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.     

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.     

Respiratory mechanics during exercise in endurance-trained men and women

The purpose of this study was to compare the mechanics of breathing including the measurement of expiratory flow limitation, end-expiratory lung volume, end-inspiratory lung volume, and the work of breathing in endurance-trained men ( n = 8) and women ( n = 10) during cycle exercise. Expiratory flow limitation was assessed by applying a negative expiratory pressure at the mouth. End-expiratory lung volume and end-inspiratory lung volume were determined by having subjects perform inspiratory capacity manoeuvres. Transpulmonary pressure, taken as the difference between oesophageal and airway opening pressure, was plotted against volume and integrated to determine the work of breathing. Expiratory flow limitation occurred in nine females (90%) and three males (43%) during the final stage of exercise. Females had a higher relative end-expiratory lung volume (42 ± 8 versus 35 ± 5% forced vital capacity (FVC)) and end-inspiratory lung volume (88 ± 5 versus 82 ± 7% FVC) compared to males at maximal exercise ( P < 0.05). Women also had a higher work of breathing compared to men across a range of ventilations. On average, women had a work of breathing that was twice that of men at ventilations above 90 l min⁻¹. These data suggest that expiratory flow limitation may be more common in females and that they experience greater relative increases in end-expiratory lung volume and end-inspiratory lung volume at maximal exercise compared to males. The higher work of breathing in women is probably attributed to their smaller lung volumes and smaller diameter airways. Collectively, these findings suggest that women utilize a greater majority of their ventilatory reserve compared to men and this is associated with a higher cost of breathing.     

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.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40?min of bench stepping (knee high step; 15 steps?·?min^?1). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150?W, with increments of 50?W every 2?min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P?V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P?P?相似文献   

Effect of carrying a weighted backpack on lung mechanics during treadmill walking in healthy men

Weighted backpacks are used extensively in recreational and occupational settings, yet their effects on lung mechanics during acute exercise is poorly understood. The purpose of this study was to determine the effects of different backpack weights on lung mechanics and breathing patterns during treadmill walking. Subjects (n = 7, age = 28 ± 6 years), completed two 2.5-min exercise stages for each backpack condition [no backpack (NP), an un-weighted backpack (NW) or a backpack weighing 15, 25 or 35 kg]. A maximal expiratory flow volume curve was generated for each backpack condition and an oesophageal balloon catheter was used to estimate pleural pressure. The 15, 25 and 35 kg backpacks caused a 3, 5 and 8% (P < 0.05) reduction in forced vital capacity compared with the NP condition, respectively. For the same exercise stage, the power of breathing (POB) requirement was higher in the 35 kg backpack compared to NP (32 ± 4.3 vs. 88 ± 9.0 J min(-1), P < 0.05; respectively). Independent of changes in minute ventilation, end-expiratory lung volume decreased as backpack weight increased. As backpack weight increased, there was a concomitant decline in calculated maximal ventilation, a rise in minute ventilation, and a resultant greater utilization of maximal available ventilation. In conclusion, wearing a weighted backpack during an acute bout of exercise altered operational lung volumes; however, adaptive changes in breathing mechanics may have minimized changes in the required POB such that at an iso-ventilation, wearing a backpack weighing up to 35 kg does not increase the POB requirement.     

The effect of resistive breathing on leg muscle oxygenation using near-infrared spectroscopy during exercise in men

