The Improvement in Exercise Performance during Reduced Muscle Mass Exercise is Associated with an Increase in Femoral Blood Flow in Older and Younger Endurance-Trained Athletes.

This study investigated whether the improved performance observed with maximal self-paced single-leg (SL), compared with double-leg (DL) cycling, is associated with enhanced femoral blood flow and/or altered tissue oxygenation. The hyperaemic response to exercise was assessed in younger and older athletes. Power output was measured in 12 older (65 ± 4 y) and 12 younger (35 ± 5 y) endurance-trained individuals performing 2 x 3 min maximal self-paced exercise using SL and DL cycling. Blood flow (BF) in the femoral artery was assessed using Doppler ultrasound and muscle oxygenation was measured using near-infrared spectroscopy on the vastus lateralis. SL cycling elicited a greater power output (295 ± 83 vs 265 ± 70 W, P < 0.001) and peak femoral BF (1749.1 ± 533.3 vs 1329.7 ± 391.7 ml/min, P < 0.001) compared with DL cycling. Older individuals had a lower peak BF in response to exercise (1355.4 ± 385.8 vs 1765.2 ± 559.6 ml/min, P = 0.019) compared with younger individuals. Peak BF in response to exercise was correlated with power output during SL (r = 0.655, P = 0.002) and DL (r = 0.666, P = 0.001) cycling. The greater exercise performance during SL compared with DL cycling may be partly explained by a greater hyperaemic response when reducing active muscle mass. Despite regular endurance training, older athletes had a lower femoral BF in response to maximal self-paced exercise compared with younger athletes.

Single- Versus Double-Leg Cycling: Small Muscle Mass Exercise Improves Exercise Capacity to a Greater Extent in Older Compared With Younger Population.

Manipulating the amount of muscle mass engaged during exercise can noninvasively inform the contribution of central cardiovascular and peripheral vascular-oxidative functions to endurance performance. To better understand the factors contributing to exercise limitation in older and younger individuals, exercise performance was assessed during single-leg and double-leg cycling. 16 older (67 ± 5 years) and 14 younger (35 ± 5 years) individuals performed a maximal exercise using single-leg and double-leg cycling. The ratio of single-leg to double-leg cycling power (RatioPower SL/DL) was compared between age groups. The association between fitness (peak oxygen consumption, peak power output, and physical activity levels) and RatioPower SL/DL was explored. The RatioPower SL/DL was greater in older compared with younger individuals (1.14 ± 0.11 vs. 1.06 ± 0.08, p = .041). The RatioPower SL/DL was correlated with peak oxygen consumption (r = .886, p < .001), peak power output relative to body mass (r = .854, p < .001), and levels of physical activity (r = .728, p = .003) in the younger but not older subgroup. Reducing the amount of muscle mass engaged during exercise improved exercise capacity to a greater extent in older versus younger population and may reflect a greater reduction in central cardiovascular function compared with peripheral vascular-oxidative function with aging.

Breathing a low-density gas reduces respiratory muscle force development and marginally improves exercise performance in master athletes.

INTRODUCTION: We tested the hypothesis that breathing heliox, to attenuate the mechanical constraints accompanying the decline in pulmonary function with aging, improves exercise performance. METHODS: Fourteen endurance-trained older men (67.9 ± 5.9 year, [Formula: see text]O2max: 50.8 ± 5.8 ml/kg/min; 151% predicted) completed two cycling 5-km time trials while breathing room air (i.e., 21% O2-79% N2) or heliox (i.e., 21% O2-79% He). Maximal flow-volume curves (MFVC) were determined pre-exercise to characterize expiratory flow limitation (EFL, % tidal volume intersecting the MFVC). Respiratory muscle force development was indirectly determined as the product of the time integral of inspiratory and expiratory mouth pressure (∫Pmouth) and breathing frequency. Maximal inspiratory and expiratory pressure maneuvers were performed pre-exercise and post-exercise to estimate respiratory muscle fatigue. RESULTS: Exercise performance time improved (527.6 ± 38 vs. 531.3 ± 36.9 s; P = 0.017), and respiratory muscle force development decreased during inspiration (- 22.8 ± 11.6%, P < 0.001) and expiration (- 10.8 ± 11.4%, P = 0.003) with heliox compared with room air. EFL tended to be lower with heliox (22 ± 23 vs. 30 ± 23% tidal volume; P = 0.054). Minute ventilation normalized to CO2 production ([Formula: see text]E/[Formula: see text]CO2) increased with heliox (28.6 ± 2.7 vs. 25.1 ± 1.8; P < 0.001). A reduction in MIP and MEP was observed post-exercise vs. pre-exercise but was not different between conditions. CONCLUSIONS: Breathing heliox has a limited effect on performance during a 5-km time trial in master athletes despite a reduction in respiratory muscle force development.

