Effect of inspiratory muscle work on peripheral fatigue of locomotor muscles in healthy humans

The work of breathing required during maximal exercise compromises blood flow to limb locomotor muscles and reduces exercise performance. We asked if force output of the inspiratory muscles affected exercise-induced peripheral fatigue of locomotor muscles. Eight male cyclists exercised at ≥ 90% peak O₂ uptake to exhaustion (CTRL). On a separate occasion, subjects exercised for the same duration and power output as CTRL (13.2 ± 0.9 min, 292 W), but force output of the inspiratory muscles was reduced (−56% versus CTRL) using a proportional assist ventilator (PAV). Subjects also exercised to exhaustion (7.9 ± 0.6 min, 292 W) while force output of the inspiratory muscles was increased (+80% versus CTRL) via inspiratory resistive loads (IRLs), and again for the same duration and power output with breathing unimpeded (IRL-CTRL). Quadriceps twitch force ( Q _tw), in response to supramaximal paired magnetic stimuli of the femoral nerve (1–100 Hz), was assessed pre- and at 2.5 through to 70 min postexercise. Immediately after CTRL exercise, Q _tw was reduced −28 ± 5% below pre-exercise baseline and this reduction was attenuated following PAV exercise (−20 ± 5%; P < 0.05). Conversely, increasing the force output of the inspiratory muscles (IRL) exacerbated exercise-induced quadriceps muscle fatigue ( Q _tw=−12 ± 8% IRL-CTRL versus −20 ± 7% IRL; P < 0.05). Repeat studies between days showed that the effects of exercise per se , and of superimposed inspiratory muscle loading on quadriceps fatigue were highly reproducible. In conclusion, peripheral fatigue of locomotor muscles resulting from high-intensity sustained exercise is, in part, due to the accompanying high levels of respiratory muscle work.     

Mouth pressure twitches induced by cervical magnetic stimulation to assess inspiratory muscle fatigue

This study aimed at determining whether twitch mouth pressure (TwPmo) induced by cervical magnetic stimulation (CMS) was sensitive to inspiratory muscle fatigue produced by whole body exercise (WBE) in normal subjects. Twenty subjects performed one or two of the following protocols: (i). cycling at 85% V(O(2),max) until exhaustion; (ii). inspiratory resistive load (IRL) breathing at 62% of maximal inspiratory pressure until task failure. In eight subjects, oesophageal (TwPoes), gastric (TwPga) and transdiaphragmatic (TwPdi) pressures were recorded. The TwPmo was significantly reduced (P<0.05) 20 min after both WBE and IRL, from 17.5+/-4.4 to 15.9+/-3.9 cmH(2)O and from 19.4+/-4.9 to 17.7+/-4.5 cmH(2)O, respectively. Subsequently to IRL, the TwPdi decrease was associated with a reduction in TwPoes/TwPga ratio; not after WBE. Independently of the mode of ventilatory loading, inspiratory muscle fatigue was detected. Thus, inspiratory muscle fatigue after WBE can be assessed in normal subjects with a noninvasive technique.     

Isotonic dynamometry for the assessment of power and fatigue in the knee extensor muscles of females.

Impairments in muscle power production and recovery following short-duration intense activity could lead to decreased performance and risk of injury. We developed a power test for the knee extensor muscles using torque-velocity testing and moderate isotonic loads. Twenty-eight female volunteers performed three maximal efforts at each of four isotonic loads (27.1, 40.6, 54.2 and 67.8 N. m). If the calculated regression line for the torque-velocity data had an r2 >/= 0.95 (i.e. an acceptable test), maximal power (408 +/- 56 W) was computed from the data. Immediately after torque-velocity testing, the subjects repeated maximal effort knee extensions with 33.9 N. m for three bouts of 15 repetitions with 15 s of rest to produce muscle fatigue, defined as a decrease in power output during isotonic exercise. After a 4 min rest, the torque-velocity test was repeated and power calculated (345 +/- 48 W). For the group, the recovery of maximal power after the fatigue protocol was 85%. The extremes were represented by one subject who recovered only 70% of her maximal power and another who recovered completely (>98%). Physiological differences in muscle power following repeated exercise could have an impact on the outcome of therapeutic interventions for sports injuries, fatigue syndromes and occupational over-use conditions.     