The effect of added respiratory work on leg muscle oxygenation during constant-load cycle ergometry was examined in six healthy adults. Exercise was initiated from a baseline of 20 W and increased to a power output corresponding to 90% of the estimated lactate threshold (moderate exercise) and to a power output yielding a tolerance limit of 11.8 min (+/- 1.4, S.D.) (heavy exercise). Ventilation and pulmonary gas exchange were measured breath-by-breath. Profiles of leg muscle oxygenation were determined throughout the protocol using near-infrared (NIR) spectroscopy (Hamamatsu NIRO 500) with optodes aligned midway along the vastus lateralis of the dominant leg. Four conditions were tested: (i) control (Con) where the subjects breathed spontaneously throughout, (ii) controlled breathing (Con Br) where breathing frequency and tidal volume were matched to the Con profile, (iii) increased work of breathing (Resist Br) in which a resistance of 7 cmH2O l(-1) s(-1) was inserted into the mouthpiece assembly, and (iv) partial leg blood flow occlusion (Leg Occl), where muscle perfusion was reduced by inflating a pressure cuff (approximately 90 mmHg) around the upper right thigh. During Resist Br and Leg Occl, subjects controlled their breathing pattern to reproduce the ventilatory profile of Con. An approximately 3 min period with respiratory resistance or pressure cuff was introduced approximately 4 min after exercise onset. NIR spectroscopy data for reduced haemoglobin-myoglobin (delta[Hb]) were extracted from the continuous display at specific times prior to, during and after removal of the resistance or pressure cuff. While the delta[Hb] increased during moderate- and heavy-intensity exercise, there was no additional increase in delta[Hb] with Resist Br. In contrast, delta[Hb] increased further with Leg Occl, reflecting increased muscle O2 extraction during the period of reduced muscle blood flow. In conclusion, increasing the work of breathing did not increase leg muscle deoxygenation during heavy exercise. Assuming that leg muscle O2 consumption did not decrease, this implies that leg blood flow was not reduced consequent to a redistribution of flow away from the working leg muscle.     

Characteristics of diaphragmatic fatigue during exhaustive exercise until task failure

The diaphragm was postulated to fatigue relatively early during exhaustive whole body exercise without further loss in contractility as exercise proceeds towards task failure. Diaphragmatic contractility was investigated prior/during/after exhaustive whole body exercise until task failure by using lung volume corrected twitch transdiaphragmatic pressure (TwPdi(c)) during magnetic phrenic nerve stimulation (every 45s). Eleven cyclists exercised to exhaustion (workloads ≥85% maximal oxygen uptake; 20.7±9.8min). Individual post hoc calculation of TwPdi(c) was conducted (diaphragmatic contractility versus lung volume). Diaphragmatic fatigue (i.e. TwPdi reduction baseline/recovery ≥10%) occurred in 9/11 subjects (82% "fatiguers"; baseline/recovery TwPdi(c) -16±13%, p<0.01). Fatiguers TwPdi(c) was: baseline: 2.99±0.40kPa, exercise-onset: 2.98±0.41kPa, initial third: 2.80±0.67kPa, second third: 2.54±0.55kPa, final third-task failure: 2.51±0.44kPa, recovery: 2.50±0.52kPa. Diaphragmatic contractility and lung volume (rest) were strongly related (r(2)=0.98, mean TwPdi(c) gradient 0.78kPa/l). To conclude, diaphragmatic contractility (lung volume corrected) decreases relatively early (initial two thirds) during exhaustive exercise and remains preserved towards task failure. This confirms previous assumptions postulating that respiratory performance is sustained without further fatigue of the primary inspiratory muscle.     

Compartmental chest wall volume changes during volitional hyperpnoea with constant tidal volume in healthy individuals

Prolonged high-intensity ventilation is associated with the development of rapid shallow breathing with decreased end-inspiratory volumes of all chest wall compartments. During respiratory muscle endurance training using normocapnic hyperpnoea, tidal volume (V_T) is normally kept constant. The aim of this study was to investigate possible changes in muscle recruitment during constant-V_T hyperpnoea, to assess potential mechanisms related to rapid shallow breathing. Ten healthy subjects performed 1 h of normocapnic hyperpnoea at 70% of maximal voluntary ventilation. Chest wall volume changes were assessed by optoelectronic plethysmography. End-inspiratory (1.08 ± 0.18 versus 0.96 ± 0.27 l, p = 0.017) and end-expiratory volumes (−0.13 ± 0.15 versus −0.31 ± 0.19 l, p = 0.007) of the pulmonary ribcage decreased significantly and lung function and respiratory muscle strength were reduced (all p < 0.05). Since with forced, constant V_T only the inspiratory rib cage muscles were unable to sustain end-inspiratory volume of their compartment, inspiratory rib cage muscles are the most likely candidate responsible for the development of rapid shallow breathing.     

