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Glucose phosphorylation by hexokinase (HK) is a rate-limiting step in glucose metabolism. Regulation of HK includes feedback inhibition by its product glucose-6-phosphate (G6P) and mitochondria binding. HK affinity for G6P is difficult to measure because its natural product (G6P) inhibits enzyme activity. HK phosphorylates several hexoses, and we have taken advantage of the fact that 2-deoxyglucose (2-DG)-6-phosphate does not inhibit HK activity. By this, we have developed a new method for rapid radiochemical analysis of HK activity with 2-DG as a substrate, which allows control of the concentrations of G6P to investigate HK affinity for inhibition by G6P. We verified that 2-DG serves as a substrate for the HK reaction with linear time and concentration dependency as well as expected maximal velocity and KM. This is the first simple assay that evaluates feedback inhibition of HK by its product G6P and provides a unique technique for future research evaluating the regulation of glucose phosphorylation under various physiological conditions. NEW & NOTEWORTHY Traditionally, hexokinase activity has been analyzed spectrophotometrically in which the product formation of glucose-6-phosphate (G6P) is analyzed by an indirect reaction coupled to NADPH formation during conversion of G6P to 6-P gluconolactone. By nature, this assay prevents measurements of hexokinase (HK) affinity for inhibition by G6P. We have developed a rapid radiochemical filter paper assay to study HK affinity for G6P by use of radiolabeled 2-deoxyglucose as substrate to study physiological regulation of HK affinity for G6P-induced inhibition. [ABSTRACT FROM AUTHOR]

This review follows two previous papers [Farina et al. Appl Physiol (1985) 96: 1486–1495, 2004; Farina et al. J Appl Physiol (1985) 117: 1215–1230, 2014] in which we reflected on the use of surface electromyography (EMG) in the study of the neural control of movement. This series of papers began with an analysis of the indirect approaches of EMG processing to infer the neural control strategies and then closely followed the progress in EMG technology. In this third paper, we focus on three main areas: surface EMG modeling; surface EMG processing, with an emphasis on decomposition; and interfacing applications of surface EMG recordings. We highlight the latest advances in EMG models that allow fast generation of simulated signals from realistic volume conductors, with applications ranging from validation of algorithms to identification of nonmeasurable parameters by inverse modeling. Surface EMG decomposition is currently an established state-of-the-art tool for physiological investigations of motor units. It is now possible to identify large samples of motor units, to track motor units over multiple sessions, to partially compensate for the nonstationarities in dynamic contractions, and to decompose signals in real time. The latter achievement has facilitated advances in myocontrol, by using the online decoded neural drive as a control signal, such as in the interfacing of prostheses. Looking back over the 20 yr since our first review, we conclude that the recording and analysis of surface EMG signals have seen breakthrough advances in this period. Although challenges in its application and interpretation remain, surface EMG is now a solid and unique tool for the study of the neural control of movement. [ABSTRACT FROM AUTHOR]

In 2005 the scientific misconduct case of a noted researcher concluded with, among other things, the retraction of 10 papers. However, these articles continue to be cited at relatively high rates. The objectives of this paper are: 1) to track the retraction process of these papers, 2) to assess the impact of retraction on subsequent citation rates of these papers, and 3) to compare the citation history of these retracted articles and five other high-profile retraction cases. For objective 1, all five articles to be retracted were retracted and of the four to be corrected, two were retracted and two were corrected. Eight PubMed and journal sites were identified where retraction messages could be conveyed; the number of retraction messages averaged 3.4 ± 2.5 for these nine articles. For objective 2, an absolute “cleansing” did not occur. While it initially appears there was a relative “cleansing,” as citation rates for these articles did decrease after retraction, the reductions in citation rates for these articles (−28%) were the same as those for matched nonretracted publications both by the same author (−28%) and by another investigator (−29%) over the same time frame. Relative to objective 3, the results for this case are quite different from the five other cases assessing this issue, perhaps because of this investigator’s “citation inertia” as a result of the small percentage of his papers that were retracted and the large number of citations to the articles before their retraction and to all of his published articles. NEW & NOTEWORTHY The scientific misconduct and fraud case of a noted exercise physiology researcher was concluded ~15 yr ago, and one the of the results was the retraction of 10 published manuscripts. However, based on a number of comparisons to that same author's and another investigator's citation histories for similar articles, the citation histories for these retracted articles appear to not have been affected whatsoever in the subsequent 15 yr. [ABSTRACT FROM AUTHOR]

