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We investigated whether muscle and ventilatory responses to incremental ramp exercise would be influenced by aerobic fitness status by means of a cross-sectional study with a large subject population. Sixty-four male students (age: 21.2 ± 3.2 years) with a heterogeneous peak oxygen uptake (51.9 ± 6.3 mL·min(-1)·kg(-1), range 39.7-66.2 mL·min(-1)·kg(-1)) performed an incremental ramp cycle test (20-35 W·min(-1)) to exhaustion. Breath-by-breath gas exchange was recorded, and muscle activation and oxygenation were measured with surface electromyography and near-infrared spectroscopy, respectively. The integrated electromyography (iEMG), mean power frequency (MPF), deoxygenated [hemoglobin and myoglobin] (deoxy[Hb+Mb]), and total[Hb+Mb] responses were set out as functions of work rate and fitted with a double linear function. The respiratory compensation point (RCP) was compared and correlated with the breakpoints (BPs) (as percentage of peak oxygen uptake) in muscle activation and oxygenation. The BP in total[Hb+Mb] (83.2% ± 3.0% peak oxygen uptake) preceded (P < 0.001) the BP in iEMG (86.7% ± 4.0% peak oxygen uptake) and MPF (86.3% ± 4.1% peak oxygen uptake), which in turn preceded (P < 0.01) the BP in deoxy[Hb+Mb] (88.2% ± 4.5% peak oxygen uptake) and RCP (87.4% ± 4.5% peak oxygen uptake). Furthermore, the peak oxygen uptake was significantly (P < 0.001) positively correlated to the BPs and RCP, indicating that the BPs in total[Hb+Mb] (r = 0.66; P < 0.001), deoxy[Hb+Mb] (r = 0.76; P < 0.001), iEMG (r = 0.61; P < 0.001), MPF (r = 0.63; P < 0.001), and RCP (r = 0.75; P < 0.001) occurred at a higher percentage of peak oxygen uptake in subjects with a higher peak oxygen uptake. In this study a close relationship between muscle oxygenation, activation, and pulmonary oxygen uptake was found, occurring in a cascade of events. In subjects with a higher aerobic fitness level this cascade occurred at a higher relative intensity.

Purpose: The aim of this study was to compare the muscle oxygenation between trained and untrained subjects during heavy exercise until exhaustion at two extreme pedaling cadences using a NIRS system., Methods: Nine untrained male subjects and nine male competitive triathletes cycled until exhaustion at an intensity corresponding to 90 % of the power output achieved at peak oxygen uptake at 40 and 100 rpm. Gas exchanges were measured breath-by-breath during each exercise. Muscle (de)oxygenation was monitored continuously by near-infrared spectroscopy on the Vastus Lateralis., Results: Muscle deoxygenation (∆deoxy[Hb + Mb], i.e., O2 extraction) and ∆total[Hb + Mb] were significantly higher at 40 rpm compared to 100 rpm during the exercise in untrained subjects but not in triathletes (p < 0.05). The time performed until exhaustion was significantly higher at 40 than at 100 rpm in untrained subjects (373 ± 55 vs. 234 ± 37 s, respectively) but not in triathletes (339 ± 69 vs. 325 ± 66 s)., Conclusions: These results indicate that high aerobic fitness (1) allows for better regulation between [Formula: see text]O2M and VO2M following the change in pedaling cadence, and (2) is the most important factor in the relationship between pedaling cadence and performance.

Purpose: The aim of this project was to study the impact of pedal rate on breakpoints in muscle oxygenation (deoxy[Hb + Mb] and total[Hb + Mb]) and activation (iEMG and MPF) at high intensities during ramp exercise., Methods: Twelve physically active students performed incremental ramp exercises at 60 rpm, starting either at 50 or 80 W (i.e., 60rpm50 and 60rpm80), and at 100 rpm, starting at 50 W (100rpm50). Pulmonary VO2, muscle activation (iEMG and MPF) and oxygenation were recorded with EMG and NIRS, respectively. IEMG, MPF, deoxy[Hb + Mb] and total[Hb + Mb] were expressed as functions of work rate (WR) and pulmonary VO2 (%VO2peak) and analyzed with double-linear models., Results: The breakpoints (BP) of iEMG, MPF, total[Hb + Mb] and deoxy[Hb + Mb] in %VO2peak did not differ among the pedal rate conditions (P > 0.05), whereas the BPs in WR were significantly lower in 100rpm50 compared to 60rpm50 and 60rpm80 (P < 0.01). Across the pedal rate conditions the BP (in %VO2peak) of total[Hb + Mb] (82.7 ± 1.5 %VO2peak) was significantly lower (P < 0.01) compared to the BP in iEMG (84.3 ± 1.7 %VO2peak) and MPF (84.2 ± 1.6 %VO2peak), whereas the BP in deoxy[Hb + Mb] (87.4 ± 1.4 %VO2peak) and respiratory compensation point (89.9 ± 1.8 %VO2peak) were significantly higher (P < 0.01) compared to the BP in total[Hb + Mb], iEMG and MPF. Additionally, the BPs in iEMG, MPF, total[Hb + Mb] and deoxy[Hb + Mb], and the RCP were highly correlated (r > 0.90; P < 0.001)., Conclusions: The present study showed that muscle activation and oxygenation at high intensities during incremental exercise are related to pulmonary VO2 rather than external WR, with a close interrelationship between that muscle activation, oxygenation and pulmonary VO2.

