| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Canadian Centre for Activity and Aging, 2School of Kinesiology, and 3Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada N6A 3K7
Submitted 1 December 2003 ; accepted in final form 27 April 2004
 |
ABSTRACT |
|---|
 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
O2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 ± 3 yr) and older (n = 5; 68 ± 3 yr) adults. We hypothesized that heavy warm-up would speed O2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). O2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hbtot) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). O2p (phase 2; 
) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 ± 9 µM; young subjects: 9 ± 8 µM) and Hbtot (older subjects: 12 ± 8 µM; young subjects: 14 ± 10 µM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, O2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 ± 7 s) than no warm-up (38 ± 5 s), whereas in young subjects, O2p was similar in no warm-up (26 ± 7 s) and heavy warm-up (25 ± 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, O2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery. near-infrared spectroscopy; muscle oxygen utilization; aging
O2p) kinetics are slowed in older compared with younger adults (2, 6, 13–15, 20, 41), suggesting that the rate-limiting process may be influenced by advancing age or inactivity. Training studies have demonstrated that O2p kinetics can be speeded in older and younger adults, suggesting that a chronic training stimulus may be able to alter the rate-limiting process (1, 7, 36). Additionally, several investigations (8, 28, 31) have demonstrated that a bout of prior heavy-intensity warm-up exercise can acutely alter O2p kinetics at the onset of a subsequent heavy-intensity exercise bout. Gerbino et al. (28) suggested that prior heavy-intensity warm-up exercise resulted in an improvement of muscle perfusion consequent to the vasodilatory effects of metabolic acidemia and demonstrated in young adults that a bout of prior heavy-intensity warm-up exercise resulted in a "speeding" of the overall time course of subsequent heavy-intensity exercise O2p kinetics but did not affect subsequent moderate-intensity exercise O2p kinetics. The authors interpreted these findings to suggest that, in young adults, O2p kinetics in the moderate-intensity domain are not limited by muscle blood flow and O2 delivery.
In contrast, recent evidence from our laboratory (20, 41) suggests that O2 delivery may limit O2p kinetics at the onset of exercise in older adults. Scheuermann et al. (41) reported a speeding of O2p kinetics during moderate-intensity exercise after a prior bout of heavy-intensity warm-up exercise in older adults, which combined with the observed elevation of HR before the subsequent exercise bout suggested that the adaptation of muscle blood flow may limit the rate of increase of O2p during the exercise on-transient in older adults, although an effect of prior exercise on metabolic activation could not be ruled out.
The technique of near-infrared spectroscopy (NIRS) provides noninvasive and continuous monitoring of relative concentration changes in deoxy- (HHb), oxy- (O2Hb), and total hemoglobin (Hb) and myoglobin (Mb) (Hbtot) in the microvasculature (small arterioles, capillaries, and venules) (9) of the muscle. The NIRS-derived HHb signal reflects the balance between O2 delivery and O2 utilization in the region of NIRS interrogation and, when used in combination with measurements of pulmonary O2p, provides information on the time course of local muscle O2 utilization (20, 21, 29).
Therefore, the purpose of the present study was to examine the effect of prior heavy-intensity exercise on the adaptation of O2p and muscle deoxygenation at the onset of a subsequent moderate-intensity exercise bout in young and older adults. We hypothesized that 1) after prior heavy-intensity exercise, O2p kinetics would be accelerated in older and unchanged in young adults during subsequent moderate-intensity exercise; 2) prior heavy-intensity exercise would result in an elevation of HR in older and younger adults, reflecting improved muscle perfusion and O2 delivery before the onset and throughout subsequent moderate-intensity exercise in both groups; and 3) after heavy-intensity warm-up exercise, muscle deoxygenation would adapt at a slower rate in older adults (despite faster O2p kinetics) and be unchanged in young adults, reflecting an improvement in local muscle perfusion in older adults. Collectively, these results would suggest that the adaptation of muscle blood flow may limit the adaptation of O2p [and muscle O2 uptake (O2)] in older adults during the on-transient of moderate-intensity exercise without prior warm-up exercise.
|
METHODS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
Protocol.