Breathing effort is important to quantify to understand mechanisms underlying central and obstructive sleep apnea, respiratory-related arousals, and the timing and effectiveness of invasive or noninvasive mechanically assisted ventilation. Current quantitative methods to evaluate breathing effort rely on inspiratory esophageal or epiglottic pressure swings or changes in diaphragm electromyographic (EMG) activity, where units are problematic to interpret and compare between individuals and to measured ventilation. This paper derives a novel method to quantify breathing effort in units directly comparable with measured ventilation by applying respiratory mechanics first principles to convert continuous transpulmonary pressure measurements into "attempted" airflow expected to have arisen without upper airway obstruction. The method was evaluated using data from 11 subjects undergoing overnight polysomnography, including six patients with obesity with severe obstructive sleep apnea (OSA), including one who also had frequent central events, and five healthy-weight controls. Classic respiratory mechanics showed excellent fits of airflow and volume to transpulmonary pressures during wake periods of stable unobstructed breathing (means ± SD, r2 = 0.94 ± 0.03), with significantly higher respiratory system resistance in patients compared with healthy controls (11.2 ± 3.3 vs. 7.1 ± 1.9 cmH2O·L−1·s, P = 0.032). Subsequent estimates of attempted airflow from transpulmonary pressure changes clearly highlighted periods of acute and prolonged upper airway obstruction, including within the first few breaths following sleep onset in patients with OSA. This novel technique provides unique quantitative insights into the complex and dynamically changing interrelationships between breathing effort and achieved airflow during periods of obstructed breathing in sleep. NEW & NOTEWORTHY: Ineffective breathing efforts with snoring and obstructive sleep apnea (OSA) are challenging to quantify. Measurements of esophageal or epiglottic pressure swings and diaphragm electromyography are useful, but units are problematic to interpret and compare between individuals and to measured ventilation. This paper derives a novel method that uses esophageal pressure and respiratory mechanics first principles to quantify breathing effort as "attempted" flow and volume in units directly comparable with measured airflow, volume, and ventilation. [ABSTRACT FROM AUTHOR]

Research on world-class athletes in endurance events, such as cycling Grand Tours, has reported extreme levels of total energy expenditure. However, it has been argued that over extended periods, such as months, sustained energy expenditure is capped at approximately 2.5 times the basal metabolic rate. Triathlon is particularly notable for its high energetic demands due to its multimodal nature, requiring athletes to maintain high training volumes. In this case study, we analyzed the total energy expenditure of world-class triathlete Kristian Blummenfelt using doubly labeled water over two specific periods, along with 3 yr of training data. Total energy expenditure ranged from 7,019 to 8,506 kcal/day. Reported energy intake ranged from 4,899 to 6,360 kcal/day. The annual training volumes for the years 2020–2022 were 1,480, 1,350, and 1,308 h, respectively, following a pyramidal intensity distribution. Approximately 53% of the entire three-year period matched with the doubly labeled water measurement periods in terms of training volume, indicating that the recorded total energy expenditure is representative of the majority of the observed data. Hence, the greater part of the 3-yr period likely exceeds the proposed metabolic ceiling for sustained total energy expenditure. This not only questions the validity of the current metabolic limits but also suggests a new perspective on what is physiologically achievable in world-class athletes. NEW & NOTEWORTHY: The current paper presents unprecedented data on the training volume and intensity distribution of a world-class triathlete. Furthermore, using doubly labeled water measurements and training data, we argue that our findings challenge the proposed alimentary limit for sustained energy expenditure, thereby raising the upper boundary of what is physiologically possible in humans. [ABSTRACT FROM AUTHOR]