Effects of continuous positive- and negative-pressure breathing on the pattern of breathing in man during exercise

Breathing pattern and static lung volumes were studied in 10 subjects at rest and during incremental-load cycle ergometry under three different conditions, viz. with normal pressure in the airways (control) and during continuous positive- and negative-pressure breathing (CPPB, CNPB) of +15 and -15 cmH2O. End-expiratory, end-inspiratory and mid-expiratory volumes were increased by CPPB and decreased by CNPB; these effects were especially pronounced at rest and during mild exercise. Both at rest and during exercise mean inspiratory flow (VT/TI) was exaggerated by CPPB and attenuated by CNPB. At rest these changes were due mainly to concomitant changes in tidal volume (VT) which was increased by CPPB and decreased by CNPB, while inspiratory time duration (TI) was relatively unaffected by pressure breathing. The transition from rest to loadless pedalling induced an increase in VT but no change in TI in the control condition, whereas in the CPPB and CNPB conditions TI decreased and VT remained unaltered. This CPPB- and CNPB-induced change in the volume-time threshold relationship at the onset of pedalling is attributed to increased stretch receptor activity in the extrathoracic portion of the trachea as a result of the increments in transmural pressure. During the course of exercise there was an inverse relationship between the slope of the VT-TI curve and the mid-expiratory volume in that the slope was greater in the control than in the CPPB condition and greatest during CNPB, suggesting that in exercise hyperpnoea the VT-TI relationship is also determined by pulmonary and/or thoracic wall stretch receptors capable of sensing the absolute lung volume.     

Impact of breathing pattern on work of breathing in healthy subjects and patients with COPD

The impact of the respiratory pattern on respiratory muscle workload represents an unresolved controversy and is important for the treatment of patients with respiratory disorders and respiratory muscle failure. We designed this study to investigate the relationship of respiratory pattern and inspiratory workload. We measured esophageal pressure and inspiratory flow and calculated work of breathing, tidal volume and respiratory rate. Ten healthy subjects and 10 COPD patients participated and performed five different breathing patterns starting from respiratory rate 12 and tidal volume 1l or quiet breathing, respectively. They were instructed to increase respiratory rate by 50 and 100% as well as tidal volume by 50 and 100% while maintaining constant minute-ventilation. In healthy subjects Delta VT was the single best parameter to predict Delta WOB (R=0.958, R(2)=0.918, p<0.0001). The relationships of changes in tidal volume, respiratory rate and rapid shallow breathing index to changes in WOB were linear. In the COPD Delta VT was also the single best parameter to predict changes in work of breathing (R=0.777, R(2)=0.604, p<0.0001), however the relation of respiratory rate and rapid shallow breathing index to work of breathing was exponential (e-function) with lower indices generating higher workload. We conclude that rapid shallow breathing might be a strategy to compensate for burdensome respiratory mechanics. In COPD patients however we observed a critical threshold where any further increases in rapid shallow breathing index will be of no further benefit.     

The role of the vagus nerves in the respiratory and circulatory responses to intravenous histamine and phenyl diguanide in rabbits

1. The responses of rabbits, anaesthetized with pentobarbitone sodium, to intravenous injections of histamine and phenyl diguanide have been studied. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The role of vagal afferent nerves was determined by observing the responses before and after bilateral vagotomy, and before and during cooling the vagus nerves to 8-10 degrees C; such cooling selectively blocks some vagal afferent pathways.3. Histamine decreased conductance (bronchoconstriction), in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. The responses were considerably reduced or abolished by vagal cooling and vagotomy and are thought to be mainly vagal reflexes due to stimulation by histamine of irritant receptors in the lungs.4. Phenyl diguanide also decreased conductance, in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. Vagotomy abolished the respiratory changes and considerably reduced the bronchoconstriction. Vagal cooling caused an equal reduction of the bronchoconstriction but an increase in minute volume persisted. This respiratory response to phenyl diguanide which persists during vagal cooling is thought to be due to stimulation of deflation receptors in the lungs; it was associated with vagal reflex hypotension and bradycardia.5. Both histamine and phenyl diguanide decreased lung compliance when vagal conduction was unimpaired. The effects were largely secondary to changes in the pattern of breathing, although histamine also had a weak direct action on lung tissue leading to a fall in compliance.6. Both histamine and phenyl diguanide decreased end-tidal CO(2)% and increased right atrial pressure by direct (non-vagal) actions on lung tissues. Histamine also caused a non-vagal hypertension.     