Submaximal fatiguing eccentric contractions of knee flexors alter leg extrapersonal representation.

This study assessed the immediate and prolonged effects of eccentric-induced fatigue on position sense, utilizing position-pointing tasks, which had not been previously implemented for this purpose. Fifteen healthy adults underwent a fatiguing eccentric protocol that entailed sets of unilateral submaximal contractions of knee flexor muscles until reaching a 20% decrease in maximal isometric torque production. Evaluations of knee flexor neuromuscular function as well as position-pointing tasks at 40° and 70° of knee flexion were conducted prior to the fatiguing eccentric protocol, immediately after (POST), and 24 h after (POST24) exercise termination. To assess neuromuscular fatigue etiology, electrical myostimulations were administered during and after maximal voluntary isometric contractions. At POST, the voluntary activation level and evoked potentiated doublet amplitude at 100 Hz were significantly reduced. In addition, position-pointing errors exhibited a significant increase at POST regardless of the tested angle, with participants positioning the pointer in a more extended position compared to their hidden exercised limb. At POST24, neuromuscular function and position sense parameters had reverted to their baseline levels. The findings of this experiment demonstrate that position-pointing accuracy was impaired immediately after the fatiguing eccentric protocol, manifesting in the presence of both central and peripheral fatigue. As position-pointing accuracy relies heavily on extrapersonal representation of the body at the brain level, acute changes in exercised limb's extrapersonal representation might have resulted from central fatigue-related mechanisms altering the cognitive processes responsible for converting kinesthetic signals into extrapersonal coordinates.

Knee position sense and knee flexor neuromuscular function are similarly altered after two submaximal eccentric bouts.

PURPOSE: This study examined eccentric-induced fatigue effects on knee flexor (KF) neuromuscular function and on knee position sense. This design was repeated across two experimental sessions performed 1 week apart to investigate potential repeated bout effects. METHODS: Sixteen participants performed two submaximal bouts of KF unilateral eccentric contractions until reaching a 20% decrease in maximal voluntary isometric contraction force. Knee position sense was evaluated with position-matching tasks in seated and prone positions at 40° and 70° of knee flexion so that KF were either antagonistic or agonistic during the positioning movement. The twitch interpolation technique was used to assess KF neuromuscular fatigue. Perceived muscle soreness was also assessed. Measurements were performed before, immediately (POST) and 24 h after (POST24) each eccentric bout. RESULTS: No repeated bout effect on neuromuscular function and proprioceptive parameters was observed. At POST, central and peripheral factors contributed to the force decrement as shown by significant decreases in voluntary activation level (- 3.8 ± 4.8%, p < 0.01) and potentiated doublet torque at 100 Hz (- 10 ± 15.8%, p < 0.01). At this time point, position-matching errors significantly increased by 1.7 ± 1.9° in seated position at 40° (p < 0.01). At POST24, in presence of muscle soreness (p < 0.05), although KF neuromuscular function had recovered, position-matching errors increased by 0.6 ± 2.6° in prone position at 40° (p < 0.01). CONCLUSION: These results provide evidence that eccentric-induced position sense alterations may arise from central and/or peripheral mechanisms depending on the testing position.

Relationship between neuromuscular fatigue, muscle activation and the work done above the critical power during severe-intensity exercise.

