scholarly journals Exercise-induced diaphragmatic fatigue in healthy humans.

1993 ◽  
Vol 460 (1) ◽  
pp. 385-405 ◽  
Author(s):  
B D Johnson ◽  
M A Babcock ◽  
O E Suman ◽  
J A Dempsey
1995 ◽  
Vol 78 (1) ◽  
pp. 82-92 ◽  
Author(s):  
M. A. Babcock ◽  
B. D. Johnson ◽  
D. F. Pegelow ◽  
O. E. Suman ◽  
D. Griffin ◽  
...  

We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83–77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.


2019 ◽  
Vol 7 (22) ◽  
Author(s):  
Christopher L. Axelrod ◽  
Connery J. Brennan ◽  
Gail Cresci ◽  
Deborah Paul ◽  
Michaela Hull ◽  
...  

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  

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.


2018 ◽  
Vol 50 (5S) ◽  
pp. 744 ◽  
Author(s):  
Anastassios Philippou ◽  
Roxane Tenta ◽  
Maria Maridaki ◽  
Michael Koutsilieris

2018 ◽  
Vol 125 (2) ◽  
pp. 624-633 ◽  
Author(s):  
Tania Atanasovska ◽  
Robert Smith ◽  
Claus Graff ◽  
Cao T. Tran ◽  
Jacob Melgaard ◽  
...  

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.


2010 ◽  
Vol 108 (5) ◽  
pp. 1061-1068 ◽  
Author(s):  
Federico Lavorini ◽  
Giovanni A. Fontana ◽  
Elisa Chellini ◽  
Chiara Magni ◽  
Roberto Duranti ◽  
...  

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.


2014 ◽  
Vol 39 (2) ◽  
pp. 266-269 ◽  
Author(s):  
Paolo B. Dominelli ◽  
Glen E. Foster ◽  
Giulio S. Dominelli ◽  
William R. Henderson ◽  
Michael S. Koehle ◽  
...  

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.


2008 ◽  
Vol 104 (5) ◽  
pp. 1418-1425 ◽  
Author(s):  
Andrew T. Lovering ◽  
Lee M. Romer ◽  
Hans C. Haverkamp ◽  
David F. Pegelow ◽  
John S. Hokanson ◽  
...  

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.


1994 ◽  
Vol 86 (5) ◽  
pp. 505-510 ◽  
Author(s):  
P. O. Iversen ◽  
B. L. Arvesen ◽  
H. B. Benestad

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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