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1.
Int J Exerc Sci ; 15(6): 1457-1471, 2022.
Article in English | MEDLINE | ID: mdl-36619236

ABSTRACT

The purpose of this study was to determine whether changes in collegiate weightlifters' external training load, biochemical markers, and jumping performance correlate to changes in items of the Short Recovery and Stress Scale (SRSS) throughout four microcycles. Twelve well-trained weightlifters (8 males, 4 females; age 24.30 ± 4.36 yr; height 170.28 ± 7.09 cm; body mass 81.73 ± 17.00 kg) with at least one year of competition experience participated in the study. Measurements included hydration, SRSS, biochemical analysis of blood (cortisol [C], creatine kinase [CK]), and unloaded and loaded squat jumps (SJ), and volume-load displacement. Pearson correlation coefficients were calculated between the changes in SRSS items and all other variables. The alpha criterion for all analyses was set at p ≤ 0.05. Negative relationships were observed between changes in SRSS recovery items and C (r = -0.608 to -0.723), and unloaded and loaded SJ height and peak power (r = -0.587 to -0.636). Positive relationships were observed between changes in several SRSS stress items and C (r = 0.609 to 0.723), CK (r = 0.922), and unloaded and loaded SJ height and peak power (r = 0.583 to 0.839). Relationships between changes in some SRSS items and cortisol agree with previous findings highlighting C as an indicator of training stress. Nonetheless, the non-significant relationships between changes in SRSS items, training volume and biochemical markers disagree with previous findings. This may partly be explained by the smaller undulations in training volume in the current study, which were characteristic of typical training. Further, relationships between changes in some SRSS items and jumping performance were opposite of what was expected indicating athletes' perception of their stress and recovery state does not always correspond with their ability to perform.

2.
Cell Host Microbe ; 23(1): 134-143.e6, 2018 Jan 10.
Article in English | MEDLINE | ID: mdl-29290574

ABSTRACT

Leishmania donovani parasites are the cause of visceral leishmaniasis and are transmitted by bites from phlebotomine sand flies. A prominent feature of vector-transmitted Leishmania is the persistence of neutrophils at bite sites, where they protect captured parasites, leading to enhanced disease. Here, we demonstrate that gut microbes from the sand fly are egested into host skin alongside Leishmania parasites. The egested microbes trigger the inflammasome, leading to a rapid production of interleukin-1ß (IL-1ß), which sustains neutrophil infiltration. Reducing midgut microbiota by pretreatment of Leishmania-infected sand flies with antibiotics or neutralizing the effect of IL-1ß in bitten mice abrogates neutrophil recruitment. These early events are associated with impairment of parasite visceralization, indicating that both gut microbiota and IL-1ß are important for the establishment of Leishmania infections. Considering that arthropods harbor a rich microbiota, its potential egestion after bites may be a shared mechanism that contributes to severity of vector-borne disease.


Subject(s)
Gastrointestinal Microbiome/immunology , Inflammasomes/immunology , Interleukin-1beta/immunology , Leishmania donovani/immunology , Leishmaniasis, Visceral/immunology , Leishmaniasis, Visceral/transmission , NLR Family, Pyrin Domain-Containing 3 Protein/immunology , Psychodidae/parasitology , Animals , Antiparasitic Agents/pharmacology , Cricetinae , Female , Insect Bites and Stings/parasitology , Insect Vectors/parasitology , Leishmania donovani/drug effects , Leishmaniasis, Visceral/parasitology , Mice , Mice, Inbred BALB C , Neutrophil Infiltration/drug effects , Neutrophil Infiltration/immunology , Neutrophils/immunology
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