NEW FINDINGS: What is the central question of this study? Does the work done above critical power (W') or muscle activation determine the degree of peripheral fatigue induced by cycling time trials performed in the severe-intensity domain? What is the main finding and its importance? Peripheral fatigue increased when power output and muscle activation increased, whereas W' did not change between the time trials. Therefore, no relationship was found between W' and exercise-induced peripheral fatigue such as previously postulated in the literature. In contrast, we found a significant association between EMG amplitude during exercise and exercise-induced reduction in the potentiated quadriceps twitch, suggesting that muscle activation plays a key role in determining peripheral fatigue during severe-intensity exercise. ABSTRACT: In order to determine the relationship between peripheral fatigue, muscle activation and the total work done above critical power (W'), 10 men and four women performed, on separated days, self-paced cycling time trials of 3, 6, 10 and 15 min. Exercise-induced quadriceps fatigue was quantified using pre- to postexercise (15 s to 15 min recovery) changes in maximal voluntary contraction (MVC) peak force, voluntary activation and potentiated twitch force (QT). Voluntary activation was measured using the interpolated twitch technique, and QT was evoked by electrical stimulations of the femoral nerve. Quadriceps muscle activation was determined using the root mean square of surface EMG of vastus lateralis (VLRMS ), vastus medialis (VMRMS ) and rectus femoris (RFRMS ). Critical power and W' were calculated from the power-duration relationship from the four time trials. Mean power output and mean VLRMS , VMRMS and RFRMS were greater during shorter compared with longer exercise periods (P < 0.05), whereas no significant between-trial change in W' was found. The magnitude of exercise-induced reductions in QT increased with the increase in power output (P < 0.001) and was associated with mean VLRMS, VMRMS and RFRMS (P < 0.001, r2  > 0.369) but not W' (P > 0.150, r2  < 0.044). Reduction in voluntary activation tended (P = 0.067) to be more pronounced with the lengthening in time trial duration, whereas no significant between-trial changes in MVC peak force were found. Our data suggest that peripheral fatigue is not related to the amount of work done above the critical power but rather to the level of muscle activation during exercise in the severe-intensity domain.

Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation.

Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: -67% vs. -82%, Pi: 353% vs. 534%, pH: -0.22 vs. -0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (-3% and -36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (-15% and -33%), complex II (-36% and -23%), complex I + II (-31% and -20%), and state 3CI+CII control ratio (-24% and -39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response.

Recovery from Fatigue after Cycling Time Trials in Elite Endurance Athletes.

INTRODUCTION: We determined the recovery from neuromuscular fatigue in six professional (PRO) and seven moderately trained (MOD) cyclists after repeated cycling time trials of various intensities/durations. METHOD: Participants performed two 1-min (1minTT) or two 10-min (10minTT) self-paced cycling time trials with 5 min of recovery in between. Central and peripheral fatigue were quantified via preexercise to postexercise (15-s through 15-min recovery) changes in voluntary activation (VA) and potentiated twitch force. VA was measured using the interpolated twitch technique, and potentiated twitch force was evoked by single (QTsingle) and paired (10-Hz (QT10) and 100-Hz (QT100)) electrical stimulations of the femoral nerve. RESULTS: Mean power output was 32%-72% higher during all the time trials and decreased less (-10% vs -13%) from the first to second time trial in PRO compared with MOD (P < 0.05). Conversely, exercise-induced reduction in QTsingle and QT10/QT100 was significantly lower in PRO after every time trial (P < 0.05). Recovery from fatigue from 15 s to 2 min for QTsingle and QT10/QT100 was slower in PRO after every time trial (P < 0.05). In both groups, the reduction in QTsingle was lower after the 10minTTs compared with 1minTTs (P < 0.05). Conversely, VA decreased more after the 10minTTs compared with 1minTTs (P < 0.05). CONCLUSION: Our findings showed that excitation-contraction coupling was preserved after exercise in PRO compared with MOD. This likely contributed to the improved performance during repeated cycling time trials of various intensity/duration in PRO, despite a slower rate of recovery in its early phase. Finally, the time course of recovery from neuromuscular fatigue in PRO was dependent on the effects of prolonged low-frequency force depression.

Similar Cardioventilatory but Greater Neuromuscular Stimuli With Interval Drop Jump Than With Interval Running.