The intrinsic force production capability of human muscle can be expressed as "Specific Tension," or, the maximum force generated per cross-sectional area of muscle fibers. This value can be used to determine, for example, whether muscle quality changes during exercise, atrophy, disease, or hypertrophy. A value of 22.5 N/cm2 for mammalian muscle has generally become accepted based on detailed studies of small mammals. Determining the specific tension of human muscle is much more challenging as almost all determinations are indirect. Calculation of human muscle specific tension requires an understanding of that muscle's contribution to joint torque, its activation magnitude, tendon compliance, and joint moment arm. Determining any of these parameters is technically challenging in humans and thus, it is no surprise that human specific tension values reported vary from 2 to 73 N/cm2. In this systematic review, we screened 1,506 published papers and identified the 30 studies published between 1983 and 2023 that used appropriate methods and which reported 96 human specific tension values. We weighted each parameter based on whether it was directly measured, estimated, or calculated based on the literature, with decreasing weighting used, the more indirect the methods. Based on this exhaustive review of the relevant human literature, we suggest that the most accurate value that should be used for human muscle specific tension is 26.8 N/cm2. [ABSTRACT FROM AUTHOR]

Focuses on issues related to the American Physiological Society (APS) Legacy Project. Conception of an initiative to increase awareness and access to seminal papers in physiology; Contemplation of all the APS journals into a searchable PDF format; Decision to highlight seminal papers published in the APS research journals.

When contracting muscles are freely perfused, the acid-sensing ion channel 3 (ASIC3) on group IV afferents plays a minor role in evoking the exercise pressor reflex. We recently showed in isolated dorsal root ganglion neurons innervating the gastrocnemius muscles that two mu opioid receptor agonists, namely endomorphin 2 and oxycodone, potentiated the sustained inward ASIC3 current evoked by acidic solutions. This in vitro finding prompted us to determine whether endomorphin 2 and oxycodone, when infused into the arterial supply of freely perfused contracting hindlimb muscles, potentiated the exercise pressor reflex. We found that infusion of endomorphin 2 and naloxone in decerebrated rats potentiated the pressor responses to contraction of the triceps surae muscles. The endomorphin 2-induced potentiation of the pressor responses to contraction was prevented by infusion of APETx2, an ASIC3 antagonist. Specifically, the peak pressor response to contraction averaged 19.3 ± 5.6 mmHg for control (n = 10), 27.2 ± 8.1 mmHg after naloxone and endomorphin 2 infusion (n = 10), and 20 ± 8 mmHg after APETx2 and endomorphin 2 infusion (n = 10). Infusion of endomorphin 2 and naloxone did not potentiate the pressor responses to contraction in ASIC3 knockout rats (n = 6). Partly similar findings were observed when oxycodone was substituted for endomorphin 2. Oxycodone infusion significantly increased the exercise pressor reflex over its control level, but subsequent APETx2 infusion failed to restore the increase to its control level (n = 9). The peak pressor response averaged 23.1 ± 8.6 mmHg for control (n = 9), 33.2 ± 11 mmHg after naloxone and oxycodone were infused (n = 9), and 27 ± 8.6 mmHg after APETx2 and oxycodone were infused (n = 9). Our data suggest that after opioid receptor blockade, ASIC3 stimulation by the endogenous mu opioid, endomorphin 2, potentiated the exercise pressor reflex. NEW & NOTEWORTHY: This paper provides the first in vivo evidence that endomorphin 2, an endogenous opioid peptide, can paradoxically increase the magnitude of the exercise pressor reflex by an ASIC3-dependent mechanism even when the contracting muscles are freely perfused. [ABSTRACT FROM AUTHOR]