This study examined the effect of pedal cadence on the heterogeneity of muscle deoxygenation during exercise of moderate intensity. Twelve healthy subjects performed 6 min of cycling at 40 and 100 r · min(-1) at 80% of the workload corresponding to the gas exchange threshold. Gas exchanges were measured breath by breath during each exercise. Muscle deoxygenation (HHb, i.e., O2 extraction) was monitored continuously by near-infrared spectroscopy at eight sites on the vastus lateralis. The heterogeneity of HHb was assessed using the relative dispersion of the signal measured at the eight sites (i.e., 100 × standard deviation/mean). HHb was not altered by the pedal cadence, whereas pulmonary V̇O2 was higher at 100 r · min(-1) than at 40 r · min(-1) (p < 0.001). The relative dispersion of HHb was significantly higher at 100 r · min(-1) than at 40 r · min(-1) (p < 0.001). These results indicate that pedal cadence has no effect on O2 extraction but that an elevated cadence would increase muscle V̇O2, suggesting an increase in muscle blood flow. Elevated cadence also induced greater heterogeneity of the muscle's V̇O2/Q̇O2 delivery ratio, suggesting a change in the adequacy between O2 demand and O2 delivery in some regions of active muscle.

Objective: To determine whether erector spinae muscle oxygenation (OXY) and blood volume during a progressive isoinertial lifting evaluation (PILE) are modified by an exercise therapy program., Design: Pre- (t1) and post- (t2) exercise therapy experimental design., Setting: Hospital., Participants: Subjects with chronic low back pain (LBP group) (n=24) and healthy subjects (control group) (n=24) were evaluated., Intervention: Exercise program., Main Outcome Measures: The control group was evaluated once, and the LBP group was evaluated before (t1) the exercise therapy program and 28 days thereafter (t2). The maximal load lifted, total work, and total power were determined using the PILE test. Continuous-wave near-infrared spectroscopy was used to measure OXY and blood volume during the PILE test., Results: The maximal load lifted, total power, and total work were significantly lower in the LBP group (-42%±5%, -46%±6%, and -67%±6% at t1, respectively; P<.05) than the control group. In the LBP subjects, these parameters improved significantly after the exercise therapy program (+20%±3%, +56%±4%, and +61%±5%; P<.05). At each submaximal power (ie, 25, 50, 75, and 100% of maximal load lifted at t1), OXY and blood volume were significantly higher at t2 than t1. One-half recovery time for OXY was significantly higher in the LBP group (at t1 and t2) than in control subjects., Conclusions: The findings in this study suggest that LBP subjects present an impairment in their capacity to deliver oxygen at the level of the erector spinae muscle, which can be partly restored by an exercise therapy program., (Copyright © 2013 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.)

This study examines the effect of high-intensity interval training (HIT) on the spatial distribution of muscle deoxygenation during incremental exercise. Young untrained male adults (n = 11) performed an incremental bicycle exercise before and after a running HIT of 6 weeks. Muscle deoxygenation (HHb) and blood volume (Hb(tot)) were monitored continuously by near-infrared spectroscopy at eight sites in the vastus lateralis. The rise in HHb during incremental exercise was significantly higher after training, in comparison with before training (P = 0.020), whereas the rise in Hb(tot) was not affected by training. The standard deviation of HHb and the relative dispersion of HHb at the eight sites were not significantly different irrespective of the intensity of exercise between pre- and post-training. After training, the standard deviation of HHb was greater at 60, 70, and 80 % of VO₂(max) than at rest. Finally, training significantly increased the standard deviation of Hb(tot) (P = 0.036). These results indicate that HIT changes the muscle deoxygenation profile during incremental exercise, suggesting an improvement in the O(2) extraction with training. HIT did not reduce the spatial heterogeneity of muscle deoxygenation and blood volume during incremental exercise. This indicates that the intra-muscular distribution of the VO(2)/O(2) delivery ratio was not improved by 6 weeks HIT.