Subjects reported to the laboratory on nine separate occasions. An incremental ramp (25 W/min) exercise test to the limit of tolerance was performed by cycle ergometry on the first day of testing for the determination of the estimated lactate threshold (
L) and peak O2. L was defined as the O2 at which CO2 output began to increase out of proportion in relation to O2, with a systematic rise in minute ventilation/O2 and end-tidal PO2 while minute ventilation/CO2 output and end-tidal PCO2 were stable. The incremental ramp test also served as a medical screening of older subjects, was monitored by a physician, and included a 12-lead ECG.
After this test, subjects returned to the laboratory on eight separate occasions to perform step transitions in work rate (WR) from 20 W to a moderate-intensity WR selected to elicit a O2p corresponding to 80% L. Each moderate-intensity WR transition was 6 min in duration and was preceded by either no warm-up exercise or 6 min of heavy-intensity warm-up exercise at a WR selected to elicit a O2p equivalent to 
50% of the difference (
50%) between the O2p at L and peak O2. In the heavy-intensity warm-up condition, the heavy-intensity exercise was preceded and followed by 6 min of 20-W cycling. Four transitions were performed in each of the warm-up conditions in random order.
Measurements. Gas-exchange measurements were similar to those described previously (2). Briefly, inspired and expired flow rates were measured with a low dead-space (90 ml) bidirectional turbine (Alpha Technologies VMM 110), which was calibrated before each test with a syringe of known volume. Inspired and expired gases were sampled continuously at the mouth and analyzed for concentrations of O2, CO2, and N2 by mass spectrometry (Morgan Medical) after calibration with precision-analyzed gas mixtures. Changes in gas concentration were aligned with gas volumes by measuring the time delay for a square-wave bolus of gas passing the turbine to the resulting changes in fractional gas concentrations, as measured by the mass spectrometer. Data collected every 20 ms were transferred to a computer, which aligned concentrations with volume data to build a profile of each breath. Breath-by-breath alveolar gas exchange was calculated using algorithms of Beaver et al. (4). Heart rate (HR) was continuously monitored by electrocardiogram.
Local muscle oxygenation profiles of the quadriceps vastus lateralis muscle were made with NIRS (Hamamatsu NIRO 300, Hamamatsu Photonics). Optodes were placed on the belly of the muscle midway between the lateral epicondyle and greater trochanter of the femur. The optodes were housed in an optically dense plastic holder, thus ensuring that the position of the optodes, relative to each other, was fixed and invariant. The optode assembly was secured on the skin surface with tape and then covered with an optically dense, black vinyl sheet, thus minimizing the intrusion of extraneous light and loss of NIR-transmitted light from the field of interrogation. The thigh, with attached optodes and covering, was wrapped with an elastic bandage to minimize movement of the optodes while still permitting freedom of movement for cycling. This preparation essentially prevented any optode movement relative to the skin surface.
The theory of NIRS is described in detail by Elwell (26). Briefly, one fiber optic bundle carried the NIR light produced by the laser diodes to the tissue of interest while a second fiber optic bundle returned the transmitted light from the tissue to a photon detector (photomultiplier tube) in the spectrometer. Four different wavelength laser diodes (775, 810, 850, and 910 nm) provided the light source. The diodes were pulsed in rapid succession, and the light was detected by the photomultiplier tube. The use of four laser diodes enables more chromophores to be detected and also increases the sensitivity of the instrument, thus providing an advantage of the NIRO 300 over other simpler NIR-detection systems (5, 12, 32). The intensity of incident and transmitted light was recorded continuously at 2 Hz and, along with the relevant specific extinction coefficients and optical pathlength, used for online estimation and display of the concentration changes from the zero-set during the resting baseline of O2Hb, HHb, and Hbtot. The raw attenuation signals (in optical density units) were transferred to a computer and stored for further analysis. At present, NIRS instrumentation is unable to accurately determine the relative contribution of Mb to the total NIRS signal because the Mb absorption spectrum overlaps that of Hb (18). However, Mb levels are small relative to those of Hb, and several studies (10, 12, 32, 42) have suggested that intracellular Mb contributes <10% to the total NIRS signal. Thus the preponderance of evidence in the literature would suggest that NIRS primarily monitors changes in vascular Hb oxygenation and deoxygenation, although Tran et al. (45) have reported that, during plantar flexion exercise with pressure cuffing of the leg, NIRS deoxygenation kinetics closely matched those of 1H-magnetic resonance spectroscopy-determined Mb desaturation but not Hb desaturation.
