The ability to modify power output (PO) in response to a changing stimulus during exercise is crucial for optimizing performance involving an integration system involving a performance template and feedback from peripheral receptors. The rapidity with which PO is modified has not been established, but would be of interest relative to understanding how PO is regulated. The objective is to determine the rapidity of changes in PO in response to a hypoxic challenge, and if change in PO is linked to changes in arterial O(2) saturation (S (a)O(2)). Well-trained cyclists performed randomly ordered 5-km time trials. Subjects began the trials breathing room air and switched to hypoxic (HYPOXIC, F(I)O(2)= 0.15) or room (CONTROL, F(I)O(2)= 0.21) air at 2 km, then to room air at 4 km. The time delay to begin decreasing S (a)O(2) and PO and to recover S (a)O(2) and PO on to room air was compared, along with the half time (t (1/2)) during the HYPOXIC trial. Mean S (a)O(2) and PO between 2 and 4 km were significantly different between CONTROL and HYPOXIC (94 +/- 2 vs. 83 +/- 2% and 285 +/- 16 vs. 245 +/- 19 W, respectively). There was no difference between the time delay for S (a)O(2)(31.5 +/- 12.8 s) and in PO (25.8 +/- 14.4 s) or the recovery of S (a)O(2)(29.0 +/- 7.7 s) and PO (21.5 +/- 12.4 s). The half time for decreases in S (a)O(2)(56.6 +/- 14.4 s) and in PO (62.7 +/- 20.8 s) was not significantly different. Modifications of PO due to the abrupt administration of hypoxic air are related to the development of arterial hypoxemia, and begin within ~30 s.

We briefly summarize recent evidence pertaining to how mechanisms primarily under the control of the respiratory system-namely, arterial oxyhemoglobin desaturation, respiratory muscle work and fatigue, and cyclical fluctuations in intrathoracic pressure-may contribute to exercise limitation. Respiratory influences on cardiac output and on sympathetic vasoconstrictor activity and blood flow distribution are shown to be important determinants of performance. We also address how a compromised O2 transport exacerbates the rate of development of peripheral muscle fatigue and, in turn, precipitates central fatigue and exercise limitation.

The purpose of this study was to use a hypoxic stress as a mean to disrupt the normal coordinative pattern during cycling. Seven male cyclists pedalled at three cadence (60, 80, 100 rpm) and three power output (150, 250, 350 W) conditions in normoxia and hypoxia (15% O2). Simultaneous measurements of pedal force, joint kinematics,% oxyhaemoglobin saturation, and minute ventilation were made for each riding condition. A conventional inverse dynamics approach was used to compute the joint moments of force at the hip, knee, and ankle. The relative contribution of the joint moments of force with respect to the total moment was computed for each subject and trial condition. Overall, the ankle contributed on average 21%, the knee 29% and the hip 50% of the total moment. This was not affected by the relative inspired oxygen concentration. Results showed that the relative ankle moment of force remained at 21% regardless of manipulation. The relative hip moment was reduced on average by 4% with increased cadence and increased on average by 4% with increased power output whereas the knee moment responded in the opposite direction. These results suggest that the coordinative pattern in cycling is a dominant characteristic of cycling biomechanics and remains robust even in the face of arterial hypoxemia.

Our aim was to isolate the independent effects of a) the inspiratory muscle work (Wb) and b) arterial-hypoxemia, during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia (FIO2=0.15, SaO2=81+/-1%; 8.6+/-0.5 min, 273+/-6 W; Hypoxia-CTRL) and at the same work-rate and duration in normoxia (SaO2=95+/-1%; Normoxia-CTRL). These trials were repeated, but with a 35 to 80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps fatigue was assessed via magnetic femoral nerve stimulation pre- and 2-min post-exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO2, were revealed by comparing Hypoxia-CTRL and Hypoxia-PAV at equal levels of SaO2 (P=0.10). Immediately after hypoxic exercise, potentiated-twitch force of the quadriceps (Qtw,pot) decreased by 30+/-3% below pre-exercise baseline and this reduction was attenuated by about one-third following PAV exercise (21+/-4%; P<0.05). This effect of Wb on quadriceps fatigue occurred at exercise work-rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of SaO2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 16+/-2% below pre-exercise baseline following Normoxia-PAV and this reduction was exacerbated by about one-third following Hypoxia-PAV (-21+/-4%; P<0.05). We conclude that both arterial-hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work-rates during which, in normoxia, the Wb has no effect on peripheral fatigue. Key words: Work of breathing, arterial oxygen content, altitude, expiratory flow limitation, limb blood flow.