This study examines the effect of prior heavy exercise on the spatial distribution of muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Young untrained male adults (n = 16) performed two consecutive bouts of 6 min of high intensity cycle exercise separated by 6 min at 35 W. Muscle deoxygenation (HHb) was monitored continuously by near-infrared spectroscopy at eight sites in the quadriceps. Prior heavy exercise reduced the delay before the increase in HHb (9 +/- 2 vs. 5 +/- 2 s; P < 0.001). The standard deviation of TD HHb of the eight sites was decreased by the performance of prior exercise (1.1 +/- 0.5 vs. 0.8 +/- 0.4 s; P < 0.05). The transient decrease in HHb during the first 10 s of exercise was less during the second bout than during the first bout (0.6 +/- 0.6 vs. 0.3 +/- 0.3 A.U.; P < 0.01). The standard deviation of this decrease was also reduced by prior exercise (0.5 +/- 0.3 vs. 0.3 +/- 0.2 A.U.; P < 0.01). Lastly, prior exercise decreased significantly the standard deviation of the HHb rise during the time period corresponding to the pulmonary VO(2) slow component. These results indicate that prior heavy exercise reduced the spatial heterogeneity of muscle deoxygenation kinetics at the early onset of heavy exercise and during the development of the pulmonary VO(2) slow component. It indicates that the distribution of the VO(2)/O(2) delivery ratio within muscle was improved by the performance of a prior exercise.

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.

Purpose: We investigated the potential effect of respiratory muscle work on leg muscle oxygenation without artificial intervention in non-endurance-trained young subjects and searched for the range of intensity when this effect could occur., Methods: We simultaneously monitored accessory respiratory and leg muscle oxygenation patterns with near-infrared spectroscopy (NIRS) in 15 healthy young men performing maximal incremental exercise on a cycle ergometer. Pulmonary gas exchange was measured. The respiratory compensation point (RCP) was determined. Oxygenation (RMO2) and blood volume (RMBV) of the serratus anterior (accessory respiratory muscle) and of the vastus lateralis (LegO2 and LegBV) were monitored with NIRS. The breakdown point of accessory respiratory muscle oxygenation (BPRMO2) and the accelerated (BP1LegO2) and attenuated fall (BP2LegO2) in leg muscle oxygenation were detected., Results: BPRMO2 occurred at approximately 85% .VO2max and was related to RCP (r = 0.88, P < 0.001). BP2LegO2 appeared at approximately 83% .VO2max and was related to RCP (r = 0.57, P < 0.05) and with BPRMO2 (r = 0.64, P = 0.01). From BP2LegO2 to maximal exercise, LegBV was significantly reduced (P < 0.05)., Conclusion: In active subjects exercising at heavy exercise intensities, we observed that the appearance of the accelerated drop in accessory respiratory muscle oxygenation-associated with high ventilatory level-was related with the attenuated fall in leg muscle oxygenation detected with near-infrared spectroscopy. This suggests that the high oxygen requirement of respiratory muscle leads to limited oxygen use by locomotor muscles as demonstrated in endurance-trained subjects. The phenomenon observed was associated with reduced leg blood volume, supporting the occurrence of leg vasoconstriction. These events appeared not only at maximal exercise but onward above the respiratory compensation point.

The objective of the present study was to relate changes in certain muscle characteristics and indicators of metabolism in response to endurance training to the concomitant changes in time to exhaustion (T(lim)) at a work rate corresponding to maximal oxygen uptake VO(2speak). Eight healthy sedentary subjects pedalled on a cycle ergometer 2 h a day, 6 days a week, for 4 weeks. Training caused increases in VO(2peak) (by 8%), T(lim) (from 299 +/- 23 s before to 486 +/- 63 s after training), citrate synthase and 3-hydroxyl-acyl-CoA dehydrogenase (HAD) activities (by 54% and 16%, respectively) and capillary density (by 31%). Decreases in activity of lactate dehydrogenase (LDH) and muscle type of LDH (by 24% and 28%, respectively) and the phosphofructokinase/citrate synthase ratio (by 37%) were also observed. Respiratory exchange ratio (RER) tended to be lower (P < 0.1) at all relative work rates after training while the corresponding ventilation rates (VE) were unchanged. At the same absolute work rate, RER and (VE) were lower after training (P < 0.05). The improvement of T(lim) with training was related to the increases in HAD activity (r = 0.91, P = 0.0043), and to the decreases in RER calculated for Pa(peak) (r = 0.71, P = 0.0496). The present results suggest that the training-induced adaptations in fat metabolism might influence T(lim) at a work rate corresponding to VO(2peak) and stimulate the still debated and incompletely understood role of fat metabolism during short high-intensity exercise.

