Although a state of anemia is perceived to be associated with spaceflight, to date a peripheral blood hematologic assessment of red blood cell (RBC) indices has not been performed during long-duration space missions. This investigation collected whole blood samples from astronauts participating in up to 6-months orbital spaceflight, and returned those samples (ambient storage) to Earth for analysis. As samples were always collected near undock of a returning vehicle, the delay from collection to analysis never exceeded 48 h. As a subset of a larger immunologic investigation, a complete blood count was performed. A parallel stability study of the effect of a 48 h delay on these parameters assisted interpretation of the in-flight data. We report that the RBC and hemoglobin were significantly elevated during flight, both parameters deemed stable through the delay of sample return. Although the stability data showed hematocrit to be mildly elevated at +48 h, there was an in-flight increase in hematocrit that was ~3-fold higher in magnitude than the anticipated increase due to the delay in processing. While susceptible to the possible influence of dehydration or plasma volume alterations, these results suggest astronauts do not develop persistent anemia during spaceflight.

Background: The renal sympathetic nervous system modulates systemic blood pressure, cardiac performance, and renal function. Pathological increases in renal sympathetic nerve activity contribute to the pathogenesis of heart failure with preserved ejection fraction (HFpEF). We investigated the effects of renal sympathetic denervation performed at early or late stages of HFpEF progression. Methods and Results: Male ZSF1 obese rats were subjected to radiofrequency renal denervation (RF‐RDN) or sham procedure at either 8 weeks or 20 weeks of age and assessed for cardiovascular function, exercise capacity, and cardiorenal fibrosis. Renal norepinephrine and renal nerve tyrosine hydroxylase staining were performed to quantify denervation following RF‐RDN. In addition, renal injury, oxidative stress, inflammation, and profibrotic biomarkers were evaluated to determine pathways associated with RDN. RF‐RDN significantly reduced renal norepinephrine and tyrosine hydroxylase content in both study cohorts. RF‐RDN therapy performed at 8 weeks of age attenuated cardiac dysfunction, reduced cardiorenal fibrosis, and improved endothelial‐dependent vascular reactivity. These improvements were associated with reductions in renal injury markers, expression of renal NLR family pyrin domain containing 3/interleukin 1β, and expression of profibrotic mediators. RF‐RDN failed to exert beneficial effects when administered in the 20‐week‐old HFpEF cohort. Conclusions: Our data demonstrate that early RF‐RDN therapy protects against HFpEF disease progression in part due to the attenuation of renal fibrosis and inflammation. In contrast, the renoprotective and left ventricular functional improvements were lost when RF‐RDN was performed in later HFpEF progression. These results suggest that RDN may be a viable treatment option for HFpEF during the early stages of this systemic inflammatory disease.

Background/Objectives: Exertional rhabdomyolysis (ER) is a possibly fatal condition resulting from extreme or novel exercise that causes substantial muscle breakdown. ER has been observed during preseason football; however, prospective research has yet to characterize normal versus ER responses using a repeated measures design. This study characterized ER biomarker responses related to muscle damage, and renal and hepatic stress, after two NCAA Division I preseason football scrimmages. Methods: Following a prospective, repeated measures design, blood and urine samples from 17 players were collected immediately (IPS) and 24 h post-scrimmage (24hPS). A subset (n = 13) provided samples after 48 h of rest as a non-exertion (NE) comparator group. A Comprehensive Metabolic Panel was run on serum samples, and urine samples were analyzed for myoglobin and creatinine. Values were compared with reference ranges, mixed models evaluated time effects, and linear regressions examined associations between CPK and renal and hepatic biomarkers. Results: No participants were diagnosed with ER. A time effect was observed for CPK (p < 0.01), with CPK greater IPS (991.6 ± 560.8 IU/L) compared to NE (267.7 ± 205.3 IU/L), and remaining elevated above reference ranges at 24hPS (739.2 ± 442.6 IU/L). Similar time effects were observed with LDH, AST, and ALT (p < 0.01). Serum creatinine increased above reference values and NE concentrations (p < 0.01). CPK correlated (p < 0.01 for all) with LDH (r = 0.69), serum myoglobin (r = 0.57), creatinine (r = 0.42), AST (r = 0.77), and ALT (r = 0.38). Conclusions: Biomarkers of muscle damage, renal stress, and liver function were higher IPS, with only partial recovery by 24hPS. These findings provide preliminary reference patterns for biomarker fluctuations and support individualized, serial monitoring to identify abnormal responses and promote early detection of ER.