We examined the effects of hypoxia severity on peripheral vs. central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various levels of inspired O2 fraction (FIO2 0.21/0.15/0.10). At task-failure (pedal-frequency <70% target) arterial-hypoxemia was surreptitiously reversed via acute O2 supplementation (FIO2=0.30) and subjects were encouraged to continue exercising. Peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (Qtw,pot) as measured pre- vs. post-exercise in response to supra-maximal femoral nerve stimulation. At task-failure in normoxia [hemoglobin saturation (SpO2)~94%, 656+/-82s] or moderate-hypoxia (SpO2 ~82%, 278+/-16s), hyperoxygenation had no significant effect on prolonging endurance-time. However, following task-failure in severe-hypoxia (SpO2 ~67%; 125+/-6s), hyperoxygenation elicited a significant prolongation of time-to-exhaustion (171+/-61%). The magnitude of Qtw,pot at exhaustion was not different among the three trials (-35 to -36%, P=0.8). Furthermore, quadriceps integrated EMG, blood-lactate, heart-rate, and effort-perceptions all rose significantly throughout exercise and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe-hypoxia, we repeated this trial and assessed peripheral-fatigue following task-failure prior to hyperoxygenation (125+/-6s). Although the magnitude of Qtw,pot was reduced from pre-exercise baseline (-23%; P<0.01), peripheral-fatigue was substantially less (P<0.01) than that observed at task-failure in normoxia and moderate-hypoxia. We conclude that across the range of normoxia to severe-hypoxia the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxic-sensitive central component of fatigue, likely involving brain hypoxic effects on effort perception.

The effect of various levels of oxygenation on quadriceps muscle fatigability during isolated muscle exercise was assessed in six male subjects. Twitch force (Qtw) was assessed using supra-maximal magnetic femoral nerve stimulation. In Experiment I, maximal voluntary contraction (MVC) and Qtw of resting quadriceps muscle were measured in nomoxia [inspired O2 fraction (FIO2)= 0.21, arterial O2 saturation (SpO2)= 98.4%, estimated arterial O2 content (CaO2)= 20.8 ml.dl(-1); NORM], acute-hypoxia (FIO2 = 0.11, SpO2 = 74.6%, CaO2 = 15.7 ml.dl(-1); HYPO), and acute-hyperoxia (FIO2= 1.0, SpO2 = 100%, CaO2 = 22.6 ml.dl(-1); HYPER). No significant differences were found for MVC and Qtw among the three FIO2s. In Experiment II, the subjects performed three sets of nine, intermittent, isometric, unilateral, submaximal quadriceps contractions (62% MVC followed by one MVC in each set) while breathing each FIO2. Qtw was assessed before and after exercise, and myoelectrical activity of the vastus lateralis was obtained during exercise. The percent reduction of twitch force (potentiated Qtw) in HYPO (-27.0%) was significantly (P<0.05) greater than those in NORM (-21.4%) and HYPER (-19.9%); as were the changes in intra-twitch measures of contractile properties. The increase in integrated electromyogram over the course of the nine contractions in HYPO (15.4%) was higher (P<0.05) than in NORM (7.2%) or HYPER (6.7%). These results demonstrate that quadriceps muscle fatigability during isolated muscle exercise is exacerbated in acute hypoxia, and these effects were independent of the relative exercise intensity. Key words: hypoxia, magnetic femoral nerve stimulation, arterial oxygenation, isolated muscle.