Differences in cardiorespiratory and neuromuscular responses between voluntary and stimulated contractions of the quadriceps femoris muscle

The aim of this study was to compare respiratory gas exchange variables and muscle fatigue between equal-intensity (i.e., same force output) electrostimulated and voluntary contractions of the quadriceps muscle (46+/-10% of maximal voluntary force). Twelve healthy men served as volunteers. Oxygen consumption, ventilation and respiratory exchange ratio were recorded during the exercise bouts. Muscle fatigue was quantified as the exercise-induced reduction in maximal voluntary force. The average oxygen consumption (11+/-3 versus 8+/-2 mL min(-1)kg(-1)), ventilation (23+/-4 versus 16+/-2 L min(-1)) and respiratory exchange ratio (0.96+/-0.02 versus 0.85+/-0.01) were significantly higher during electrostimulation compared with voluntary exercise (P<0.05-0.001). Maximal voluntary force decreased significantly after electrostimulation (-21+/-10%; P<0.001), while no changes were observed following voluntary exercise. Electrostimulation-resistance exercise of the quadriceps muscle elicited greater cardiorespiratory demand and muscle fatigue compared with voluntary contractions of the same intensity. These findings probably reflect differences in the patterns of motor unit recruitment between stimulated and voluntary contractions, despite equal force productions.     

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise

We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac(-)](B)) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation ([Formula: see text]). Prior to the intervention, the MLSS [lac(-)](B) was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L(-1) in the IMT and control groups, respectively. During volitional hyperpnoea, [Formula: see text] increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min(-1) at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min(-1) in IMT and control groups, respectively; [lac(-)](B) concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L(-1) (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.     

Impaired exercise ventilatory mechanics with the self-contained breathing apparatus are improved with heliox

The effect of the self-contained breathing apparatus (SCBA) with compressed air (BA-A) on ventilatory mechanics, work of breathing (WOB), pulmonary function, and respiratory muscle fatigue, was compared with that of a low resistance breathing valve (LRV). Further, the effect of unloading the respiratory muscles with heliox with the SCBA (BA-H) was compared with BA-A and LRV. Twelve men completed three randomized exercise trials on separate days, each consisting of three 10 min bouts of stepping exercise (Bouts 1, 2, and 3) separated by a 5 min recovery. Subjects wore firefighter protective equipment including the SCBA. At rest, FEV₁ and peak expiratory flow rates were lower with BA-A than with LRV, but were higher with BA-H than either with BA-A or LRV. After Bout 3, expiratory reserve volume, expiratory resistive WOB, and inspiratory elastic WOB were increased in BA-A compared to LRV but these were lower with BA-H compared to BA-A. After Bout 3, maximal inspiratory and expiratory pressures were reduced with BA-A, but not with LRV or BA-H. In summary, we found that the SCBA reduced resting pulmonary function, and increased expiratory reserve volume, work of breathing, and respiratory muscle fatigue during stepping exercise, and these changes can be reduced with the use of heliox.     

Ventilatory threshold characterizations during incremental rowing and cycling exercises in older subjects.

