UCC118 supplementation reduces exercise‐induced gastrointestinal permeability and remodels the gut microbiome in healthy humans

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.

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Hormonal Responses after Exercise-induced Muscle Damage in Healthy Humans

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000538452.48469.4d ◽

2018 ◽

Vol 50 (5S) ◽

pp. 744 ◽

Cited By ~ 1

Author(s):

Anastassios Philippou ◽

Roxane Tenta ◽

Maria Maridaki ◽

Michael Koutsilieris

Keyword(s):

Muscle Damage ◽

Hormonal Responses ◽

Healthy Humans ◽

Exercise Induced

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The Oral and Gut Bacterial Microbiomes: Similarities, Differences, and Connections

Biological Research For Nursing ◽

10.1177/1099800420941606 ◽

2020 ◽

Vol 23 (1) ◽

pp. 7-20

Author(s):

Katherine A. Maki ◽

Narjis Kazmi ◽

Jennifer J. Barb ◽

Nancy Ames

Keyword(s):

Gut Microbiome ◽

Alpha Diversity ◽

Oral Microbiome ◽

Taxonomic Resolution ◽

Future Research ◽

Sequencing Analysis ◽

Systemic Diseases ◽

Shotgun Metagenomics ◽

Healthy Humans ◽

Microbiome Research

Background: The oral cavity is associated with local and systemic diseases, although oral samples are not as commonly studied as fecal samples in microbiome research. There is a gap in understanding between the similarities and differences in oral and gut microbiomes and how they may influence each other. Methods: A scoping literature review was conducted comparing oral and gut microbiome communities in healthy humans. Results: Ten manuscripts met inclusion criteria and were examined. The oral microbiome sites demonstrated great variance in differential bacterial abundance and the oral microbiome had higher alpha diversity as compared to the gut microbiome. Studies using 16S rRNA sequencing analysis resulted in overall community differences between the oral and gut microbiomes when beta diversity was analyzed. Shotgun metagenomics sequencing increased taxonomic resolution to strain level (intraspecies) and demonstrated a greater percentage of shared taxonomy and oral bacterial translocation to the gut microbiome community. Discussion: The oral and gut microbiome bacterial communities may be more similar than earlier research has suggested, when species strain is analyzed through shotgun metagenomics sequencing. The association between oral health and systemic diseases has been widely reported but many mechanisms underlying this relationship are unknown. Although future research is needed, the oral microbiome may be a novel interventional target through its downstream effects on the gut microbiome. As nurse scientists are experts in symptom characterization and phenotyping of patients, they are also well posed to lead research on the connection of the oral microbiome to the gut microbiome in health and disease.

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Protection against severe hypokalemia but impaired cardiac repolarization after intense rowing exercise in healthy humans receiving salbutamol

Journal of Applied Physiology ◽

10.1152/japplphysiol.00680.2017 ◽

2018 ◽

Vol 125 (2) ◽

pp. 624-633 ◽

Cited By ~ 3

Author(s):

Tania Atanasovska ◽

Robert Smith ◽

Claus Graff ◽

Cao T. Tran ◽

Jacob Melgaard ◽

...

Keyword(s):