It is commonly assumed that changes in plasma strong ion difference (SID) result in equal changes in whole blood base excess (BE). However, at varying pH, albumin ionic-binding and transerythrocyte shifts alter the SID of plasma without affecting that of whole blood (SIDwb), i.e., the BE. We hypothesize that, during acidosis, 1) an expected plasma SID (SIDexp) reflecting electrolytes redistribution can be predicted from albumin and hemoglobin's charges, and 2) only deviations in SID from SIDexp reflect changes in SIDwb, and therefore, BE. We equilibrated whole blood of 18 healthy subjects (albumin = 4.8 ± 0.2 g/dL, hemoglobin = 14.2 ± 0.9 g/dL), 18 septic patients with hypoalbuminemia and anemia (albumin = 3.1 ± 0.5 g/dL, hemoglobin = 10.4 ± 0.8 g/dL), and 10 healthy subjects after in vitro-induced isolated anemia (albumin = 5.0 ± 0.2 g/dL, hemoglobin = 7.0 ± 0.9 g/dL) with varying CO2 concentrations (2–20%). Plasma SID increased by 12.7 ± 2.1, 9.3 ± 1.7, and 7.8 ± 1.6 mEq/L, respectively (P < 0.01) and its agreement (bias[limits of agreement]) with SIDexp was strong: 0.5[−1.9; 2.8], 0.9[−0.9; 2.6], and 0.3[−1.4; 2.1] mEq/L, respectively. Separately, we added 7.5 or 15 mEq/L of lactic or hydrochloric acid to whole blood of 10 healthy subjects obtaining BE of −6.6 ± 1.7, −13.4 ± 2.2, −6.8 ± 1.8, and −13.6 ± 2.1 mEq/L, respectively. The agreement between ΔBE and ΔSID was weak (2.6[−1.1; 6.3] mEq/L), worsening with varying CO2 (2–20%): 6.3[−2.7; 15.2] mEq/L. Conversely, ΔSIDwb (the deviation of SID from SIDexp) agreed strongly with ΔBE at both constant and varying CO2: −0.1[−2.0; 1.7], and −0.5[−2.4; 1.5] mEq/L, respectively. We conclude that BE reflects only changes in plasma SID that are not expected from electrolytes redistribution, the latter being predictable from albumin and hemoglobin's charges. NEW & NOTEWORTHY: This paper challenges the assumed equivalence between changes in plasma strong ion difference (SID) and whole blood base excess (BE) during in vitro acidosis. We highlight that redistribution of strong ions, in the form of albumin ionic-binding and transerythrocyte shifts, alters SID without affecting BE. We demonstrate that these expected SID alterations are predictable from albumin and hemoglobin's charges, or from the noncarbonic whole blood buffer value, allowing a better interpretation of SID and BE during in vitro acidosis. [ABSTRACT FROM AUTHOR]

Skeletal muscle is a highly complex tissue that is studied by scientists from a wide spectrum of disciplines, including motor control, biomechanics, exercise science, physiology, cell biology, genetics, regenerative medicine, orthopedics, and engineering. Although this diversity in perspectives has led to many important discoveries, historically, there has been limited overlap in discussions across fields. This has led to misconceptions and oversimplifications about muscle biology that can create confusion and potentially slow scientific progress across fields. The purpose of this synthesis paper is to bring together research perspectives across multiple muscle fields to identify common assumptions related to muscle fiber type that are points of concern to clarify. These assumptions include 1) classification by myosin isoform and fiber oxidative capacity is equivalent, 2) fiber cross-sectional area (CSA) is a surrogate marker for myosin isoform or oxidative capacity, and 3) muscle force-generating capacity can be inferred from myosin isoform. We address these three fiber-type traps and provide some context for how these misunderstandings can and do impact experimental design, computational modeling, and interpretations of findings, from the perspective of a range of fields. We stress the dangers of generalizing findings about "muscle fiber types" among muscles or across species or sex, and we note the importance for precise use of common terminology across the muscle fields. [ABSTRACT FROM AUTHOR]

Emphysema is one of the pathological hallmarks of chronic obstructive pulmonary disease. We have recently reported that radiofrequency therapy improves lung function in rodent models of emphysema. However, preclinical data using large animals is necessary for clinical translation. Here, we describe the work performed to establish a unilateral porcine emphysema model. Different doses of porcine pancreatic elastase (PPE) were instilled into the left lung of 10 Yucatan pigs. Three additional pigs were used as controls. Six weeks after instillation, lungs were harvested. Lung compliance was measured by a water displacement method and plethysmography. Systematic uniform random sampling of the left and right lungs was performed independently to measure alveolar surface area using micro-computed tomography (micro-CT) and histology. In pigs instilled with 725-750 U/kg of PPE (PPE group, n = 6), the compliance of the left lung was significantly higher by 37.6% than that of the right lung (P = 0.03) using the water displacement method. With plethysmography, the volume of the left lung was significantly larger than that of the right lung at 3, 5, and 10 cmH2O. Measurements from either micro-CT or histology images showed a significant decrease in alveolar surface area by 14.2% or 14.5% (P = 0.031) in the left lung compared with the right lung of the PPE group. A unilateral model for mild emphysema in Yucatan pigs has been established, which can now be used for evaluating novel therapeutics and interventional strategies. NEW & NOTEWORTHY For clinical translation, preclinical data using large animal models is necessary. However, papers describing an emphysema model in pigs, which are anatomically and physiologically similar to humans, are lacking. Here, we report success in creating a unilateral mild-emphysema model in pigs with only one single dose of porcine pancreatic elastase. This model will be useful in bringing novel technologies and therapies from small animals to humans with emphysema. [ABSTRACT FROM AUTHOR]

