Respiratory Muscle Fatigue Research Articles

Pulmonary complications of neuromuscular disease: A Respiratory mechanics perspective

Paediatric neuromuscular disease compromises both the gas exchange and pump functions of the respiratory system. This can have profound implications for both growth and development of the respiratory system, as well as morbidity and mortality. Aspiration lung disease is common, and leads to increasingly restrictive pulmonary physiology over time. Abnormal lung and chest wall mechanics, and weak respiratory muscles, can combine to cause respiratory failure. Improving the balance between the work of breathing (by decreasing the respiratory load) and the respiratory pump (by improving respiratory muscle strength and decreasing respiratory muscle fatigue) can help prevent the onset of respiratory failure. Airway clearance techniques and non-invasive ventilation are two important tools in this effort. Better ways of assessing the respiratory pump, mechanical function, control and fatigue are needed especially in children.

Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia

Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO(2)). Acute metabolic acidosis was induced by administration of ammonium chloride (NH(4)Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33.2 +/- 11.5 years; FEV(1) 108.3 +/- 16.2% predicted), 14 asthma patients (5 male; age 48.1 +/- 16.1 years; FEV(1) 101.6 +/- 15.3% predicted), and 15 moderate to severe COPD patients (9 male; age 62.8 +/- 6.8 years; FEV(1) 50.0 +/- 11.8% predicted). An acute metabolic acidemia of BE -3.1 mmol x L(-1) was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference -0.1 kPa x sec x L(-1) [95%-CI: -0.1 - -0.02]. In COPD patients PaCO(2) was significantly lowered during metabolic acidemia (mean difference -1.73 mmHg [-3.0 - -0.08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure.

Infection decreases fatty acid oxidation and nuclear hormone receptors in the diaphragm

Respiratory failure is a major cause of mortality during septic shock and is due in part to decreased ventilatory muscle contraction. Ventilatory muscles have high energy demands; fatty acid (FA) oxidation is an important source of ATP. FA oxidation is regulated by nuclear hormone receptors; studies have shown that the expression of these receptors is decreased in liver, heart, and kidney during sepsis. Here, we demonstrate that lipopolysaccharide (LPS) decreases FA oxidation and the expression of lipoprotein lipase (LPL), FA transport protein 1 (FATP-1), CD36, carnitine palmitoyltransferase beta, medium chain acyl-CoA dehydrogenase (MCAD), and acyl-CoA synthetase, key proteins required for FA uptake and oxidation, in the diaphragm. LPS also decreased mRNA levels of PPARalpha and beta/delta, RXRalpha, beta, and gamma, thyroid hormone receptor alpha and beta, and estrogen related receptor alpha (ERRalpha) and their coactivators PGC-1alpha, PGC-1beta, SRC1, SRC2, Lipin 1, and CBP. Zymosan resulted in similar changes in the diaphragm. Finally, in PPARalpha deficient mice, baseline CPT-1beta and FATP-1 levels were markedly decreased and were not further reduced by LPS suggesting that a decrease in the PPARalpha signaling pathway plays an important role in inducing some of these changes. The decrease in FA oxidation in the diaphragm may be detrimental, leading to decreased diaphragm contraction and an increased risk of respiratory failure during sepsis.

Effects of different respiratory muscle training regimes on fatigue-related variables during volitional hyperpnoea

We compared the effects of the most commonly used respiratory muscle (RM) training regimes: RM endurance training (RMET; normocapnic hyperpnoea) and inspiratory resistive training (IMT), on RM performance. Twenty-six healthy men were randomized into 3 groups performing 4 weeks of RMET, IMT or sham-training. Lung function, RM strength and endurance were tested before and after training. RM fatigue during intermittent hyperpnoea was assessed by twitch oesophageal (P(oes,tw)) and gastric pressures with cervical and thoracic magnetic stimulation. Respiratory sensations (visual analogue scale, 0-10) and blood lactate concentrations ([La]) were assessed during hyperpnoea. RMET increased maximal voluntary ventilation while IMT increased maximal inspiratory pressure. Both RMET and IMT increased vital capacity and RM endurance, but only RMET improved the development of inspiratory muscle fatigue (from -31% to -21% P(oes,tw)), perception of respiratory exertion (4.2+/-0.1 to 2.3+/-2.3 points) and [La] (1.8+/-0.4 to 1.3+/-0.3 mmol l(-1)) during hyperpnoea. Whether these specific RMET-induced adaptations observed during hyperpnoea would translate into greater improvements in exercise performance compared to IMT remains to be investigated.