The interoptode spacing was 5 cm. Although values exist for differential pathlength factors in muscle for calf and forearm (25, 47), there are presently no published values for the quadriceps muscle. In the present study, we used a value for differential pathlength factors of 3.83; thus values for O2Hb, HHb, and Hbtot are reported as a change from pretransition (20-W cycling) baseline in micromolar units.
The HHb signal can be regarded as being essentially blood volume insensitive during exercise (16, 27); thus it was assumed to be a reliable estimator of changes in intramuscular oxygenation status and O2 extraction in the field of interrogation (17, 27).
Analysis.
Breath-by-breath gas-exchange data were filtered for aberrant data points, interpolated to 1-s intervals, ensemble averaged, and then averaged into 5-s time bins to yield a single response for each subject. Phase 2 O2p kinetics were determined by the use of a monoexponential model of the form
 | (1) |
O2p at any time (t), b is the baseline value of Y at the point in time from which the data were fitted, A is the amplitude of the increase in Y above the baseline value, is the time constant defined as the duration of time through which Y increases to a value equivalent to 63% of A, and TD is the time delay. Data were fit from the phase 1-phase 2 interface to minute 4 of exercise.
The NIRS-derived O2Hb, HHb, and Hbtot data were time aligned and ensemble averaged to 5-s time bins to yield a single response for each subject. The time delay before an increase in HHb after exercise onset was determined as the first point greater than one standard deviation above the mean of the pretransition (20 W) baseline. This analysis was performed on the second-by-second data for each of the individual trials; the time delay was calculated as the average of the four trials for each subject. HHb data were fit from the time of initial increase in HHb to 180 s with a monoexponential model of the form in Eq. 1 to determine the time course of muscle deoxygenation. Although we are not certain that the underlying processes determining muscle deoxygenation are exponential in nature, visual inspection of the NIRS-derived HHb signal and analysis of least squares residuals suggested that fitting with a monoexponential model would provide a reasonable estimate of the time course of muscle deoxygenation (i.e., effective ). The time course for the overall change in HHb was also determined as the sum of the time delay before an increase in HHb and effective -HHb [mean response time (MRT)]. In addition, the time course of increase of HHb during the on-transient was also determined as the time to reach 63% (t63%) of the steady-state response observed at 3–4 min. The O2Hb and Hbtot signals did not approximate an exponential response as changes in local blood volume will influence these signals, whereas the HHb signal is essentially blood volume insensitive (16). The O2Hb and Hbtot signals were not modeled; however, the response of these signals was compared qualitatively to the HHb data at corresponding time intervals.
Beat-by-beat HR data were filtered for aberrant beats, time-aligned, and averaged to 5-s time bins. These data were then fit from exercise onset with a monoexponential model of the form in Eq. 1.
Statistical analysis.
Analysis of the effects of age and warm-up on O2p, HR, and HHb kinetics was by two-way repeated-measures ANOVA. Significant differences were further tested by Student-Newman-Keuls post hoc analysis. Comparisons of O2p, HR, and HHb kinetics within a group (young vs. older) and within condition (no warm-up vs. heavy-intensity warm-up) was by independent t-test. Relationships among key variables were determined by Pearson product correlation. All data are presented as means ± SD. A P value of <0.05 was considered statistically significant.
|
RESULTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
O2p peak (2.3 ± 0.3 l/min; 27 ± 4 ml·kg–1·min–1) and peak WR (220 ± 29 W) of older adults was lower (P < 0.05) than that of young adults (3.6 ± 0.6 l/min; 48 ± 7 ml·kg–1·min–1 at 343 ± 63 W).
O2 kinetics.