Research to date provides equivocal evidence regarding the influence of heat stress, heat strain, and more specifically, elevated exercise-induced core temperature on cognitive performance. This review sought to identify differences in how specific cognitive tasks were affected by increases in core body temperatures. Included papers (n = 31) measured cognitive performance and core temperature during exercise, while experiencing heightened thermal stress. Cognitive tasks were classified as cognitive inhibition, working memory, or cognitive flexibility tasks. Independently, core temperature changes were not sufficient predictors of cognitive performance. However, reaction time, memory recall, and Stroop tasks appeared to be most effective at identifying cognitive changes during heightened thermal strain. Alterations in performance were more likely to arise under increased thermal loads, which were typically associated with cumulative physiological stressors, such as elevated core temperatures, occurring alongside dehydration, and prolonged exercise durations. Future experimental designs should consider the relevance, or futility of assessing cognitive performance in activities that do not elicit a considerable degree of heat strain, or physiological load. [ABSTRACT FROM AUTHOR]

Circulatory shock is the inadequacy to supply mitochondria with enough oxygen to sustain aerobic energy metabolism. A novel noninvasive bedside measurement was recently introduced to monitor the mitochondrial oxygen tension in the skin (mitoP o2). As the most downstream marker of oxygen balance in the skin, mitoPo2 may provide additional information to improve shock management. However, a physiological basis for the interpretation of mitoPo2 values has not been established yet. In this paper, we developed a mathematical model of skin mitoPo2 using a network of parallel microvessels, based on Krogh's cylinder model. The model contains skin blood flow velocity, heterogeneity of blood flow, hematocrit, arteriolar oxygen saturation, and mitochondrial oxygen consumption as major variables. The major results of the model show that normal physiological mitoPo2 is in the range of 40-60 mmHg. The relationship of mitoPo2 with skin blood flow velocity follows a logarithmic growth curve, reaching a plateau at high skin blood flow velocity, suggesting that oxygen balance remains stable while peripheral perfusion declines. The model shows that a critical range exists where mitoPo2 rapidly deteriorates if skin perfusion further decreases. The model intuitively shows how tissue hypoxia could occur in the setting of septic shock, due to the profound impact of microcirculatory disturbance on mitoPo2, even at sustained cardiac output. MitoPo2 is the result of a complex interaction between all factors of oxygen delivery and microcirculation. This mathematical framework can be used to interpret mitoPo2 values in shock, with the potential to enhance personalized clinical trial design. [ABSTRACT FROM AUTHOR]

Postactivation potentiation refers to an acute enhancement of contractile properties following muscle activity. Previously, the effects of prior muscle activation on eccentric force at tetanic activation frequencies have only been sparsely reported. This paper aimed to study acute activity-induced effects on eccentric force of slow and fast-twitch muscles and characterize them in relation to postactivation potentiation. We elicited eccentric contractions in isolated rat extensor digitorum longus and soleus muscles by actively lengthening muscles at a constant velocity. We assessed contractile properties by measuring force over shortly interspaced, identical eccentric, and isometric contractions. We then analyzed stretch force, isometric peak force, rate of force development, and relaxation times. Finally, we compared the time courses for the development and cessation of changes in stretch force to known features of postactivation potentiation. In extensor digitorum longus, muscles stretch force consistently increased in a contraction-to-contraction manner by up to 49% [95% confidence interval (CI): 35-64%] whereas isometric peak force simultaneously showed minor declines (8%, 95% CI: 5-10%). The development and cessation of eccentric force potentiation coincided with the development of twitch potentiation and increases in rate of force development. In soleus muscles we found no consistent eccentric potentiation. Characterization of the increase in eccentric force revealed that force only increased in the very beginning of an active stretch. Eccentric force at tetanic activation frequencies potentiates substantially in extensor digitorum longus muscles over consecutive contractions with a time course coinciding with postactivation potentiation. Such eccentric potentiation may be important in sport performance. NEW & NOTEWORTHY Force during eccentric contractions can increase to a magnitude that may have profound consequences for our understanding of skeletal muscle locomotion. This increase in eccentric force occurs over consecutive, shortly interspaced, tetanic contractions in rat extensor digitorum longus muscles--not in rat soleus muscles--and coincides with well-known traits of postactivation potentiation. Eccentric force potentiation may significantly enhance muscle performance in activities involving stretch-shortening cycles. [ABSTRACT FROM AUTHOR]

