Development of respiratory muscle contractile fatigue in the course of hyperpnoea

To assess the development of inspiratory and expiratory muscle fatigue during normocapnic hyperpnoea, we studied fourteen healthy men performing 8 min hyperpnoea, 6 min pause, 8 min hyperpnoea, etc., until task failure. Twitch transdiaphragmatic (P_di,tw) and gastric (P_ga,tw) pressures were measured during cervical and thoracic magnetic nerve stimulation, before hyperpnoea, after every 8 min of hyperpnoea, and at task failure (i.e., at 25.3 ± 4.7 min). P_di,tw decreased during the first 16 min (−28 ± 7%, p < 0.001) and P_ga,tw during the first 8 min (−20 ± 7%, p < 0.001) of hyperpnoea without further change until task failure. During inspiration, the pressure–time-product of oesophageal pressure (PTP_oes) increased relative to PTP_di during the first 16 min (+11 ± 21%, p < 0.05). Similarly, during expiration, PTP_oes increased relative to PTP_ga during the first 8 min (+10 ± 16%, p < 0.05). Also, blood lactate concentration and respiratory sensations significantly increased during the first 8 min (+1.0 ± 0.5 mmol l⁻¹, p < 0.001) and 16 min (breathlessness +1.6 ± 1.8 points, respiratory effort +5.9 ± 2.2 points, p < 0.001), respectively. We conclude that, during hyperpnoea, contractile fatigue of the diaphragm and abdominal muscles develops long before task failure and may trigger an increased recruitment of rib cage muscles.     

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO₂ retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate ( f_R), paced at 18 min^–1, with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P_es,tw), gastric (P_ga,tw), and transdiaphragmatic (P_di,tw) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P_di,tw significantly decreased from 33.1 to 25.9 cmH₂O in the first run, partially recovered (27.6 cmH₂O), and decreased further in the second run (23.4 cmH₂O). P_es,tw also decreased significantly (–5.1 and –2.4 cmH₂O), while P_ga,tw did not change significantly (–2.0 and –1.9 cmH₂O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO₂ (P_ETCO₂) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (S_aO₂) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in P_ETCO₂, and/or decreases in S_aO₂, probably contributed to task-failure.     

Expiratory effort enhancement and peak expiratory flow in humans

Peak expiratory flow (PEF) has previously been considered an effort-dependent, non flow-limited parameter that is constrained by the force–velocity relationship of the respiratory muscles. It has also been assumed that, if the muscles were able to augment the expiratory pressure, the PEF would increase. We tested the validity of this notion in normal volunteers who were able to enhance their expiratory pressure with maneuvers utilizing the stretch-shortening cycle (greater force when contractions were immediately preceded by eccentric contractions). Five healthy volunteers [35 (2) years] performed two successive maximal expiratory flow-volume maneuvers (MEFV) in rapid sequence. MEFV1 was a standard maneuver, whereas MEFV2 included a forceful inspiration to total lung capacity; a strategy designed to augment expiratory pressure via the stretch-shortening cycle. Neither maneuver included a post-inspiratory pause. We measured PEF, esophageal pressure (P_es), and the electromyographic activity of the abdominal muscles. Compared to MEFV1, MEFV2 produced greater activation of the abdominal muscles during inspiration (eccentric contraction), greater peak expiratory P_es, greater rate of rise of P_es, shorter time to PEF, but similar PEF. Our findings directly demonstrate the inability of the augmented expiratory effort to increase PEF and thus support the notion that PEF is determined by a flow-limiting mechanism and not by the velocity of muscle shortening.     

