Studies of the physiological response to exercise in different age groups, particularly in the young and old, have demonstrated age-related differences in cardiorespiratory fitness, as determined by changes in maximal oxygen uptake (V·O2max) (23,30,46). In addition, comparisons of highly trained versus more sedentary groups of different ages have allowed assessment as to whether age-related changes in V·O2max may be due partly to lack of physical activity or whether long-term physical activity prevents or reduces these losses (36,46). With respect to V·O2 kinetics, although several studies have examined differences in the rate of adjustment of oxidative phosphorylation between older and young individuals (10,13,28,29) as well as the effects of exercise training interventions (8,28,29), there is a dearth of information on the acute dynamic V·O2 responses to submaximal exercise across age groups (young, middle-age, and older individuals) in chronically trained and untrained men.
It has been shown that V·O2 kinetics during the transition to moderate-intensity exercise is typically slower in older compared with that in young healthy men (2,13,29); thus, older individuals rely more on nonoxidative sources for energy production during exercise on-transients, which could lead to intracellular disturbance of homeostasis and premature fatigue (14). Importantly, a relatively slow rate of adjustment in the V·O2 response has also been observed in some young healthy men (33). Although the precise mechanisms determining the rate of adjustment of oxidative phosphorylation are yet to be fully elucidated, recent studies have proposed that a limitation in O2 delivery and/or distribution to the exercising muscles play a critical role in this sluggish response (29,33,34). Considering that endurance training exercise has been shown to speed V·O2 kinetics in young (24,29), middle-age (8,19), and older (1,7,29) men and that “late” middle-age adults of similar physical fitness as young adults exhibited similar V·O2 kinetics responses (26), it remains unclear whether the age-related slowing of V·O2 kinetics is due to aging per se or lack of physical activity. Understanding this issue could help further our knowledge on the mechanisms controlling the dynamic adjustment of oxidative phosphorylation.
Thus, the main goal of this study was to examine the age-related differences in V·O2 kinetics of untrained young, middle-age, and older groups of men, compared with age-matched groups of chronically endurance-trained men, and to further explain the mechanisms controlling those responses. We hypothesized that there would be a continuous increase in the phase II V·O2p time constant ([tau]V·O2p) from young to middle-age to older men, in both the trained and untrained groups; it was further hypothesized that in groups with slower V·O2 kinetics, there would be an O2 delivery limitation, as indicated by a greater mismatch in the adjustment of V·O2 and O2 extraction.
Healthy men (n = 34) volunteered and gave a written consent to participate in this study. In addition, the data of 17 healthy men from studies completed previously (<=3 yr ago) in the laboratory and using similar equipment and exercise protocols were retrieved (Spencer et al. (40), n = 9; Murias et al. (29), n = 4; unpublished, n = 4). Subjects were separated into three groups: young (20–39 yr), middle-age (40–59 yr), and older (60–85 yr) men. Each group was further separated into two categories, trained and untrained, yielding six groups: young trained (YT) and untrained (YuT), middle-age trained (MT) and untrained (MuT), and older trained (OT) and untrained (OuT) men. All procedures were approved by the University of Western Ontario Research Ethics Board for Health Sciences Research Involving Human Subjects. All participants were nonsmokers and were not taking medications that would affect the cardiorespiratory or hemodynamic responses to exercise.
Subject training status.
The untrained (recreationally active) men were not actively training or participating in an exercise training program and were recruited by publicly posted flyers. The endurance-trained men were competitive and/or actively training cyclists and were recruited by flyers posted at their cycling clubs. All trained cyclists had been training for >=3, 7, and 15 yr for YT, MT, and OT, respectively, and typically cycled at least five times per week for >300 km·wk-1.