In order to individualize the intensity of an aerobic training program on different ergometers in healthy elderly subjects using a single test of muscular exercise, we analysed cardiorespiratory responses in 8 men (65.7 +/- 4.5 yrs) and 10 women (63.3 +/- 4.8 yrs). The heart rate corresponding to the ventilatory threshold was defined as individualised exercise intensity. All subjects carried out two incremental exercise tests on the cycle and rowing ergometers. For men, the results on the cycle ergometer and rowing ergometer demonstrated that, at ventilatory threshold, heart rates were not significantly different (114.6 +/- 13.7 and 115.6 +/- 14.2 beats x min (-1), respectively), but ventilation was significantly higher in rowing (p < 0.05). At ventilatory threshold, heart rates for women were not significantly different between the cycle ergometer and rowing ergometer (121.3 +/- 12.4 and 125.1 +/- 15.2 beats x min (-1 ), respectively), but ventilation was significantly higher in rowing (p< 0.01). At maximal exercise, maximal tidal volume for men (p < 0.01) and women (p < 0.05) was significantly higher in rowing. In spite of alterations of breathing patterns on the rowing ergometer, it is possible to design an individualized training program for healthy elderly subjects based on a single muscle evaluation exercise in order to diversify and optimize the cardiorespiratory benefits following an aerobic training program.     

Contractile properties of the human triceps surae following prolonged exercise and beta-blockade

Sixteen healthy males volunteered to perform both an incremental maximal and prolonged submaximal treadmill test with beta-blockade (2 X 80 mg oral propranolol per day) or matched placebo in a blind crossover design. Prior to and following the prolonged exercise, electrical stimulation of the triceps surae was performed to examine contractile properties. During the maximal test, the heart rate (HR) was reduced at all times by beta-blockade. The time to exhaustion in this test was significantly reduced by beta-blockade (P less than 0.03), while the maximal oxygen uptake (VO2 max) was not significantly lower (P = 0.06). In response to prolonged treadmill walking at 60% of VO2 max, the HR was reduced but VO2, respiratory quotient and ventilation were not affected by beta-blockade relative to placebo. Plasma concentrations of free fatty acids increased during exercise in the placebo but not beta-blocked treatment (P less than 0.0001). Plasma noradrenalin and adrenalin increased with exercise; the increase in adrenalin with beta-blockade was greater than that with placebo (P less than 0.0001). The RPE obtained at intervals during the prolonged exercise were greater for beta-blockades than placebo. Eight of 16 subjects were unable to complete full 90 min with beta-blockade; but all 16 completed the test with placebo. The electrically evoked twitches in the triceps surae muscle group after exercise did not differ in peak torque or one-half relaxation time compared to pre-exercise. The time to peak twitch torque was significantly shorter after exercise. No differences in twitch were observed due to beta-blockade. The tetanic responses at 10, 20, 50 and 100 Hz were not affected by either exercise or the beta-blockade. In conclusion, an increased subjective estimate of fatigue (RPE) was observed during prolonged exercise with beta-blockade. This subjective fatigue did not relate to altered peripheral muscle force production during electrical stimulation. The results suggest either a central rather than peripheral origin of fatigue, or fatigue in a muscle group not examined by stimulation of the triceps surae.     

Local metabolite accumulation augments passive muscle stretch-induced modulation of carotid-cardiac but not carotid-vasomotor baroreflex sensitivity in man.

We examined the effects of muscle mechanoreflex stimulation by passive calf muscle stretch, at rest and during concurrent muscle metaboreflex activation, on carotid baroreflex (CBR) sensitivity. Twelve subjects either performed 1.5 min one-legged isometric plantarflexion at 50% maximal voluntary contraction with their right or left calf [two ischaemic exercise (IE) trials, IER and IEL] or rested for 1.5 min [two ischaemic control (IC) trials, ICR and ICL]. Following exercise, blood pressure elevation was partly maintained by local circulatory occlusion (CO). 3.5 min of CO was followed by 3 min of CO with passive stretch (STR-CO) of the right calf in all trials. Carotid baroreflex function was assessed using rapid pulses of neck pressure from +40 to -80 mmHg. In all IC trials, stretch did not alter maximal gain of carotid-cardiac (CBR-HR) and carotid-vasomotor (CBR-MAP) baroreflex function curves. The CBR-HR curve was reset without change in maximal gain during STR-CO in the IEL trial. However, during the IER trial maximal gain of the CBR-HR curve was smaller than in all other trials (-0.34 +/- 0.04 beats min(-1) mmHg(-1) in IER versus -0.76 +/- 0.20, -0.94 +/- 0.14 and -0.66 +/- 0.18 beats min(-1) mmHg(-1) in ICR, IEL and ICL, respectively), and significantly smaller than in IEL (P < 0.05). The CBR-MAP curves were reset from CO values by STR-CO in the IEL and IER trials with no changes in maximal gain. These results suggest that metabolite sensitization of stretch-sensitive muscle mechanoreceptive afferents modulates baroreflex control of heart rate but not blood pressure.     