Maximal dynamic expiratory pressures with fast and slow inspirations

Maximal dynamic expiratory pressures are higher when forced expiration is preceded by a fast inspiration to total lung capacity (TLC) than when preceded by a slow inspiration and a few seconds pause at TLC. We hypothesized that these pressure differences are due to the stretch-shorten cycle (SSC), which refers to enhancement of muscle force when a concentric muscle contraction is immediately preceded by an eccentric contraction. Seven volunteers [36 (2) years; mean (SEM)] performed maximal forced expirations against minimal resistance with fast (F) or slow (S) maneuvers. F maneuvers consisted of a fast inspiration to TLC followed immediately by a fast expiration, whereas S consisted of a slow inspiration to TLC and a 4- to 5-s pause at TLC prior to forced expiration. We measured esophageal pressure (P _es), peak expiratory flow rate (PEFR), and the EMG activity of the transversus abdominis (Tr) by means of intramuscular fine-wire electrodes. The subjects performed several runs of each maneuver in a random order, and runs with the greatest expiratory P _es were analyzed. In comparison with S, F yielded greater P _es [182 (15) versus 167 (15) cmH₂O; P=0.003)] but similar PEFR [9.8 (0.7) versus 9.6 (0.7) l/s, P>0.05] and EMG activity of the Tr during forced expiration [221 (31) versus 208 (34) a.u., P>0.05]. Further analysis revealed significant EMG activity of Tr during end-inspiration (eccentric contraction) with F maneuvers only [73 (22) versus 32 (17) a.u., P<0.05]. We conclude that the ability of expiratory muscles to generate greater P _es with F maneuvers is related to the sequence of an eccentric contraction, which is followed immediately by concentric contraction in a manner analogous to SSC described in skeletal muscles. Electronic Publication     

Central and peripheral components of diaphragmatic fatigue during inspiratory resistive load in cats

The development of fatigue was investigated in the diaphragm of anaesthetized, tracheostomized, spontaneously breathing cats during restricted air flow. Ventilation, transdiaphragmatic pressure (P_di), integrated electrical activity of diaphragm (E_di) and phrenic nerve (E_ph) were measured simultaneously and expressed as a percentage of values at unloaded breathing. Inspiratory loads were 60, 70 and 80% of P_{di max}. The P_{di max} was measured by airway occlusion at functional residual capacity. The duration of loads was 40–60 min. The diaphragmatic fatigue developed only during heavy inspiratory loading (80% P_{di max}). During the first 10 min of heavy load P_di, E_di and E_ph increased to 905 ± 60%, 248 ± 20% and 229 ± 24%, respectively (P < 0.01), and then began to fall gradually. Ventilation declined to 39 ± 3% after 60 min of heavy load (P < 0.01), resulting in acute hypercapnia and hypoxia. Initial fatigue appeared as a decrease in P_di (to 781 ± 63%) and parallel decline in E_di (to 233 ± 21%) after 30 min of load (P < 0.05). Phrenic nerve activity did not change during this stage. These data suggest a peripheral basis of diaphragmatic fatigue, related to disorders in neuromuscular transmission. After 60 min of heavy load, P_di fell to 675 ± 49%, E_di declined to 209 ± 28% and E_ph decreased to 189 ± 25%. We interpret the decrease in phrenic nerve activity as a weakening of central inspiratory drive and development of the central component of diaphragmatic fatigue in the last stage.     

Locomotor and diaphragm muscle fatigue in endurance athletes performing time-trials of different durations

Purpose

Fatigue in leg muscles might differ between running and cycling due to inherent differences in muscle activation patterns. Moreover, postural demand placed upon the diaphragm during running could augment the development of diaphragm fatigue.

Methods

We investigated quadriceps and diaphragm fatigue in 11 runners and 11 cyclists (age: 29 ± 5 years; \(\dot{V}\) O_2,peak: 66.9 ± 5.5 ml min^?1 kg^?1) by assessing quadriceps twitch force (Q _tw) and transdiaphragmatic twitch pressure (P _di,tw) before and after 15- and 30-min time-trials (15TT, 30TT). Inspiratory muscle fatigue was also obtained after volitional normocapnic hyperpnoea (NH) where postural demand is negligible. We hypothesized that running and cycling would induce different patterns of fatigue and that runners would develop less respiratory muscle fatigue when performing NH.

Results

The reduction in Q _tw was greater in cyclists (32 ± 6 %) compared to runners (13 ± 8 %, p < 0.01), but not different for 15TTs (23 ± 13 %) and 30TTs (21 ± 11 %, p = 0.34). Overall P _di,tw was more reduced after 15TTs (24 ± 8 %) than after 30TTs (20 ± 9 %, p = 0.04) while being similar for runners and cyclists (p = 0.78). Meanwhile, breathing duration in NH and the magnitude of inspiratory muscle fatigue were also not different (both p > 0.05).