We hypothesized that severe hypoxia limits exercise performance via decreased contractility of limb locomotor muscles. Nine male subjects (mean +/- SEM maximum oxygen uptake [VO2max]= 56.5 +/- 2.7 ml kg(-1) min(-1)) cycled at >/=90% VO2max to exhaustion in normoxia (NORM-EXH; inspired O2 fraction [FIO2]= 0.21, arterial O2 saturation [SpO2]= 93 +/- 1%) and hypoxia (HYPOX-EXH; FIO2 = 0.13, SpO2 = 76 +/- 1%). The subjects also exercised in normoxia for a time equal to that achieved in hypoxia (NORM-CTRL; SpO2 = 96 +/- 1%). Quadriceps twitch force, in response to supramaximal single (non-potentiated and potentiated 1 Hz) and paired magnetic stimuli of the femoral nerve (10-100 Hz), was assessed pre- and at 2.5, 35 and 70 min post-exercise. Hypoxia exacerbated exercise-induced peripheral fatigue, as evidenced by a greater decrease in potentiated twitch force in HYPOX-EXH vs. NORM-CTRL (-39 +/- 4 vs.-24 +/- 3%, P < 0.01). Time-to-exhaustion was reduced by more than two-thirds in HYPOX-EXH vs. NORM-EXH (4.2 +/- 0.5 vs. 13.4 +/- 0.8 min, P < 0.01); however, peripheral fatigue was not different in HYPOX-EXH vs. NORM-EXH (-34 +/- 4 vs.-39 +/- 4%, P > 0.05). Blood lactate concentration and perceptions of limb discomfort were higher throughout HYPOX-EXH vs. NORM-CTRL, but were not different at end-exercise in HYPOX-EXH vs. NORM-EXH. We conclude that severe hypoxia exacerbates peripheral fatigue of limb locomotor muscles and that this effect may contribute, in part, to the early termination of exercise. Key words: hypoxemia, muscle fatigue, exercise performance.

We investigated the role of somatosensory feedback from locomotor muscles on central motor drive (CMD) and the development of peripheral fatigue during high-intensity endurance exercise. In a double-blind, placebo-controlled design, eight cyclists randomly performed three 5 km time-trials: control, interspinous ligament injection of saline (5KPlac, L3-L4), or intrathecal fentanyl (5KFent, L3-L4) to impair cortical projection of opioid-mediated muscle afferents. Peripheral quadriceps fatigue was assessed via changes in force output pre- vs post-exercise in response to supra-maximal magnetic femoral nerve stimulation (DeltaQtw). CMD during the time-trials was estimated via quadriceps electromyogram (iEMG). Fentanyl had no effect on quadriceps strength. Impairing neural feedback from the locomotor muscles increased iEMG during the first 2.5 km of 5KFent vs 5KPlac by 12 +/- 3%(P < 0.05); during the second 2.5 km iEMG was similar between trials. Power output was also 6 +/- 2% higher during the first and 11 +/- 2% lower during the second 2.5 km of 5KFent vs 5KPlac (both P < 0.05). VE/VCO2 was on average 7 +/- 2% lower during 5KFent. Capillary blood lactate was higher (16.3 +/- 0.5% vs 12.6 +/- 1.0%) and arterial HbO2 saturation was lower (89 +/- 1% vs 94 +/- 1%) during 5KFent vs 5KPlac. Exercise-induced DeltaQtw was greater following 5KFent vs 5KPlac (-46 +/- 2% vs -33 +/- 2%, P < 0.001). Our results emphasize the critical role of somatosensory feedback from working muscles on the centrally mediated determination of CMD and power output. Attenuated afferent feedback from exercising locomotor muscles results in an overshoot in CMD and power output normally chosen by the athlete, thereby causing a greater rate of accumulation of muscle metabolites and excessive development of peripheral muscle fatigue.

We investigated whether somatosensory feedback from contracting limb muscles exerts an inhibitory influence on the determination of central command during closed-loop cycling exercise in which the subject voluntarily determines his second-by-second central motor drive. Eight trained cyclists performed two 5 km time trials either without (5KCtrl) or with lumbar epidural anesthesia (5KEpi; 24 ml of 0.5% lidocaine, vertebral interspace L3-L4). Percent voluntary quadriceps muscle activation was determined at rest using a superimposed twitch technique. Epidural lidocaine reduced pre-time trial maximal voluntary quadriceps strength (553 +/- 45 N; MVC) by 22 +/- 3%. Percent voluntary quadriceps activation was also reduced from 97 +/- 1% to 81 +/- 3% via epidural lidocaine and this was unchanged following the 5KEpi indicating a sustained level of neural impairment throughout the trial. Power output was reduced by 9 +/- 2% throughout the race (P < 0.05). We found three types of significant effects of epidural lidocaine which supported a substantial role for somatosensory feedback from the exercising limbs as a determinant of central command throughout high intensity closed-loop cycling exercise: a) relative integrated electromyogram of the vastus lateralis was significantly increased; b) pedal forces were similar despite reduced number of fast-twitch muscle fibers available for activation; c) ventilation was increased out of proportion to a reduced VCO2 and heart rate and blood pressure were increased out of proportion to power output and VO2. These findings demonstrate the inhibitory influence of somatosensory feedback from contracting locomotor muscles on the conscious and/or subconscious determination of the magnitude of central motor drive during high intensity closed-loop endurance exercise. Key words: nociception, exercise hyperpnea, muscle metaboreflex, ascending sensory pathway.

