Abstract

PURPOSE: Increased extracellular potassium reduces peak diaphragm force, as do various reactive oxygen species (ROS). At physiologic pH levels, diaphragm contractility is unaffected by acidosis, but at lower levels (pH 6.8) diaphragm contractility decreases. During exercise, however, the diaphragm is exposed to arterial blood with a milieu of metabolites. This study was designed to determine whether acidosis or ROS exacerbate the effects of potassium on diaphragm contractility. METHODS: In study one, rat diaphragm strips were subjected to four conditions: 1) pH 7.4, normal K+ (CTRL) 2) pH 7.2, high (12mM) K+ (K7.2) 3) pH 7.1, high K+ (K7.1) 4) pH 7.0 high K+ (K7.0). In the second study, strips were exposed to either the control solution or 9mM K+ with 10–3MH2O2. A baseline force frequency relationship (FF1) was measured from each strip. The treatment solution was introduced and a second force frequency relationship (FF2) was obtained. Differences between FF1 and FF2 were compared for each group. RESULTS: and Conclusions: With regards to pH, K7.2, K7.1, and K7.0 all differed between FF1 and FF2, but CTRL did not. At lower frequencies (tw - 40Hz), force production of K+ groups exceeded that of CTRL. At 120 – 200 Hz, K+ groups produced less force than control with no difference across pH. This is the same pattern we have previously noted with increased K+ alone. In the H2O2 study, we found a significant overall decrease in force in FF2, however, there was still a slight but significant increase in force at twitch − 20 Hz. Force at the highest frequencies was dramatically (50–75%) decreased. This suggests that alterations (increases in force) at lower stimulation frequencies are influenced by increased K+, without any added influence from either acidosis or ROS. Decreases in force elicited by K+ at higher frequencies are not affected by pH at physiological levels, but are exacerbated by ROS. This may provide some clarification of causes of loss of diaphragm contractility during and following maximal exercise.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.