Psychological changes in athletes infected with Omicron after return to training: fatigue, sleep, and mood.

Background: This study aims to analyze the changes of approximately 1 month in fatigue, sleep, and mood in athletes after returning to training following infection with the COVID-19 Omicron strain and provide recommendations for returning to training after infection. Methods: Two hundred and thirty professional athletes who had returned to training after being infected with COVID-19 in December 2022 were recruited to participate in three tests conducted from early January 2023. The second test was completed approximately 1 week after the first, and the third was completed about 2 weeks after the second. Each test consisted of completing scales and the exercise-induced fatigue measure. The scales included a visual analog scale, the Athens Insomnia Scale for non-clinical application, and the Depression-Anxiety-Stress scale. The exercise task was a six-minute stair climb test, and athletes evaluated subjective fatigue levels before and after exercise using another Visual Analog Scale and the Karolinska Sleepiness Scale. Results: After returning to training, athletes' physical fatigue decreased initially but increased as training progressed. Cognitive fatigue did not change significantly. The exercise task led to elevated levels of physical fatigue after a longer duration of training. Sleep quality problems decreased rapidly after the start of training but remained stable with prolonged training. Depression levels continued to decline, while anxiety levels only reduced after a longer duration of training. Stress levels decreased rapidly after the start of training but did not change with prolonged training. Conclusion: Athletes who return to training after recovering from COVID-19 experience positive effects on their fatigue, sleep, and mood. It is important to prioritize anxiety assessment and interventions during the short period after returning and to continue monitoring fatigue levels and implementing recovery interventions over a longer period of time.

Differential impact of heat and hypoxia on dynamic oxygen uptake and deoxyhemoglobin parameters during incremental exhaustive exercise.

Purpose: This study aims to explore the relationship between the dynamic changes in oxygen uptake (V˙O2) and deoxyhemoglobin (HHb) and peripheral fatigue in athletes during incremental exhaustive exercise under different environmental conditions, including high temperature and humidity environment, hypoxic environment, and normal conditions. Methods: 12 male modern pentathlon athletes were recruited and performed incremental exhaustive exercise in three different environments: normal condition (23°C, 45%RH, FiO2 = 21.0%, CON), high temperature and humidity environment (35°C, 70%RH, FiO2 = 21.0%, HOT), and hypoxic environment (23°C, 45%RH, FiO2 = 15.6%, HYP). Gas metabolism data of the athletes were collected, and muscle oxygen saturation (SmO2) and total hemoglobin content in the vastus lateralis muscles (VL) were measured to calculate the deoxyhemoglobin content. Linear and nonlinear function models were used to fit the characteristic parameters of V˙O2 and HHb changes. Results: The results showed that compared to the CON, V˙O2, V˙CO2, and exercise time were decreased in the HOT and HYP (p < 0.05). ΔEV˙O2 and OUES were reduced in the HOT and HYP compared to the CON (p < 0.05). The Gas exchange threshold in the CON corresponded to higher V˙O2 than in the HYP and HOT (p < 0.05). ΔEV˙O2-1 was reduced in the HOT compared to the HYP (p < 0.05). ΔEHHb was higher in the HOT compared to the CON (p < 0.05). ΔEHHb-1 was increased in the HYP compared to the CON (p < 0.05). There was a negative correlation between ΔEHHb and corresponding V˙O2⁡max in the HOT (r = -0.655, p < 0.05), and a negative correlation between ΔEHHb-1 and corresponding V˙O2⁡max in the HYP (r = -0.606, p < 0.05). Conclusion: Incremental exhaustive exercise in hypoxic environment and high temperature and humidity environments inhibits gas exchange and oxygen supply to skeletal muscle tissue in athletes. For athletes, the accelerated deoxygenation response of skeletal muscles during incremental exhaustive exercise in high temperature and humidity environments, as well as the excessive deoxygenation response before BP of deoxyhemoglobin in hypoxic environment, may be contributing factors to peripheral fatigue under different environmental conditions.

Anti-Inflammatory Effects of Cajaninstilbene Acid and Its Derivatives.