The total compliance of the respiratory system during the first year of life

Respiratory system compliance (Crs) was measured in 34 spontaneously breathing infants during the first year of life. An occlusion technique was used whereby several expiratory occlusions were performed at different lung volumes within the tidal range. The airway opening pressure generated during a plateau after occlusion was related to the volume included above the end-tidal level by a regression equation. The slope of this equation represented the compliance of the infant's respiratory system; the intercept was significantly different for preterm (-0.5 ml) and post-term (-5.5 ml) infants and may represent the difference between end-expiratory lung volume during tidal breathing and the relaxed functional residual capacity. The values for respiratory system compliance were similar to those previously reported for infants during muscle relaxation. As a function of body length, Crs = 1.58 X length3.13 X 10(-4) ml . kPa-1. The technique described is simple to apply and is independent of oesophageal pressure measurements.     

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.     

Increases in central blood volume modulate carotid baroreflex resetting during dynamic exercise in humans

We sought to determine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated by changes in central blood volume (CBV). CBV was increased during exercise by altering: (1) subject posture (supine versus upright) and (2) pedal frequency (80 versus 60 revolutions min⁻¹ (r.p.m.)); while oxygen uptake (     ) was kept constant. Eight male subjects performed three exercise trials: upright cycling at 60 r.p.m. (control); supine cycling at 60 r.p.m. (SupEX) and upright cycling at 80 r.p.m. to enhance the muscle pump (80EX). During each condition, carotid baroreflex (CBR) function was determined using the rapid neck pressure (NP) and neck suction (NS) protocol. Although mean arterial pressure (MAP) was significantly elevated from rest (88 ± 2 mmHg) during all exercise conditions ( P < 0.001), the increase in MAP was lower during SupEX (94 ± 2 mmHg) and 80EX (95 ± 2 mmHg) compared with control (105 ± 2 mmHg, P < 0.05). Importantly, the blood pressure responses to NP and NS were maintained around these changed operating points of MAP. However, in comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and leftward when CBV was increased during SupEX and 80EX. These alterations in CBR resetting occurred without any differences in     or heart rate between the exercise conditions. Thus, increasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced increases in MAP and CBR resetting. These findings suggest that changes in cardiopulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.     

Ventilatory responses to exercise training in obese adolescents

The aim of this study was to examine ventilatory responses to training in obese adolescents. We assessed body composition, pulmonary function and ventilatory responses (among which expiratory flow limitation and operational lung volumes) during progressive cycling exercise in 16 obese adolescents (OB) before and after 12 weeks of exercise training and in 16 normal-weight volunteers. As expected, obese adolescents' resting expiratory reserve volume was lower and inversely correlated with thoraco-abdominal fat mass (r=-0.74, p<0.0001). OB presented lower end expiratory (EELV) and end inspiratory lung volumes (EILV) at rest and during submaximal exercise, and modest expiratory flow limitation. After training, OB increased maximal aerobic performance (+19%) and maximal inspiratory pressure (93.7±31.4 vs 81.9±28.2cmH(2)O, +14%) despite lack of decrease in trunk fat and body weight. Furthermore, EELV and EILV were greater during submaximal exercise (+11% and +9% in EELV and EILV, respectively), expiratory flow limitation delayed but was not accompanied by increased V(T). However, submaximal exertional symptoms (dyspnea and leg discomfort) were significantly decreased (-71.3% and -70.7%, respectively). Our results suggest that exercise training can improve pulmonary function at rest (static inspiratory muscle strength) and exercise (greater operating lung volumes and delayed expiratory flow limitation) but these modifications did not entirely account for improved dyspnea and exercise performance in obese adolescents.     