Conclusion

Different levels of leg muscle fatigue in runners and cyclists could in part be related to the specific muscle activation patterns including concentric contractions in both modalities but eccentric contractions in runners only. Diaphragm fatigue likely resulted from the large ventilatory load which is characteristic for both exercise modalities and which was higher in 15TTs than in 30TTs (+27 %, p < 0.01) while postural demand appears to be of less importance.     

The influence of inspiratory and expiratory muscle training upon rowing performance

We investigated the effect of 4 week of inspiratory (IMT) or expiratory muscle training (EMT), as well as the effect of a subsequent 6 week period of combined IMT/EMT on rowing performance in club-level oarsmen. Seventeen male rowers were allocated to either an IMT (n = 10) or EMT (n = 7) group. The groups underwent a 4 week IMT or EMT program; after interim testing, both groups subsequently performed a 6 week program of combined IMT/EMT. Exercise performance and physiological responses to exercise were measured at 4 and 10 week during an incremental rowing ergometer ‘step-test’ and a 6 min all-out (6MAO) effort. Pressure threshold respiratory muscle training was undertaken at the 30 repetition maximum load (∼50% of the peak inspiratory and expiratory mouth pressure, P _Imax or P _Emax, respectively). P _Imax increased during the IMT phase of the training in the IMT group (26%, P < 0.001) and was accompanied by an improvement in mean power during the 6MAO (2.7%, P = 0.015). Despite an increase in P _Emax by the end of the intervention (31%, P = 0.03), the EMT group showed no significant changes in any performance parameters during either the ‘step-test’ or 6MAO. There were no significant changes in breathing pattern or the metabolic response to the 6MAO test in either group, but the IMT group showed a small decrease in HR (2–5%, P = 0.001). We conclude that there were no significant additional changes following combined IMT/EMT. IMT improved rowing performance, but EMT and subsequent combined IMT/EMT did not.     

Effects of obesity on breathing pattern, ventilatory neural drive and mechanics

The purpose of this study was to assess whether obesity induces changes in breathing pattern and ventilatory neural drive and mechanics. Measurements performed in 34 male obese subjects (BMI, 39 ± 6 kg/m²) and 18 controls (BMI, 23 ± 3 kg/m²) included anthropometric parameters, spirometry, breathing patterns, mouth occlusion pressure, maximal inspiratory pressure and work of breathing. The results show that spirometric flow (FEV₁% pred, FVC% pred) and maximal inspiratory pressure (P_Imax) were significantly lowers (p < 0.001) in obese subjects compared to controls. The (fR/VT) ratio was higher in obese subjects than in controls (p < 0.001). The increase in (fR/VT) was associated with an increase in the ratio of mean inspiratory pressure to maximal inspiratory pressure (P_I/P_Imax) and the duty cycle (T_I/T_TOT) (p < 0.001). The energy cost of breathing (W_rest/W_crit), which reflects the oxygen consumed by the respiratory muscle was greater in obese subject than in controls (p < 0.001) inducing an increase in the effective inspiratory impedance on the respiratory muscles. It is concluded that obese subjects show impairment in breathing pattern and respiratory mechanics as assessed by rapid shallow breathing leading to ventilatory failure.     

Pulmonary blood flow generates cardiogenic oscillations

Cardiogenic oscillations are small waves produced by heartbeats, which are superimposed on the pressure and flow signals at the airway opening. The aim of this study was to investigate the role of the two main factors believed to generate these oscillations: (1) contact between heart and lungs and (2) pulmonary blood flow. We studied 15 heart surgery patients on cardiopulmonary bypass so both factors could be manipulated independently.At minimal heart–lung contact pressure and flow oscillations were larger than during maximal contact (1.20 ± 0.17 cmH₂O and 2.36 ± 0.08 L min⁻¹ vs 0.92 ± 0.15 cmH₂O and 1.78 ± 0.26 L min⁻¹, mean ± SD, p < 0.05). Cardiogenic oscillations for pressure and flow were smaller at 50% compared to 100% pulmonary blood flow (0.80 ± 0.12 cmH₂O and 1.56 ± 0.34 L min⁻¹ vs 1.19 ± 0.14 cmH₂O and 2.38 ± 0.19 L min⁻¹). We conclude that the amount of pulmonary blood flow and not the contact between heart and lungs is the main factor determining the amplitude of cardiogenic oscillations.     