CONTEXT: Drop jumps and high-intensity interval running are relevant training methods to improve explosiveness and endurance performance, respectively. Combined training effects might, however, be achieved by performing interval drop jumping. PURPOSE: To determine the acute effects of interval drop jumping on oxygen uptake (V˙O2)-index of cardioventilatory/oxidative stimulation level and peripheral fatigue-a limiting factor of explosiveness. METHODS: Thirteen participants performed three 11-minute interval training sessions during which they ran 15 seconds at 120% of the velocity that elicited maximal V˙O2 (V˙O2max) (ITrun), or drop jumped at 7 (ITDJ7) or 9 (ITDJ9) jumps per 15 seconds, interspersed with 15 seconds of passive recovery. V˙O2 and the time spent above 90% of V˙O2max (V˙TO2max) were collected. Peripheral fatigue was quantified via preexercise to postexercise changes in evoked potentiated quadriceps twitch (ΔQT). Power output was estimated during ITDJs using optical sensors. RESULTS: All participants reached 90% of V˙O2max or higher during ITrun and ITDJ9, but only 11 did during ITDJ7. V˙TO2max was not different between ITrun and ITDJ9 (145 [76] vs 141 [151] s; P = .92) but was reduced during ITDJ7 (28 [26] s; P = .002). Mean ΔQT in ITDJ9 and ITDJ7 was not different (-17% [9%] vs -14% [8%]; P = .73) and greater than in ITrun (-8% [7%]; P = .001). No alteration in power output was found during ITDJs (37 [10] W·kg-1). CONCLUSION: Interval drop jumping at a high work rate stimulated the cardioventilatory and oxidative systems to the same extent as interval running, while the exercise-induced increase in fatigue did not compromise drop jump performance. Interval drop jumping might be a relevant strategy to get concomitant improvements in endurance and explosive performance.

Acute High-Intensity Exercise Impairs Skeletal Muscle Respiratory Capacity.

PURPOSE: The effect of an acute bout of exercise, especially high-intensity exercise, on the function of mitochondrial respiratory complexes is not well understood, with potential implications for both the healthy population and patients undergoing exercise-based rehabilitation. Therefore, this study sought to comprehensively examine respiratory flux through the different complexes of the electron transport chain in skeletal muscle mitochondria before and immediately after high-intensity aerobic exercise. METHODS: Muscle biopsies of the vastus lateralis were obtained at baseline and immediately after a 5-km time trial performed on a cycle ergometer. Mitochondrial respiratory flux through the complexes of the electron transport chain was measured in permeabilized skeletal muscle fibers by high-resolution respirometry. RESULTS: Complex I + II state 3 (state 3CI + CII) respiration, a measure of oxidative phosphorylation capacity, was diminished immediately after the exercise (pre, 27 ± 3 ρm·mg·s; post, 17 ± 2 ρm·mg·s; P < 0.05). This decreased oxidative phosphorylation capacity was predominantly the consequence of attenuated complex II-driven state 3 (state 3CII) respiration (pre, 17 ± 1 ρm·mg·s; post, 9 ± 2 ρm·mg·s; P < 0.05). Although complex I-driven state 3 (3CI) respiration was also lower (pre, 20 ± 2 ρm·mg·s; post, 14 ± 4 ρm·mg·s), this did not reach statistical significance (P = 0.27). In contrast, citrate synthase activity, proton leak (state 2 respiration), and complex IV capacity were not significantly altered immediately after the exercise. CONCLUSIONS: These findings reveal that acute high-intensity aerobic exercise significantly inhibits skeletal muscle state 3CII and oxidative phosphorylation capacity. This, likely transient, mitochondrial defect might amplify the exercise-induced development of fatigue and play an important role in initiating exercise-induced mitochondrial adaptations.

Increased Fatigue Response to Augmented Deceptive Feedback during Cycling Time Trial.