Intercostal muscle blood flow limitation in athletes during maximal exercise

We investigated whether, during maximal exercise, intercostal muscle blood flow is as high as during resting hyperpnoea at the same work of breathing. We hypothesized that during exercise, intercostal muscle blood flow would be limited by competition from the locomotor muscles. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle perfusion were measured simultaneously in ten trained cyclists by near-infrared spectroscopy using indocyanine green dye. Measurements were made at several exercise intensities up to maximal (WRmax) and subsequently during resting isocapnic hyperpnoea at minute ventilation levels up to those at WRmax. During resting hyperpnoea, intercostal muscle blood flow increased linearly with the work of breathing (R2 = 0.94) to 73.0 +/- 8.8 ml min-1 (100 g)-1 at the ventilation seen at WRmax (work of breathing approximately 550-600 J min-1), but during exercise it peaked at 80% WRmax (53.4 +/- 10.3 ml min-1 (100 g)-1), significantly falling to 24.7 +/- 5.3 ml min-1 (100 g)-1 at WRmax. At maximal ventilation intercostal muscle vascular conductance was significantly lower during exercise (0.22 +/- 0.05 ml min-1 (100 g)-1 mmHg-1) compared to isocapnic hyperpnoea (0.77 +/- 0.13 ml min-1 (100 g)-1 mmHg-1). During exercise, both cardiac output and vastus lateralis muscle blood flow also plateaued at about 80% WRmax (the latter at 95.4 +/- 11.8 ml min-1 (100 g)-1). In conclusion, during exercise above 80% WRmax in trained subjects, intercostal muscle blood flow and vascular conductance are less than during resting hyperpnoea at the same minute ventilation. This suggests that the circulatory system is unable to meet the demands of both locomotor and intercostal muscles during heavy exercise, requiring greater O2 extraction and likely contributing to respiratory muscle fatigue.

Theophylline in Weaning Adult Patients From Mechanical Ventilation

Abstract: The methylxanthines, theophylline, and aminophylline, have been used traditionally in patients with airway disease, primarily for their bronchodilating and central nervous stimulatory effects. In the context that these drugs have been shown to favorably affect respiratory muscle contractility and endurance, their use has also been advocated for liberating difficult-to-wean patients from mechanical ventilation and, in our experience, has been used with moderate frequency for this purpose. This article reviews the in vitro, animal, human, and clinical data regarding use of methylxanthines to facilitate adult patients' liberation from mechanical ventilation. A substantial volume of studies support the favorable effects of methylxanthines on respiratory muscle strength and endurance, including specific benefits in patients with chronic obstructive pulmonary disease, in the postoperative setting, and in settings of respiratory muscle fatigue. Surprisingly, much less attention has been given to using methylxanthines in the specific context of liberating patients from mechanical ventilation, with, to our knowledge, only 2 available case reports. Overall, available data and experience suggest a role for methylxanthines in facilitating liberation from mechanical ventilation of adult patients, though the paucity of available studies invites further research regarding this specific application.