We briefly summarize recent evidence pertaining to how mechanisms primarily under the control of the respiratory system-namely, arterial oxyhemoglobin desaturation, respiratory muscle work and fatigue, and cyclical fluctuations in intrathoracic pressure-may contribute to exercise limitation. Respiratory influences on cardiac output and on sympathetic vasoconstrictor activity and blood flow distribution are shown to be important determinants of performance. We also address how a compromised O2 transport exacerbates the rate of development of peripheral muscle fatigue and, in turn, precipitates central fatigue and exercise limitation.

BACKGROUND: Asthma is an inflammatory disease of the airways that can lead to impaired arterial blood oxygenation during exercise. OBJECTIVE: We asked whether treatment of airway inflammation in asthmatic subjects would improve arterial blood gases during whole-body exercise. METHODS: By using a double-blind parallel-group design, 19 asthmatic subjects completed treadmill exercise to exhaustion on 2 occasions:(1) before and (2) after 6 weeks' treatment with an inhaled corticosteroid (ICS; n = 9) or placebo (n = 10). RESULTS: The ICS group had improved resting pulmonary function, decreased exercise-induced bronchospasm, and decreased postexercise sputum histamine during the posttreatment study compared with that during the pretreatment study. In the ICS group exercise Pao(2) was significantly increased after treatment (84.8 to 93.8 mm Hg). Increased alveolar ventilation (arterial Pco(2) decreased from 36.9 to 34.1 mm Hg) accounted for 37% of the increased Pao(2) and improved gas exchange efficiency (alveolar-to-arterial Po(2) difference decreased from 22.5 to 16.3 mm Hg) accounted for the remaining 63% of the increased Pao(2) after treatment. In the ICS group exercise time to exhaustion was increased from 9.9 minutes during the pretreatment study to 14.8 minutes during the posttreatment study. CONCLUSION: Treatment of airway inflammation in asthmatic subjects can improve arterial blood oxygenation during exercise by (1) improving airway function, thereby allowing increased alveolar ventilation during exercise, and (2) improving the efficiency of alveolar-to-arterial blood O(2) exchange. CLINICAL IMPLICATIONS: In asthmatic patients ICSs not only attenuate exercise-induced bronchospasm but also improve arterial blood oxygenation during exercise.

We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed six incremental exercise tests. For three trials, subjects exercised with proportional assist ventilation (PAV). For the remaining three trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (P(mus)) was reduced with PAV (-35.9+/-2.3% versus placebo; P<0.05). Furthermore,[Formula: see text] and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak power output, however, was not different between placebo and PAV (324+/-4W versus 326+/-4W; P>0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise.