Pulmonary flow-resistive work during hydrostatic loading

This paper focuses upon flow-resistive pulmonary work during upright immersion, and during changes in the air delivery pressure. Nine male non-smokers (aged 26.2 +/- 3.5 years), with normal lung function history, performed spontaneous respiration while seated in air (control) and during total immersion. During the immersed state subjects were supplied with air at four hydrostatic pressures: mouth pressure (PM; simulating a mouth-held demand regulator), lung centroid pressure (PLC; + 1.33 kPa relative to the sternal notch), and 0.98 kPa (10 cmH2O) above and below the lung centroid pressure. Inspiratory, expiratory and total flow-resistive pulmonary work were computed from the integration of transpulmonary pressure (difference between oesophageal and mouth pressure) with respect to lung volume change. When breathing air delivered at mouth pressure, immersion significantly elevated all total flow-resistive pulmonary work components (P less than 0.05). Each increment in breathing pressure resulted in a progressive reduction in expiratory and total flow-resistive pulmonary work, so that when air was provided at lung centroid pressure and lung centroid pressure +0.98 kPa both components were similar to control values (P greater than 0.05). Inspiratory was always less than expiratory pulmonary work. During immersion inspiratory pulmonary work was significantly reduced when air supply pressure was increased above mouth pressure (P less than 0.05). Subsequent pressure increments failed to produce further changes in inspiratory pulmonary work. The difference in response between the inspiratory and expiratory components of total flow resistive pulmonary work was attributed primarily to the volume-dependence of the expiratory component.     

Partial blockade of skeletal muscle somatosensory afferents attenuates baroreflex resetting during exercise in humans

During exercise, the carotid baroreflex is reset to operate around the higher arterial pressures evoked by physical exertion. The purpose of this investigation was to evaluate the contribution of somatosensory input from the exercise pressor reflex to this resetting during exercise. Nine subjects performed seven minutes of dynamic cycling at 30 % of maximal work load and three minutes of static one-legged contraction at 25 % maximal voluntary contraction before (control) and after partial blockade of skeletal muscle afferents with epidural anaesthesia. Carotid baroreflex function was assessed by applying rapid pulses of hyper- and hypotensive stimuli to the neck via a customised collar. Using a logistic model, heart rate (HR) and mean arterial pressure (MAP) responses to carotid sinus stimulation were used to develop reflex function stimulus-response curves. Compared with rest, control dynamic and static exercise reset carotid baroreflex-HR and carotid baroreflex-MAP curves vertically upward on the response arm and laterally rightward to higher operating pressures. Inhibition of exercise pressor reflex input by epidural anaesthesia attenuated the bi-directional resetting of the carotid baroreflex-MAP curve during both exercise protocols. In contrast, the effect of epidural anaesthesia on the resetting of the carotid baroreflex-HR curve was negligible during dynamic cycling whereas it relocated the curve in a laterally leftward direction during static contraction. The data suggest that afferent input from skeletal muscle is requisite for the complete resetting of the carotid baroreflex during exercise. However, this neural input appears to modify baroreflex control of blood pressure to a greater extent than heart rate.     

Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise

We hypothesized that the role of stroke volume (SV) in the metaboreflex-induced cardiac output (CO) increase was blunted when the metaboreflex was stimulated by exercise muscle ischemia (EMI) compared with post-exercise muscle ischemia (PEMI), because during EMI heart rate (HR) increases and limits diastolic filling. Twelve healthy volunteers were recruited and their hemodynamic responses to the metaboreflex evoked by EMI, PEMI, and by a control dynamic exercise were assessed. The main finding was that the blood pressure increment was very similar in the EMI and PEMI settings. In both conditions the main mechanism used to raise blood pressure was a CO elevation. However, during the EMI test CO was increased as a result of HR elevation whereas during the PEMI test CO was increased as a result of an increase in SV. These results were explainable on the basis of the different HR behavior between the two settings, which in turn led to different diastolic time and myocardial performance.