The adaptation of O2p at the onset of moderate-intensity exercise after no warm-up and heavy-intensity warm-up for a representative older and young subject is illustrated in Fig. 1. To confirm that a moderate-intensity steady-state O2p had been achieved and that a slow component of O2p characteristic of heavy-intensity exercise performed above L did not exist, the slopes of the O2p responses between 3 and 6 min of no warm-up and heavy-intensity warm-up in older and young adults were calculated. The O2p slope was not different from zero for the older or young adults during either no warm-up (older: 4 ± 4 ml/min; young: 8 ± 4 ml/min) or heavy-intensity warm-up (older: 2 ± 5 ml/min; young: 8 ± 13 ml/min) conditions. Additionally, end-exercise O2p (calculated as the average O2p during the last 30 s of the exercise transient) was similar to the sum of the O2p baseline and amplitude from modeling in older and young adults after no warm-up and heavy-intensity warm-up exercise.
|
O2p was similar in older and young adults in the no warm-up condition. Heavy-intensity warm-up resulted in a higher (P < 0.01) pretransition baseline O2p in both older and young adults. As expected in relation to the lower absolute WR during heavy-intensity warm-up in older adults, the increase in baseline O2p after heavy-intensity warm-up exercise was smaller in older (0.11 l/min) than in young adults (0.17 l/min), such that baseline O2p was lower (P = 0.046) in older compared with young adults after heavy-intensity warm-up (Table 1). The amplitude of the increase in O2p was lower (P < 0.01) in older compared with young adults after both warm-up conditions, reflecting the lower absolute moderate-intensity WR in older adults. The amplitude of the increase in O2p was lower (P < 0.01) after heavy-intensity warm-up compared with no warm-up in young subjects, whereas the increase in O2p was not different between warm-up conditions in older adults (Table 1). The resulting end-exercise O2p was lower (P < 0.05) in no warm-up compared with heavy-intensity warm-up in older (no warm-up: 1.16 ± 0.15 l/min; heavy-intensity warm-up: 1.24 ± 0.17 l/min) and young adults (no warm-up: 1.70 ± 0.28 l/min; heavy-intensity warm-up: 1.78 ± 0.29 l/min); end-exercise O2p was lower (P < 0.01) in older compared with young adults in both warm-up conditions. The end-exercise change in O2p-to-change in WR ratio (
2/WR) was similar in older and young adults for both no warm-up (older: 10 ± 1 ml/W; young: 11 ± 4 ml/W) and heavy-intensity warm-up (older: 9 ± 1 ml/W; young: 9 ± 3 ml/W).
|
O2p was greater (P < 0.01) in older compared with young adults in the no warm-up condition (Fig. 1, Table 1). After heavy-intensity warm-up, O2p was reduced (P < 0.01) in older adults but was unchanged in the young adults, such that after heavy-intensity warm-up O2p was similar in older and young adults (Table 1).
HR.
The adaptation of HR at the onset of moderate-intensity exercise after no warm-up and heavy-intensity warm-up for a representative older and young subject is illustrated in Fig. 2. Baseline HR during no warm-up was similar in older and young adults (Table 2) and was elevated (P < 0.001) after heavy-intensity warm-up in older (17 beats/min) and young (18 beats/min) adults. The amplitude of the increase in HR was lower (P < 0.01) in older compared with young adults during both warm-up conditions (Table 2). The rate of adaptation of HR (HR) was not statistically different in older (47 ± 24 s) and young adults (23 ± 12 s) in the no warm-up condition (Table 2). When the HR data in the no warm-up condition were analyzed separately by independent t-test, the apparent difference in HR between older and young adults was significant (P < 0.05). After heavy-intensity warm-up, HR was similar to the no warm-up condition in older adults, but in young adults HR was 22 s greater (P < 0.05), resulting in a similar HR in older and young adults after heavy-intensity warm-up (older: 51 ± 31 s; young: 45 ± 36 s).