Effects of oral N-acetylcysteine on fatigue, critical power, and W' in exercising humans

The accumulation of reactive oxygen species (ROS) is associated with muscular fatigue. The antioxidant N-acetylcysteine (NAC) can extend time to fatigue (TTF), but the effect appears to be exercise intensity dependent. The purpose of this study was to determine the effects of an acute oral dose of NAC on time to fatigue (TTF), critical power (CP), W' (curvature constant), V(O2) kinetics and muscle EMG during cycling exercise. Male (n=7) subjects performed four tests at power outputs corresponding to 80, 90, 100, and 110% of the peak power output achieved during the incremental test (Pmax) under NAC and placebo (PLA) conditions. TTF was increased only in the 80% Pmax trial (p=0.033). CP was higher with NAC (NAC: 232±28 W versus PLA: 226±31 W; p=0.032), but W' tended to decrease (NAC: 15.5±3.8 kJ versus W': 16.4±4.5 kJ; p=0.10). The change in W' was negatively related to the change in CP (r = -0.96). MdPF and RMS of EMG tended to change less with NAC. There were no significant differences in V(O2) kinetics. These results demonstrate that oral NAC was successful in extending time to fatigue at 80% Pmax but not at higher work rates.     

Inspiratory muscles experience fatigue faster than the calf muscles during treadmill marching

The possibility that respiratory muscles may fatigue during extreme physical activity and thereby become a limiting factor leading to exhaustion is debated in the literature. The aim of this study was to determine whether treadmill marching exercise induces respiratory muscle fatigue, and to compare the extent and rate of respiratory muscle fatigue to those of the calf musculature. To identify muscle fatigue, surface electromyographic (EMG) signals of the inspiratory (sternomastoid, external intercostals), expiratory (rectus abdominis and external oblique) and calf (gastrocnemius lateralis) muscles were measured during a treadmill march of 2 km at a constant velocity of 8 km/h. The extent of fatigue was assessed by determining the increase in root-mean-square (RMS) of EMG over time, and the rate of fatigue was assessed from the slope of the EMG RMS versus time curve. Results indicated that (i) the inspiratory and calf muscles are the ones experiencing the most dominant fatigue during treadmill marching, (ii) the rate of fatigue of each muscle group was monotonic between the initial and terminal phases of exercise, and (iii) the inspiratory muscles fatigue significantly faster than the calf at the terminal phase of exercise, and are likely to fatigue faster during the initial exercise as well. Accordingly, this study supports the hypothesis that fatigue of the inspiratory muscles may be a limiting factor during exercise.     

The effect of oral creatine supplementation on the curvature constant parameter of the power-duration curve for cycle ergometry in humans.

For high-intensity cycle ergometer exercise, the tolerable duration (t) is well characterized as a hyperbolic function of power output, P : t = W'/(P-thetaF), where thetaF may be termed the "fatigue threshold." The purpose of this study was to determine the effect of oral creatine (Cr) supplementation on the curvature constant parameter (W') of the power-duration curve. A double-blind research method and a cross-over design were employed for creatine/placebo supplementation. Eight healthy male subjects (aged 18 to 22 years) each performed four or five high-intensity square-wave exercise bouts on an electrically braked cycle ergometer after 5 d of Cr monohydrate (CR: 20 g of Cr with artificial sweetener/d) or placebo (PL: 6 g of glucose/d) supplementation. Each subject performed a single high-intensity exercise trial per day for four or five successive days to determination the P-t hyperbolic relation. After 6 weeks (the washout time of Cr from the muscles), each subject performed the other condition (i.e., PL or CR) and repeated the same experimental procedure. There was no significant difference for thetaF between PL and CR conditions (PL: 214.4 +/- 23.6, CR: 207.0 +/- 19.8 W, mean +/- SD). In contrast, W' was significantly increased by the Cr supplementation (PL: 10.9 +/- 2.7, CR: 13.7 +/- 3.0 kJ; p<0.05). The results indicated that Cr and/or PCr content in muscles seems to be one of the important determinants of the curvature constant parameter (W') of the power-duration hyperbolic curve for cycle ergometry.     

