Suppression of Abdominal Motor Activity during Swallowing in Cats and Humans

Diseases affecting pulmonary mechanics often result in changes to the coordination of swallow and breathing. We hypothesize that during times of increased intrathoracic pressure, swallow suppresses ongoing expiratory drive to ensure bolus transport through the esophagus. To this end, we sought to determine the effects of swallow on abdominal electromyographic (EMG) activity during expiratory threshold loading in anesthetized cats and in awake-healthy adult humans. Expiratory threshold loads were applied to recruit abdominal motor activity during breathing, and swallow was triggered by infusion of water into the mouth. In both anesthetized cats and humans, expiratory cycles which contained swallows had a significant reduction in abdominal EMG activity, and a greater percentage of swallows were produced during inspiration and/or respiratory phase transitions. These results suggest that: a) spinal expiratory motor pathways play an important role in the execution of swallow, and b) a more complex mechanical relationship exists between breathing and swallow than has previously been envisioned.     

Effects of changes in inspiratory muscle strength on the sensation of respiratory force

The sensation of respiratory muscle force was compared in seven normal subjects before and after inspiratory muscle strength training. Subjects performed 20 sustained maximal inspiratory maneuvers daily for 6-18 wk. Maximal inspiratory pressures (MIP) increased from 124 +/- 10 to 187 +/- 9 (SE) cmH2O (P less than 0.005). Exponents of the power function relationships between mouth pressure (Pm) and the intensity of the sensation of force, corrected for inspiratory duration, during magnitude scaling of resistive and elastic ventilatory loads were the same before and after training (P greater than 0.05). However, absolute sensation intensity (S) during resistive and elastic loading was reduced significantly after strength training but returned toward baseline levels greater than or equal to 8 wk after the cessation of training when the MIP had fallen to 150 +/- 5 cmH2O. The absolute S at a given Pm during ventilatory loading changed inversely with changes in MIP (P less than 0.001). Furthermore the relationship between absolute S and Pm expressed as a proportion of the MIP (Pm/MIP) was constant over testing periods. These results suggest that the sensation of respiratory muscle force reflects the proportion of the maximum force utilized in breathing and may be based on the level of respiratory motor command signals.     

An apparatus for altering the mechanical load of the respiratory system

We describe an apparatus for altering the mechanical load against which the respiratory muscles operate in humans. A closed system incorporates a rolling seal spirometer. The spirometer piston shaft is coupled to a fast-responding linear actuator that develops force in proportion to desired command signals. The command signal may be flow (resistive loading or unloading), volume (elastic loading or unloading), constant voltage (continuous positive or negative pressure), or any external function. Combinations of loads can be applied. Logic circuits permit application of the load at specific times during the respiratory cycle, and the magnitude of the loads is continuously adjustable. Maximum pressure output is +/- 20 cmH2O. The apparatus permits loading or unloading over a range of ventilation extending from resting levels to those observed during high levels of exercise (over 100 l/min). In response to a square-wave input, pressure rises exponentially with a time constant of 20 ms.     

Cardiac output and O2 consumption during inspiratory threshold loaded breathing

In this study, noninvasive measurements of cardiac output and O2 consumption were performed to estimate the blood flow to and efficiency of the respiratory muscles that are used in elevated inspiratory work loads. Five subjects were studied for 4.5 min at a respiratory rate of 18 breaths/min and a duty cycle of 0.5. Studies were performed at rest without added respiratory loads and at elevated inspiratory work loads with the use of an inspiratory valve that permitted flow only when a threshold pressure was maintained. Cardiac output and O2 consumption were calculated using a rebreathing technique. Respiratory muscle blood flow and O2 consumption were estimated as the difference between resting and loaded breathing. Work of breathing was calculated by integrating the product of mouth pressure and volume. Increases in cardiac output and O2 consumption in response of 4.5 min loaded breathing averaged 1.84 l/min and 108 ml/min, respectively. No increases were seen in response to 20-s loaded breathing. In a separate series of experiments on four subjects, though, cardiac output increased for the first 2 min then leveled off. These results indicate that the increase in cardiac output was a metabolic effect of the increased work load and was not caused primarily by the influence of the highly negative intrathoracic pressure on venous return. Efficiency of the respiratory muscles during inspiratory threshold loading averaged 5.9%, which was similar to measurements of efficiency of respiratory muscles using whole-body O2 consumption that have been reported previously in humans and in dogs.     