Sudden Cardiac Death ◽

Cardiac Death ◽

Plasma Potassium ◽

Protective Mechanism ◽

Cardiac Repolarization ◽

Early Recovery ◽

Double Blind ◽

Healthy Humans ◽

Increased Risk ◽

Exercise Induced

Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the β2 agonist salbutamol attenuated the exercise hyperkalemia and exacerbated the postexercise hypokalemia, and whether hypokalemia was associated with impaired cardiac repolarization (QT hysteresis). Eleven healthy adults participated in a randomized, counterbalanced, double-blind trial receiving either 1,000 µg salbutamol (SAL) or placebo (PLAC) by inhalation. Arterial plasma potassium concentration ([K+]a) was measured at rest, during 3 min of intense rowing exercise, and during 60 min of recovery. QT hysteresis was calculated from ECG ( n = 8). [K+]a increased above baseline during exercise (rest, 3.72 ± 0.7 vs. end-exercise, 6.81 ± 1.4 mM, P < 0.001, mean ± SD) and decreased rapidly during early recovery to below baseline; restoration was incomplete at 60 min postexercise ( P < 0.05). [K+]a was less during SAL than PLAC (4.39 ± 0.13 vs. 4.73 ± 0.19 mM, pooled across all times, P = 0.001, treatment main effect). [K+]a was lower after SAL than PLAC, from 2 min preexercise until 2.5 min during exercise, and at 50 and 60 min postexercise ( P < 0.05). The postexercise decline in [K+]a was correlated with QT hysteresis ( r = 0.343, n = 112, pooled data, P = 0.001). Therefore, the decrease in [K+]a from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. Although salbutamol lowered [K+]a during exercise, no additive hypokalemic effects occurred in early recovery, suggesting there may be a protective mechanism against severe or prolonged hypokalemia after exercise when treated by salbutamol. This is important because postexercise hypokalemia impaired cardiac repolarization, which could potentially trigger arrhythmias and sudden cardiac death in susceptible individuals with preexisting hypokalemia and/or heart disease. NEW & NOTEWORTHY Intense rowing exercise induced a marked increase in arterial potassium, followed by a pronounced decline to hypokalemic levels. The β2 agonist salbutamol lowered potassium during exercise and late recovery but not during early postexercise, suggesting a protective effect against severe hypokalemia. The decreased potassium in recovery was associated with impaired cardiac QT hysteresis, suggesting a link between postexercise potassium and the heart, with implications for increased risk of cardiac arrhythmias and, potentially, sudden cardiac death.

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Desensitization of the cough reflex by exercise and voluntary isocapnic hyperpnea

Journal of Applied Physiology ◽

10.1152/japplphysiol.00423.2009 ◽

2010 ◽

Vol 108 (5) ◽

pp. 1061-1068 ◽

Cited By ~ 22

Author(s):

Federico Lavorini ◽

Giovanni A. Fontana ◽

Elisa Chellini ◽

Chiara Magni ◽

Roberto Duranti ◽

...

Keyword(s):

Cough Reflex ◽

Control Value ◽

Cognitive Component ◽

Cognitive Components ◽

Healthy Humans ◽

Thoracic Muscles ◽

Exercise Induced ◽

Relationship Of ◽

Isocapnic Hyperpnea ◽

The Relationship

Little is known about the effects of exercise on the sensory and cognitive aspects of coughing evoked by inhalation of tussigenic agents. The threshold for the cough reflex induced by inhalation of increasing nebulizer outputs of ultrasonically nebulized distilled water (fog), an index of cough reflex sensitivity, was assessed in twelve healthy humans in control conditions, during exercise and during voluntary isocapnic hyperpnea (VIH) at the same ventilatory level as the exercise. The intensity of the urge to cough (UTC), a cognitive component of coughing, was recorded throughout the trials on a linear scale. The relationships between inhaled fog nebulizer outputs and the correspondingly evoked UTC values, an index of the perceptual magnitude of the UTC sensitivity, were also calculated. Cough appearance was always assessed audiovisually. At an exercise level of 80% of anaerobic threshold, the median cough threshold was increased from a control value of 0.73 to 2.22 ml/min ( P < 0.01), i.e., cough sensitivity was downregulated. With VIH, the threshold increased from 0.73 to 2.22 ml/min ( P < 0.01), a similar downregulation. With exercise and VIH compared with control, mean UTC values at cough threshold were unchanged, i.e., control, 3.83 cm; exercise, 3.12 cm; VIH, 4.08 cm. The relationship of the fog nebulizer output/UTC value was linear in control conditions and logarithmic during both exercise and VIH. The perception of the magnitude of the UTC seems to be influenced by signals or sensations arising from exercising limb and thoracic muscles and/or by higher nervous (cortical) mechanisms. The results indicate that the adjustments brought into action by exercise-induced or voluntary hyperpnea exert inhibitory influences on the sensory and cognitive components of fog-induced cough.