The article focuses on the assessment of peripheral hypercapnic chemosensitivity (PHC) during different exercise intensities. Topics include the evaluation of PHC responses at rest, during low and high-intensity exercise, and post-exercise, the lack of significant variation in PHC across these conditions, and the relationship between end-tidal PCO2 and PHC at high exercise intensity.

John O. Holloszy, as perhaps the world's preeminent exercise biochemist/physiologist, published >400 papers over his 50+ year career, and they have been cited >41,000 times. In 1965 Holloszy showed for the first time that exercise training in rodents resulted in a doubling of skeletal muscle mitochondria, ushering in a very active era of skeletal muscle plasticity research. He subsequently went on to describe the consequences of and the mechanisms underlying these adaptations. Holloszy was first to show that muscle contractions increase muscle glucose transport independent of insulin, and he studied the mechanisms underlying this response throughout his career. He published important papers assessing the impact of training on glucose and insulin metabolism in healthy and diseased humans. Holloszy was at the forefront of rodent studies of caloric restriction and longevity in the 1980s, following these studies with important cross-sectional and longitudinal caloric restriction studies in humans. Holloszy was influential in the discipline of cardiovascular physiology, showing that older healthy and diseased populations could still elicit beneficial cardiovascular adaptations with exercise training. Holloszy and his group made important contributions to exercise physiology on the effects of training on numerous metabolic, hormonal, and cardiovascular adaptations. Holloszy's outstanding productivity was made possible by his mentoring of ~100 postdoctoral fellows and substantial NIH grant funding over his entire career. Many of these fellows have also played critical roles in the exercise physiology/biochemistry discipline. Thus it is clear that exercise biochemistry and physiology will be influenced by John Holloszy for numerous years to come. [ABSTRACT FROM AUTHOR]

Historical aspects of respiratory reflexes from the lungs and airways are reviewed, up until about 10 yr ago. For most of the 19th century, the possible reflex inputs into the ‘respiratory center,’ the position of which had been identified, were very speculative. There was little concept of reflex control of the pattern of breathing. Then, in 1868, Breuer published his paper on ‘The self-steering of respiration via the Nervus Vagus.’ For the first time this established the role of vagal inflation and deflation reflexes in determining the pattern of breathing. Head later extended Breuer's work, and Kratschmer laid a similar basis for reflexes from the nose and larynx. Then, 50–60 yr later, the development of the thermionic valve and the oscilloscope allowed recording action potentials from single nerve fibers in the vagus. In 1933, Adrian showed that slowly adapting pulmonary stretch receptors were responsible for the inflation reflex. Later, Knowlton and Larrabee described rapidly adapting receptors and showed that they mediated deep augmented breaths and the deflation reflex. Still later, it was established that rapidly adapting receptors were, at least in part, responsible for cough. In 1954, Paintal began his study of C-fiber receptors (J receptors), work greatly extended by the Coleridges. Since ∼10 yr ago, when the field of this review stops, there has been an explosion of research on lung and airway receptors, many aspects of which are dealt with in other papers in this series. [ABSTRACT FROM AUTHOR]

The article discusses the implications of rethinking force steadiness, particularly focusing on the metric of yank magnitude as a more accurate indicator of force unsteadiness compared to coefficient variation of force (CVF). It addresses the need for normalization of yank magnitude and compares the effectiveness of yank and CVF in predicting movement instability, advocating for further research in this area.