Exercise-induced respiratory muscle fatigue: implications for performance.

It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O(2) and CO(2) transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles.     

Effects of respiratory muscle work on exercise performance.

The normal respiratory muscle effort at maximal exercise requires a significant fraction of cardiac output and causes leg blood flow to fall. We questioned whether the high levels of respiratory muscle work experienced in heavy exercise would affect performance. Seven male cyclists [maximal O(2) consumption (VO(2)) 63 +/- 5 ml. kg(-1). min(-1)] each completed 11 randomized trials on a cycle ergometer at a workload requiring 90% maximal VO(2). Respiratory muscle work was either decreased (unloading), increased (loading), or unchanged (control). Time to exhaustion was increased with unloading in 76% of the trials by an average of 1.3 +/- 0.4 min or 14 +/- 5% and decreased with loading in 83% of the trials by an average of 1.0 +/- 0.6 min or 15 +/- 3% compared with control (P < 0.05). Respiratory muscle unloading during exercise reduced VO(2), caused hyperventilation, and reduced the rate of change in perceptions of respiratory and limb discomfort throughout the duration of exercise. These findings demonstrate that the work of breathing normally incurred during sustained, heavy-intensity exercise (90% VO(2)) has a significant influence on exercise performance. We speculate that this effect of the normal respiratory muscle load on performance in trained male cyclists is due to the associated reduction in leg blood flow, which enhances both the onset of leg fatigue and the intensity with which both leg and respiratory muscle efforts are perceived.     

Maturational and anesthetic effects on apneic thresholds in lambs

Periods of apnea are relatively common in newborns but rare in older infants. Postnatal changes in the response of the central neural respiratory circuits to afferent inputs may have a role in the age-related incidence of apnea. Therefore we determined the central neural apneic threshold to CO2 and superior laryngeal nerve (SLN) stimulation in halothane-anesthetized newborn (4- to 7-day-old) and older (45- to 56-day-old) lambs. The animals were vagotomized, paralyzed, and mechanically ventilated with hyperoxic gas. Phrenic nerve activity served as a monitor of central respiratory output. The CO2 and SLN apneic thresholds were defined as the arterial PCO2 when phrenic activity began after hyperventilation, and the quantity of current applied to the SLN that abolished phrenic activity, respectively. At equivalent concentrations of halothane, newborn lambs had higher CO2 apneic thresholds (P less than 0.05) and lower SLN apneic thresholds (P less than 0.05) than did older lambs. Increasing concentrations of halothane decreased (P less than 0.05) the SLN apneic threshold and increased (P less than 0.05) the CO2 apneic threshold. Equal incremental changes in halothane concentration induced similar changes in the apneic thresholds of both ages of lambs. The data suggest that with maturation, the central neural respiratory circuits become more responsive to CO2 and less responsive to SLN afferents. Halothane alters central neural responsiveness to these inputs in both ages similarly.     

Probabilistic Estimate of a Threshold for Eutrophication

Regime shifts, or massive changes in ecosystems, are often associated with thresholds in drivers such as climate, land-use change, nutrient fluxes, or other factors. A frequently studied example is eutrophication, which is a serious environmental problem of lakes and reservoirs associated with phosphorus (P) enrichment above a threshold. We estimated probability distributions of thresholds for eutrophication of Lake Mendota, Wisconsin, USA using 30 years of annual P budgets. Although thresholds were likely to influence eutrophication of the lake (probability 96.6%), the probability distributions of thresholds spanned a wide range of P loading rates. Management recommendations are consistent with simpler models that recommend P load targets near or below the lowest P loads observed in the past 30 years. If loads increase, there is considerable risk of crossing a threshold to sustained eutrophication with high in-lake P concentrations and poor water quality. On the other hand, if loads decrease there is a chance of crossing a mitigation threshold, causing substantial reductions in P concentrations and improvements in water quality. Consideration of these risks will increase estimates of the net economic benefits of lower P loading. Our analysis illustrates a process for estimating probability distributions for thresholds of ecosystem regime shifts. Even though threshold probability distributions may be wide with thick tails, they provide crucial information about potential consequences of alternative policy choices. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Inspiratory resistive load detection in conscious dogs