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Exercise-induced arterial hypoxemia is unaffected by intense physical training: a case report

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2013-0341 ◽

2014 ◽

Vol 39 (2) ◽

pp. 266-269 ◽

Cited By ~ 3

Author(s):

Paolo B. Dominelli ◽

Glen E. Foster ◽

Giulio S. Dominelli ◽

William R. Henderson ◽

Michael S. Koehle ◽

...

Keyword(s):

Oxygen Consumption ◽

Case Report ◽

Aerobic Training ◽

Maximal Exercise ◽

Maximal Oxygen Consumption ◽

Severe Hypoxemia ◽

Exercise Tests ◽

Arterial Hypoxemia ◽

Healthy Humans ◽

Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) occurs in some healthy humans at sea-level, whereby the most aerobically trained individuals develop the most severe hypoxemia. A female competitive runner completed 2 maximal exercise tests. Maximal oxygen consumption increased by 15% between testing days, but the degree of hypoxemia remained similar (PaO2, SaO2; 82 and 80 mm Hg; 93.8% and 92.8%; first and second test, respectively). Our case indicates that EIAH does not necessarily worsen with aerobic training.

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Intrapulmonary shunting and pulmonary gas exchange during normoxic and hypoxic exercise in healthy humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00208.2007 ◽

2008 ◽

Vol 104 (5) ◽

pp. 1418-1425 ◽

Cited By ~ 88

Author(s):

Andrew T. Lovering ◽

Lee M. Romer ◽

Hans C. Haverkamp ◽

David F. Pegelow ◽

John S. Hokanson ◽

...

Keyword(s):

Gas Exchange ◽

Contrast Echocardiography ◽

Pulmonary Gas Exchange ◽

Pulmonary Vasculature ◽

Long Term Effects ◽

Arteriovenous Shunting ◽

Healthy Humans ◽

Intrapulmonary Shunting ◽

Exercise Induced

Exercise-induced intrapulmonary arteriovenous shunting, as detected by saline contrast echocardiography, has been demonstrated in healthy humans. We have previously suggested that increases in both pulmonary pressures and blood flow associated with exercise are responsible for opening these intrapulmonary arteriovenous pathways. In the present study, we hypothesized that, although cardiac output and pulmonary pressures would be higher in hypoxia, the potent pulmonary vasoconstrictor effect of hypoxia would actually attenuate exercise-induced intrapulmonary shunting. Using saline contrast echocardiography, we examined nine healthy men during incremental (65 W + 30 W/2 min) cycle exercise to exhaustion in normoxia and hypoxia (fraction of inspired O2 = 0.12). Contrast injections were made into a peripheral vein at rest and during exercise and recovery (3–5 min postexercise) with pulmonary gas exchange measured simultaneously. At rest, no subject demonstrated intrapulmonary shunting in normoxia [arterial Po2 (PaO2) = 98 ± 10 Torr], whereas in hypoxia (PaO2 = 47 ± 5 Torr), intrapulmonary shunting developed in 3/9 subjects. During exercise, ∼90% (8/9) of the subjects shunted during normoxia, whereas all subjects shunted during hypoxia. Four of the nine subjects shunted at a lower workload in hypoxia. Furthermore, all subjects continued to shunt at 3 min, and five subjects shunted at 5 min postexercise in hypoxia. Hypoxia has acute effects by inducing intrapulmonary arteriovenous shunt pathways at rest and during exercise and has long-term effects by maintaining patency of these vessels during recovery. Whether oxygen tension specifically regulates these novel pathways or opens them indirectly via effects on the conventional pulmonary vasculature remains unclear.