Cajaninstilbene acid (CSA) is one of the active components isolated from pigeon pea leaves. In this study, anti-inflammatory effects of CSA and its synthesized derivatives were fully valued with regard to their activities on the production of nitric oxide (NO) and pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in vitro cell model, as well as their impacts on the migration of neutrophils and macrophages in fluorescent protein labeled zebrafish larvae model by live image analysis. Furthermore, the anti-inflammatory mechanism of this type of compounds was clarified by western-blot and reverse transcription-polymerase chain reaction (RT-PCR). The results showed that CSA, as well as its synthesized derivatives 5c, 5e and 5h, exhibited strong inhibition activity on the release of NO and inflammatory factor TNF-α and IL-6 in lipopolysaccharides (LPS)-stimulated murine macrophages. CSA and 5c greatly inhibited the migration of neutrophils and macrophages in injury zebrafish larvae. CSA and 5c treatment greatly inhibited the phosphorylation of proteins involved in nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. Moreover, we found that peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662 could reverse partly the roles of CSA and 5c, and CSA and 5c treatment greatly resist the decrease of PPARγ mRNA and protein induced by LPS stimulation. Our results identified the promising anti-inflammatory effects of CSA and its derivatives, which may serve as valuable anti-inflammatory lead compound. Additionally, the mechanism studies demonstrated that the anti-inflammatory activity of CSA and its derivative is associated with the inhibition of NF-κB and MAPK pathways, relying partly on resisting the LPS-induced decrease of PPARγ through improving its expression.

Novel cajaninstilbene acid derivatives as antibacterial agents.

Discovery of novel antibacterial agents with new structural scaffolds that combat drug-resistant pathogens is an urgent task. Cajaninstilbene acid, which is isolated from pigeonpea leaves, has shown antibacterial activity. In this study, a series of cajaninstilbene acid derivatives were designed and synthesized. The antibacterial activities of these compounds against gram-negative and gram-positive bacteria, as well as nine strains of methicillin-resistant staphylococcus aureus (MRSA) bacteria are evaluated，and the related structure-activity relationships are discussed. Assays suggest that some of the synthetic cajaninstilbene acid derivatives exhibit potent antibacterial activity against gram-positive bacterial strains and MRSA. Among these compounds, 5b, 5c, 5j and 5k show better antibacterial activity than the positive control compounds. The results of MTT assays illustrate the low cytotoxicity of the active compounds.

Essential roles of p53 and MAPK cascades in microcystin-LR-induced germline apoptosis in Caenorhabditis elegans.

Hepatotoxin microcystin-LR (MC-LR) can induce apoptosis in a variety of cells. However, the underlying pathways of MC-LR-induced apoptosis have not been well elucidated yet. To find out the roles of underlying pathways in apoptosis signaling in response to MC-LR, germ cell corpses were scored in Caenorhabditis elegans N2 wild type and strains carrying mutated alleles homologous to their mammalian counterparts. We found that exposure to MC-LR at 1.0 µg/L significantly increased germline apoptosis in N2. Germline apoptosis was absent at all doses in ced-3 and ced-4 loss-of-function strains. MC-LR-induced apoptosis was blocked in Bcl-2 gain-of-function strain ced-9(n1950), whereas it showed a slight increase in BH3-only protein EGL-1 mutated strain. The null mutation of cep-1, which is the homologue of p53 tumor suppressor gene, significantly inhibited MC-LR-induced cell death, and checkpoint proteins HUS-1 and CLK-2 exerted proapoptotic effects. Apoptosis in loss-of-function members of ERK, JNK, and p38 MAPK signaling pathways reduced significantly under MC-LR exposure, and members of MAPKK subgroup JKK-1, MEK-1, and SEK-1 worked cooperatively. Our results show that the caspase protein CED-3 and Apaf-1 protein CED-4 were absolutely required for the apoptotic processes, and that the p53/CEP-1 and MAPKs cascades played essential roles in modulating MC-LR-induced germline apoptosis in C. elegans.