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and [Formula: see text] Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at [Formula: see text] (IHE group, SaO(2) at [Formula: see text] baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise [Formula: see text] Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamuM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of [Formula: see text] was reduced (-0.9 +/- 0.8 DeltamuM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged [Formula: see text] following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.     

Restrictions in systemic and locomotor skeletal muscle perfusion, oxygen supply and VO2 during high-intensity whole-body exercise in humans

Perfusion to exercising skeletal muscle is regulated to match O(2) delivery to the O(2) demand, but this regulation might be compromised during or approaching maximal whole-body exercise as muscle blood flow for a given work rate is blunted. Whether muscle perfusion is restricted when there is an extreme metabolic stimulus to vasodilate during supramaximal exercise remains unknown. To examine the regulatory limits of systemic and muscle perfusion in exercising humans, we measured systemic and leg haemodynamics, O(2) transport, and , and estimated non-locomotor tissue perfusion during constant load supramaximal cycling (498 +/- 16 W; 110% of peak power; mean +/- S.E.M.) in addition to both incremental cycling and knee-extensor exercise to exhaustion in 13 trained males. During supramaximal cycling, cardiac output (Q), leg blood flow (LBF), and systemic and leg O(2) delivery and reached peak values after 60-90 s and thereafter levelled off at values similar to or approximately 6% (P < 0.05) below maximal cycling, while upper body blood flow remained unchanged (approximately 5.5 l min(-1)). In contrast, Q and LBF increased linearly until exhaustion during one-legged knee-extensor exercise accompanying increases in non-locomotor tissue blood flow to approximately 12 l min(-1). At exhaustion during cycling compared to knee-extensor exercise, Q, LBF, leg vascular conductance, leg O(2) delivery and leg for a given power were reduced by 32-47% (P < 0.05). In conclusion, locomotor skeletal muscle perfusion is restricted during maximal and supramaximal whole-body exercise in association with a plateau in Q and limb vascular conductance. These observations suggest that limits of cardiac function and muscle vasoconstriction underlie the inability of the circulatory system to meet the increasing metabolic demand of skeletal muscles and other tissues during whole-body exercise.     

Effects of aminophylline upon the exercise performance of patients with stable chronic airflow obstruction

To assess the effects of aminophylline upon the exercise performance of patients with chronic airflow obstruction (CAO), we performed ramp exercise tests (1 W/3 s) on six CAO subjects before and after intravenous aminophylline (6 mg X kg-1). The subjects had airflow obstruction (mean FEV1/FVC = 0.53) which did not improve following the inhalation of aerosolized isoetharine. After intravenous aminophylline, maximal oxygen uptake, maximal work rate and exercise duration increased (p less than 0.03) and the subjective dyspnea scores during exercise decreased (p less than 0.05). These changes were not accompanied by increases of FEV1 or peak expiratory flow rate, but maximal inspiratory pressure and peak inspiratory flow rate during exercise increased (p less than 0.05). These observations suggest that aminophylline acutely improves the maximal exercise performance of CAO subjects by mechanisms other than bronchodilation.     

