Athletes are susceptible to acute respiratory tract infections, including SARS-CoV-2, which can affect cardiovascular function. We aimed to evaluate the impact of COVID-19 infection and quarantine on cardiac function in male and female collegiate athletes. We conducted a single-center, prospective, case-control study and performed transthoracic echocardiography in a diverse group of convalescent SARS-CoV-2-positive athletes following a 10-14-day quarantine, matched to non-SARS-CoV-2 athletes. Data collection occurred from August 1, 2020, to May 31, 2021. We evaluated 61 SARS-CoV-2-positive athletes (20 ± 1 years, 39% female) and 61 controls (age 20 ± 2 years, 39% female). Echocardiography in SARS-CoV-2-positive athletes was performed on average 40 ± 38 days after infection diagnosis. All SARS-CoV-2-positive athletes had clinically normal systolic left ventricular function (LVEF > 50%). However, SARS-CoV-2-positive athletes exhibited mildly lower LVEF compared to controls (65 ± 6% vs. 72 ± 8%, respectively, p < 0.001), which remained significant when evaluated separately for female and male athletes. Sub-analysis revealed these differences occurred only when imaging occurred within a mean average of 27 days of infection, with a longer recovery period (≥27 days) resulting in no differences. SARS-CoV-2-positive male athletes exhibited higher left ventricular end-diastolic volume and mitral filling velocities compared to male controls. Our study reveals unique sex-specific cardiac changes in collegiate athletes following SARS-CoV-2 infection and quarantine compared to controls. Despite a mild reduction in LVEF, which was only observed in the first weeks following infection, no clinically significant cardiac abnormalities were observed. Further research is required to understand if the changes in LVEF are directly attributed to the infection or indirectly through exercise restrictions resulting from quarantine.

Alzheimer’s disease (AD) is the third leading cause of death among older adults with nearly 6 million diagnosed annually. In the race for a cure, one thing is certain—exercise can reduce your risk. However, the mechanisms responsible for this reduced risk are unknown. Several studies have linked exercise to improved memory, reduced amyloid beta plaques, and tau hyperphosphorylation in AD. Background/Objectives: By utilizing a novel rat model of AD, TgF344-AD, we evaluated the time course of behavioral shifts as well as the protective effect of exercise. Methods: TgF344-AD animals (61 total, 31 females and 30 males) were assessed every 3 months from 3 to 12 months of age and then assessments were increased to monthly until they reached 18 months of age. A progressive treadmill protocol was administered at 12 months of age and continued until 18 months. Pre-intervention and post-intervention data were analyzed. Results: Females had greater grip strength relative to body mass compared to males and exercise attenuated the age-related and AD-induced decline. Also, female AD-impaired memory was rescued with exercise, while males had no exercise-induced improvements. Conclusions: There is a sex difference present in the TgF344-AD rat model of Alzheimer’s disease and this should be studied further; in addition, sex differences across all models of AD and the human pathology need to be evaluated. Exercise neuroprotection, while more prominent in females, is an important factor in AD research, and further work to understand the mechanisms of neuroprotection is warranted.

Dehydration in the human body arises due to inadequate replenishment of fluids. An appropriate level of hydration is essential for optimal functioning of the human body, and complications ranging from mild discomfort to, in severe cases, death, could result from a neglected imbalance in fluid levels. Regular and accurate monitoring of hydration status can provide meaningful information for people operating in stressful environmental conditions, such as athletes, military professionals and the elderly. In this study, we propose a non-invasive hydration monitoring technique employing non-ionizing electromagnetic power in the microwave band to estimate the changes in the water content of the whole body. Specifically, we investigate changes in the attenuation coefficient in the frequency range 2–3.5 GHz between a pair of planar antennas positioned across a participant’s arm during various states of hydration. Twenty healthy young adults (10M, 10F) underwent controlled hypohydration and euhydration control bouts. The attenuation coefficient was compared among trials and used to predict changes in body mass. Volunteers lost $1.50\pm 0.44\%$ and $0.49\pm 0.54\%$ body mass during hypohydration and euhydration, respectively. The microwave transmission-based attenuation coefficient (2–3.5 GHz) was accurate in predicting changes in hydration status. The corresponding regression analysis demonstrates that building separate estimation models for dehydration and rehydration phases offer better predictive performance (88%) relative to a common model for both the phases (76%).

Evidence supports that exercise defends against age‐associated declines in brain health and protects against neurodegenerative disease. To help understand the molecular basis for the neuroprotection, we examined the impact of training on mitochondrial protein expression within the exercise–brain axis. Thirty‐two F344 rats (50% male/female) were assigned randomly to 10‐week treadmill training or sedentary groups. Grip strength, Morris water maze and rotarod were used to assess muscular strength, spatial learning and motor coordination, respectively. Jess automated western blotting was used to quantify mitochondrial complex expression in hippocampus and soleus skeletal muscle samples. Values are means and standard deviation. Exercised females had better spatial memory (9.16 ± 8.70 vs. 32.7 ± 22.7 s, P = 0.043) and motor coordination (69.0 ± 16.1 vs. 47.5 ± 15.6 s, P = 0.042) as well as increased soleus mass (0.043 ± 0.003 vs. 0.039 ± 0.002% body mass, P = 0.039), hippocampal mitochondrial complex II expression (1.96 ± 0.38 vs. 1.11 ± 0.33 a.u., P = 0.007), and soleus mitochondrial complex III expression (6.68 ± 1.40 vs. 4.65 ± 1.26 a.u., P = 0.025) in comparison to sedentary females. Cognitive performance and hippocampal metabolic enzyme expression were concordantly increased following the 10‐week exercise intervention in females but not males. These results provide novel support for the putative involvement of cerebral mitochondrial function in the beneficial relationship between exercise and brain health.