PURPOSE: This study aimed to investigate the effect of different magnitudes of deception on performance and exercise-induced fatigue during cycling time trial. METHODS: After three familiarization visits, three women and eight men performed three 5-km cycling time trials while following a simulated dynamic avatar reproducing either 100% (5K100%), 102% (5K102%), or 105% (5K105%) of the subject's previous fastest trial. Quadriceps muscle activation was quantified with surface electromyography. Fatigue was quantified by preexercise to postexercise (10 s through 15 min recovery) changes in quadriceps maximal voluntary contraction (MVC) force, potentiated twitch force evoked by electrical femoral nerve stimulation (QTSingle) and voluntary activation (VA, twitch interpolation technique). RESULTS: Greater quadriceps muscle activation in 5K102% versus 5K100% (12% ± 11%) was found in parallel with a 5% ± 2% and 2% ± 1% improvement in power output and completion time, respectively (P < 0.01). Exercise-induced reduction in MVC force and VA were 14% ± 19% and 28% ± 31% greater at exercise termination (at 10 s), whereas QTSingle recovery (from 10 s to 15 min) was 5% ± 5% less in 5K102% versus 5K100% (P < 0.01). No difference in performance or fatigue indices measured at exercise termination was found between 5K100% and 5K105%. CONCLUSIONS: Muscle activation and performance improvements during a deceptive cycling time trial were achieved only with a 2% magnitude of deception and were associated with a further impairment in MVC force, QTSingle recovery and VA compared to control. Performance improvement during cycling time trial with augmented deceptive feedback therefore resulted in exacerbated exercise-induced peripheral and central fatigue.

Group III/IV muscle afferents limit the intramuscular metabolic perturbation during whole body exercise in humans.

KEY POINTS: The purpose of this study was to determine the role of group III/IV muscle afferents in limiting the endurance exercise-induced metabolic perturbation assayed in muscle biopsy samples taken from locomotor muscle. Lumbar intrathecal fentanyl was used to attenuate the central projection of µ-opioid receptor-sensitive locomotor muscle afferents during a 5 km cycling time trial. The findings suggest that the central projection of group III/IV muscle afferent feedback constrains voluntary neural 'drive' to working locomotor muscle and limits the exercise-induced intramuscular metabolic perturbation. Therefore, the CNS might regulate the degree of metabolic perturbation within locomotor muscle and thereby limit peripheral fatigue. It appears that the group III/IV muscle afferents are an important neural link in this regulatory mechanism, which probably serves to protect locomotor muscle from the potentially severe functional impairment as a consequence of severe intramuscular metabolic disturbance. ABSTRACT: To investigate the role of metabo- and mechanosensitive group III/IV muscle afferents in limiting the intramuscular metabolic perturbation during whole body endurance exercise, eight subjects performed 5 km cycling time trials under control conditions (CTRL) and with lumbar intrathecal fentanyl impairing lower limb muscle afferent feedback (FENT). Vastus lateralis muscle biopsies were obtained before and immediately after exercise. Motoneuronal output was estimated through vastus lateralis surface electromyography (EMG). Exercise-induced changes in intramuscular metabolites were determined using liquid and gas chromatography-mass spectrometry. Quadriceps fatigue was quantified by pre- to post-exercise changes in potentiated quadriceps twitch torque (ΔQTsingle ) evoked by electrical femoral nerve stimulation. Although motoneuronal output was 21 ± 12% higher during FENT compared to CTRL (P < 0.05), time to complete the time trial was similar (∼8.8 min). Compared to CTRL, power output during FENT was 10 ± 4% higher in the first half of the time trial, but 11 ± 5% lower in the second half (both P < 0.01). The exercise-induced increase in intramuscular inorganic phosphate, H(+) , adenosine diphosphate, lactate and phosphocreatine depletion was 55 ± 30, 62 ± 18, 129 ± 63, 47 ± 14 (P < 0.001) and 27 ± 14% (P < 0.01) greater in FENT than CTRL. ΔQTsingle was greater following FENT than CTRL (-52 ± 2 vs -31 ± 1%, P < 0.001) and this difference was positively correlated with the difference in inorganic phosphate (r(2)  = 0.79; P < 0.01) and H(+) (r(2)  = 0.92; P < 0.01). In conclusion, during whole body exercise, group III/IV muscle afferents provide feedback to the CNS which, in turn, constrains motoneuronal output to the active skeletal muscle. This regulatory mechanism limits the exercise-induced intramuscular metabolic perturbation, preventing an abnormal homeostatic challenge and excessive peripheral fatigue.

