To test the hypothesis that, during exercise, substantial heterogeneity of muscle hemoglobin and myoglobin deoxygenation [deoxy(Hb + Mb)] dynamics exists and to determine whether such heterogeneity is associated with the speed of pulmonary O(2) uptake (pVo(2)) kinetics, we adapted multi-optical fibers near-infrared spectroscopy (NIRS) to characterize the spatial distribution of muscle deoxygenation kinetics at exercise onset. Seven subjects performed cycle exercise transitions from unloaded to moderate [GET) work rates and the relative changes in deoxy(Hb + Mb), at 10 sites in the quadriceps, were sampled by NIRS. At exercise onset, the time delays in muscle deoxy(Hb + Mb) were spatially inhomogeneous [intersite coefficient of variation (CV), 3~56% for GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O(2) extraction were also spatially inhomogeneous (intersite CV, 6~48% for GET) and faster (P < 0.05) than those of phase 2 pVo(2). However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pVo(2) kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of Vo(2) and O(2) delivery increase across the regions sampled.

It is presently unclear how the fast and slow components of pulmonary oxygen uptake (VO(2)) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (VO(2) equal to 50% of the difference between LT and peak VO(2)) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in VO(2) was similar in the two positions, but VO(2) kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of VO(2) to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component of VO(2), without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise VO(2) was the same in the two positions. The changes in VO(2) kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for VO(2) but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.

The relationship between muscle deoxygenation and activation was examined in three different muscles of the quadriceps during cycling ramp exercise. Seven young male adults (24 ± 3 yr; mean ± SD) pedaled at 60 rpm to exhaustion, with a work rate (WR) increase of 20 W/min. Pulmonary oxygen uptake was measured breath-by-breath, while muscle deoxygenation (HHb) and activity were measured by time-resolved near-infrared spectroscopy (NIRS) and surface electromyography (EMG), respectively, at the vastus lateralis (VL), rectus femoris (RF), and vastus medialis (VM). Muscle deoxygenation was corrected for adipose tissue thickness and normalized to the amplitude of the HHb response, while EMG signals were integrated (iEMG) and normalized to the maximum iEMG determined from maximal voluntary contractions. Muscle deoxygenation and activation were then plotted as a percentage of maximal work rate (%WR(max)). The HHb response for all three muscle groups was fitted by a sigmoid function, which was determined as the best fitting model. The c/d parameter for the sigmoid fit (representing the %WR(max) at 50% of the total amplitude of the HHb response) was similar between VL (47 ± 12% WR(max)) and VM (43 ± 11% WR(max)), yet greater (P < 0.05) for RF (65 ± 13% WR(max)), demonstrating a "right shift" of the HHb response compared with VL and VM. The iEMG also showed that muscle activation of the RF muscle was lower (P < 0.05) compared with VL and VM throughout the majority of the ramp exercise, which may explain the different HHb response in RF. Therefore, these data suggest that the sigmoid function can be used to model the HHb response in different muscles of the quadriceps; however, simultaneous measures of muscle activation are also needed for the HHb response to be properly interpreted during cycle ramp exercise.

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.

We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (Ve) and core temperature during prolonged exercise in the heat. Thirteen subjects exercised for 60 min on a cycle ergometer at 50% of peak oxygen uptake while wearing a suit perfused with water at 10 degrees C (T10), 35 degrees C (T35), or 45 degrees C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), Ve, tidal volume, respiratory frequency (f), respiratory gases, blood pressure (BP), and blood lactate were all measured. We found that oxygen uptake, carbon dioxide output, BP, and blood lactate did not differ among the sessions. Tes, HR, Ve, and f remained nearly constant from minute 10 onward in the T10 session, but all of these parameters progressively increased in the T35 and T45 sessions, and significantly higher levels were seen in the T45 than the T35 session. For all but two subjects in the T35 and T45 sessions, plotting Ve as a function of Tes revealed no threshold for hyperventilation; instead, increases in Ve were linearly related to Tes, and there were no significant differences in the slopes or intercepts between the T35 and T45 sessions. Thus, during prolonged submaximal exercise in the heat, Ve increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between Ve and Tes are apparently small.