Cross talk is an important source of error in interpreting surface electromyography (EMG) signals. Here, we aimed at characterizing cross talk for three groups of synergistic muscles by the identification of individual motor unit action potentials. Moreover, we explored whether spatial filtering (single and double differential) of the EMG signals influences the level of cross talk. Three experiments were conducted. Participants (total 25) performed isometric contractions at 10% of the maximal voluntary contraction (MVC) with digit muscles and knee extensors and at 30% MVC with plantar flexors. High-density surface EMG signals were recorded and decomposed into motor unit spike trains. For each muscle, we quantified the cross talk induced to neighboring muscles and the level of contamination by the nearby muscle activity. We also estimated the influence of cross talk on the EMG power spectrum and intermuscular correlation. Most motor units (80%) generated significant cross-talk signals to neighboring muscle EMG in monopolar recording mode, but this proportion decreased with spatial filtering (50% and 42% for single and double differential, respectively). Cross talk induced overestimations of intermuscular correlation and has a small effect on the EMG power spectrum, which indicates that cross talk is not reduced with high-pass temporal filtering. Conversely, spatial filtering reduced the cross-talk magnitude and the overestimations of intermuscular correlation, confirming to be an effective and simple technique to reduce cross talk. This paper presents a new method for the identification and quantification of cross talk at the motor unit level and clarifies the influence of cross talk on EMG interpretation for muscles with different anatomy. [ABSTRACT FROM AUTHOR]

The word "hypoxia" has recently come to the attention of the general public on two occasions, the Nobel Prize in Medicine or Physiology in 2019 and the recent COVID-19 pandemic. In the academic environment, hypoxia is a current topic of research in biology, physiology, and medicine: in October 2020, there were more than 150,000 occurrences of "hypoxia" in the PubMed database. However, the first occurrence is dated to 1945, while the interest for the effects of oxygen lack on the living organisms started in the mid-19th century, when scientists explored high altitude regions and mainly used the terms "anoxia" or "anoxemia." I therefore researched online through multiple databases to look for the first appearance of "hypoxia" and related terms "hypoxemia" and "hypoxybiosis" in scientific literature published in English, German, French, Italian, and Spanish. Viault and Jolyet used "Hypohématose" in 1894, but this term has not been used since. Hypoxybiosis first appeared in 1909 in Germany, then hypoxemia in 1923 in Austria, and hypoxia in 1938 in Holland. It was then exported to the United States where it appeared in 1940 in cardiology and anesthesiology. The clinical distinction between anoxia and hypoxia was clearly defined by Carl Wiggers in 1941. Hypoxia (decrease in oxygen), by essence variable in time and in localization in the body, in contrast with anoxia (absence of oxygen), illustrates the concept of homeodynamics that defines a living organism as a complex system in permanent instability, exposed to environmental and internal perturbations. [ABSTRACT FROM AUTHOR]

The worldwide pandemic caused by the SARS-CoV-2 virus has resulted in over 84,407,000 cases, with over 1,800,000 deaths when this paper was submitted, with comorbidities such as gender, race, age, body mass, diabetes, and hypertension greatly exacerbating mortality. This review will analyze the rapidly increasing knowledge of COVID-19-induced lung pathophysiology. Although controversial, the acute respiratory distress syndrome (ARDS) associated with COVID-19 (CARDS) seems to present as two distinct phenotypes: type L and type H. The "L" refers to low elastance, ventilation/perfusion ratio, lung weight, and recruitability, and the "H" refers to high pulmonary elastance, shunt, edema, and recruitability. However, the LUNG-SAFE (Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure) and ESICM (European Society of Intensive Care Medicine) Trials Groups have shown that ~13% of the mechanically ventilated non-COVID-19 ARDS patients have the type-L phenotype. Other studies have shown that CARDS and ARDS respiratory mechanics overlap and that standard ventilation strategies apply to these patients. The mechanisms causing alterations in pulmonary perfusion could be caused by some combination of 1) renin-angiotensin system dysregulation, 2) thrombosis caused by loss of endothelial barrier, 3) endothelial dysfunction causing loss of hypoxic pulmonary vasoconstriction perfusion control, and 4) hyperperfusion of collapsed lung tissue that has been directly measured and supported by a computational model. A flowchart has been constructed highlighting the need for personalized and adaptive ventilation strategies, such as the time-controlled adaptive ventilation method, to set and adjust the airway pressure release ventilation mode, which recently was shown to be effective at improving oxygenation and reducing inspiratory fraction of oxygen, vasopressors, and sedation in patients with COVID-19. [ABSTRACT FROM AUTHOR]

