Biology subjects

Hodzic, D.

Publications and source records attributed to Hodzic, D..

3 recordsLinked to original sources

bioRxiv2023

Physiological Profiles of Male and Female CrossFit Athletes

ObjectiveTo 1) establish extensive physiological profiles of highly-trained CrossFit athletes using gold-standard tests and 2) investigate which physiological markers best correlate with CrossFit(R) Open performance. MethodsThis study encompassed sixty participants (30 males and 30 females), all within the top 5% of the CrossFit(R) Open, including 7 CrossFit(R) Semi-finalists and 3 Games finalists. Isokinetic dynamometers were employed to measure maximum isometric and isokinetic leg and trunk strength. Countermovement jump height and maximum isometric mid-thigh pull strength were assessed on a force plate. V{square}O2peak was measured by a cardiopulmonary exercise test, while critical power and W were evaluated during a 3-minute all-out test, both on a cycle ergometer. ResultsMale and female athletes median (IQR) V{square}O2peak was 4.64 (4.43, 4.80) and 3.21 (3.10, 3.29) (L{middle dot}min-1), critical power 314.5 (285.9, 343.6) and 221.3 (200.9, 238.9) (W) and mid-thigh pull 3158 (2690, 3462) and 2035 (1728, 2347) (N). Linear regression analysis shows strong evidence for associations between different anthropometric variables and CrossFit(R) Open performance in men and women, whereas for markers of cardiorespiratory fitness such as V{square}O2peak this was only true for women but not men. Conventional laboratory evaluations of strength, however, manifest minimal evidence for associations with Open performance across both sexes. ConclusionsThis study provides the first detailed insights into the physiology of high-performing CrossFit(R) athletes and informs training optimization. Further the results emphasize the advantage of athletes with shorter limbs and suggests potential modifications to Open workout designs to level the playing field for athletes across different anthropometrics characteristics.

physiology↗

bioRxiv2022

Mouse NEMP1 is required for erythropoiesis, nuclear envelope openings and enucleation of erythroblasts

Nuclear Envelope Membrane Proteins (NEMP) are a conserved family of nuclear envelope proteins that reside within the inner nuclear membrane. Even though Nemp1 knockout (KO) mice are overtly normal, they display a pronounced splenomegaly. This phenotype and recent reports describing a requirement for nuclear envelope openings during erythroblasts terminal maturation led us to examine a potential role for Nemp1 in erythropoiesis. Here, we report that Nemp1 knockout (KO) mice show peripheral blood defects, anemia in neonates, ineffective erythropoiesis, splenomegaly and stress erythropoiesis. The erythroid lineage of Nemp1 KO mice is overrepresented until the pronounced apoptosis of polychromatophilic erythroblasts. We show that NEMP1 localizes to the nuclear envelope of erythroblasts and their progenitors. Mechanistically, we discovered that NEMP1 accumulates into aggregates that localize near or at the edge of nuclear envelope openings and Nemp1 deficiency leads to a marked decrease of both nuclear envelope openings and ensuing enucleation. Together, our results for the first time demonstrate that NEMP1 is essential for nuclear envelope openings and erythropoietic maturation in vivo and provide the first mouse model of defective erythropoiesis directly linked to the loss of an inner nuclear membrane protein.

cell biology↗

bioRxiv2022

Lem2 is essential for cardiac development by maintaining nuclear integrity

Nuclear envelope integrity is essential for compartmentalisation of nucleus and cytoplasm. Importantly, mutations in nuclear envelope-encoding genes are the second-highest cause of familial dilated cardiomyopathy. One such nuclear envelope protein that causes cardiomyopathy in humans and affects mouse heart development is Lem2. However, its role in mechanically active tissue such as heart remains poorly understood. We generated mice in which Lem2 was specifically ablated in cardiomyocytes and carried out detailed physiological, tissue and cellular analyses. Importantly, our data showed that Lem2 was essential for cardiac development, and hearts from Lem2 cKO mice were morphologically and transcriptionally underdeveloped. Lem2 cKO hearts displayed high levels of DNA damage, nuclear rupture, and apoptosis. Crucially, we found that these defects were driven by muscle contraction as they were ameliorated by inhibiting myosin contraction and conversely were exacerbated upon myosin activation. Our data suggest that Lem2 is critical for integrity at the nascent nuclear envelope in fetal hearts, and protects the nucleus from the mechanical forces of muscle contraction. Taken together, these data provide novel insight into mechanisms underlying striated muscle diseases caused by altered nuclear envelope integrity.

cell biology↗