|
|
HHb) at the onset of moderate-intensity exercise after no warm-up and heavy-intensity warm-up for a representative older and young subject is illustrated in Fig. 3. The time delay before an increase NIRS-derived HHb was similar in older and young adults in both warm-up conditions (Table 3). The time delay before an increase in HHb was shorter (P < 0.05) after heavy-intensity warm-up compared with no warm-up in older and young adults (Table 3). After the time delay, HHb increased, with the effective HHb and MRT-HHb being similar in older and young adults after no-warm-up; in older adults with heavy-intensity warm-up exercise, the effective HHb and MRT-HHb were greater (P < 0.01) compared with young and compared with the no warm-up condition (Table 3). The t63% of the steady-state HHb response (HHb-t63%) was also calculated. Consistent with the results from modeling of the HHb signal, after heavy-warm-up, HHb-t63% was greater (P < 0.05; 34 ± 12 s) in older adults compared with no warm-up (22 ± 3 s) and compared with the young adults after either warm-up condition. The HHb-t63% in young adults was not affected by warm-up (no warm-up: 25 ± 4 s; heavy-intensity warm-up: 21 ± 3 s). The amplitude of increase in HHb was similar in older and young adults in both warm-up conditions. Additionally, the increase in HHb for a given increase in O2p (O2p) was similar in older and young adults after no warm-up [older: 13 ± 4 µM·l–1·min–1; young: 7 ± 2 µM (l/min)], whereas after heavy-intensity warm-up the HHb-to-O2p ratio was greater (P = 0.044) in older compared with young adults [older: 16 ± 9 µM/(l/min); young: 10 ± 4 µM/(l/min)]; the HHb-to-O2p ratio was similar after both warm-up conditions in older [no warm-up: 13 ± 4 µM/(l/min); heavy-intensity warm-up: 16 ± 9 µM/(l/min)] and young adults [no warm-up: 7 ± 2 µM/(l/min); heavy-intensity warm-up: 10 ± 4 µM/(l/min)]. After heavy-intensity warm-up, baseline O2Hb and Hbtot were elevated before the onset of subsequent moderate-intensity exercise compared with the no warm-up baseline in both older (O2Hb: 13 ± 9 µM increase; P < 0.05; Hbtot: 12 ± 8 µM increase; P < 0.05) and young (O2Hb: 9 ± 8 µM increase; P < 0.05; Hbtot: 14 ± 10 µM increase; P < 0.05) adults. The increase in O2Hb and Hbtot was similar in older and young adults. The pretransition baseline HHb concentration was not different in young and older adults with no warm-up (older: –4 ± 2 µM; young: –7 ± 3 µM) or after heavy-intensity warm-up (older: –5 ± 2 µM; young: –4 ± 3 µM)
|
|
O2p, HR, and HHb kinetics.
The effective HHb during the on-transient of exercise was less than (P < 0.001) the O2p in older and young subjects after no warm-up and heavy-intensity warm-up exercise (Tables 1 and 3). The MRT-HHb was less (P < 0.001) than the O2p in older adults after no warm-up, whereas after heavy-intensity warm-up the MRT-HHb and O2p were similar. In young adults, the MRT-HHb and O2p were similar in both warm-up conditions. In older adults, O2p was not correlated with the MRT-HHb after no warm-up; however, the O2p was negatively correlated with the MRT-HHb (r = –0.889; P = 0.043) after heavy-intensity warm-up. In contrast, the O2p was not correlated with the MRT-HHb after either warm-up in young adults. |
DISCUSSION |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
O2p and muscle HHb at the onset of a subsequent bout of moderate-intensity leg-cycling exercise in older and young adults. The main findings were 1) without prior warm-up exercise, O2p kinetics were slower (P < 0.01) in older compared with young adults; 2) after heavy-intensity warm-up, O2p kinetics were similar in older and young adults as a consequence of a faster (P < 0.05) adaptation in older adults; 3) the adaptation of HHb at exercise onset (i.e., HHb and MRT-HHb) was similar in older and young adults without warm-up; and 4) with heavy-intensity warm-up, the adaptation of HHb was slowed (P < 0.01) in older but not in young adults. Collectively, these results suggest that faster moderate-intensity O2p kinetics in older adults after heavy-intensity warm-up were related to an improvement in local muscle perfusion and O2 delivery at the onset of exercise. Furthermore, the slower O2p kinetics in older adults without prior warm-up exercise may be due to an O2 delivery limitation.
