Journal Overview

The Journal of Physiology publishes original research in all areas of physiology and pathophysiology that illustrates new physiological principles or mechanisms. Papers on work at the molecular level, cell membrane, single cells, tissues or organs and on systems physiology are all encouraged. We are particularly keen to publish papers that have a clinical or translational focus, to help further our understanding of the role physiology plays in health and disease.

Featured in The Journal of Physiology

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Adipose tissue browning and thermogenesis under physiologically energetic challenges: a remodelled thermogenic system

  •  29 November 2023

Graphical Abstract

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Abstract figure legend Physiological energetic challenges including cold stress, exercise and caloric restriction remodel the thermogenic system of the organism, leading to an increased non-shivering thermogenesis in the adipose tissue and a decreased shivering thermogenesis in the skeletal muscle. The remodelled thermogenic system improves the utilization of fatty acids, which both elevates thermogenic endurance and conserves glucose, enabling the organism to maintain body temperature in a more economical and sustainable manner during periods of energy deprivation. Created with BioRender.com.

Loss of mitochondrial Ca2+ uptake protein 3 impairs skeletal muscle calcium handling and exercise capacity

  •  28 November 2023

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Abstract figure legend Role of MICU3 in skeletal muscle physiology. Deletion of MICU3 leads to a decline in exercise capacity in mice, along with an accelerated onset of muscle fatigue. The mitochondria from skeletal muscle lacking MICU3 exhibited lower calcium uptake. Furthermore, skeletal muscle from MICU3-KO mice shows reduced net oxidation of NADH and membrane potential (ΔΨ) during electrically stimulated muscle contraction in comparison to wild-type mice. These findings collectively underscore the important role of MICU3 in regulating mitochondrial calcium uptake, which impacts the synchronization of energy demand and supply in skeletal muscle physiology.

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Efficacy of morning versus afternoon aerobic exercise training on reducing metabolic syndrome components: A randomized controlled trial

  •  28 November 2023

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Abstract figure legend Exercise training can be used as a non-pharmacological treatment to halt, or at least reduce, the progression of the cardiovascular and metabolic derangements that compose the metabolic syndrome. Recent studies using intense interval training have spurred interest in other exercise factors that may increase exercise training effectiveness. For example, the time of day at which training takes place could modulate the health outcome. The present study randomly assigned 175 individuals with metabolic syndrome to train in the morning or afternoon, or to remain untrained. The novel finding was that working out in the morning further improved, systolic blood pressure, insulin resistance and, in general, the metabolic syndrome (i.e. Z score) compared to training in the afternoon. Thus, morning training is somewhat more effective in maximizing health promotion in individuals with metabolic syndrome.

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Simultaneous control of forward and backward locomotion by spinal sensorimotor circuits

  •  28 November 2023

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Abstract figure legend Simultaneous control of forward and backward locomotion by spinal sensorimotor circuits. Sensory feedback from the hindimbs interacts with neuronal circuits of the lumbosacral cord to coordinate the left and right hindlimbs, allowing one hindlimb to step forward while the other steps backward on a split-belt treadmill.

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Everything old is new again

  •  28 November 2023
No abstract is available for this article.

Targeting mitochondrial Ca2+ uptake for the treatment of amyotrophic lateral sclerosis

  •  27 November 2023

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Abstract figure legend Contribution of excessive mitochondrial Ca2+ uptake to amyotrophic lateral sclerosis (ALS) pathology. Left, under physiological condition, mitochondria located in different tissues (from top to bottom: upper motor neuron, astrocytes, lower motor neurons, neuromuscular junction (NMJ) and skeletal muscle) take up Ca2+ during neuronal and muscle activity and produce ATP through oxidative phosphorylation to support physiological activities of the cells. Right, under diseased condition, mitochondria in the same tissues take up excessive amount of Ca2+ during neuronal and muscle activity, which triggers the opening of the mitochondrial membrane permeability transition pore, mitochondrial membrane depolarization, mitochondrial swelling and increased reactive oxygen species generation; Ca2+-induced mitochondrial dysfunction then results, consequently leading to decreased ATP production and energy stress. Swollen mitochondria undergo apoptosis and eventually cell death occurs. The two curved arrows pointing to the NMJ indicate that the initial NMJ destruction in ALS likely results from the insult from both motor neurons (orthograde signalling) and skeletal muscle (retrograde signalling). (The figure was created with BioRender.com.)

Interstitial cells of Cajal – pacemakers of the gastrointestinal tract

  •  23 November 2023

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Abstract figure legend Electrical slow waves recorded directly from ICC-MY of the Guinea pig gastric antrum. A, interval between slow waves: small amplitude spontaneous transient depolarizations (STDs) summate to generate upstroke. B, upstroke phase: activation of voltage-dependent Ca2+ conductance and Ca2+ entry. C, plateau phase: Ca2+ entry initiates Ca2+-induced Ca2+ release and activation of Ca2+-activated Cl conductance (ANO1 or a Ca2+-dependent non-selective cation conductance). D, repolarization: when Ca2+ release from ER is exhausted, ANO1 is deactivated and cells repolarize to the inter-slow wave potential.

Open access

Reduced in utero substrate supply decreases mitochondrial abundance and alters the expression of metabolic signalling molecules in the fetal sheep heart

  •  23 November 2023

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Abstract Figure legend Fetal growth restriction (FGR) results in altered cardiac metabolism in the late gestation fetus. This includes reduced glucose and fatty acid transporter expression, which has downstream effects on molecular markers of metabolism, including lower abundance of mitochondria and complexes II and IV of the electron transport chain (ETC).

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