Peripheral and Central Fatigue Development during All-Out Repeated Cycling Sprints.

PURPOSE: We investigated the development and recovery of peripheral and central fatigue during repeated cycling sprints and its influence on power output. METHODS: On six separate days, 12 healthy males performed the following tests: 1, 4, 6, 8, and 10 × 10 s sprints with 30 s of passive recovery between sprints, as well as 8 × 10 s sprints with 10 s of passive recovery. Peripheral and central fatigue levels were quantified via changes in preexercise- to postexercise-potentiated quadriceps twitch force, as evoked by supramaximal electrical stimulation of the femoral nerve (30 s through 6 min recovery), and quadriceps voluntary activation (VA), respectively. Root mean square of the vastus lateralis and the vastus medialis electromyogram during sprints were normalized by maximal M wave amplitude (RMS·Mmax). RESULTS: From the first to the sixth sprint, we found significant and gradual reductions in power output (-25% ± 7%), RMS·Mmax (-7% ± 4%), twitch force (-47% ± 11%) and VA (-11% ± 6%). During the subsequent sprints, no additional reduction in power output, RMS·Mmax, twitch force or VA, was found. Reduction in between-sprints recovery duration led to a significant reduction in power output and RMS·Mmax but no change in peripheral and central fatigue. CONCLUSION: These findings are consistent with the hypothesis that central motor command and power output during all-out repeated sprints are limited in order to prevent excessive locomotor muscle fatigue. They also demonstrate that both the peripheral and central fatigue contribute significantly to the decline in power output elicited via repeated sprints.

Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO2 : role of carotid body CO2.

We asked if the type of carotid body (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2 . The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 ≈ 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors was studied in seven awake dogs with vascularly-isolated and extracorporeally-perfused CBs. Chemosensitivity with one CB was similar to that in intact dogs. In four CB-denervated dogs, absence of hyper-/hypoventilatory responses to CB perfusion with PCO2 of 19-75 mmHg confirmed separation of the perfused CB circulation from the brain. The group mean central CO2 response slopes were increased 303% for minute ventilation (V̇I)(P ≤ 0.01) and 251% for mean inspiratory flow rate (VT /TI ) (P ≤ 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes for tidal volume (VT ), breathing frequency (fb ) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group mean changes did not reach statistical significance. Group mean central CO2 response slopes were also increased 237% for V̇I(P ≤ 0.01) and 249% for VT /TI (P ≤ 0.05) when the CB was normocapnic vs. hypocapnic, but no significant differences in any of the central ventilatory response indices were found between CB normocapnia and hypercapnia. These hyperadditive effects of CB hyper-/hypocapnia agree with previous findings using CB hyper-/hypoxia.We propose that hyperaddition is the dominant form of chemoreceptor interaction in quiet wakefulness when the chemosensory control system is intact, response gains physiological, and carotid body chemoreceptors are driven by a wide range of O2 and/or CO2 .

Exercise performance is regulated during repeated sprints to limit the development of peripheral fatigue beyond a critical threshold.

We hypothesized that exercise performance is adjusted during repeated sprints in order not to surpass a critical threshold of peripheral fatigue. Twelve men randomly performed three experimental sessions on different days, i.e. one single 10 s all-out sprint and two trials of 10 × 10 s all-out sprints with 30 s of passive recovery in between. One trial was performed in the unfatigued state (CTRL) and one following electrically induced quadriceps muscle fatigue (FTNMES). Peripheral fatigue was quantified by comparing pre- with postexercise changes in potentiated quadriceps twitch force (ΔQtw-pot) evoked by supramaximal magnetic stimulation of the femoral nerve. Central fatigue was estimated by comparing pre- with postexercise voluntary activation of quadriceps motor units. The root mean square (RMS) of the vastus lateralis and vastus medialis EMG normalized to maximal M-wave amplitude (RMS.Mmax (-1)) was also calculated during sprints. Compared with CTRL condition, pre-existing quadriceps muscle fatigue in FTNMES (ΔQtw-pot = -29 ± 4%) resulted in a significant (P < 0.05) reduction in power output (-4.0 ± 0.9%) associated with a reduction in RMS.Mmax (-1). However, ΔQtw-pot postsprints decreased by 51% in both conditions, indicating that the level of peripheral fatigue was identical and independent of the degree of pre-existing fatigue. Our findings show that power output and cycling EMG are adjusted during exercise in order to limit the development of peripheral fatigue beyond a constant threshold. We hypothesize that the contribution of peripheral fatigue to exercise limitation involves a reduction in central motor drive in addition to the impairment in muscular function.