O2p kinetics were slower during moderate-intensity exercise (without prior warm-up) in older adults consistent with previous reports from our laboratory (2, 6, 13, 14, 20, 41). In agreement with Scheuermann et al. (41), after heavy-intensity warm-up, O2p kinetics were speeded in older (P < 0.05), but not in young adults, and resulted in similar O2p kinetics in older and young adults. Thus this influence of heavy-intensity warm-up exercise on O2p kinetics in older but not in young adults suggests that the limitation to the adaptation of O2p (and presumably muscle O2) is different in older and young adults in the moderate-intensity exercise domain.
Previous studies have attributed slower O2p kinetics in older adults to 1) a slower adaptation of muscle blood flow/O2 delivery (20, 41) and/or 2) a slower rate of activation and a slowing of the biochemical processes regulating oxidative phosphorylation (7). Heavy-intensity warm-up has been presumed to increase muscle blood flow (28) with the implication that the faster O2p kinetics after heavy-intensity warm-up in older adults in the present study may be the result of an improvement in muscle perfusion and O2 delivery before exercise onset. Previous studies have demonstrated the potential for an O2 delivery limitation in older adults at the onset of moderate-intensity exercise. Age-related changes, which suggest a potential O2 delivery limitation in older adults, include 1) a lower resting cardiac output (
) (39) and lower exercise relative to O2p (33, 44), 2) a lower resting limb blood flow and limb vascular conductance (22–24), 3) lower leg blood flow during submaximal exercise (38, 40, 48), 4) an impaired ability to redistribute blood flow from the splanchnic and renal circulations to muscle during exercise (30), and 5) decrements in endothelium-dependent vasodilation (35, 43) and myogenic responsiveness (34), which have implications for blood flow distribution.
In the present study, the adaptation of HR was used as an indicator of the rate of adaptation of and presumably muscle O2 delivery. HR kinetics during moderate-intensity exercise were slower in older (HR, 47 s) compared with young adults (HR, 23 s) without warm-up, in agreement with others (41). Nevertheless, after heavy-intensity warm-up, baseline HR was significantly elevated compared with the no warm-up condition, suggesting that , muscle blood flow, and O2 delivery were elevated before the onset of the subsequent exercise bout in both older and young adults. An inherent limitation to the use of HR kinetics is that it provides an indirect estimate of the adaptation of local muscle blood flow. However, the adaptation of HR is commonly used to examine the adaptation of because stroke volume probably changes little after the initial adaptation from rest to the initial WR (20 W in the present study), and further increases in stroke volume during the exercise transient likely occur over the first heart beats of the transient secondary to the muscle pump effect on end-diastolic volume. Therefore, HR kinetics provide a reasonable approximation of kinetics, as suggested by the data of De Cort et al. (19) and Yoshida and Whipp (49).
To date, technical limitations have precluded study of muscle blood flow and O2 delivery at the level of the microvasculature within the active muscle in the exercising human. NIRS, however, allows the relative concentration changes of HHb, O2Hb, and Hbtot to be monitored noninvasively and continuously throughout the transition to and into the steady state of dynamic exercise (21). NIRS measurements primarily reflect changes in the small arterioles, capillaries, and venules (9), and, assuming that the largest proportion of vascular volume resides in the capillaries (37), any change in HHb reflects the balance between O2 delivery and O2 utilization in the microvasculature of the region of muscle being interrogated. In contrast to measurement of an arteriovenous O2 difference calculated across the limb, NIRS provides an indirect estimate of muscle O2 extraction. However, Bangsbo et al. (3) have reported that the measurement of venous PO2 may not accurately reflect the dynamics of O2 in active muscle due to the need to correct for tissue-to-sampling site delays and the influence of blood draining vascular beds from inactive tissues. In agreement, Van Beekvelt et al. (46) have reported that the Fick method of determining metabolic rate provides a global assessment of muscle O2, and, on the basis of the presence of metabolism/perfusion mismatching in an exercising limb, agreement between NIRS estimates of O2 utilization in an active area of muscle tissue and the more global Fick estimate is unlikely. NIRS data have also been shown to closely reflect the muscle metabolic rate as determined by magnetic resonance spectroscopy-derived PCr changes (a proxy for muscle O2) (11). Thus the ability to noninvasively monitor the balance between O2 delivery and utilization in the microvasculature of the exercising human with NIRS is a significant advance in the study of muscle O2. In the present study, NIRS data provided further evidence in support of an increase in muscle blood flow and O2 delivery. Relative to no warm-up, after heavy-intensity warm-up, O2Hb and Hbtot concentrations were significantly elevated in both older (O2Hb: 13 ± 9 µM; Hbtot: 12 ± 8 µM) and young (O2Hb: 9 ± 8 µM; Hbtot: 14 ± 10 µM) adults, suggesting improved local muscle oxygenation in the region of NIRS interrogation before exercise onset.