On day 1, participants reported to the laboratory to perform a ramp incremental test (30 W·min-1 for YT and MT, 25 W·min-1 for YuT, MuT, and OT, and 20 W·min-1 for OuT) to the limit of tolerance on a cycle ergometer (model H-300-R Lode; Lode B.V., Groningen, Holland) for determination of V·O2max and the estimated lactate threshold ([theta] L); the ramp portion of the protocol was initiated after 4 min of cycling at 20 W. V·O2max was determined as the maximal 20 s averaged V·O2 value during the last 60 s of the ramp incremental test. The HRmax and RER values during the ramp incremental test were obtained during the same 20-s period as that for the V·O2max. The [theta] L was determined by visual inspection as the V·O2 at which CO2 output (V·CO2) began to increase out of proportion in relation to V·O2, with a systematic rise in minute ventilation/V·O2 ratio and end-tidal PO2 (partial pressure of O2), whereas minute ventilation/V·CO2 ratio and end-tidal PCO2 (partial pressure of CO2) were stable (5).
From the results of this ramp test, a moderate-intensity work rate (WR) was selected to elicit V·O2 equivalent to approximately 80% of the V·O2 at [theta] L (MOD). On the second laboratory session, subjects completed three successive transitions from cycling at baseline (20 W) to cycling at MOD, each for 6 min. The cycling transitions between baseline and MOD were initiated as a “step” change. Subjects were instructed to maintain a pedal rate between 60 and 70 rpm throughout the trial.
Gas exchange measurements were similar to those previously described (2). Briefly, inspired and expired flow rates were measured using a low dead space (90 mL) bidirectional turbine (Alpha Technologies VMM 110), which was calibrated before each test using a syringe of known volume. Inspired and expired gases were continuously sampled (50 Hz) at the mouth and analyzed for concentrations of O2, CO2, and N2 by mass spectrometry (AMIS 2000; Innovision, Odense, Denmark) after calibration with precision-analyzed gas mixtures. Changes in gas concentrations 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 were transferred to a computer, which aligned concentrations with volume information to build a profile of each breath. Breath-by-breath alveolar gas exchange was calculated by using algorithms of Beaver et al. (4).
HR was monitored continuously by ECG (three-lead arrangement) using PowerLab (ML132/ML880; ADInstruments, Colorado Springs, CO). Data were recorded using LabChart version 6.1 (ADInstruments, Colorado Springs, CO) on a separate computer.
Local muscle deoxygenation ([HHb]) of the vastus lateralis muscle was monitored continuously with a frequency-domain multidistance near-infrared spectroscopy (NIRS) system (Oxiplex TS, Model 95205; ISS, Champaign, IL) as previously described (40). Briefly, the arrangement for the present study included a single channel consisting of eight laser diodes operating at two wavelengths ([lambda] = 690 and 828 nm, four at each wavelength), which were pulsed in a rapid succession (frequency modulation of laser intensity was 110 MHz), and a photomultiplier tube. The lightweight plastic NIRS probe (connected to laser diodes and photomultiplier tube by optical fibers) consisted of two parallel rows of light emitter fibers and one detector fiber bundle; the source–detector separations for this probe were 2.0, 2.5, 3.0, and 3.5 cm for both wavelengths. The probe was placed on the belly of the muscle midway between the lateral epicondyle and greater trochanter of the femur; it was covered with an optically dense, black vinyl sheet, thus minimizing the intrusion of extraneous light and was secured in place with an elastic strap tightened to prevent movement of the probe. NIRS measurements were collected continuously for the entire duration of each trial. This allowed for continuous measurement of absolute concentration changes of the deoxyhemoglobin [HHb] signal.
The near-infrared spectrometer was calibrated at the beginning of each testing session after a warm-up period of at least 20 min. The calibration was done with the probe placed on a calibration block (phantom) with absorption (μ A) and reduced scattering coefficients (μ s') previously measured; thus, correction factors were determined and were automatically implemented by the manufacturer’s software for the calculation of the μ A and μ s' for each wavelength during the data collection. Calculation of [HHb] reflected continuous measurements of μ s' made throughout each testing session (i.e., constant scattering value was not assumed). Data were stored online at an output frequency of 25 Hz but were reduced to 1-s bins for all subsequent analyses within the present study.