Interacción paciente-ventilador en ventilación mecánica no invasiva

Noninvasive mechanical ventilation is one more step in the treatment of patients with acute respiratory failure. In addition to gas exchange disorders, its primary indication to initiate it is the presence of signs of respiratory muscles fatigue. To assure successful mechanical ventilation, the ventilator and patient must be synchronized, that is, the effort the patient makes to start inspiration is recognized by the ventilator and it quickly delivers gas flow, that the flow provided by the ventilator adapts to the flow need of the patient during delivery of gas phase and that the ventilator recognizes the cessation of inspiratory activity by the patient, ends the delivery of gas and opens the expiratory valve to allow the patient expiration. This sequence of events, which seem so logical, is almost never achieved in the clinical practice, commonly observing some asynchrony in ventilated patients. The presence of patient-ventilator asynchrony leads to increased breathing work, which would lead to the failure of the main objective of ventilatory support, that is none other than decline in the patient's respiratory work.

Assessment of thoraco-abdominal asynchrony

Thoraco-abdominal asynchrony is often observed in many respiratory disorders and/or respiratory muscle dysfunctions and clinically assessed as a sign of respiratory distress and increased work of breathing. This review describes the assessment of thoraco-abdominal asynchrony by respiratory inductance plethysmography. Visual inspection of the Konno-Mead plot yields information about the relative contribution of the RC and the ABD to respiration and about respiratory muscle dysfunction in selected patients. The monitoring of thoraco-abdominal asynchrony is a useful, non-invasive indicator of respiratory muscle load or respiratory muscle dysfunction and can be used to determine response to therapy in individual patients. The technique is limited by the fact that it does not detect respiratory muscle fatigue and that the occurrence of TAA does not always correspond to a clinically relevant respiratory problem, especially in the neonatal period.

Response of the respiratory muscles to rehabilitation in COPD

Respiratory rehabilitation is known to improve outcomes in patients with chronic obstructive pulmonary disease (COPD). The question addressed in the present review is whether these beneficial effects are related to improvements in inspiratory muscle function. Respiratory muscle fatigue often did not occur during exercise in patients with COPD, since exercise limitation usually occurred when significant force reserve in the inspiratory muscles was still present. Notwithstanding, a number of observations may provide indirect evidence that respiratory muscle fatigue may occur during exercise. Some evidence is present that, in normal humans, whole body exercise training improved inspiratory muscle endurance, but no studies are available in patients with COPD. Animal studies invariably demonstrated that exercise training increased the number of oxidative fibers and oxidative enzyme activity in inspiratory muscles. These effects, however, were considerably smaller than the effects found on peripheral muscles with similar fiber composition. Clear evidence indicated that inspiratory muscle training (IMT) improved inspiratory muscle function. Two large meta-analyses indicated that, if the training load was properly controlled, IMT alone or combined with general exercise reconditioning improved inspiratory muscle strength and endurance and dyspnea. The combination did not result in greater improvements in functional exercise capacity. Animal studies and one patient study confirmed the occurrence of structural remodeling of the inspiratory muscles in response to IMT. The final question is whether improvements in inspiratory muscle function produced by IMT lead to improved outcomes in COPD. In all five studies in which training load was adequately controlled, a significant reduction of dyspnea during activities of daily living was found. Eight randomized studies examined the effects of the combination. Greater improvements in exercise capacity were only found in three studies, and none showed a greater reduction in dyspnea.

Noninvasive Determination of the Tension-Time Index in Duchenne Muscular Dystrophy

Noninvasive determination of the tension-time index of the inspiratory muscles (TT MUS) can identify predisposition to respiratory muscle fatigue in neuromuscular disease. We correlated TT MUS with age and extent of need of ventilator use for patients with Duchenne muscular dystrophy. Maximal inspiratory pressure, inspiratory pressure 0.1 sec after the onset of inspiration (P 0.1), and the breathing pattern during spontaneous breathing were measured in 46 subjects with Duchenne muscular dystrophy and in 46 healthy males of the same age. TT MUS (TT MUS = T I/T TOT x P I/MIP) was determined by calculating P I from P 0.1 (P I = 5 x P 0.1 x T I). The data were compared with normal values and related to age and ventilator use. TT MUS was significantly higher in the entire Duchenne muscular dystrophy group than in controls (0.21 +/- 0.11 vs. 0.06 +/- 0.02, P < 0.001) and increased with age in the patients (P < 0.001). TT MUS was significantly higher in subjects ventilated 8-20 hrs per day than in nocturnal-only users and in patients ventilated >20 hrs per day than in those ventilated 8-20 hrs per day (P < 0.001). TT MUS surpassed 0.23 in 95% of subjects ventilated 8-20 hrs. TT MUS exceeded 0.37 in 95% of individuals ventilated >20 hrs per day, whereas it was less than this value in 95% of patients ventilated 8-20 hrs. TT MUS increases significantly with disease progression and is a sensitive indicator of risk of inspiratory muscle fatigue and ventilator use. Longitudinal determination of TT MUS in patients with Duchenne muscular dystrophy may help to justify the extent of need for mechanical ventilation.