Ultrasound has risen to the forefront as one of the primary tools in tendon research, with benefits including its relatively low cost, ease of use, and high safety. Moreover, it has been shown that cine ultrasound can be used to evaluate tendon deformation by tracking the motion of anatomical landmarks during physical movement. Estimates from landmark tracking, however, are typically limited to global tissue properties, such that clinically relevant regional nonuniformities may be missed. Fortunately, advancements in ultrasound scanning have led to the development of speckle-tracking algorithms, which enable the noninvasive measurement of in vivo local deformation patterns. Despite the successes in other fields, the adaptation of speckle-tracking to tendon research has presented some unique challenges as a result of tissue anisotropy and microstructural changes under load. With no generally accepted standards for its use, current methodological approaches vary substantially between studies and research groups. Therefore, the goal of this paper is to provide a summative review of the technical complexities and variations of speckle-tracking approaches being used and the impact these decisions may have on measured results and their interpretation. Variations in these approaches currently being used with relevant technical aspects are discussed first (for the technician), followed by a discussion of the more clinical considerations (for the clinician). Finally, a summary table of common challenges encountered when implementing speckle-tracking is provided, with suggested recommendations for minimizing the impact of such potential sources of error. [ABSTRACT FROM AUTHOR]

This document will take you through all the major steps of preparing your manuscript for submission to the American Physiological Society Journals, from how best to format and organize the paper itself, to how to create digital images suitable for print and web publication, to advice on how to present supplemental data files such as video clips and long tables. The full, HTML version of these Instructions is located at www.the-aps.org/publications/i4a/prep-manuscript.htm, and is linked to additional information on PDF5, image file formats, etc. These instructions pertain to all of the American Journal of Physiology sections, as well as the Journal of Applied Physiology, the Journal of Neurophysiology, and Physiological Genomics. Please note that Advances in Physiology Education, Physiology (invited only), and Physiological Reviews (invited only) have specific instructions that you should review if you are submitting to them. [ABSTRACT FROM AUTHOR]

This paper assessed the blood pressure, heart rate, and mouth-pressure responses to indoor rock climbing (bouldering) and associated training exercises. Six well-trained male rock climbers (mean ± SD age, 27.7 ± 4.7 yr; stature, 177.7 ± 7.3 cm; mass, 69.8 ± 12.1 kg) completed two boulder problems (6b and 7a+ on the Fontainebleau Scale) and three typical training exercises [maximum voluntary contraction (MVC) isometric pull-up, 80% MVC pull-ups to fatigue, and campus board to fatigue]. Blood pressure and heart rate were measured via an indwelling femoral arterial catheter, and mouth pressure via a mouthpiece manometer. Bouldering evoked a peak systolic pressure of 200 ± 17 mmHg (44 ± 21% increase from baseline), diastolic pressure of 142 ± 26 mmHg (70 ± 32% increase), mean arterial pressure of 163 ± 18 mmHg (56 ± 25% increase), and heart rate of 176 ± 22 beats/min (76 ± 35% increase). The highest systolic pressure was observed during the campus board exercise (218 ± 33 mmHg), although individual values as high as 273/189 mmHg were recorded. Peak mouth pressure during climbing was 31 ± 46 mmHg, and this increased independently of climb difficulty. We concluded that indoor rock climbing and associated exercises evoke a substantial pressor response resulting in high blood pressures that may exceed those observed during other upper-limb resistance exercises. These findings may inform risk stratification for climbers. NEW & NOTEWORTHY This case study provides original data on the exercise pressor response to indoor rock climbing and associated training exercises through the use of an indwelling femoral arterial catheter. Our subjects exhibited systolic/diastolic blood pressures that exceeded values often reported during upper-limb resistance exercise. Our data extend the understanding of the cardiovascular stress associated with indoor rock climbing. [ABSTRACT FROM AUTHOR]