Pulmonary V·O2 (V·O2p) data were edited by removing aberrant data points that lay four SD outside of the local mean. Data for each repetition were then linearly interpolated to 1-s intervals, time-aligned such that time 0 represented the onset of each transition, and ensemble-averaged to yield a single averaged response for each subject. These averaged responses were further time-averaged into 5-s bins. The on-transient responses for V·O2p were modeled using the following equation:
where Y ( t ) represents the V·O2p at any given time (t), Y BSLN is the steady-state baseline value of Y before an increase in WR, A is the amplitude of the increase in Y above Y BSLN; [tau] represents the time required to attain 63% of the steady-state amplitude, and TD represents the mathematically generated time delay through which the exponential model is predicted to intersect Y BSLN. After excluding the initial 20 s of data from the model, while still allowing TD to vary freely (to optimize accuracy of parameter estimates), V·O2p data were modeled to 4 min (240 s) of the step transition; this ensured that each subject had attained a V·O2p steady state yet did not bias the model fit during the on-transient (7). The model parameters were estimated by least-square nonlinear regression (Origin; OriginLab Corp., Northampton, MA) in which the best fit was defined by minimization of the residual sum of squares and minimal variation of residuals around the Y-axis (Y = 0). The 95% confidence interval for the estimated time constant was determined after preliminary fit of the data with Y BSLN, A, and TD constrained to the best-fit values and the [tau] allowed to vary. HR data were fit in the same manner but from the onset (time 0) of exercise.
The [HHb] profile has been described to consist of a time delay at the onset of exercise, followed by an increase in the signal with an “exponential-like” time course. This calculated time delay for the [HHb] response (CTD[HHb]) was determined using second-by-second data and corresponded to the time, after the onset of exercise, at which the [HHb] signal began a systematic increase from its nadir value. The [HHb] data were modeled using equation 1; the fitting window for the “exponential” response spanned from the end of the CTD[HHb] to 90 s into each transition. As described previously (15), different fitting strategies ranging from 90 to 180 s into a transition resulted in minimal differences in estimates of [tau][HHb]. Baseline [HHb] ([HHb]BSLN) values were computed as the mean value in the 60 s before a transition. Whereas the [tau][HHb] described the time course for the increase in [HHb], the overall change of the effective [HHb] ([tau]'[HHb] = TD[HHb] + [tau][HHb]) described the overall time course of the [HHb] from the onset of the step transition.
Calculations of the normalized [HHb]/V·O2p ratio were similar to those previously described (33,35). Briefly, the second-by-second [HHb] and V·O2p data were normalized for each subject (0% representing the 20-W baseline value and 100% representing the posttransition steady state of the response). This normalization procedure was undertaken so that the specific time course of adjustment in the respective signals could be considered without concern for signal amplitude. The normalized V·O2p was left-shifted 20 s to account for the phase I–phase II transition. This procedure minimizes the risks of including data points that belong to the phase I of the response, without affecting the parameter estimates of the Phase II V·O2p fitting (32), which has been previously described to correspond with muscle V·O2 (V·O2m) within approximately 10% (20). Data were further averaged into 5-s bins for statistical comparison of the rate of adjustment for [HHb] and V·O2p responses. In addition, an overall average [HHb]/V·O2p ratio for the adjustment period during the exercise on-transient was derived for each individual as the average of the twenty-one 5-s ratio values from 20 to 120 s (approximating the start of the [HHb]/V·O2p “overshoot” to the time point at which the ratio reached the steady-state value of 1.0 in all groups). The rationale, benefits, and limitations of this analysis have been detailed elsewhere (33,35).
Data are presented as means ± SD. Two-way ANOVA was used to determine statistical significance for the dependent variables. Tukey post hoc tests were used when significant differences were found for the main effects and when interaction effects were present. All statistical analyses were performed using SPSS version 18.0 (SPSS Inc., Chicago, IL). Statistical significance was declared when P < 0.05.
