Biometric approximation of diaphragmatic contractility during sustained hyperpnea

Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and appl...

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Published in	Respiratory physiology & neurobiology Vol. 176; no. 3; pp. 90 - 97
Main Authors	Kabitz, Hans-Joachim, Walker, David Johannes, Schwoerer, Anja, Schlager, Daniel, Walterspacher, Stephan, Storre, Jan Hendrik, Roecker, Kai, Windisch, Wolfram, Vergès, Samuel, Spengler, Christina M.
Format	Journal Article
Language	English
Published	Amsterdam Elsevier B.V 31.05.2011 Elsevier
Subjects	Adult Biological and medical sciences Biometry - methods Diaphragm - physiology Diaphragmatic fatigue Fundamental and applied biological sciences. Psychology Humans Hyperventilation - physiopathology Male Medical Education Muscle Contraction - physiology Muscle Fatigue - physiology Oxygen Consumption - physiology Pulmonary/Respiratory Respiratory Mechanics - physiology Respiratory muscle Time Factors Twitch transdiaphragmatic pressure Vertebrates: respiratory system Young Adult Respiratory muscle Twitch transdiaphragmatic pressure Diaphragmatic fatigue Biometrics Vertebrata Mammalia Contractility Fatigue Respiratory system Hyperpnea Pressure
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Abstract	Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30–60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery −19 ± 17% and −30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay ( r 2 = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.
AbstractList	Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30–60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery −19 ± 17% and −30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay ( r 2 = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea. Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea. Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea. Abstract Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30–60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery −19 ± 17% and −30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay ( r2 = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.
Author	Schlager, Daniel Walker, David Johannes Walterspacher, Stephan Schwoerer, Anja Storre, Jan Hendrik Vergès, Samuel Roecker, Kai Windisch, Wolfram Kabitz, Hans-Joachim Spengler, Christina M.
Author_xml	– sequence: 1 givenname: Hans-Joachim surname: Kabitz fullname: Kabitz, Hans-Joachim email: hans-joachim.kabitz@uniklinik-freiburg.de organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 2 givenname: David Johannes surname: Walker fullname: Walker, David Johannes organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 3 givenname: Anja surname: Schwoerer fullname: Schwoerer, Anja organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 4 givenname: Daniel surname: Schlager fullname: Schlager, Daniel organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 5 givenname: Stephan surname: Walterspacher fullname: Walterspacher, Stephan organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 6 givenname: Jan Hendrik surname: Storre fullname: Storre, Jan Hendrik organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 7 givenname: Kai surname: Roecker fullname: Roecker, Kai organization: Sports-Medicine, University Hospital Freiburg, Germany – sequence: 8 givenname: Wolfram surname: Windisch fullname: Windisch, Wolfram organization: Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany – sequence: 9 givenname: Samuel surname: Vergès fullname: Vergès, Samuel organization: HP2 Laboratory (INSERM ERI17), Joseph Fourier University, Grenoble, France – sequence: 10 givenname: Christina M. surname: Spengler fullname: Spengler, Christina M. organization: Exercise Physiology, Institute of Human Movement Sciences, ETH Zurich, Switzerland
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Keywords	Respiratory muscle Twitch transdiaphragmatic pressure Diaphragmatic fatigue Biometrics Vertebrata Mammalia Contractility Fatigue Respiratory system Hyperpnea Pressure
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Snippet	Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off... Abstract Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels...
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SubjectTerms	Adult Biological and medical sciences Biometry - methods Diaphragm - physiology Diaphragmatic fatigue Fundamental and applied biological sciences. Psychology Humans Hyperventilation - physiopathology Male Medical Education Muscle Contraction - physiology Muscle Fatigue - physiology Oxygen Consumption - physiology Pulmonary/Respiratory Respiratory Mechanics - physiology Respiratory muscle Time Factors Twitch transdiaphragmatic pressure Vertebrates: respiratory system Young Adult
Title	Biometric approximation of diaphragmatic contractility during sustained hyperpnea
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