Non-invasive tension-time-index and ventilator use in Duchenne muscular dystrophy

Non-invasive determination of the tension-time-index (TTMUS) can identify predisposition to respiratory muscle fatigue in neuromuscular disease. We correlated TTMUS with age and extent of need of ventilator use for patients with Duchenne muscular dystrophy (DMD).

The Influence of Respiratory Muscle Training Upon Intermittent Exercise Performance

The purpose of this study was to determine the effect of respiratory muscle training (RMT) on intermittent exercise performance, respiratory muscle strength (PI (max)), respiratory muscle fatigue (RMF), and dyspnea in soccer athletes. Collegiate soccer athletes (20 male, 7 female) were randomly divided into either a RMT or control condition during off-season conditioning. The RMT group performed a 30RM protocol (10 times weekly) for 5 weeks using a commercially-available training device, while the controls received no RMT. Performance was evaluated utilizing Level 1 of the Yo-Yo Intermittent Recovery Test (IRT) and dyspnea was assessed during and immediately following the IRT. RMF was quantified within 2 minutes (RMF2) and 10 minutes (RMF10) after completing the IRT. Following training, the RMT group significantly increased IRT performance by 216.6 +/- 231.0 meters (p = .008) while the 49.2 +/- 75.1 meter increase observed in the controls was not significant. PI (max) in the RMT group increased from 138.1 +/- 19.6 to 165.3 +/- 23.5 cmH (2)O (p < .001), with no significant change observed in the controls. RMT did not significantly affect RMF or dyspnea. In conclusion, RMT improved intermittent exercise performance in these soccer athletes. The mechanisms by which RMT improves performance warrant further study.

Effects of N-acetylcysteine on respiratory muscle fatigue during heavy exercise

Respiratory muscle fatigue (RMF) occurs during heavy exercise in humans. N-acetylcysteine (NAC) infusion has been shown to reduce RMF, suggesting that oxidative stress is a contributing factor. The purpose of the present study was to determine the effect of an acute oral dose of NAC on RMF during heavy exercise. Subjects (n=8) were given either placebo (PLA) or NAC (1,800 mg) 45 min prior to a 30 min constant load (85V(O)(2peak)), discontinuous exercise test. Maximum respiratory pressures (inspiratory, PI(max); expiratory, PE(max)) and venous blood samples were made prior to and following each 5 min of exercise. There was no difference (p>0.05) in PI(max) between NAC (127.9+/-34.1 cm H(2)O) or PLA (134.1+/-28.1cm H(2)O) at rest. During exercise, PI(max) was significantly lower with PLA ( approximately 14%) compared to NAC at 25 and 30 min suggesting less RMF with NAC. There were no differences (p>0.05) between groups in PE(max), V(O)(2), V(E), or heart rate at rest or throughout exercise. These results suggest that an acute dose of NAC reduces RMF during heavy exercise.