Influence of expiratory flow-limitation during exercise on systemic oxygen delivery in humans

To determine the effects of exercise with expiratory flow-limitation (EFL) on systemic O₂ delivery, seven normal subjects performed incremental exercise with and without EFL at ~0.8 l s^–1 (imposed by a Starling resistor in the expiratory line) to determine maximal power output under control (W_max,c) and EFL (W_max,e) conditions. W_max,e was 62.5% of W_max,c, and EFL exercise caused a significant fall in the ventilatory threshold. In a third test, after exercising at W_max,e without EFL for 4 min, EFL was imposed; exercise continued for 4 more minutes or until exhaustion. O₂ consumption was measured breath-by-breath for the last 90 s of control, and for the first 90 s of EFL exercise. Assuming that the arterio-mixed venous O₂ content remained constant immediately after EFL imposition, we used as a measure of cardiac output (Q_c). Q_c was also calculated by the pulse contour method with blood pressure measured continuously by a photo-plethysmographic device. Both sets of data showed a decrease of Q_c due to a decrease in stroke volume by 10% with EFL and remained decreased for the full 90 s. Concurrently, arterial O₂ saturation decreased by 5%, abdominal, pleural and alveolar pressures increased, and duty cycle decreased by 43%. We conclude that this combination of events led to a decrease in venous return secondary to high expiratory pressures, and a decreased duty cycle which decreased O₂ delivery to working muscles by ~15%.     

Expiratory muscle fatigue impairs exercise performance

High-intensity, exhaustive exercise may lead to inspiratory as well as expiratory muscle fatigue (EMF). Induction of inspiratory muscle fatigue (IMF) before exercise has been shown to impair subsequent exercise performance. The purpose of the present study was to determine whether induction of EMF also affects subsequent exercise performance. Twelve healthy young men performed five 12-min running tests on a 400-m track on separate days: a preliminary trial, two trials after induction of EMF, and two trials without prior muscle fatigue. Tests with and without prior EMF were performed in an alternate order, randomly starting with either type. EMF was defined as a ≥20% drop in maximal expiratory mouth pressure achieved during expiratory resistive breathing against 50% maximal expiratory mouth pressure. The average distance covered in 12 min was significantly smaller during exercise with prior EMF compared to control exercise (2872 ± 256 vs. 2957 ± 325 m; P = 0.002). Running speed was consistently lower (0.13 m s⁻¹) throughout the entire 12 min of exercise with prior EMF. A significant correlation was observed between the level of EMF (decrement in maximal expiratory mouth pressure after resistive breathing) and the reduction in running distance (r ² = 0.528, P = 0.007). Perceived respiratory exertion was higher during the first 800 m and heart rate was lower throughout the entire test of running with prior EMF compared to control exercise (5.3 ± 1.6 vs. 4.5 ± 1.7 points, P = 0.002; 173 ± 10 vs. 178 ± 7 beats min⁻¹, P = 0.005). We conclude that EMF impairs exercise performance as previously reported for IMF.     