Subject characteristics and exercise values at the end of the ramp incremental test are listed in Table 1. As expected by design, age was different between older, middle-age, and young participants in both trained and untrained groups (P < 0.05). Subjects reached volitional fatigue during the ramp incremental test, with the mean HRmax not different from the age-predicted maximum and mean RER data greater than 1.2 for all groups. Absolute V·O2max was lower in the untrained groups compared with that in the trained groups in young, middle-age, and older participants (P < 0.05), and it was lower in both the OT and OuT compared with that in MT, MuT, YT, and YuT (P < 0.05). V·O2max normalized to body mass was also lower in the untrained compared with that in the trained groups in young, middle-age, and older subjects (P < 0.05), and it was lower in OT and OuT compared with that in their middle-age and younger counterparts as well as in MT and MuT compared with that in YT and YuT (P < 0.05) (Fig. 1a). The endurance-trained men reported cycling 6.1 ± 0.7 rides per week for 435 ± 180 km·wk-1, 5.0 ± 0.9 rides per week for 309 ± 84 km·wk-1, and 4.8 ± 0.4 rides per week for 304 ± 71 km·wk-1 in the YT, MT, and OT groups, respectively. The trained cyclists were also long-term endurance athletes and had been training for 6 ± 3, 15 ± 7, and 23 ± 7 yr before testing in the YT, MT, and OT groups, respectively.
Individual [tau]V·O2p data and group means and SD are displayed in Figure 1b and detailed in Table 2. Phase II [tau]V·O2p was similar among the trained groups (P > 0.05). However, there was an effect of aging in the untrained group, such that [tau]V·O2p was significantly greater in OuT compared with that in YuT and MuT (P < 0.05). Similarly, [tau]V·O2p was greater in OuT compared with that in YT, MT, and OT (P < 0.05); [tau]V·O2p was not different between YuT and MuT (Table 2). On the basis of the assigned MOD WR, the V·O2p amplitude decreased with age in both trained and untrained groups (P < 0.05) and was greater in each trained group compared with that in the corresponding age-matched untrained group (P < 0.05) (Table 2). The gain ([DELTA]V·O2p/[DELTA]WR) was similar in all groups (Table 2).
Kinetic parameters for HR are presented in Table 2. The overall [tau]HR was greater in the untrained compared with that in the trained groups (P < 0.05). Although no differences in [tau]HR were observed in the trained groups (P > 0.05), the OuT had a greater [tau]HR compared with that of the MuT, YuT, OT, MT, and YT. The [tau]HR was greater than the [tau]V·O2p in all groups (P < 0.05), although averaging only 4 s longer (range per group, 2–6 s).
[tau][HHb], and [tau]'[HHb], was longer (P < 0.05) in the untrained compared with that in the trained groups (for M and O) (Table 2). The CTD[HHb] was longer (P < 0.05) in the OT and OuT compared with those in the YT and YuT groups, respectively.
Figures 2 and 3 depict the normalized (%) responses of [HHb] and V·O2p adjustments to the step transition in WR and the [HHb]/V·O2 ratio, respectively. Although a small transient “overshoot” in the [HHb]/V·O2p ratio was observed for YuT, MT, and OT, these overshoots were not significantly different from 1.0 (Fig. 3). However, the overshoot displayed in OuT was not only significantly greater than 1.0 but also resulted in an [HHb]/V·O2 ratio that was significantly larger than that observed in MuT and YuT as well as in OT, MT, and YT (P < 0.05). Figure 4 displays the adjustment of V·O2p and muscle deoxygenation (with model fits) during the transition to MOD in a representative YT and OuT adults.
