Exercise-induced Expiratory Muscle Fatigue in Healthy Humans

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S381-S382
Author(s):  
Bryan J. Taylor ◽  
Stephen C. How ◽  
Lee M. Romer ◽  
Alison McConnell
Keyword(s):  
Muscle Fatigue ◽  
Expiratory Muscle ◽  
Healthy Humans ◽  
Exercise Induced

scholarly journals Effect of expiratory muscle fatigue on exercise tolerance and locomotor muscle fatigue in healthy humans

2008 ◽  
Vol 104 (5) ◽  
pp. 1442-1451 ◽  
Author(s):  
Bryan J. Taylor ◽  
Lee M. Romer
Keyword(s):  
Muscle Fatigue ◽  
Exercise Tolerance ◽  
Quadriceps Muscle ◽  
Peak Power Output ◽  
Exercise Time ◽  
Expiratory Muscle ◽  
Healthy Humans ◽  
Resistive Breathing ◽  
Gastric Pressure ◽  
Exercise Induced

High-intensity exercise (≥90% of maximal O2 uptake) sustained to the limit of tolerance elicits expiratory muscle fatigue (EMF). We asked whether prior EMF affects subsequent exercise tolerance. Eight male subjects (means ± SD; maximal O2 uptake = 53.5 ± 5.2 ml·kg−1·min−1) cycled at 90% of peak power output to the limit of tolerance with (EMF-EX) and without (CON-EX) prior induction of EMF and for a time equal to that achieved in EMF-EX but without prior induction of EMF (ISO-EX). To induce EMF, subjects breathed against an expiratory flow resistor until task failure (15 breaths/min, 0.7 expiratory duty cycle, 40% of maximal expiratory gastric pressure). Fatigue of abdominal and quadriceps muscles was assessed by measuring the reduction relative to prior baseline values in magnetically evoked gastric twitch pressure (Pgatw) and quadriceps twitch force (Qtw), respectively. The reduction in Pgatw was not different after resistive breathing vs. after CON-EX (−27 ± 5 vs. −26 ± 6%; P = 0.127). Exercise time was reduced by 33 ± 10% in EMF-EX vs. CON-EX (6.85 ± 2.88 vs. 9.90 ± 2.94 min; P < 0.001). Exercise-induced abdominal and quadriceps muscle fatigue was greater after EMF-EX than after ISO-EX (−28 ± 9 vs. −12 ± 5% for Pgatw, P = 0.001; −28 ± 7 vs. −14 ± 6% for Qtw, P = 0.015). Perceptual ratings of dyspnea and leg discomfort (Borg CR10) were higher at 1 and 3 min and at end exercise during EMF-EX vs. during ISO-EX ( P < 0.05). Percent changes in limb fatigue and leg discomfort (EMF-EX vs. ISO-EX) correlated significantly with the change in exercise time. We propose that EMF impaired subsequent exercise tolerance primarily through an increased severity of limb locomotor muscle fatigue and a heightened perception of leg discomfort.

Pulmonary Function Subsequent to Expiratory Muscle Fatigue in Healthy Humans

2001 ◽  
Vol 22 (7) ◽  
pp. 498-503 ◽  
Author(s):  
H. C. Haverkamp ◽  
M. Metelits ◽  
J. Hartnett ◽  
K. Olsson ◽  
J. R. Coast
Keyword(s):  
Pulmonary Function ◽  
Muscle Fatigue ◽  
Expiratory Muscle ◽  
Healthy Humans

scholarly journals Expiratory muscle fatigue does not regulate operating lung volumes during high-intensity exercise in healthy humans

2013 ◽  
Vol 114 (11) ◽  
pp. 1569-1576 ◽  
Author(s):  
Bryan J. Taylor ◽  
Stephen C. How ◽  
Lee M. Romer
Keyword(s):  
Muscle Fatigue ◽  
High Intensity ◽  
Expiratory Flow Limitation ◽  
Lung Volumes ◽  
Expiratory Muscle ◽  
Healthy Humans ◽  
Resistive Breathing ◽  
Expiratory Muscles ◽  
Expiratory Flow ◽  
Pressure Changes