Thus, after heavy-intensity warm-up, there was a similar increase in muscle O2 delivery (evidenced by elevation of baseline HR and local oxygenation) in young and older adults, but a significant speeding of O2p kinetics was observed only in older adults. These results are consistent with the hypothesis that muscle O2 delivery imposed a limitation to O2p kinetics in older adults during moderate-intensity upright cycle exercise, whereas in young adults O2p kinetics may be limited by factors other than blood flow and O2 delivery.
Further support for an increase in local muscle O2 delivery being responsible for the speeding of O2p in older adults is evidenced by the adaptation of the local muscle HHb. Despite slower O2p kinetics (and presumably muscle O2) in older compared with young adults without warm-up, the adaptation of HHb was similar in older and young adults. After heavy-intensity warm-up, O2p was not changed in young, but the heavy-intensity warm-up was associated with a faster adaptation of O2p in older adults, whereas HHb adapted at a slower rate in older compared with young adults and compared with the no warm-up condition. Reflecting the balance between local O2 delivery and utilization, the slower adaptation of HHb during the exercise-transient in older adults after heavy-intensity warm-up suggests that O2 delivery was increasing at a faster rate than O2 utilization.
As discussed by Scheuermann et al. (41), factors such as substrate provision and changes in the activation and/or rate of metabolic processes regulating oxidative phosphorylation cannot be overlooked when the mechanisms responsible for the speeding of O2p are considered in older adults after heavy-intensity warm-up. However, as argued in that study, there is little evidence supporting a greater metabolic limitation to mitochondrial respiration in older compared with young adults during moderate-intensity exercise. Presumably, an increase in substrate provision and/or metabolic activation would impact primarily on the ability of the muscle to utilize O2 and, as such, would be reflected in the NIRS-HHb signal as a faster rate of muscle deoxygenation at the onset of exercise. However, in the present study, a slower, not faster, adaptation of HHb was observed in older adults after heavy-intensity warm-up.
Thus an increase in local muscle O2 delivery before the onset of exercise may be particularly important to the older adult because it may serve to alleviate decrements in the ability to deliver and distribute blood flow and O2 delivery to active skeletal muscles during the exercise on-transient.
Also, after no warm-up, a similar time delay before an increase in the NIRS-derived HHb signal above preexercise baseline levels was observed in older (11 ± 2 s) and young (12 ± 2 s) adults. After heavy-intensity warm-up, this time delay was shorter in both older (8 ± 2 s) and young (10 ± 2 s) adults. We (21) and others (29) have previously documented a delay before an increase in HHb in young subjects at the onset of moderate-intensity cycling exercise, and the potential explanations for this delay have been discussed in detail (21). We believe that the HHb delay reflects a complex balance between Hb/Mb deoxygenation, O2 delivery, and the effect of muscle contraction on microvascular volume, such that muscle O2 is actually increasing during the delay, and an increase in HHb is "masked" by other factors, which impact on the volume of Hb in the field of NIRS interrogation.
