammatory melanocortin receptors (MCRs) may play a role in modulating exercise-induced decreases in chronic inflammation. Here, we present a study designed to determine the effect of intense, resistance exercise training on systemic monocyte MCR expression. Because low-grade chronic inflammation is associated with elevated cardiometabolic risk in healthy populations and exercise decreases chronic inflammation, we investigated the associations between systemic monocyte cell surface expression of MCRs and inflammatory markers as a possible mechanism for the beneficial anti-inflammatory effects of resistance training. To this end, the present study includes 40 adults (aged 19-27 yr) and implements a 12-wk periodized, intensive resistance training intervention. Melanocortin 1 and 3 receptor expression on systemic monocytes and inflammatory markers, including C-reactive protein (CRP), interleukin (IL)-6, IL-1ß, and IL-10, were measured before and after the intervention. Resistance training significantly altered MCR systemic monocyte cell surface expression, had no chronic effects on IL-6, IL-1ß, or IL-10 expression, but significantly decreased CRP levels from a moderate to a low cardiovascular disease risk category. More specifically, decreased melanocortin 3 receptor expression significantly correlated with decreased CRP, independent of changes in adiposity. These data suggest that the observed responses in MCR expression and decreases in cardiovascular disease risk in response to resistance training represent an important anti-inflammatory mechanism in regulating exercise-induced decreases in chronic inflammation that occur independent of chronic changes in systemic cytokines.