To determine whether expiratory muscle fatigue (EMF) is involved in regulating operating lung volumes during exercise, nine recreationally active subjects cycled at 90% of peak work rate to the limit of tolerance with prior induction of EMF (EMF-ex) and for a time equal to that achieved in EMF-ex without prior induction of EMF (ISO-ex). EMF was assessed by measuring changes in magnetically evoked gastric twitch pressure. Changes in end-expiratory and end-inspiratory lung volume (EELV and EILV) and the degree of expiratory flow limitation (EFL) were quantified using maximal expiratory flow-volume curves and inspiratory capacity maneuvers. Resistive breathing reduced gastric twitch pressure (−24 ± 14%, P = 0.004). During EMF-ex, EELV decreased from rest to the 3rd min of exercise [39 ± 8 vs. 27 ± 7% of forced vital capacity (FVC), P = 0.001] before increasing toward baseline (34 ± 8% of FVC end exercise, P = 0.073 vs. rest). EILV increased from rest to the 3rd min of exercise (54 ± 8 vs. 84 ± 9% of FVC, P = 0.006) and remained elevated to end exercise (88 ± 9% of FVC). Neither EELV ( P = 0.18) nor EILV ( P = 0.26) was different at any time point during EMF-ex vs. ISO-ex. Four subjects became expiratory flow limited during the final minute of EMF-ex and ISO-ex; the degree of EFL was not different between trials (37 ± 18 vs. 35 ± 16% of tidal volume, P = 0.38). At end exercise in both trials, EELV was greater in subjects without vs. subjects with EFL. These findings suggest that 1) contractile fatigue of the expiratory muscles in healthy humans does not regulate operating lung volumes during high-intensity sustained cycle exercise; and 2) factors other than “frank” EFL cause the terminal increase in EELV.

scholarly journals Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

2006 ◽  
Vol 290 (2) ◽  
pp. R365-R375 ◽  
Author(s):  
Lee M. Romer ◽  
Hans C. Haverkamp ◽  
Andrew T. Lovering ◽  
David F. Pegelow ◽  
Jerome A. Dempsey
Keyword(s):  
Muscle Fatigue ◽  
Femoral Nerve ◽  
Quadriceps Muscle ◽  
Cycle Ergometer ◽  
Arterial Hypoxemia ◽  
Healthy Humans ◽  
Peripheral Mechanism ◽  
Evoked Force ◽  
Exercise Induced ◽  
Intensity Of Exercise

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (V̇o2 peak) = 56.4 ± 2.8 ml·kg−1·min−1; mean ± SE]. Subjects exercised on a cycle ergometer at ≥90% V̇o2 peak to exhaustion (13.2 ± 0.8 min), during which time arterial O2 saturation (SaO2) fell from 97.7 ± 0.1% at rest to 91.9 ± 0.9% (range 84–94%) at end exercise, primarily because of changes in blood pH (7.183 ± 0.017) and body temperature (38.9 ± 0.2°C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (FiO2) = 0.25–0.31] that prevented EIAH (SaO2 = 97–99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1–100 Hz). Immediately after exercise at FiO2 0.21, the mean force response across 1–100 Hz decreased 33 ± 5% compared with only 15 ± 5% when EIAH was prevented ( P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at FiO2 0.21 (SaO2 = 95.3 ± 0.7%), the decrease in evoked force was exacerbated by 35% ( P < 0.05) in response to further desaturation induced via FiO2 0.17 (SaO2 = 87.8 ± 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (−6 ± 1% ΔSaO2 from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.

scholarly journals Influence of inspiratory resistive loading on expiratory muscle fatigue in healthy humans

2017 ◽  
Vol 102 (9) ◽  
pp. 1221-1233 ◽  
Author(s):  
Carli M. Peters ◽  
Joseph F. Welch ◽  
Paolo B. Dominelli ◽  
Yannick Molgat-Seon ◽  
Lee M. Romer ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Expiratory Muscle ◽  
Healthy Humans ◽  
Resistive Loading

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

2019 ◽  
Vol 7 (22) ◽  
Author(s):  
Christopher L. Axelrod ◽  
Connery J. Brennan ◽  
Gail Cresci ◽  
Deborah Paul ◽  
Michaela Hull ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Healthy Humans ◽  
Exercise Induced ◽  
Gastrointestinal Permeability

Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Light Chain ◽  
Human Skeletal Muscle ◽  
Transgenic Animal ◽  
Dependent Manner ◽  
Healthy Humans ◽  
Transgenic Animal Models ◽  
Exercise Induced

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.

scholarly journals Hormonal Responses after Exercise-induced Muscle Damage in Healthy Humans

2018 ◽  
Vol 50 (5S) ◽  
pp. 744 ◽  
Author(s):  
Anastassios Philippou ◽  
Roxane Tenta ◽  
Maria Maridaki ◽  
Michael Koutsilieris
Keyword(s):  
Muscle Damage ◽  
Hormonal Responses ◽  
Healthy Humans ◽  
Exercise Induced
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