PURPOSE:: The purpose was to test whether the higher DeltaV O2/DeltaW in aerobically trained subjects compared to less trained counterparts during a ramp protocol is related to changes in muscle fibre activation. METHODS:: Ten cyclists and ten physically active students (PAstudents) performed two ramp exercises (ramp 25-protocol and relative ramp protocol, leading to exhaustion in 12 minutes) and a step protocol (20-60-100-140-180-220Watt). Pulmonary gas exchange was measured and muscle fibre activity recorded with surface electromyography (EMG) of the M. Vastus Lateralis. V O2 and integrated EMG (iEMG) were described as functions of work rate up to the gas exchange threshold and linear regression analysis was used to determine DeltaV O2/DeltaW and DeltaiEMG/DeltaW. RESULTS:: The statistical analysis revealed a higher DeltaV O2/DeltaW in cyclists compared to PAstudents in ramp exercises (ramp 25: 9.98+/-0.51 vs. 9.18+/-0.59 ml.min.Watt; relative ramp: 9.87+/-0.30 vs. 9.16+/-0.33 ml.min.Watt in the cyclists and PA students, respectively; P<0.05) but not in step exercise (9.97+/-0.32 and 9.83+/-0.37 ml.min.Watt in cyclists and PAstudents, respectively; P>0.05). Additionally, cyclists demonstrated a higher DeltaiEMG/DeltaW in ramp exercises (0.96+/-0.14 and 0.98 +/-0.14 %.Watt in ramp 25 and relative ramp, respectively) compared to step exercise (0.75+/-0.12 %.Watt, P<0.05) whereas in the PAstudents DeltaiEMG/DeltaW did not differ between the ramp (0.75+/-0.10 and 0.70+/-0.12 %.Watt in ramp 25 and relative ramp, respectively) and step protocol (0.77+/-0.17 %. Watt, P>0.05). CONCLUSION:: The present study reveals that trained cyclists demonstrate reduced mechanical efficiency in the ramp protocol and that this phenomenon is associated with an 'over-activation' of muscle fibres.

An MR-compatible ergometer was developed for in-magnet whole-body human exercise testing. Designed on the basis of conventional mechanically braked bicycle ergometers and constructed from nonferrous materials, the ergometer was implemented on a 1.5-T whole-body MR scanner. A spectrometer interface was constructed using standard scanner hardware, complemented with custom-built parts and software to enable gated data acquisition during exercise. High-quality (31)P NMR spectra were reproducibly obtained from the medial head of the quadriceps muscle of the right leg of eight healthy subjects during two-legged high-frequency pedaling (80 revolutions per minute) at three incremental workloads, including maximal. Muscle phosphocreatine content dropped 82%, from 32.2 +/- 1.0 mM at rest to 5.7 +/- 1.1 mM at maximal workload (mean +/- standard error; n = 8), indicating that the majority of quadriceps motor units were recruited. The cardiovascular load of the exercise was likewise significant, as evidenced by heart rates of 150 (+/-10%) beats per minute, measured immediately afterward. As such, the newly developed MR bicycling exercise equipment offers a powerful new tool for clinical musculoskeletal and cardiovascular MR investigation. The basic design of the ergometer is highly generic and adaptable for application on a wide selection of whole-body MR scanners. Magn Reson Med, 2009.(c) 2009 Wiley-Liss, Inc.

The object of the the present study involved determining of rate of the inspiratory muscles fatigue development in healthy humans during increasing exercise under resistive loaded breathing with the air, oxygen, or hypoxic gas mixtures (FIO2 = 0.21, 1.0 and 0.13 respectively). 6 normal male subjects were studied. Volume/time parameters of breathing and parasternal integrated EMG activities were recorded under inspiratory-expiratory resistive loading 12 cm H2O/I s(-1) during increasing exercise in the air, oxygen, or hypoxic gas mixtures. The degree of inspiratory muscle fatigue was assessed by the "tension-time" index P(ml)/P(ml max) Tl/T(T) as well as by ratio of the mean amplitudes of the EMG signal spectrum in the hight-frequency (H) range to the mean spectrum amplitudes in the low-frequency (L) range (H/L). The signs of inspiratory muscle fatigue were most conspicuous during inhalation of the hypoxic mixture, compared to air. This was supported by the increased "tension-time" index, the hurried shallow breathing, and the decreased H/L ratio on 37%(p < 0.001). Only starting signs of inspiratory muscle fatigue were revealed during oxygen inhalation, although the maximum working capacity was higher than the control one (exercise in air). The results indicate that the oxygen contained in the inhaled gas mixture affects on the total working capacity total working capacity and influences the rate of inspiratory muscle fatigue development in exercising healthy men during resistive load 12 cm H2O/l s(-1). The decreased energy supply to respiratory muscles accelerates functional failure and results in fatigue, whereas the increased energy supply decelerates the development of inspiratory muscle fatigue.