Role of chemoreception in cardiorespiratory acclimatization to, and deacclimatization from, hypoxia.

During sojourn to high altitudes, progressive time-dependent increases occur in ventilation and in sympathetic nerve activity over several days, and these increases persist upon acute restoration of normoxia. We discuss evidence concerning potential mediators of these changes, including the following: 1) correction of alkalinity in cerebrospinal fluid; 2) increased sensitivity of carotid chemoreceptors; and 3) augmented translation of carotid chemoreceptor input (at the level of the central nervous system) into increased respiratory motor output via sensitization of hypoxic sensitive neurons in the central nervous system and/or an interdependence of central chemoreceptor responsiveness on peripheral chemoreceptor sensory input. The pros and cons of chemoreceptor sensitization and cardiorespiratory acclimatization to hypoxia and intermittent hypoxemia are also discussed in terms of their influences on arterial oxygenation, the work of breathing, sympathoexcitation, systemic blood pressure, and exercise performance. We propose that these adaptive processes may have negative implications for the cardiovascular health of patients with sleep apnea and perhaps even for athletes undergoing regimens of "sleep high-train low"!

Are type III-IV muscle afferents required for a normal steady-state exercise hyperpnoea in humans?

When tested in isolation, stimuli associated with respiratory CO2 exchange, feedforward central command and type III-IV muscle afferent feedback have each been shown to be capable of eliciting exercise-like cardio-ventilatory responses, but their relative contributions in a setting of physiological exercise remains controversial. We reasoned that in order to determine whether any of these regulators are obligatory to the exercise hyperpnoea each needs to be removed or significantly diminished in a setting of physiological steady-state exercise, during which all recognized stimuli (and other potential modulators) are normally operative. In the past few years we and others have used intrathecal fentanyl, a µ-opiate receptor agonist, in humans to reduce the input from type III-IV opiate-sensitive muscle afferents. During various types of intensities and durations of exercise a sustained hypoventilation, as well as reduced systemic pressure and cardioacceleration, were consistently observed with this blockade. These data provide the basis for the hypothesis that type III-IV muscle afferents are obligatory to the hyperpnoea of mild to moderate intensity rhythmic, large muscle, steady-state exercise. We discuss the limitations of these studies, the reasons for their disagreement with previous negative findings, the nature of the muscle afferent feedback stimulus and the need for future investigations.

Role of central/peripheral chemoreceptors and their interdependence in the pathophysiology of sleep apnea.

Unstable periodic breathing with intermittent ventilatory overshoots and undershoots commonly occurs in chronic heart failure, in hypoxia, with chronic opioid use and in certain types of obstructive sleep apnea. Sleep promotes breathing instability because it unmasks a highly sensitive dependence of the respiratory control system on chemoreceptor input, because transient cortical arousals promote ventilatory overshoots and also because upper airway dilator muscle tonicity is reduced and airway collapsibility enhanced. We will present data in support of the premise that carotid chemoreceptors are essential in the pathogenesis of apnea and periodicity; however it is the hyperadditive influence of peripheral chemoreceptor sensory input on central chemosensitivity that accounts for apnea and periodic breathing. This chemoreceptor interdependence also provides a significant portion of the normal drive to breathe in normoxia (i.e. eupnea) and in acute hypoxia. Finally, we discuss the effects of preventing transient hypocapnia (via selective increases in FICO(2)) on centrally mediated types of periodic breathing and even some varieties of cyclical obstructive sleep apnea.