The present study examined the V·O2 kinetics profiles of young, middle-age, and older endurance-trained and untrained men. The main findings were as follows. First, in the middle-age groups, V·O2 kinetics are not slower in comparison with those observed in young adults; a noticeably slower rate of adjustment of V·O2 is evident only after 60 yr of age, but this is counteracted by chronic endurance training exercise, so that the older untrained men display the slowest V·O2 kinetics compared with all other groups, whereas the older trained men are not different from young and middle-age trained men. Thus, this is the first study to show that prolonged exercise training can prevent the declines in V·O2 kinetics normally associated with aging. Second, chronic endurance exercise training is associated with faster V·O2 kinetics in each age group tested. Third, poorer matching of O2 delivery to O2 utilization is an important factor determining the slower V·O2 kinetics response in older untrained individuals. Fourth, there seems to be dissociation between the mechanisms controlling changes in V·O2max and V·O2 kinetics with aging and training, as the progressive decline in V·O2max observed with aging independently of the training status is not evident for the V·O2 kinetics response.
Several studies evaluating V·O2 kinetics responses in older (8,10,13,21,29,41) and young (9,21,24,29,33,40,42) untrained individuals have shown [tau]V·O2p values in the range of 40–55 s and 20–35 s, respectively. The V·O2 kinetics responses reported in the present investigation for older (approximately 42 s) and young (approximately 26 s) untrained individuals are in line with those reports. Furthermore, a number of training studies examining the change in [tau]V·O2p after endurance-training exercise programs lasting <=12 wk have shown a speeding of V·O2 kinetics to an average of approximately 20–25 s in young (9,29) and approximately 30–35 s in older (19,29) men. Although speeding of V·O2 kinetics in these studies was substantial, those [tau]V·O2p values are still larger than those observed in the present study for the chronically trained young (17 s) and, particularly, older (20 s) men. One likely reason for this differential response between long-term (several years) versus short-term (approximately 12 wk) training resides in the type of adaptations that might occur as a result of the duration of training. For instance, it has been proposed that improvement in the matching of O2 delivery to O2 distribution was responsible for the faster V·O2 kinetics response after 12 wk of endurance exercise training (28,29). Similarly, the present investigation proposes that appropriate matching of O2 delivery and/or distribution to the metabolic needs in the active fibers is an important factor determining the rate of adjustment of oxidative phosphorylation, supported by the fact that only the older untrained individuals showed a significant overshoot in the [HHb]/V·O2 ratio. Although the idea that adequate provision of O2 to the active tissues is improved by exercise training applies to both long- and short-term endurance exercise training interventions, the mechanistic reasons for this ameliorated response might be different.
From a central delivery of O2 perspective, the present study showed that [tau]HR, previously used as a proxy of the dynamic adjustment of cardiac output (13), was significantly smaller in the trained compared with that in the untrained individuals. It is likely that with training, cardiac adaptations to exercise such as improved left ventricular filling (25) (leading to a more compliant left ventricle and thus improved Frank–Starling mechanism) and/or enhanced contractility related to enlargement of the left ventricle (16,39) would elicit greater stroke volume. However, with greater stroke volume response at exercise onset, a faster HR response would not be evident or required in the trained group. The present data indicated that the older untrained participants had the greatest [tau]HR of all groups. This would suggest that an O2 provision limitation that originates at the central level might be partly responsible for the slower adjustment of V·O2 observed in the older untrained individuals. However, it should be noted that a slower adjustment of HR was present even in the groups with the fastest V·O2 kinetics. In addition, it has been suggested that even in the presence of slower adjustment of HR in the elderly, some compensatory mechanisms might occur to redirect a larger portion of the cardiac output to the active regions to provide sufficient blood flow to those areas (37). In support of this idea, it has been shown that the adjustment of femoral artery blood flow in the older is as fast or even faster than that of V·O2 (14). In fact, a training study performed in older adults showed a faster V·O2 kinetics after training with no changes in the kinetics of femoral artery mean blood velocity (7). Thus, it is likely that if an O2 delivery limitation determines the dynamic adjustment of oxidative phosphorylation, this constraint occurs within the microcirculation and not at the “bulk” delivery of O2 level. A slower HR response in the untrained might not be the cause but rather the consequence of the slower V·O2 kinetics.