The physiological mechanisms mediating the detection of mechanical loads are unknown. This is, in part, due to the lack of an animal model of load detection that could be used to investigate specific sensory systems. We used American Foxhounds with tracheal stomata to behaviorally condition the detection of inspiratory occlusion and graded resistive loads. The resistive loads were presented with a loading manifold connected to the inspiratory port of a non-rebreathing valve. The dogs signaled detection of the load by lifting their front paw off a lever. Inspiratory occlusion was used as the initial training stimulus, and the dogs could reliably respond within the first or second inspiratory effort to 100% of the occlusion presentations after 13 trials. Graded resistances that spanned the 50% detection threshold were then presented. The detection threshold resistances (delta R50) were 0.96 and 1.70 cmH2O.l-1.s. Ratios of delta R50 to background resistance were 0.15 and 0.30. The near-threshold resistive loads did not significantly change expired PCO2 or breathing patterns. These results demonstrate that dogs can be conditioned to reliably and specifically signal the detection of graded inspiratory mechanical loads. Inspiration through the tracheal stoma excludes afferents in the upper extrathoracic trachea, larynx, pharynx, nasal passages, and mouth from mediating load detection in these dogs. It is unknown which remaining afferents (vagal or respiratory muscle) are responsible for load detection.     

Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads.

The sensation of increased respiratory resistance or effort is likely to be important for the initiation of alerting or arousal responses, particularly in sleep. Hypoxia, through its central nervous system-depressant effects, may decrease the perceived magnitude of respiratory loads. To examine this, we measured the effect of isocapnic hypoxia on the ability of 10 normal, awake males (mean age = 24.0 +/- 1.8 yr) to magnitude-scale five externally applied inspiratory resistive loads (mean values from 7.5 to 54.4 cmH(2)O. l(-1). s). Each subject scaled the loads during 37 min of isocapnic hypoxia (inspired O(2) fraction = 0.09, arterial O(2) saturation of approximately 80%) and during 37 min of normoxia, using the method of open magnitude numerical scaling. Results were normalized by modulus equalization to allow between-subject comparisons. With the use of peak inspiratory pressure (PIP) as the measure of load stimulus magnitude, the perception of load magnitude (Psi) increased linearly with load and, averaged for all loaded breaths, was significantly lower during hypoxia than during normoxia (20.1 +/- 0.9 and 23.9 +/- 1.3 arbitrary units, respectively; P = 0. 048). Psi declined with time during hypoxia (P = 0.007) but not during normoxia (P = 0.361). Our result is remarkable because PIP was higher at all times during hypoxia than during normoxia, and previous studies have shown that an elevation in PIP results in increased Psi. We conclude that sustained isocapnic hypoxia causes a progressive suppression of the perception of the magnitude of inspiratory resistive loads in normal subjects and could, therefore, impair alerting or arousal responses to respiratory loading.     

Occlusion pressure response to inspiratory flow-resistive loading in anesthetized swine.