Changes in respiratory muscle and lung function following marathon running in man

Respiratory muscle fatigue has been reported following short bouts of high-intensity exercise, and prolonged, moderate-intensity exercise, as evidenced by decrements in inspiratory and expiratory mouth pressures. However, links to functionally relevant outcomes such as breathing effort have been lacking. The present study examined dyspnoea and leg fatigue during a treadmill marathon in nine experienced runners. Maximal inspiratory and expiratory pressure, peak inspiratory and expiratory flow, forced vital capacity, and forced expiratory volume in one second were assessed before, immediately after, and four and 24 hours after a marathon. During the run, leg effort was rated higher than respiratory effort from 18 through 42 km (P < 0.05). Immediately after the marathon, there were significant decreases in maximal inspiratory pressure and peak inspiratory flow (from 118 ± 20 cm H2O and 6.3 ± 1.4 litres · s−1 to 100 ± 22 cm H2O and 4.9 ± 1.5 litres · s−1 respectively; P < 0.01), while expiratory function remained unchanged. Leg maximum voluntary contraction force was significantly lower post-marathon. Breathing effort correlated significantly with leg fatigue (r = 0.69), but not inspiratory muscle fatigue. Our results confirm that prolonged moderate-intensity exercise induces inspiratory muscle fatigue. Furthermore, they suggest that the relative intensity of inspiratory muscle work during exercise makes some contribution to leg fatigue.

Non‐invasive tension time index in relation to severity of disease in children with cystic fibrosis

The non-invasive tension-time index of the inspiratory muscles at rest (TTMUS) can be used for assessing respiratory muscle function in children with cystic fibrosis (CF). This study aimed to investigate how TTMUS becomes altered with increasing pulmonary impairment, and which factors determine TTMUS changes in CF. We assessed TTMUS in 47 patients with stable CF ranging in age from 9 to 26 years and in 47 controls of same age and gender. Pulmonary impairment was assessed by the pulmonary function score (PFS) according to Cropp (PFS 0-2 = no, 3-7 = mild, 8-12 = moderate, and 13-18 = severe dysfunction). Median TTMUS was significantly higher in the entire CF-group than in controls ((0.112 (0.079-0.174) vs. 0.07 (0.052-0.094), P < 0.001)). It was nearly identical in CF-patients without (0.079 (0.056-0.114)) and mild (0.080 (0.059-0.128)) pulmonary dysfunction. It was non-significantly higher in subjects with moderate (0.118 (0.103-0.173)) and grossly elevated in individuals with severe (0.232 (0.211-0.31), P < 0.001)) respiratory impairment when compared to the other PFS-groups. TTMUS was significantly related to percent predicted airway resistance (Raw%pred) (r = 0.60, P < 0.001), percent predicted Forced Expiratory Volume in 1 sec (r = -0.49, P < 0.001), percent predicted Vital Capacity (-0.57, P < 0.001), Functional Residual Capacity in percent Total Lung Capacity (r = 0.42, P = 0.003), and transcutaneous oxygen saturation (r = -0.49, P < 0.001). By contrast, Raw%pred was the only variable that had a significant effect on TTMUS (P = 0.01), when a multivariate logistic regression was applied, using the median of the entire CF-cohort to dichotomise TTMUS. These findings suggest that subjects with stable CF and severe pulmonary dysfunction are prone to respiratory muscle fatigue, and that airway obstruction is an important factor contributing to the increase of TTMUS in CF. Regular determination of TTMUS may be clinically useful during course of disease, and may aid the decision to institute therapies like respiratory muscle training or non-invasive intermittent ventilation.

Mechanisms of improvement of respiratory failure in patients with COPD treated with NIV