New physiological insights into exercise-induced diaphragmatic fatigue

Data on the dynamic process and time-point of manifestation of exercise-induced diaphragmatic fatigue (DF) are lacking. Therefore, this study was aimed assessing dynamic changes of diaphragmatic strength during exercise and determining the time-point of DF manifestation. Fourteen trained subjects (maximal oxygen uptake (VO2(max)) 59.3+/-5.5 ml/min/kg) performed standardized exercise protocols (maximal workload: 85% VO2(max)) followed by recovery (6 min). Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF was induced (TwPdi-rest: 2.34+/-0.26 versus TwPdi-end-recovery 2.01+/-0.21 kPa, p<0.01). TwPdi progressively increased during exercise (TwPdi-rest: 2.34+/-0.26 versus TwPdi-maximal-workload: 3.28+/-0.38 kPa, p<0.001). DF was detectable immediately after exercise-termination (TwPdi-maximal-workload: 3.28+/-0.38 versus TwPdi-early-recovery 2.55+/-0.34 kPa, p<0.001). TwPdi during exercise was highly correlated to workload, VO2(max) and dyspnea (r=0.96/r=0.92/r=0.97; all p<0.0001). In conclusion, diaphragmatic strength progressively increases with increasing workload, and DF manifests after - rather than during - exercise. In addition, TwPdi is highly correlated to key-measures of ergospirometry, approving the physiological thesis that muscle strength is progressively enhanced and escapes fatiguing failure during high-intensity exercise performance.     

Leg uptake of calcitonin gene-related peptide during exercise in spinal cord injured humans.

Exercise-induced increases in cardiac output (CO) and oxygen uptake (VO2) are tightly coupled, as also in absence of central motor activity and neural feedback from skeletal muscle. Neuromodulators of vascular tone and cardiac function - such as calcitonin gene related peptide (CGRP) - may be of importance. Spinal cord injured individuals (six tetraplegic and four paraplegic) performed electrically induced cycling (FES) with their paralyzed lower limbs for 29 +/- 2 min to fatigue. Voluntary cycling performed both at VO2 similar to FES and at maximal exercise in six healthy subjects served as control. In healthy subjects, CGRP in plasma increased only during maximal exercise (33.8 +/- 3.1 pmol l(-1) (rest) to 39.5 +/- 4.3 (14%, P<0.05)) with a mean extraction over the working leg of 10% (P<0.05). Spinal cord injured individuals had more pronounced increase in plasma CGRP (33.2 +/- 3.8 to 46.9 +/- 3.6 pmol l-1, P<0.05), and paraplegic and tetraplegic individuals increased in average by 23% and 52%, respectively, with a 10% leg extraction in both groups (P<0.05). The exercise induced increase in leg blood flow was 10-12 fold in both spinal cord injured and controls at similar VO2 (P<0.05), whereas CO increased more in the controls than in spinal man. Heart rate (HR) increased more in paraplegic subjects (67 +/- 7 to 132 +/- 15 bpm) compared with controls and tetraplegics (P<0.05). Mean arterial pressure (MAP) was unchanged during submaximal exercise and increased during maximal exercise in healthy subjects, but decreased during the last 15 min of exercise in the tetraplegics. It is concluded that plasma CGRP increases during exercise, and that it is taken up by contracting skeletal muscle. The study did not allow for a demonstration of the origin of the CGRP, but its release does not require activation of motor centres. Finally, the more marked increase in plasma CGRP and the decrease in blood pressure during exercise in tetraplegic humans may indicate a role of CGRP in regulation of vascular tone during exercise.     