Acute effects of inspiratory pressure threshold loading upon airway resistance in people with asthma

Large inspiratory pressures may impart stretch to airway smooth muscle and modify the response to deep inspiration (DI) in asthmatics. Respiratory system resistance (Rrs) was assessed in response to 5 inspiratory manoeuvres using the forced oscillation technique: (a) single unloaded DI; (b) single DI at 25 cmH₂O; (c) single DI at 50% maximum inspiratory mouth pressure [MIP]; (d) 30 DIs at 50% MIP; and (e) 30 DIs at 50% MIP with maintenance of normocapnia. Rrs increased after the unloaded DI and the DI at 25 cmH₂O but not after a DI at 50% MIP (3.6 ± 1.6 hPa L s⁻¹ vs. 3.6 ± 1.5 hPa L s⁻¹; p = 0.95), 30 DIs at 50% MIP (3.9 ± 1.5 hPa L s⁻¹ vs. 4.2 ± 2.0 hPa L s⁻¹; p = 0.16) or 30 DIs at 50% MIP under normocapnic conditions (3.9 ± 1.5 hPa L s⁻¹ vs. 3.9 ± 1.5 hPa L s⁻¹; p = 0.55). Increases in Rrs in response to DI were attenuated after single and multiple loaded breaths at 50% MIP.     

Inspiratory versus expiratory efforts in pigeons: A search for selective drug influence

Respiratory activity of anaesthetized pigeons was stimulated by occluding the trachea. Inspiratory and expiratory efforts were measured in an early and in the agonal period of prolonged tracheal occlusions.In the early period the mean change in intratracheal pressure amounted to –0.79 cm H₂O and +0.73 cm H₂O per breath. These mean pressures are considered to represent an equivalent of the mean inspiratory and expiratory activity of that period. The corresponding figures in the agonal period were –1.18 and +2.48 cm H₂O, respectively.A palette of 10 drugs was tested to see whether they could alter respiratory efforts. None of the drugs, including the CNS-stimulants, was able to increase the efforts in either of the two periods. Some of the drugs (ethylurethane, pentobarbitone, codeine and 37059¹)) led to an impairment of the efforts performed in the early period, to about the same extent in both inspiration and expiration. One drug (37059) led to an impairment of the expiratory efforts in the agonal period and to an increase of the inspiratory efforts at the same time.     

Ventilation in Pacific hagfish (Eptatretus stoutii) during exposure to acute hypoxia or hypercapnia

A technique was developed to measure ventilation in unrestrained Pacific hagfish (Eptatretus stoutii) by inserting and fastening into the nostril a flexible tube fitted with an ultrasonic flow probe. This technique permitted the continuous measurement of ventilation (respiratory) frequency (fR), stroke volume and minute ventilation () in real time in fish exposed to acute hypoxia or hypercapnia. Exposing fish to acute hypoxia (final Pw_O2=21.0±3.4 mm Hg) caused hypoxaemia and a marked increase in of 350 ± 71 ml min⁻¹ kg⁻¹ (from 235 to 585 ml min⁻¹ kg⁻¹) owing exclusively to an increase in fR of 44 ± 7 min⁻¹ (from 19 to 63 min⁻¹). Because O₂ consumption (0.4 mmol kg⁻¹ h⁻¹) was unaltered during hypoxia, there was an associated marked increased in the ventilation convection requirement from 36.7 to 81.8 l mmol⁻¹. Injecting the O₂ chemoreceptor stimulant NaCN into inspired water (external CN⁻) or pre-branchial blood (internal CN⁻) evoked ventilatory responses that were similar to those observed during hypoxia although of a lesser magnitude. With external CN⁻, increased maximally by 146 ± 46 ml min⁻¹ kg⁻¹ and fR increased by 20 ± 2 min⁻¹. With internal CN⁻, the maximal increase in was 93 ± 30 ml min⁻¹ kg⁻¹ and fR increased maximally by 19 ± 6 min⁻¹. Exposure to acute hypercapnia (final PwC = 7.0 ± 0.2 mm Hg) caused an increase in of 169 ± 60 ml min⁻¹ kg⁻¹. These results provide compelling evidence for chemoreceptor-mediated control of breathing in hagfish and suggest that ventilatory responses to environmental hypoxia and hypercapnia in the vertebrates arose in the myxine lineage.     

Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

In acute heart failure, systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (P _LA) have to be controlled within acceptable ranges. Under this condition, cardiac energetic efficiency should also be improved. Theoretically, if heart rate (HR) is reduced while AP, CO, and P _LA are maintained by preserving the functional slope of left ventricular (LV) Starling’s curve (S _L) with precisely increased LV end-systolic elastance (E _es), it is possible to improve cardiac energetic efficiency and reduce LV oxygen consumption per minute (MVO ₂). We investigated whether this hemodynamics can be accomplished in acute heart failure using an automated hemodynamic regulator that we developed previously. In seven anesthetized dogs with acute heart failure (CO < 70 mL min⁻¹ kg⁻¹, P _LA > 15 mmHg), the regulator simultaneously controlled S _L with dobutamine, systemic vascular resistance with nitroprusside and stressed blood volume with dextran or furosemide, thereby controlling AP, CO, and P _LA. Normal hemodynamics were restored and maintained (CO; 88 ± 3 mL min⁻¹ kg⁻¹, P _LA; 10.9 ± 0.4 mmHg), even when zatebradine significantly reduced HR (−27 ± 3%). Following HR reduction, E _es increased (+34 ± 14%), LV mechanical efficiency (stroke work/oxygen consumption) increased (+22 ± 6%), and MVO ₂ decreased (−17 ± 4%) significantly. In conclusion, in a canine acute heart failure model, computationally managed bradycardia improved cardiac energetic efficiency while restoring normal hemodynamic conditions.     

Ammonia as a stimulant to ventilation in rainbow trout Oncorhynchus mykiss

Ammonia is the third most important respiratory gas in ammoniotelic fish after oxygen and carbon dioxide. We here investigated the effects of elevated plasma ammonia on ventilation in freshwater rainbow trout. Intact trout fitted with indwelling dorsal aortic catheters were given injections (over 5 min) of Cortland saline, isotonic high ammonia solutions (NH₄HCO₃, (NH₄)₂SO₄, NH₄OH at pH 8.0, and NH₄OH at pH 9.0), and other solutions as controls for acid–base effects, while ventilatory rate (VR) and buccal pressure amplitude (ΔP_buccal) were recorded. All high ammonia solutions resulted in immediate elevations of plasma Tamm_a, Pa_NH3, and [NH₄⁺]_a, and increases in ventilatory ΔP_buccal and VR to different degrees. However, while Pa_O2 remained constant, in every case there was a confounding change in one or more components of acid–base status (decreases in pH_a or increases in [HCO₃⁻]_a or Pa_CO2 in different treatments), although the ventilatory responses to ammonia injections were generally larger than could be explained by changes in acid–base status. Therefore a series was performed in which normal blood perfusion of the gills was replaced by ventral aortic perfusion with either Cortland saline or Cortland saline plus high ammonia in which pH, [HCO₃⁻], P_CO2, and P_O2 remained unchanged. Although ventilation was depressed in these anaesthetized, spontaneously ventilating preparations, perfusion with high ammonia saline increased ΔP_buccal. In a final series, trout were infused for 24 h with Cortland saline, isotonic NH₄HCO₃, or isotonic (NH₄)₂SO₄ solutions. The two ammonia solutions both caused persistent elevations in VR and ΔP_buccal, together with similar large increases in plasma Tamm_a, Pa_NH3, and [NH₄⁺]_a. As there was no changes in Pa_O2, pH_a, Pa_CO2, or [HCO₃⁻]_a in the (NH₄)₂SO₄ infusion series, this, together with the ventral aortic perfusion experiment, provides the most convincing evidence that ammonia stimulates ventilation. We suggest several circumstances (post-feeding, post-exercise) where the role of ammonia as a ventilatory stimulant may have adaptive benefits for O₂ uptake, and propose that ammonia-induced hyperventilation may also facilitate ammonia excretion in rainbow trout.     