Purpose: The aim of this study was to compare the muscle deoxygenation measured by near infrared spectroscopy in endurance athletes who presented or not with exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic conditions., Methods: Nineteen male endurance sportsmen performed an incremental test on a cycle ergometer to determine maximal oxygen consumption (VO2max) and the corresponding power output (P(max)). Arterial O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between rest and the end of the exercise. Muscle deoxygenation of the right vastus lateralis was monitored by near infrared spectroscopy and was expressed in percentage according to the ischemia-hyperemia scale., Results: Ten athletes exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic (NEIH group). Training volume, competition level, VO2max, Pmax, and lactate concentration were similar in the two groups. Nevertheless, muscle deoxygenation at the end of the exercise was significantly greater in the EIH group (P < 0.05)., Conclusion: Greater muscle deoxygenation at maximal exercise in hypoxemic athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to working muscle added to the metabolic demand. In addition, our finding is also consistent with the hypothesis of greater muscle oxygen extraction in order to counteract reduced O2 availability.

Purpose: Endurance training improves the oxygen delivery and muscle metabolism. Muscle oxygen saturation measured by near infrared spectroscopy (IR-SO(2)), which is primarily influenced by the local delivery/demand balance, should thus be modified by training. We examined this effect by determining the influence of change in blood lactate and muscle capillary density with training on IR-SO(2) in seven healthy young subjects., Methods: Two submaximal exercise tests at 50% (Ex1) and 80% pretraining VO(2max) (Ex2) were performed before and after a 4-wk endurance-training program., Results: VO(2max) increased only slightly (+8%, NS) with training but the training effect was confirmed by the increased capillary density (+31%, P < 0.01) and citrate synthase activity (50%, P < 0.01), determined from muscle biopsy samples. Before training, blood lactate increased during the first 5 min of Ex1 and then remained constant (3.8 +/- 0.5 mmol x L(-1), P < 0.01), whereas it increased continuously during Ex2 (8.9 +/- 1.8 mmol x L(-1), P < 0.001). After training, lactate decreased significantly and remained constant during the two bouts of exercise (2.0 +/- 0.4 and 3.7 +/- 1.2 at the end of Ex1 and Ex2, respectively, both P < 0.001). During Ex1, IR-SO(2) dropped initially at the onset of exercise and recovered progressively without reaching the resting level. Training did not change this pattern of IR-SO(2). During Ex2, IR-SO(2) decreased progressively during the 15 min of exercise (P < 0.05); IR-SO2 kept constant after the initial drop after training. We found a significant relationship (r = 0.42, P = 0.03) between blood lactate and IR-SO(2) at the end of both bouts of exercise; this relationship was closer before training. By contrast, IR-SO(2) or IR-BV was not related to the capillary density., Conclusion: The training-induced adaptation in blood lactate influences IR-SO(2) during mild- to hard-intensity exercise. Thus, NIRS could be used as a noninvasive monitoring of training-induced adaptations.

The influence of ageing on the capacity to increase muscle oxygen delivery during exercise is unclear. This was investigated by comparing the evolution of Near InfraRed Spectroscopy (NIRS) in 10 old (67 +/- 5 years, Old group) and 13 young subjects (27 +/- 4 years, Young group), during a progressive maximal exercise. The NIRS probe was placed on the vastus lateralis; muscle oxygen saturation - IR-SmO(2) - values were expressed on a scale using an arterial occlusion as the lower reference point and the subsequent reactive hyperaemia as the upper reference point. Resting IR-SmO( 2) was found to be significantly lower in the Old as co mpared to the Young group. During exercise, VO(2) increased similarly as a function of the workload whereas IR-SmO(2) decreased faster in old subjects than in young ones. Conversely, when expressed at the same percentage of VO( 2max), IR-SmO(2) followed a similar evolution in both groups from rest to maximal exercise (27.3 +/- 16.7 vs 24.3 +/- 12.9% decrease, in Old and Young group, respectively, NS). Thus, the initial difference remained constant between the two groups. During recovery, the time to recover the signal variation was not different between the two groups. We concluded that Old subjects demonstrate a systematic lower muscle oxygen saturation than Young ones. This difference could be explained by an age related decrease in muscle blood flow limiting O(2) supply.