Noninvasive ventilation (NIV) improves gas-exchange and symptoms in selected chronic obstructive pulmonary disease (COPD) patients with hypercapnic respiratory failure. We hypothesized NIV reverses respiratory failure by one or all of increased ventilatory response to carbon-dioxide, reduced respiratory muscle fatigue, or improved pulmonary mechanics. Nineteen stable COPD patients (forced expiratory volume in one second 35% predicted) were studied at baseline (DO), 5-8 days (D5) and 3 months (3M) after starting NIV. Ventilator use was 6.2 (3.7) hours per night at D5 and 3.4 (1.6) at 3M (p = 0.12). Mean (SD) daytime arterial carbon-dioxide tension (PaCO2) was reduced from 7.4 (1.2) kPa to 7.0 (1.1) kPa at D5 and 6.5 (1.1) kPa at 3M (p = 0.001). Total lung capacity decreased from 107 (28) % predicted to 103 (28) at D5 and 103 (27) % predicted at 3M (p = 0.035). At D5 there was an increase in the hypercapnic ventilatory response and some volitional measures of inspiratory and expiratory muscle strength, but not isolated diaphragmatic strength whether assessed by volitional or nonvolitional methods. These findings suggest decreased gas trapping and increased ventilatory sensitivity to CO2 are the principal mechanism underlying improvements in gas-exchange in patients with COPD following NIV. Changes in some volitional but not nonvolitional muscle strength measures may reflect improved patient effort.

Modulation of ventilatory mechanics during exercise in ventilation-limited populations

The aim of this thesis was to examine the impact of modifications to ventilatory constraint in populations who have reductions in expiratory flow and ventilatory limitations during exercise. The first study examined the effect of the self-contained breathing apparatus (SCBA) regulator on work of breathing (WOB) and lung volume changes in healthy subjects. The second study further examined the effect of the SCBA on the above outcomes, as well as on pulmonary function and respiratory muscle fatigue during stair-stepping (in healthy subjects). In addition, the effect of breathing heliox on the aforementioned variables was studied. The third thesis study examined the effect of heliox on ventilatory constraint, exercise tolerance, and leg muscle fatigue in patients with chronic obstructive pulmonary disease (COPD). The main results of the first study were that, compared with a low-resistance breathing valve (RV), the SCBA regulator increased inspiratory elastic (32%), expiratory resistive (59%), and total WOB (13%), and increased end-expiratory lung volume creating a plateau in end-inspiratory lung volume at approximately 90% of vital capacity. When these variables were examined with the full SCBA and compared with the RV in the second study, similar results were found. In addition, resting pulmonary function was reduced with the SCBA. Exercise with the SCBA induced reductions in both inspiratory and expiratory maximal pressures indicating the presence of respiratory muscle fatigue. When compressed air was replaced with heliox in the SCBA, end-expiratory lung volume, total WOB, and respiratory muscle fatigue were reduced. These observations regarding the effect of heliox on ventilatory function led to the third study, which found that heliox increased exercise tolerance (53%) and leg muscle fatigue (15%) in patients with COPD, but only in those limited by ventilatory constraints and who did not have a significant level of leg fatigue while breathing room air. Those patients who did have leg fatigue on room air did not increase exercise tolerance despite reduced ventilatory constraint. Together, these findings indicate that reducing ventilatory constraint during exercise can have specific positive effects on exercise performance in populations who are ventilatory limited and have implications for occupational or rehabilitation exercise training.

Influence of Baseline Respiratory Muscle Strength on Respiratory Muscle Fatigue Following Exhaustive Intermittent Exercise