Conscious animals subjected to inspiratory flow-resistive loading augment respiratory drive [as measured by airway occlusion pressure (P100)] independently of changes in chemical drive. Past studies of anesthetized subjects, however, have failed to demonstrate this response, and investigators have concluded that its presence depends on a state of consciousness. We tested the hypothesis that respiratory depression due to anesthesia or endogenous opioids rather than unconsciousness per se was responsible for this observation. Miniature piglets were anesthetized with ketamine and xylazine and subjected to hyperoxic CO2 rebreathing trials with and without added inspiratory resistance, before and after treatment with the opioid antagonist naltrexone. Before naltrexone there was a parallel leftward shift in the occlusion pressure vs. PCO2 relationship without a change in slope (delta P100/delta PCO2). After naltrexone there was a 45.5 +/- 15% increase in slope with loading. Addition of incremental doses of pentobarbital markedly reduced this increase in slope. We conclude that anesthetized animals can demonstrate flow-resistive load compensation in the form of augmented neuromuscular output not due to increased chemical drive. Failure to observe this response in past studies may reflect respiratory depression due to the anesthetic agents employed.     

Transient cervical nerve root compression modulates pain: load thresholds for allodynia and sustained changes in spinal neuropeptide expression

Nerve root compression produces chronic pain and altered spinal neuropeptide expression. This study utilized controlled transient loading in a rat model of painful cervical nerve root compression to investigate the dependence of mechanical allodynia on load magnitude. Injury loads (0-110mN) were applied quasistatically using a customized loading device, and load thresholds to produce maintained mechanical allodynia were defined. Bilateral spinal expression of substance P (SP) and calcitonin gene-related peptide (CGRP) was assessed 7 days following compression using immunohistochemistry to determine relationships between these neuropeptides and compression load. A three-segment change point model was implemented to model allodynia responses and their relationship to load. Load thresholds were defined at which ipsilateral and contralateral allodynia were produced and sustained. The threshold for increased allodynia was lowest for acute (day 1) ipsilateral responses (26.29mN), while thresholds for allodynia on day 7 were similar for the ipsilateral (38.16mN) and contralateral forepaw (38.26mN). CGRP, but not SP, significantly decreased with load; the thresholds for ipsilateral and contralateral CGRP decreases corresponded to 19.52 and 24.03mN, respectively. These thresholds suggest bilateral allodynia may be mediated by spinal mechanisms, and that these mechanisms depend on the magnitude of load.     

Importance of ventilation in modulating interaction between sympathetic drive and cardiovascular variability

Chemoreflex stimulation elicits both hyperventilation and sympathetic activation, each of which may have different influences on oscillatory characteristics of cardiovascular variability. We examined the influence of hyperventilation on the interactions between changes in R-R interval (RR) and muscle sympathetic nerve activity (MSNA) and changes in neurocirculatory variability, in 14 healthy subjects. We performed spectral analysis of RR and MSNA variability during each of the following interventions: 1) controlled breathing, 2) maximal end-expiratory apnea, 3) isocapnic voluntary hyperventilation, and 4) hypercapnia-induced hyperventilation. MSNA increased from 100% during controlled breathing to 170 +/- 25% during apnea (P = 0.02). RR was unchanged, but normalized low-frequency (LF) variability of both RR and MSNA increased markedly (P < 0.001). During isocapnic hyperventilation, minute ventilation increased to 20.2 +/- 1.4 l/min (P < 0.0001). During hypercapnic hyperventilation, minute ventilation also increased (to 19.7 +/- 1.7 l/min) as did end-tidal CO(2) (both P < 0.0001). MSNA remained unchanged during isocapnic hyperventilation (104 +/- 7%) but increased to 241 +/- 49% during hypercapnic hyperventilation (P < 0.01). RR decreased during both isocapnic and hypercapnic hyperventilation (P < 0.05). However, normalized LF variability of RR and of MSNA decreased (P < 0.05) during both isocapnic and hypercapnic hyperventilation, despite the tachycardia and heightened sympathetic nerve traffic. In conclusion, marked respiratory oscillations in autonomic drive induced by hyperventilation may induce dissociation between RR, MSNA, and neurocirculatory variability, perhaps by suppressing central genesis and/or inhibiting transmission of LF cardiovascular rhythms.     

