Acute cardiovascular responses to resistance exercise in anabolic steroids users: A preliminary investigation

Objectives: Anabolic steroid (AS) use has increased in recent years, but the cardiovascular consequences for users is not fully understood. Equipment and Methods: Resistance trained males (AS = 7, age = 29 ± 5; NAS = 6, age = 25 ± 1 yrs) undertook a resistance exercise session with echocardiographic measures and cardiac biomarkers taken pre and post exercise (cTnI, NT-proBNP). Results: A significant decrease in early diastolic tissue velocity (E’) (AS = 13 ± 1 vs 11 ± 3, NAS = 13 ± 2 vs12 ± 1 cm.s−1), late diastolic tissue velocity (A’) (AS = 9 ± 2 vs 8 ± 1, NAS = 8 ± 1 vs 8 ± 1 cm.s−1), E’:A’ (AS = 1.63 vs 1.21, NAS = 1.71 vs 1.62) and E:A (AS = 1.61 vs 1.19, NAS = 1.63 vs 1.29) with an increase in late dia < stolic filling velocity (A) (AS = 53 ± 8 vs 65 ± 11, NAS = 51 ± 3 vs 57 ± 9 cm.s−1) were seen in both groups post-exercise. A significant decrease in left ventricular end-systolic volume (LVESV) (AS = 48 ± 16 vs 45 ± 12, NAS = 51 ± 9 vs 43 ± 11 ml) was seen post-exercise with maintenance of ejection fraction (EF). There was a significant group effect on diastolic blood pressure (BP) (AS = 74 ± 11 vs 66 ± 7, NAS = 68 ± 6 vs 58 ± 2 mmHg) and basal systolic rotation rate (AS = −61.69 ± 18.38 vs −86.65 ± 17.99, NAS = −63.69 ± 14.72 vs −56.50 ± 2.15.s−1). Conclusion: Despite significant reductions in diastolic measures, with maintenance of systolic function, there was no altered cardiovascular response in the AS users following resistance exercise. © 2018 Elsevier Masson SA

Pion contamination in the MICE muon beam

The international Muon Ionization Cooling Experiment (MICE) will perform a systematic investigation of ionization cooling with muon beams of momentum between 140 and 240\,MeV/c at the Rutherford Appleton Laboratory ISIS facility. The measurement of ionization cooling in MICE relies on the selection of a pure sample of muons that traverse the experiment. To make this selection, the MICE Muon Beam is designed to deliver a beam of muons with less than $\sim$1\% contamination. To make the final muon selection, MICE employs a particle-identification (PID) system upstream and downstream of the cooling cell. The PID system includes time-of-flight hodoscopes, threshold-Cherenkov counters and calorimetry. The upper limit for the pion contamination measured in this paper is $f_\pi < 1.4\%$ at 90\% C.L., including systematic uncertainties. Therefore, the MICE Muon Beam is able to meet the stringent pion-contamination requirements of the study of ionization cooling.Department of Energy and National Science Foundation (U.S.A.), the Instituto Nazionale di Fisica Nucleare (Italy), the Science and Technology Facilities Council (U.K.), the European Community under the European Commission Framework Programme 7 (AIDA project, grant agreement no. 262025, TIARA project, grant agreement no. 261905, and EuCARD), the Japan Society for the Promotion of Science and the Swiss National Science Foundation, in the framework of the SCOPES programme

Performance of the MICE diagnostic system

Muon beams of low emittance provide the basis for the intense, well-characterised neutrino beams of a neutrino factory and for multi-TeV lepton-antilepton collisions at a muon collider. The international Muon Ionization Cooling Experiment (MICE) has demonstrated the principle of ionization cooling, the technique by which it is proposed to reduce the phase-space volume occupied by the muon beam at such facilities. This paper documents the performance of the detectors used in MICE to measure the muon-beam parameters, and the physical properties of the liquid hydrogen energy absorber during running

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

The endurance athletes heart: acute stress and chronic adaptation

The impact of endurance exercise training on the heart has received significant research and clinical attention for well over a century. Despite this, many issues remain controversial and clinical interpretation can be complex of biomarkers of cardiomyocyte insult. This review assesses the current state of knowledge related to two areas of research where problems with clinical decision making may arise: (1) the impact of chronic endurance exercise training on cardiac structure, function and electrical activity to the point where the athletic heart phenotype may be similar to the expression of some cardiac pathologies (a diagnostic dilemma referred to as the ‘grey-zone’) and (2) the impact of acute bouts of prolonged exercise on cardiac function and the presentation of biomarkers and cardiomyocyte insult in the circulatory system. The combination of acute endurance exercise stress on the heart and prolonged periods of training are considered together in the final section

Conduit diameter and wall remodeling in elite athletes and spinal cord injury.

PURPOSE: This study aimed to investigate localized and systemic effects of chronic exercise and inactivity on conduit artery remodeling in humans. METHODS: We recruited elite athletes engaged in predominantly lower limb (LL runners/cyclists, n = 10) or upper limb (UL canoe paddlers, n = 12) exercise and matched able-bodied, recreationally active, controls (C, n = 16). We also studied wheelchair controls (spinal cord injury, n = 9) and athletes (spinal cord injury, n = 1; spina bifida, n = 4). Carotid, brachial, and superficial femoral (SF) artery diameter and wall thickness were assessed using high-resolution ultrasound. RESULTS: Brachial diameters were significantly larger in UL and wheelchair users (athletes and controls) compared with C (both P < 0.05). SF artery diameter in wheelchair controls was significantly smaller compared with the other groups, with LL athletes having significantly greater lumen diameter than controls (both P < 0.05). In all arteries, a lower wall thickness was found in able-bodied athletes compared with C, including wheelchair athletes compared with wheelchair controls (P < 0.001). In the SF artery, wall-to-lumen-ratio was significantly lower in able-bodied athletes and higher in wheelchair controls compared with able-bodied controls (P < 0.001). In the brachial and carotid arteries, able-bodied and wheelchair athletes demonstrated lower wall-to-lumen-ratio than less active wheelchair controls and able-bodied controls (P < 0.001). CONCLUSIONS: These findings suggest that remodeling of the arterial wall occurs systemically in response to exercise training and is unrelated to exercise type in humans. Conversely, localized effects are evident with respect to the effect of exercise on arterial diameter. These findings have implications for our understanding of the effects of exercise on arterial structure and function in humans