PURPOSE: The purpose of this study was to determine the severity of inspiratory muscle fatigue (IMF) and expiratory muscle fatigue (EMF) following exhaustive intermittent exercise in female athletes. The study also addressed the question of whether higher values of inspiratory muscle strength (PImax) or expiratory muscle strength (PEmax) relate to the severity of respiratory muscle fatigue (RMF) after intermittent exercise. METHODS: Female collegiate soccer athletes (N = 16) from a NCAA Division II university volunteered to participate in the study. PImax and PEmax were assessed from participants using a portable mouth pressure meter. Participants completed the Yo-Yo Intermittent Recovery test (IRT) to exhaustion. Upon completion of the IRT, PImax and PEmax were measured to determine levels of RMF in participants. RESULTS: Average PImax and PEmax values were 118.6 ± 8.0 and 128.3 ± 28.1 cmH2O, respectively. There was a significant drop in both PImax (-15.4 ± 12.4%; p =.000) and PEmax (-12.8 ± 9.7%, p = .000) following the completion of the IRT. PImax and level of IMF were inversely related, although not significantly (r = -.40; p = .061). PEmax and EMF were not significantly related (r = .004; p = .494). RMF was compared between participants (n = 4) exhibiting the highest PImax (HPI) to the lowest (LPI, n = 4), (140.3 ± 8.8 cmH20 vs. 96.3 ± 13.6 cmH20). HPI experienced a -20 ± 16.1 cmH20 (-13.9 ± 11.3%) drop in PImax post exercise compared to a -25.5 ± 8.4 cmH20 (-27.7 ± 12.9%) drop in LPI. No significant differences were found between these two subgroups in absolute loss of PImax (p = .567) or percentage loss (p = .161). In addition, no significant correlations were found between baseline PImax or PEmax and performance in the IRT. CONCLUSIONS: These data support existing evidence of RMF following intense exercise and that RMF occurs after intermittent exercise in female athletes. Mean percentage values of IMF were less in individuals with higher baseline values of PImax suggesting "protection" from IMF, but statistical differences were not observed. Baseline PEmax does not appear to relate to severity of EMF post-exercise. In addition, baseline PImax and PEmax did not appear to predict intermittent exercise performance. The relationships between respiratory muscle strength, RMF, and exercise performance warrant further study.

The Effects of N-Acetylcysteine on Respiratory Muscle Fatigue During Heavy Exercise

Diaphragmatic fatigue is known to limit endurance performance during heavy exercise. Previous reports have shown that diaphragmatic fatigue is reduced in rats with N-acetylcysteine (NAC; a nonspecific antioxidant) infusion suggesting that oxidative stress contributes to this fatigue. However, it is not know if oral supplementation of NAC will reduce respiratory muscle fatigue during heavy exercise in humans. PURPOSE: To determine the effect of an acute oral dose of NAC on respiratory muscle fatigue during whole body heavy exercise. METHODS: Eight healthy men (22+2 yrs; VO2peak: 43+5 ml/kg/min) initially completed baseline pulmonary function tests followed by an incremental cycle VO2peak test. Subjects then performed a randomized, double blind crossover study where subjects were given either placebo (PLA) or NAC (1800 mg) 45 min prior to a constant load (85% VO2peak), discontinuous, 30 minute cycle exercise test. Tests were separated by one week. Maximum pressures (inspiratory, PImax; expiratory, PEmax) and venous blood samples (lactate and total glutathione) were made prior to- and following each 5-min of exercise. RESULTS: There was no difference (p>0.05) in PImax between NAC (127.9+34.1 cmH2O) or PLA (134.1+28.1 cmH2O) at rest. During exercise, PImax was significantly lower (~14%) in 6 of 8 subjects with PLA compared to NAC at minutes 25 and 30; whereas with NAC, PImax did not change (p>0.05) from rest throughout exercise indicating no respiratory muscle fatigue. There was no difference (p>0.05) in PEmax, plasma glutathione, lactate, VO2, VE, or HR between PLA and NAC at rest or during exercise. CONCLUSIONS: These results suggest that an acute dose of NAC reduces respiratory muscle fatigue during high intensity exercise but does not alter other ventilatory or metabolic indices. These data indicate that NAC's affect on respiratory muscles may favorably influence endurance exercise performance. Support from Kansas State University Research Grant

Respiratory System Determinants of Peripheral Fatigue and Endurance Performance

We briefly summarize recent evidence pertaining to how mechanisms primarily under the control of the respiratory system-namely, arterial oxyhemoglobin desaturation, respiratory muscle work and fatigue, and cyclical fluctuations in intrathoracic pressure-may contribute to exercise limitation. Respiratory influences on cardiac output and on sympathetic vasoconstrictor activity and blood flow distribution are shown to be important determinants of performance. We also address how a compromised O2 transport exacerbates the rate of development of peripheral muscle fatigue and, in turn, precipitates central fatigue and exercise limitation.