Acute effects of paroxetine on genioglossus activity in obstructive sleep apnea

STUDY OBJECTIVE: To determine the acute effects of paroxetine on genioglossus activity during NREM sleep. DESIGN: A single dose of Paroxetine (40 mg) or placebo was administered four hours before bedtime on nights separated by one week in a double blind randomized crossover manner. The moving time average of genioglossus muscle activity (EMGgg) expressed as a percentage of maximum was measured using a mouthpiece electrode customized for each subject. The peak inspiratory and tonic values of EMGgg and the corresponding esophageal pressure deflections (DP) during the last three occluded breaths of obstructive apneas during NREM sleep were analyzed. SETTING: NA. PARTICIPANTS: 8 adult men with severe obstructive sleep apnea (OSA). INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Paroxetine increased the peak inspiratory EMGgg (29.8+/-2.4 (SE) versus 24.4+/-2.7 % max, p<0.05) and peak EMGgg/DP ratio (0.78+/-0.12 versus 0.65+/-0.11 % max/cm H2O, p<0.01) but not the tonic EMGgg (11.6+/-0.9 versus 9.8+/-0.7 % max) nor the DP (39.4+/-2.2 versus 38.2+/-2.8 cm H2O). Linear regression analysis of the peak inspiratory EMGgg versus DP relationship showed that paroxetine increased the slope (0.62+/-0.11 versus 0.49+/-0.09 % max/cm H2O, p<0.01). However, the apnea + hypopnea index (paroxetine: 75.2+/-5.5 versus placebo: 73.7+/-6.9 events/hour) did not differ. CONCLUSIONS: Paroxetine augmented peak inspiratory genioglossus activity during NREM sleep but this effect was not sufficient to decrease the frequency of obstructive apnea in this group with severe OSA.     

Effect of acute hyperoxia during exercise on quadriceps electrical activity in active COPD patients

AIMS: This study investigated whether acute hyperoxia improves electrical muscle activity in active chronic obstructive pulmonary disease (COPD) patients with mild hypoxemia (rest PaO(2) = 9.1 +/- 0.4 kPa). METHODS: Two identical incremental exercise tests were performed by nine patients while breathing either air or 30% oxygen. Pulmonary gas exchanges, venous concentrations of lactate and pyruvate, and the electromyographic signal of the quadriceps muscle (vastus lateralis and vastus medialis) were sampled each minute. RESULTS: Peak working capacity increased significantly in hyperoxia (94.4 +/- 5.2W) compared with normoxia (85.4 +/- 5.8W, P < 0.01). During hyperoxic exercise and for a given work load, oxygen uptake was increased (P < 0.001) and ventilation decreased (P < 0.05). Lactate concentration was significantly decreased (P < 0.01) at isowork level and during recovery (respectively - 26% and at least - 15%). In the quadriceps muscle, M-wave amplitude (P < 0.05), root mean square (P < 0.01) and root mean square/oxygen uptake ratio (P < 0.001) were significantly increased during hyperoxic exercise compared with room air. Although median frequency values did not differ between conditions, the median frequency was significantly decreased for higher exercise intensity in hyperoxic condition. These modifications reflected better aerobic metabolism, later emergence of muscle fatigue, and greater muscle excitability and activation for the same level of exercise under hyperoxic condition. CONCLUSION: These data suggest that the acute addition of oxygen in active COPD patients improves their muscle electrical activity during dynamic exercise. Hypoxemia-induced skeletal muscle dysfunction most probably acts through mechanisms based on oxygen availability.     

Chest wall volume changes during inspiratory loaded breathing

We assessed the effect of inspiratory loaded breathing (ILB) on respiratory muscle strength and investigated the extent to which respiratory muscle fatigue is associated with chest wall volume changes during ILB. Twelve healthy subjects performed ILB at 76 ± 11% of maximal inspiratory mouth pressure (MIP) for 1h. MIP and breathing pattern during 3 min of normocapnic hyperpnea (NH) were measured before and after ILB. Breathing pattern and chest wall volume changes were assessed by optoelectronic plethysmography. After ILB, six subjects decreased MIP significantly (-16 ± 10%; p < 0.05), while the other six subjects did not (0 ± 7%, p = 0.916). Only subjects with decreased MIP after ILB lowered end-expiratory rib cage volume (volume at which inspiration is initiated) below resting values during ILB. During NH after ILB, tidal volume was smaller in subjects with decreased MIP (-19 ± 16%, p < 0.05), while it remained unchanged in the other group (-3 ± 11%, p = 0.463). These results suggest that respiratory muscle fatigue depends on the lung volume from which inspiratory efforts are made during ILB.