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Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

Clinical Science ◽

10.1042/cs19990080 ◽

2000 ◽

Vol 98 (1) ◽

pp. 39 ◽

Cited By ~ 9

Author(s):

D. ROBERTS ◽

D. J. SMITH ◽

S. DONNELLY ◽

S. SIMARD

Keyword(s):

Plasma Volume ◽

Volume Contraction ◽

Healthy Humans ◽

Erythropoietin Production ◽

Exercise Induced

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No Mandatory Role for the Spleen in the Exercise-Induced Leucocytosis in Man

Clinical Science ◽

10.1042/cs0860505 ◽

1994 ◽

Vol 86 (5) ◽

pp. 505-510 ◽

Cited By ~ 13

Author(s):

P. O. Iversen ◽

B. L. Arvesen ◽

H. B. Benestad

Keyword(s):

Plasma Concentrations ◽

Blood Concentrations ◽

Healthy Humans ◽

Strenuous Physical Exercise ◽

Eosinophilic Granulocytes ◽

Cell Sources ◽

Exercise Induced ◽

Factor Α ◽

Stimulating Factor ◽

Necrosis Factor

1. Short-lasting strenuous physical exercise leads to a marked increase in the blood concentration of leucocytes in healthy humans. The cell sources of this leucocytosis have not been definitely identified, neither has the contribution made by the various subtypes of leucocytes. 2. We have compared the exercise-induced leucocytosis in six splenectomized and six intact subjects. The blood concentrations of leucocytes as well as of most subtypes, except monocytes and eosinophilic granulocytes, increased substantially at the end of a 5 min exercise (200 W) bout. 3. The increases were similar in the splenectomized subjects and in the control subjects. Thirty minutes after completion of the exercise the various leucocyte blood concentrations had returned to pre-exercise levels. 4. The plasma concentrations of several cytokines (interleukins-1α and −6; tumour necrosis factor-α and granulocyte colony-stimulating factor) known to affect leucocyte kinetics did not change appreciably with exercise in either group. 5. We conclude that exercise-induced leucocytosis can take place in the absence of the spleen. There was no evidence that cytokines known to affect leucocyte formation, mobilization and activity are involved in this leucocytosis.

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Recent advances in modulating the microbiome

F1000Research ◽

10.12688/f1000research.20204.1 ◽

2020 ◽

Vol 9 ◽

pp. 46 ◽

Cited By ~ 2

Author(s):

Eamonn M.M Quigley ◽

Prianka Gajula

Keyword(s):

Gut Microbiome ◽

Fecal Microbiota Transplantation ◽

Fecal Microbiota ◽

Human Phenotype ◽

Host Interactions ◽

Healthy Humans ◽

Probiotic Strains ◽

The Many ◽

Definition Of

We are in the midst of “the microbiome revolution”—not a day goes by without some new revelation on the potential role of the gut microbiome in some disease or disorder. From an ever-increasing recognition of the many roles of the gut microbiome in health and disease comes the expectation that its modulation could treat or prevent these very same diseases. A variety of interventions could, at least in theory, be employed to alter the composition or functional capacity of the microbiome, ranging from diet to fecal microbiota transplantation (FMT). For some, such as antibiotics, prebiotics, and probiotics, an extensive, albeit far from consistent, literature already exists; for others, such as other dietary supplements and FMT, high-quality clinical studies are still relatively few in number. Not surprisingly, researchers have turned to the microbiome itself as a source for new entities that could be used therapeutically to manipulate the microbiome; for example, some probiotic strains currently in use were sourced from the gastrointestinal tract of healthy humans. From all of the extant studies of interventions targeted at the gut microbiome, a number of important themes have emerged. First, with relatively few exceptions, we are still a long way from a precise definition of the role of the gut microbiome in many of the diseases where a disturbed microbiome has been described—association does not prove causation. Second, while animal models can provide fascinating insights into microbiota–host interactions, they rarely recapitulate the complete human phenotype. Third, studies of several interventions have been difficult to interpret because of variations in study population, test product, and outcome measures, not to mention limitations in study design. The goal of microbiome modulation is a laudable one, but we need to define our targets, refine our interventions, and agree on outcomes.

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