The Journal of Physiology publishes 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 on research that has a clinical or translational focus, to help further our understanding of the role physiology plays in health and disease.

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Daily blood flow restriction does not preserve muscle mass and strength during 2 weeks of bed rest

  •  27 February 2024

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Abstract figure legend Two weeks of bed rest lowers skeletal muscle mass and strength. Daily passive blood flow restriction during bed rest does not modulate daily muscle protein synthesis and does not preserve skeletal muscle mass or strength. Created with BioRender.com.

Right ventricular performance during acute hypoxic exercise

  •  26 February 2024

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Abstract figure legend The purpose of this study was to characterize the impact of hypoxia on right ventricular (RV) performance during exercise. Ten healthy individuals underwent invasive cardiopulmonary exercise testing with upright cycle ergometry, under normoxic and hypoxic conditions at a fraction of inspired oxygen ( F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) of 0.12. Participants were randomized to exercise with either a Swan–Ganz catheter (to characterize traditional cardiac and pulmonary haemodynamics) or a conductance catheter (to characterize RV performance by generation of real-time pressure–volume loops). Exercise at an F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$  = 0.12 was associated with a significant reduction in exercise capacity as determined by maximal oxygen uptake and workload on cycle ergometry. Compared to normoxic exercise, hypoxic exercise led to systemic hypoxaemia, increased pulmonary arterial pressures and pulmonary vascular resistance, and ventilatory inefficiency. RV contractility was maintained during submaximal hypoxic exercise. Ventricular–arterial coupling was also preserved.

Open access

Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2

  •  26 February 2024

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Abstract figure legend We aimed to (i) develop a method to prevent hypoxia-induced nocturnal periodic breathing (nPB) via an increased inspiratory CO2 fraction ( F iC O 2 ${{F}_{{\mathrm{iC}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ ) and (ii) use this method to investigate the effects of nPB on sleep architecture at high altitude. Healthy participants susceptible to hypoxia-induced nPB (confirmed during a screening night) underwent two sojourns in a hypobaric chamber simulating 4000 m altitude, one with increased (CO2 sojourn) and one with normal (placebo sojourn) nocturnal F iC O 2 ${{F}_{{\mathrm{iC}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ , and with polysomnography during the first and third night. The increased F iC O 2 ${{F}_{{\mathrm{iC}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ effectively reduced nPB without significantly changing sleep macro-architecture. Created with BioRender.com.

Open access

Conserved mammalian muscle mechanics during eccentric contractions

  •  24 February 2024

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Abstract figure legend The biphasic force response seen during active muscle lengthening is conserved over three orders of magnitude of mammalian skeletal muscle mass. Using mice with a small deletion in titin (mdm), we show that the phase-2 portion (blue) of the biphasic force profile in response to muscle lengthening is reliant on normal titin activation. The rate of force development during muscle stretch may be a more reliable way to describe the forces experienced during eccentric muscle contractions compared to the traditional hyperbolic curve fitting, and functions as a novel predictor of force–velocity characteristics that may be used to better inform musculoskeletal models and assess pathophysiological remodelling.

Death by hypoxia: what were they thinking?

  •  24 February 2024
No abstract is available for this article.
Open access

Role of CFTR in diabetes-induced pancreatic ductal fluid and HCO3 secretion

  •  22 February 2024

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Abstract figure legend Putative mechanism by which diabetes causes increased ductal secretion. The activity of the Cl/HCO3 exchanger is enhanced in diabetes through the overexpression of ductal acid–base transporters, namely, the cystic fibrosis transmembrane conductance regulator (CFTR), the Na+/H+ exchanger-1 (NHE-1), anoctamine-1 (ANO-1) and the aquaporin-1 (AQP-1) water channel. Furthermore, high extracellular glucose directly stimulates NHE-1, which may also contribute to increased secretion. Diabetes also causes the upregulation of secretin receptors (SCTRs) at the mRNA level, but the exact role of secretin in the stimulatory effect of diabetes requires further investigations.

Open access

Neuropilin‐1 regulates renin synthesis in juxtaglomerular cells

  •  21 February 2024

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Abstract figure legend In the present study, we investigated the role of the conserved membrane-bound receptor neuropilin-1 (NRP1) in the development and function of kidney juxtaglomerular (JG) cells. We used a genetic approach to abrogate Nrp1 constitutively in P0-Cre lineage-labelled progenitors and analysed the subsequent changes of renal structures and physiological defects in Nrp1 knockout (Nrp1-ko) mice. Our work identified NRP1 as a key regulator of JG cell development and renin production. Nrp1-ko mutant mice present with renin paucity in JG cells and struggle to adapt to a homeostatic challenge to sodium balance. Our results support the versatility of renin-producing cells in the kidney and may open new avenues for therapeutic approaches.

Open access

Residual force depression is not related to positive muscle fascicle work during submaximal voluntary dorsiflexion contractions in humans

  •  21 February 2024

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Abstract figure legend Accurately predicting muscle force is challenging because active muscle shortening depresses force output. We explored whether the residual force depression (rFD) following active shortening could be predicted by fascicle work. Once the optimal angle of active torque production was determined, we reduced tibialis anterior muscle fascicle shortening during EMG-amplitude-matched contractions through muscle–tendon unit (MTU) lengthening (LEN) over small and medium amplitudes without a preload. We also increased fascicle shortening through MTU LEN with a preload over a large amplitude (not shown), and through MTU shortening (SHO) over small and large amplitudes without (not shown) and with a preload. Relative to fixed-end reference (REF) contractions at similar EMG amplitudes and fascicle lengths, MTU LEN reduced fascicle shortening and enhanced steady-state active dorsiflexion torque. However, increased fascicle shortening during MTU SHO with a preload depressed steady-state output, whereas MTU SHO without a preload did not depress steady-state output relative to REF. Consequently, active fascicle shortening induced rFD, but rFD was not well predicted by fascicle work.

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