yasu T. Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise. J Appl Physiol 104: 998-1005, 2008. First published January 3, 2008 doi:10.1152/japplphysiol.00146.2007.-We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a waterperfused suit were used to increase esophageal temperature (T es) in 19 healthy male subjects; in the exercise trial, T es was increased by prolonged submaximal cycling [50% peak O 2 uptake (V O2)] in the heat (35°C). Minute ventilation (V E), ventilatory equivalent for V O2 (V E/V O2) and CO2 output (V E/V CO2), tidal volume (VT), and respiratory frequency (f) were plotted as functions of T es. In the exercise trial, V E increased linearly with increases (from 37.0 to 38.7°C) in Tes in all subjects; in the rest trial, 14 of the 19 subjects showed a Tes threshold for hyperpnea (37.8 Ϯ 0.5°C). Above the threshold for hyperpnea, the slope of the regression line relating V E and Tes was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating V E/V O2, V E/V CO2, and Tes were significantly greater for the rest than the exercise trial. The increase in V E reflected increases in VT and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to VT. Finally, the slope of the regression line relating Tes and VT or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity. thermoregulation; evaporative heat loss; ventilatory pattern IN MANY SPECIES OF MAMMALS and birds, an elevation in body temperature stimulates ventilation and increases evaporative heat loss for thermoregulation with a two-phase panting response (26,33). In animals such as the sheep and dog, this panting response can include two distinct patterns of breathing, often referred to as first-and second-phase panting (7,12,13,26,33). In the first phase, respiratory frequency (f) is maximized, while tidal volume (VT) is minimized, and arterial blood gases are not perturbed (33). The second phase is only evident with an increase in core temperature, and VT and f are increased, so that alveolar ventilation is increased, resulting in hypocapnia and respiratory alkalosis (33). In 1905, Haldane (11) was the first to report that hyperthermia also increases ventilation in humans. The recent review by White (33) suggested that since increased ventilation by hyperthermia in humans increases alveolar ventilation so that respiratory alkalosis occurs, a hyperthermia-induced increase in ventilation in humans is likely to be the second phase of panting. However, the mechanisms and the physiological significance of this response in humans are not fully understood.When body tem...

-The conventional continuous wave near-infrared spectroscopy (CW-NIRS) has enabled identification of regional differences in muscle deoxygenation following onset of exercise. However, assumptions of constant optical factors (e.g., path length) used to convert the relative changes in CW-NIRS signal intensity to values of relative concentration, bring the validity of such measurements into question. Furthermore, to justify comparisons among sites and subjects, it is essential to correct the amplitude of deoxygenated hemoglobin plus myoglobin [deoxy(HbϩMb)] for the adipose tissue thickness (ATT). We used two time-resolved NIRS systems to measure the distribution of the optical factors directly, thereby enabling the determination of the absolute concentrations of deoxy(HbϩMb) simultaneously at the distal and proximal sites within the vastus lateralis (VL) and the rectus femoris muscles. Eight subjects performed cycle exercise transitions from unloaded to heavy work rates (Ͼgas exchange threshold). Following exercise onset, the ATT-corrected amplitudes (Ap), time delay (TDp), and time constant (p) of the primary component kinetics in muscle deoxy(Hb ϩ Mb) were spatially heterogeneous (intersite coefficient of variation range for the subjects: 10 -50 for Ap, 16 -58 for TDp, 14 -108% for p). The absolute and relative amplitudes of the deoxy(HbϩMb) responses were highly dependent on ATT, both within subjects and between measurement sites. The present results suggest that regional heterogeneity in the magnitude and temporal profile of muscle deoxygenation is a consequence of differential matching of O 2 delivery and O2 utilization, not an artifact caused by changes in optical properties of the tissue during exercise or variability in the overlying adipose tissue. near-infrared spectroscopy; oxygen uptake kinetics; muscle oxygen delivery; muscle oxygen utilization MUSCLE OXYGENATION/DEOXYGENATION reflects the balance between O 2 delivery (Q o 2 ) and O 2 utilization (V O 2 ), i.e., Q o 2 /V O 2 ratio (or V O 2 /Q o 2 as deoxygenation). Thus, the profile of muscle deoxygenation, for example, following the onset of exercise can provide important information regarding the adequacy of the vascular response and the O 2 pressures essential for driving blood-muscle O 2 flux (1, 4 -8, 11, 13, 15-17, 25, 32, 39, 43, 47).Recently, we found that the dynamics of muscle microvascular deoxygenation [deoxy(Hb ϩ Mb)] measured by continuous wave near-infrared spectroscopy (CW-NIRS) were spatially heterogeneous within the quadriceps muscles in transient states where metabolic rate was changing rapidly (25, 43). However, the spatial heterogeneity of the muscle deoxygenation dynamics may have been related to intra-and intersubject variability in unmeasured optical factors such as path length, absorption, and scattering coefficients inherent in CW-NIRS technology (15). Thus, it remains unknown to what extent the absolute amplitude of muscle deoxygenation of the different regions reflects the temporal profile of the mean muscle oxygen pressur...

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