In conclusion, this study demonstrated slower O2p kinetics but a similar adaptation of muscle HHb in older compared with young adults during a moderate-intensity WR transition without prior warm-up exercise. After heavy-intensity warm-up exercise, O2p kinetics were accelerated in older adults, and the adaptation of HHb was slowed during subsequent moderate-intensity exercise. Prior heavy-intensity warm-up did not alter the adaptation of O2p kinetics and HHb in young adults. These results suggest that heavy-intensity warm-up exercise resulted in an improvement in local muscle perfusion and O2 delivery at the onset of a subsequent moderate-intensity exercise bout and that the speeding of O2p kinetics in older adults is due to an improvement in muscle O2 delivery. Furthermore, these results suggest that, without prior warm-up exercise, muscle blood flow in older compared with young subjects may be lower and adapt at a slower rate, and thus the slower O2p kinetics observed in older adults may be the result of a lower O2 delivery in older relative to young adults. These results also demonstrate that, in young adults, heavy-intensity warm-up exercise does not alter the adaptation of O2p kinetics and muscle deoxygenation at the onset of a subsequent moderate-intensity exercise bout, and thus blood flow and O2 delivery are unlikely to limit O2p kinetics in young adults during moderate-intensity exercise.
|
GRANTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
|
FOOTNOTES |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
|
REFERENCES |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
|---|
O2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J Appl Physiol 83: 1318–1325, 1997.
O2 kinetics at the onset of submaximal exercise. J Appl Physiol 79: 1914–1920, 1995.
This article has been cited by other articles:
|
|
 |
|
  A. Borghi-Silva, C. Carrascosa, C. C. Oliveira, A. C. Barroco, D. C. Berton, D. Vilaca, E. B. Lira-Filho, D. Ribeiro, L. E. Nery, and J. A. Neder Effects of respiratory muscle unloading on leg muscle oxygenation and blood volume during high-intensity exercise in chronic heart failure Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2465 - H2472. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. R. Chiappa, A. Borghi-Silva, L. F. Ferreira, C. Carrascosa, C. C. Oliveira, J. Maia, A. C. Gimenes, F. Queiroga Jr, D. Berton, E. M. V. Ferreira, et al. Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics J Appl Physiol, May 1, 2008; 104(5): 1341 - 1350. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Jones, J. Fulford, and D. P. Wilkerson Influence of prior exercise on muscle [phosphorylcreatine] and deoxygenation kinetics during high-intensity exercise in men Exp Physiol, April 1, 2008; 93(4): 468 - 478. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. S. DeLorey, J. M. Kowalchuk, A. P. Heenan, G. R. duManoir, and D. H. Paterson Prior exercise speeds pulmonary O2 uptake kinetics by increases in both local muscle O2 availability and O2 utilization J Appl Physiol, September 1, 2007; 103(3): 771 - 778. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. H. Raymer, S. C. Forbes, J. M. Kowalchuk, R. T. Thompson, and G. D. Marsh Prior exercise delays the onset of acidosis during incremental exercise J Appl Physiol, May 1, 2007; 102(5): 1799 - 1805. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Gurd, S. J. Peters, G. J. F. Heigenhauser, P. J. LeBlanc, T. J. Doherty, D. H. Paterson, and J. M. Kowalchuk Prior heavy exercise elevates pyruvate dehydrogenase activity and speeds O2 uptake kinetics during subsequent moderate-intensity exercise in healthy young adults J. Physiol., December 15, 2006; 577(3): 985 - 996. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Burnley, J. H. Doust, and A. M. Jones Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise J Appl Physiol, November 1, 2006; 101(5): 1320 - 1327. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Jones, N. J. A. Berger, D. P. Wilkerson, and C. L. Roberts Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions J Appl Physiol, November 1, 2006; 101(5): 1432 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. D. Paterson, J. M. Kowalchuk, and D. H. Paterson Effects of prior heavy-intensity exercise during single-leg knee extension on vO2 kinetics and limb blood flow J Appl Physiol, October 1, 2005; 99(4): 1462 - 1470. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. F. Ferreira, D. K. Townsend, B. J. Lutjemeier, and T. J. Barstow Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy J Appl Physiol, May 1, 2005; 98(5): 1820 - 1828. [Abstract] [Full Text] [PDF]
|
|