Effect of pressure assist on ventilation and respiratory mechanics in heavy exercise

To assess the effect of the normal respiratory resistive load on ventilation (VE) and respiratory motor output during exercise, we studied the effect of flow-proportional pressure assist (PA) (2.2 cmH2O.l-1.s) on various ventilatory parameters during progressive exercise to maximum in six healthy young men. We also measured dynamic lung compliance (Cdyn) and lung resistance (RL) and calculated the time course of respiratory muscle pressure (Pmus) during the breath in the assisted and unassisted states at a sustained exercise level corresponding to 70-80% of the subject's maximum O2 consumption. Unlike helium breathing, resistive PA had no effect on VE or any of its subdivisions partly as the result of an offsetting increase in RL (0.78 cmH2O.1-1.s) and partly to a reduction in Pmus. These results indicate that the normal resistive load does not constrain ventilation during heavy exercise. Furthermore, the increase in exercise ventilation observed with helium breathing, which is associated with much smaller degrees of resistive unloading (ca. -0.6 cmH2O.l-1.s), is likely the result of factors other than respiratory muscle unloading. The pattern of Pmus during exercise with and without unloading indicates that the use of P0.1 as an index of respiratory motor output under these conditions may result in misleading conclusions.     

Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise.

We determined the effects of augmented expiratory intrathoracic pressure (P(ITP)) production on cardiac output (Q(TOT)) and blood flow distribution in healthy dogs and dogs with chronic heart failure (CHF). From a control expiratory P(ITP) excursion of 7 +/- 2 cmH2O, the application of 5, 10, or 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 47 +/- 23, 67 +/- 32, and 118 +/- 18% (P < 0.05 for all). Stroke volume (SV) rapidly decreased (onset <10 s) with increases in the expiratory P(ITP) excursion (-2.1 +/- 0.5%, -2.4 +/- 0.9%, and -3.6 +/- 0.7%, P < 0.05), with slightly smaller reductions in Q(TOT) (0.8 +/- 0.6, 1.0 +/- 1.1, and 1.8 +/- 0.8%, P < 0.05) owing to small increases in heart rate. Both Q(TOT) and SV were restored to control levels when the inspiratory P(ITP) excursion was augmented by the addition of an inspiratory resistive load during 15 cmH2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by -5 +/- 2% owing to significant reductions in vascular conductance (-7 +/- 2%). After the induction of CHF by 6 wk of rapid cardiac pacing at 210 beats/min, the expiratory P(ITP) excursions during nonloaded breathing were not significantly changed (8 +/- 2 cmH2O), and the application of 5, 10, and 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 15 +/- 7, 23 +/- 7, and 31 +/- 7%, respectively (P < 0.05 for all). Both 10 and 15 cmH2O expiratory threshold loads significantly reduced SV (-3.5 +/- 0.7 and -4.2 +/- 0.7%, respectively) and Q(TOT) (-1.7 +/- 0.4 and -2.5 +/- 0.4%, P < 0.05) after the induction of CHF, with the reductions in SV predominantly occurring during inspiration. However, the augmentation of the inspiratory P(ITP) excursion now elicited further decreases in SV and Q(TOT). Only the highest level of expiratory loading significantly reduced hindlimb blood flow (-4 +/- 2%) as a result of significant reductions in vascular conductance (-5 +/- 2%). We conclude that increases in expiratory P(ITP) production-similar to those observed during severe expiratory flow limitation-reduce cardiac output and hindlimb blood flow during submaximal exercise in health and CHF.     

Volume loading reduces pulmonary vascular resistance in ventilated animals with acute lung injury: evaluation of RV afterload

