Results 131 to 140 of about 6,676 (255)

Determinants of maximal oxygen uptake in highly trained females and males: a mechanistic study of sex differences using advanced invasive methods

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The results from this study show that maximal cardiac output, stroke volume and leg blood flow are similar between highly trained females and males after normalisation to lean body mass (LBM). However, the 10% higher haemoglobin concentration ([Hb]) and arterial O2 content in males result in higher systemic and leg O2 delivery ...
Øyvind Skattebo   +11 more
wiley   +1 more source

Cardiac Myosin Protein C

open access: yesJACC: Basic to Translational Science, 2017
Robert M. Blanton, MD   +1 more
openaire   +2 more sources

Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The capillary–mitochondria–ion channel (CMIC) axis scales structural resources to match functional workload. (Left) In settings of restricted energetic capacity (e.g. cortical neurons), sparse capillary networks and modest mitochondrial pools set a lower energetic ceiling, sufficient to support phasic, low‐workload excitability. (
L. Fernando Santana, Scott Earley
wiley   +1 more source

NSAID ingestion augments training‐induced muscle hypertrophy and differentially affects muscle mRNA expression, but not strength gains, in trained men

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic outlining the impact of NSAID ingestion on resistance exercise training‐induced changes in muscle morphology, function and gene networks relative to placebo ingestion in trained males. Abstract Non‐steroidal anti‐inflammatory drugs (NSAIDs) are widely overused in sports.
Joanne E. Mallinson   +6 more
wiley   +1 more source

Hypoxia and the cytoskeleton

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic outlining the activation of hypoxia‐sensitive pathways, the influence of hypoxia and associated pathways on the cytoskeleton, and the impact of these on disease progression. Abstract A highly‐regulated and dynamic cytoskeleton is vital for functional cellular physiology and the maintenance of homeostasis.
Darragh Flood, Cormac T. Taylor
wiley   +1 more source

Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend This review utilized animal models of complicated human pregnancies that result in reduced fetal nutrient or oxygen delivery, or combined nutrient and oxygen delivery, to elucidate their independent and/or synergistic contributions to the development of high‐risk cardiac phenotypes.
Melanie R. Bertossa   +8 more
wiley   +1 more source

Demonstration of beat‐to‐beat, on‐demand ATP synthesis in ventricular myocytes reveals sex‐specific mitochondrial and cytosolic dynamics

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Beat‐locked mitochondrial ATP transients reveal modular, sex‐specific bioenergetic control during excitation–contraction coupling. A, each action potential activates L‐type CaV1.2 channels, producing a Ca2+ influx that triggers ryanodine receptors (RyR2) and elicits SR Ca2+ release.
Paula Rhana   +2 more
wiley   +1 more source

Human‐derived cardiac‐neural microtissues reveal catecholaminergic polymorphic ventricular tachycardia is also a disease of the sympathetic neuron

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic diagram illustrating the proposed pathway in which regulatory defects might occur in sympathetic neurons derived from hiPSC in catecholaminergic polymorphic ventricular tachycardia (CPVT). Specifically, enhanced calcium transients appeared to derive from three sources: enhanced membrane excitability (due to loss of ...
Ni Li   +19 more
wiley   +1 more source

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