Relations among motor unit types,generated forces and muscle length in single motor units of anaesthetized cat peroneus longus muscle

The active length-tension curves of identified single motor units (MUs) belonging to peroneus longus muscle (PL) of anaesthetized adult cats were obtained by eliciting isometric single twitches and tetani. The recorded responses were evaluated by measuring the peak tension amplitude and the tension-time area at muscle lengths extending throughout the physiological length range of the muscle (mean 5.5 mm, standard deviation ±0.8). The muscle lengths at which each tested MU developed its maximal twitch (L _tw) and tetanic (L _te) tensions were determined and compared with the muscle length (L _o) at which the stimulation of all the -axons, innervating PL and contained in L7 ventral root, developed their maximal twitch tension. The mean of single MU L _tw values was at L _o+1.08±1.1 mm. Slow MUs showed the longest values of L _tw(L _o+1.6±1.0 mm). Single MUs stimulated at tetanic frequencies presented their L _te at values shorter than L _o (L _o–2.8±1.7 mm). Slow MUs had the shortest L _te (L _o–3.4±1.5 mm). For all the units L _te was shorter than L _tw. L _tw and L _te were, respectively, negatively and positively correlated with the developed tension. Optimal length values also appeared to be related to the MU types. The possibility is discussed that the muscle and tendon compliances and the high non-linearities to the applied forces are the main factors which can determine the differences among L _o, L _tw and L _te values. The relationships between MU type and optimal length values are suggested to be, at least partly, an epiphenomenon due to the different contraction strengths of the various MU types. However, the heterogeneous distribution of the MU types is brought into account to explain the dependence of L _tw and L _te values on MU type.     

Effects of concurrent inspiratory and expiratory muscle training on respiratory and exercise performance in competitive swimmers

The efficiency of the respiratory system presents significant limitations on the bodys ability to perform exercise due to the effects of the increased work of breathing, respiratory muscle fatigue, and dyspnoea. Respiratory muscle training is an intervention that may be able to address these limitations, but the impact of respiratory muscle training on exercise performance remains controversial. Therefore, in this study we evaluated the effects of a 12-week (10 sessions week^–1) concurrent inspiratory and expiratory muscle training (CRMT) program in 34 adolescent competitive swimmers. The CRMT program consisted of 6 weeks during which the experimental group (E, n=17) performed CRMT and the sham group (S, n=17) performed sham CRMT, followed by 6 weeks when the E and S groups performed CRMT of differing intensities. CRMT training resulted in a significant improvement in forced inspiratory volume in 1 s (FIV_1.0) (P=0.050) and forced expiratory volume in 1 s (FEV_1.0) (P=0.045) in the E group, which exceeded the S groups results. Significant improvements in pulmonary function, breathing power, and chemoreflex ventilation threshold were observed in both groups, and there was a trend toward an improvement in swimming critical speed after 12 weeks of training (P=0.08). We concluded that although swim training results in attenuation of the ventilatory response to hypercapnia and in improvements in pulmonary function and sustainable breathing power, supplemental respiratory muscle training has no additional effect except on dynamic pulmonary function variables.     

Men and women exhibit a similar time to task failure for a sustained,submaximal elbow extensor contraction

Sex differences in muscle fatigue-resistance have been observed in a variety of muscles and under several conditions. This study compared the time to task failure (TTF) of a sustained isometric elbow extensor (intensity 15% of maximal strength) contraction in young men (n = 12) and women (n = 11), and examined if their neurophysiologic adjustments to fatigue differed. Motor-evoked potential amplitude (MEP), silent period duration, interference electromyogram (EMG) amplitude, maximal muscle action potential (M _max), heart rate, and mean arterial pressure were measured at baseline, during the task, and during a 2-min ischemia period. Men and women did not differ in TTF (478.2 ± 31.9 vs. 500.4 ± 41.3 s; P = 0.67). We also performed an exploratory post hoc cluster analysis, and classified subjects as low (n = 15) or high endurance (n = 8) based on TTF (415.3 ± 16.0 vs. 626.7 ± 25.8 s, respectively). The high-endurance group exhibited a lower MEP and EMG at baseline (MEP 16.3 ± 4.1 vs. 37.2 ± 3.0% M _max, P < 0.01; EMG 0.98 ± 0.18 vs. 1.85 ± 0.26% M _max, P = 0.03). These findings suggest no sex differences in elbow extensor fatigability, in contrast to observations from other muscle groups. The cluster analyses results indicated that high- and low-endurance groups displayed neurophysiologic differences at baseline (before performing the fatigue task), but that they did not differ in fatigue-induced changes in their neurophysiologic adjustments to the task.