Exercise has long been considered crucial for improving cardiometabolic health. However, recent research also highlights the benefits of exercise on improving immune function in adults of all ages (Duggal et al., 2019). Given the immune system's complexity, the mechanisms linking regular exercise to enhanced immune function are likely multi-dimensional. Cross-sectional studies have shown that individuals who participate in lifelong physical
Circulating immune cell numbers and phenotypes are impacted by high-intensity acute bouts of exercise and infection history with the latent herpesviruses cytomegalovirus (CMV). In particular, CMV infection history impairs the exercise-induced mobilization of cytotoxic innate lymphoid cells 1 (ILC1) cells, also known as NK cells, in the blood. However, it remains unknown whether exercise and CMV infection modulate the mobilization of traditionally tissue-resident non-cytotoxic ILCs into the peripheral blood compartment. To address this question, 22 healthy individuals with or without CMV (20–35 years—45% CMVpos) completed 30 min of cycling at 70% VO2 max, and detailed phenotypic analysis of circulating ILCs was performed at rest and immediately post-exercise. We show for the first time that a bout of high-intensity exercise is associated with an influx of ILCs that are traditionally regarded as tissue-resident. In addition, this is the first study to highlight that latent CMV infection blunts the exercise-response of total ILCs and progenitor ILCs (ILCPs). These promising data suggest that acute exercise facilitates the circulation of certain ILC subsets, further advocating for the improvements in health seen with exercise by enhancing cellular mobilization and immunosurveillance, while also highlighting the indirect deleterious effects of CMV infection in healthy adults.
Low energy availability (LEA) is defined as a mismatch between an individual's energy intake (EI) and energy expenditure (EE) in exercise, leaving insufficient energy to support normal physiological function and maintain metabolic homeostasis. Periods of LEA are common amongst endurance athletes and may occur due to increased EE, reduced EI, or both. While chronic exposure to LEA is associated with negative health outcomes, to date the effects of acute LEA on parameters of endurance performance have not been characterized. PURPOSE: to determine if short-term LEA exposure negatively impacts factors contributing to endurance performance. METHODS: elite race walkers (n=21, 18 male, 3 female; VO 2peak 63 ± 5 mL/min/kg) underwent a 4-stage exercise economy test and competed in a 10,000 m race prior to and following 8-d of a high energy (HEA; ~ 40 kcal/kg fat free mass (FFM); n=11) or LEA (15 kcal/kg FFM, n=10) diet during a 4-week intensified training camp. DXA and resting metabolic rate were measured to calculate energy availability, while a subset of participants also had DXA measured post intervention to assess changes in body composition. RESULTS: fat oxidation rates during the economy test increased across the training camp (n=21; p<0.001), with a reciprocal decrease in carbohydrate (CHO) oxidation (p<0.001), however there were no differences between dietary treatments. The oxygen cost of exercise (relative VO 2 , mL/min/kg) decreased across all 4 stages in both groups (p<0.001), indicating an increase in exercise economy, while there was no change in VO 2max . Athletes in the LEA intervention (n=7) displayed a decrease in body mass (68.1 ± 6.4 vs. 66.6 ± 6.3 kg, p<0.05) and fat mass (9.0 ± 2.7 vs. 7.9 ± 2.6 kg, p<0.05), but maintained total FFM. Athletes in the HEA group (n=5) displayed no changes in body mass or composition. Race performance was improved in both groups (LEA; 3 ± 2%, HEA 4 ± 2%, p<0.001) with no difference between dietary treatments. CONCLUSION: long-term performance preparation involves integration of strategies to alternatively manage training support, physique management and fuel availability. Acute 8-d exposure to LEA resulted in a decrease in total body and fat mass, but reduced training quality. However, with acute replenishment of CHO availability, there was no short-term impairment in race performance.
METHODS: Female Sprague-Dawley rats (n=52; 4-mo-old) were singly housed and randomly assigned to placebo (PL) and LARC groups, via an implanted slow-release etonogestrel pellet (0.00ug/d vs. 0.30ug/d). A week later, animals were further randomized to weight bearing (WB) and HU groups for 6 weeks. At the end of the 6-week HU period animals were euthanized. Tissues collected and snap frozen for later analysis. Western blot analysis was run to quantify markers of mitophagy (Parkin, NIX) as well as glycolytic enzymes (GAPDH). Signal values were normalized against the loading control for each gel. Statistics were conducted using RStudio. RESULTS: Despite increasing their food intake during HU (p<0.01), HU animals lost weight and weighed less than WB animals starting on HU week 2 (p<0.01). Weight wet of the gastrocnemius was significantly different after HU (WB: 2.07g +/-0.08 vs HU: 1.58g +/-0.11). A significant difference was observed between the WB and HU groups for both Parkin (1.01 +/-0.33 vs 0.74 +/-.25, p=.006) and NIX (1.10 +/-0.38 vs 0.82 +/-0.43, p=.040), respectively. No significant difference was found in GAPDH. LARC had no effect on mitophagy or glycolytic enzyme content. There was no significant interaction between HU and LARC on mitophagy or glycolytic markers. CONCLUSION: After 6-weeks of unloading, markers of mitophagy were significantly decreased. This could be due to either impairments in the mitophagy process or reduced enzyme content due to reduced muscle fiber size as indicated by reduced muscle weight after HU. LARC implantation did not alter the impact of HU on mitophagy markers. Further analysis into mitochondrial protein content as well as respiratory capacity will provide insight into mitochondrial health and function.
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