During mechanical ventilation, increased pulmonary vascular resistance (PVR) may decrease right ventricular (RV) performance. We hypothesized that volume loading, by reducing PVR, and, therefore, RV afterload, can limit this effect. Deep anesthesia was induced in 16 mongrel dogs (8 oleic acid-induced acute lung injury and 8 controls). We measured ventricular pressures, dimensions, and stroke volumes during positive end-expiratory pressures of 0, 6, 12, and 18 cmH(2)O at three left ventricular (LV) end-diastolic pressures (5, 12, and 18 mmHg). Oleic acid infusion (0.07 ml/kg) increased PVR and reduced respiratory system compliance (P < 0.05). With positive end-expiratory pressure, PVR was greater at a lower LV end-diastolic pressure. Increased PVR was associated with a decreased transseptal pressure gradient, suggesting that leftward septal shift contributed to decreased LV preload, in addition to that caused by external constraint. Volume loading reduced PVR; this was associated with improved RV output and an increased transseptal pressure gradient, which suggests that rightward septal shift contributed to the increased LV preload. If PVR is used to reflect RV afterload, volume loading appeared to reduce PVR, thereby improving RV and LV performance. The improvement in cardiac output was also associated with reduced external constraint to LV filling; since calculated PVR is inversely related to cardiac output, increased LV output would reduce PVR. In conclusion, our results, which suggest that PVR is an independent determinant of cardiac performance, but is also dependent on cardiac output, improve our understanding of the hemodynamic effects of volume loading in acute lung injury.     

Reduced nucleus pulposus glycosaminoglycan content alters intervertebral disc dynamic viscoelastic mechanics

The intervertebral disc functions over a range of dynamic loading regimes including axial loads applied across a spectrum of frequencies at varying compressive loads. Biochemical changes occurring in early degeneration, including reduced nucleus pulposus glycosaminoglycan content, may alter disc mechanical behavior and thus may contribute to the progression of degeneration. The objective of this study was to determine disc dynamic viscoelastic properties under several equilibrium loads and loading frequencies, and further, to determine how reduced nucleus glycosaminoglycan content alters dynamic mechanics. We hypothesized that (1) dynamic stiffness would be elevated with increasing equilibrium load and increasing frequency, (2) the disc would behave more elastically at higher frequencies, and finally, (3) dynamic stiffness would be reduced at low equilibrium loads under all frequencies due to nucleus glycosaminoglycan loss. We mechanically tested control and chondroitinase ABC injected rat lumbar motion segments at several equilibrium loads using oscillatory loading at frequencies ranging from 0.05 to 5 Hz. The rat lumbar disc behaved non-linearly with higher dynamic stiffness at elevated compressive loads irrespective of frequency. Phase angle was not affected by equilibrium load, although it decreased as frequency was increased. Reduced glycosaminoglycan decreased dynamic stiffness at low loads but not at high equilibrium loads and led to increased phase angle at all loads and frequencies. The findings of this study demonstrate the effect of equilibrium load and loading frequencies on dynamic disc mechanics and indicate possible mechanical mechanisms through which disc degeneration can progress.     

Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance.

The aim of this study was to investigate the effect of a high-fat diet (HFD) followed by 1 day of carbohydrate (CHO) loading on substrate utilization, heart rate variability (HRV), effort perception [rating or perceived exertion (RPE)], muscle recruitment [electromyograph (EMG)], and performance during a 100-km cycling time trial. In this randomized single-blind crossover study, eight well-trained cyclists completed two trials, ingesting either a high-CHO diet (HCD) (68% CHO energy) or an isoenergetic HFD (68% fat energy) for 6 days, followed by 1 day of CHO loading (8-10 g CHO/kg). Subjects completed a 100-km time trial on day 1 and a 1-h cycle at 70% of peak oxygen consumption on days 3, 5, and 7, during which resting HRV and resting and exercising respiratory exchange ratio (RER) were measured. On day 8, subjects completed a 100-km performance time trial, during which blood samples were drawn and EMG was recorded. Ingestion of the HFD reduced RER at rest (P < 0.005) and during exercise (P < 0.01) and increased plasma free fatty acid levels (P < 0.01), indicating increased fat utilization. There was a tendency for the low-frequency power component of HRV to be greater for HFD-CHO (P = 0.056), suggestive of increased sympathetic activation. Overall 100-km time-trial performance was not different between diets; however, 1-km sprint power output after HFD-CHO was lower (P < 0.05) compared with HCD-CHO. Despite a reduced power output with HFD-CHO, RPE, heart rate, and EMG were not different between trials. In conclusion, the HFD-CHO dietary strategy increased fat oxidation, but compromised high intensity sprint performance, possibly by increased sympathetic activation or altered contractile function.     

Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.