We investigated whether somatosensory feedback from contracting limb muscles exerts an inhibitory influence on the determination of central command during closed-loop cycling exercise in which the subject voluntarily determines his second-by-second central motor drive. Eight trained cyclists performed two 5 km time trials either without (5KCtrl) or with lumbar epidural anesthesia (5KEpi; 24 ml of 0.5% lidocaine, vertebral interspace L3-L4). Percent voluntary quadriceps muscle activation was determined at rest using a superimposed twitch technique. Epidural lidocaine reduced pre-time trial maximal voluntary quadriceps strength (553 +/- 45 N; MVC) by 22 +/- 3%. Percent voluntary quadriceps activation was also reduced from 97 +/- 1% to 81 +/- 3% via epidural lidocaine and this was unchanged following the 5KEpi indicating a sustained level of neural impairment throughout the trial. Power output was reduced by 9 +/- 2% throughout the race (P < 0.05). We found three types of significant effects of epidural lidocaine which supported a substantial role for somatosensory feedback from the exercising limbs as a determinant of central command throughout high intensity closed-loop cycling exercise: a) relative integrated electromyogram of the vastus lateralis was significantly increased; b) pedal forces were similar despite reduced number of fast-twitch muscle fibers available for activation; c) ventilation was increased out of proportion to a reduced VCO2 and heart rate and blood pressure were increased out of proportion to power output and VO2. These findings demonstrate the inhibitory influence of somatosensory feedback from contracting locomotor muscles on the conscious and/or subconscious determination of the magnitude of central motor drive during high intensity closed-loop endurance exercise. Key words: nociception, exercise hyperpnea, muscle metaboreflex, ascending sensory pathway.

Near-infrared spectroscopy (NIRS) allows non-invasive monitoring of central and peripheral changes in oxygenation during exercise and may provide valuable insight into the factors affecting fatigue. This study aimed to explore the changes in oxygenation of prefrontal cortex and active muscle tissue as limiting factors of incremental exercise performance in trained cyclists. Thirteen trained healthy subjects (mean +/- SE: age 24.9 +/- 1.5 years, body mass 70.1 +/- 1.2 kg, training 6.1 +/- 0.9 h week(-1)) performed a progressive maximal exercise to exhaustion on a cycling ergometer. Prefrontal cortex (Cox) and vastus lateralis muscle (Mox) oxygenation were measured simultaneously by NIRS throughout the exercise. Maximal voluntary isometric knee torques and quadriceps neuromuscular fatigue (M-wave properties and voluntary activation ratio) were evaluated before and after exercise. Maximal power output and oxygen consumption were 380.8 +/- 7.9 W and 75.0 +/- 2.2 ml min(-1) kg(-1), respectively. Mox decreased significantly throughout exercise while Cox increased in the first minutes of exercise but decreased markedly from the workload corresponding to the second ventilatory threshold up to exhaustion (P < 0.05). No significant difference was noted 6 min after maximal exercise in either the voluntary activation ratio or the M-wave properties. These findings are compatible with the notion that supraspinal modulation of motor output precedes exhaustion.

In contrast to their exercise trained counterparts, the maximal oxidative rate of skeletal muscle in sedentary humans appears not to benefit from supplemental O2 availability but is impacted by severe hypoxia, suggesting a metabolic limitation either at or below ambient O2 levels. However, the critical level of O2 availability at which maximal metabolic rate is reduced in sedentary humans is unknown. Using (31)P magnetic resonance spectroscopy (MRS) and arterial oximetry, PCr recovery kinetics and arterial oxygenation were assessed in 6 sedentary subjects performing 5 min bouts of plantar flexion exercise followed by 6 min of recovery. Each trial was repeated while breathing one of four different fractions of inspired O2 (FIO2)(0.10, 0.12, 0.15, and 0.21). The PCr recovery rate constant (a marker of oxidative capacity) was unaffected by reductions in FIO2, remaining at a value of 1.5 +/- 0.2 min(-1) until arterial O2 saturation (SaO2) fell to less than ~ 92%, the average value reached breathing an FIO2 of 0.15. Below this SaO2, the PCr rate constant fell significantly by 13 and 31% to 1.3 +/- 0.2 and 1.0 +/- 0.2 min(-1)(P<0.05) as SaO2 was reduced to 82 +/- 3 and 77 +/- 2 %, respectively. In conclusion, this study has revealed that O2 availability does not impact maximal oxidative rate in sedentary humans until the O2 level falls well below that of ambient air, indicating a metabolic limitation in normoxia. Key words: oxidative capacity, 31P-magnetic resonance spectroscopy, exercise.

Our aim was to isolate the independent effects of a) the inspiratory muscle work (Wb) and b) arterial-hypoxemia, during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia (FIO2=0.15, SaO2=81+/-1%; 8.6+/-0.5 min, 273+/-6 W; Hypoxia-CTRL) and at the same work-rate and duration in normoxia (SaO2=95+/-1%; Normoxia-CTRL). These trials were repeated, but with a 35 to 80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps fatigue was assessed via magnetic femoral nerve stimulation pre- and 2-min post-exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO2, were revealed by comparing Hypoxia-CTRL and Hypoxia-PAV at equal levels of SaO2 (P=0.10). Immediately after hypoxic exercise, potentiated-twitch force of the quadriceps (Qtw,pot) decreased by 30+/-3% below pre-exercise baseline and this reduction was attenuated by about one-third following PAV exercise (21+/-4%; P<0.05). This effect of Wb on quadriceps fatigue occurred at exercise work-rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of SaO2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 16+/-2% below pre-exercise baseline following Normoxia-PAV and this reduction was exacerbated by about one-third following Hypoxia-PAV (-21+/-4%; P<0.05). We conclude that both arterial-hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work-rates during which, in normoxia, the Wb has no effect on peripheral fatigue. Key words: Work of breathing, arterial oxygen content, altitude, expiratory flow limitation, limb blood flow.

There is a strong need for more studies devoted to the analysis of changes in physiological processes during the incremental bicycle exercise when increasing the intensity of physical activity, serious ischemic episodes in cardiac muscle occur. The aim of this study was a synchronous observation of physiological changes during bicycle ergometry. Participants of the study were 27 healthy male volunteers. All participants of the study performed a graded exercise test to maximal efforts. A 12-lead electrocardiogram was recorded during exercise test and the first three minutes of recovery. Heart rate and ST-segment depression (sum of negative amplitudes) was analyzed. InSpectra Standad System Model 325 (Hutchinson Technology, Hutchinson, Minnesota, USA) was used for the registration of changes in oxygen saturation during exercise and recovery. The InSpectra sensor was placed on m. vastus lateralis. The results obtained in this study showed that changes in oxygen saturation depended on the intensity of workload. During the incremental increase in workload, oxygen saturation decreased in active muscles. While performing the final stages of exercise, a gradual increase in oxygen saturation is observed in the muscles of some participants. Increasing the intensity of physical activity to maximal efforts, rise in oxygen saturation (second phase) coincides with augmentative ischemic episodes in cardiac muscle.

The aim of this study was to evaluate the effect of transcutaneous electrical acupoint stimulation (TEAS) at selected acupoints on enhancing the rate of muscle force recovery after strenuous knee extension/flexion exercise. Ten male and seven female healthy young adults participated in this study in which they performed isokinetic knee fatigue exercise on the Biodex System 3 ergometer on three separate days. After the familiarization trial on day 1, subjects underwent 15 min of either TEAS or pseudo-TEAS recovery treatment after the isokinetic exercise in the following two trials on days 2 and 3, respectively. The TEAS treatment was applied on four selected acupoints [Zusanli (ST36), Chenshan (BL57), Yanglingquan (GB34) and Sanyinjiao (SP6)] while the pseudo-TEAS treatment was applied to the points away from the true acupoints. Isometric knee extension peak torque was measured before and immediately after the test exercise, and again during the 15-min recovery period at 5-min intervals. Blood lactate and median power frequency (MF) of the vastus medialis, vastus lateralis and rectus femoris were also measured at the same time points. The results indicated that the TEAS treatment was significantly more effective than the pseudo-TEAS treatment in enhancing the rate of muscle force recovery (knee extension peak torque recovery after 15 min, from 155 to 195 Nm in TEAS group and from 155 to 182 Nm in the pseudo-TEAS group), but had no effect on lactate removal and MF restitution rate. It is proposed that pain control is a plausible mechanism to explain the benefit of TEAS treatment. As TEAS is a non-invasive and simple treatment, it is feasible to apply it during and immediately after training.