In the studies by Murias et al. (28,29), it was proposed that improved vascular responsiveness mediated by enhanced endothelium-dependent vasodilation (6,27,43,44) resulted in a rapid (<3 wk) improvement in the matching of O2 delivery to O2 distribution within the active tissues and, thus, a speeding of V·O2 kinetics that was not further improved with subsequent training despite sustained improvements in V·O2max throughout the exercise training intervention. It was suggested that the lack of further changes in [tau]V·O2p, especially in the older people who could not completely abolish the [HHb]/V·O2 ratio overshoot, was related to the lack of time to induce a sufficiently large vascular remodeling to better match O2 delivery to O2 requirement in the active muscles. In the present study, chronically trained older individuals who had been exercising for over 20 yr showed a V·O2 kinetics response that was as fast as that observed even in young trained individuals. Consequently, it seems that in older individuals, chronic endurance training can prevent the O2 delivery limitation normally observed with aging, whereas shorter-term training regimes only partially improve the V·O2 kinetic limitation. Although this study did not take measures of vascularization, it is likely that the vascular remodeling experienced as a consequence of prolonged endurance training resulted in an O2 transport system capable of adequately matching O2 delivery to the metabolic needs at least during activities performed in the moderate-intensity domain. In support of this idea, structural improvements (i.e., 20%–40% increased capillarization) have been shown in response to endurance training interventions lasting between 3 and 12 months (11,12,31). In addition, it has been shown that chronically trained master athletes showed similar capillary density as that observed in training-matched young athletes (12). These substantial improvements in capillarization would result in a larger surface area for O2 exchange and thus may have contributed to an “overshoot” in the normalized [HHb]/V·O2 ratio not being present in the older trained compared with the older untrained men.
Few studies that have measured V·O2 kinetics in the middle-age population exist. The findings from the present study are in line with the results of the study of McNarry et al. (26) who reported a [tau]V·O2p of 21 s in young and 22 s in middle-age recreationally active subjects. Similarly, Berger et al. (8) reported [tau]V·O2p values of approximately 25 s in endurance-trained middle-age master athletes. Thus, contrary to the idea of a progressive slowness of V·O2 kinetics with aging, these data collectively show that, at least in recreationally to highly active individuals, the phase II [tau]V·O2 does not need to be greater in middle- to late middle-age participants. On the contrary, Fukuoka et al. (19) observed [tau]V·O2p of approximately 47 s in untrained middle-age men. This discrepancy in [tau]V·O2p values measured in the study of Fukuoka et al. (19) compared with the data from the present investigation and the study of McNarry et al. (26) may be explained by the difference in relative physical activity of the groups, as the subjects in the present study and that of McNarry et al. (26) were recreationally active and the subjects in Fukuoka et al. (19) were sedentary. Notably, in the study of Fukuoka et al. (19), 15 days of training were enough to reduce [tau]V·O2p values to approximately 30 s, with no further changes observed thereafter up to the end of the exercise training intervention at 90 days. These data would suggest that, even though our study indicates that slower V·O2 kinetics responses are not likely to occur until later in life (i.e., after approximately 60 yr of age), it is plausible that middle-age individuals of poorer fitness level might have a slower adjustment of oxidative phosphorylation. Indeed, a limitation of the present study is the lack of truly sedentary participants in each age group so that a wider spectrum of physiological responses could be captured. In other words, slower V·O2 kinetics responses that, in this study, were suggested to be associated with poorer vascular responsiveness or deteriorated vascular structures in aging might be more likely to occur in less active or sedentary groups. Whether prevention of the slower V·O2 kinetics occurs in those undertaking serious cycling training at middle age or whether it requires lifelong training from youth cannot be discerned from the present study. In both the MT and OT groups, although they had taken up their cycling in their 40s, most reported that this was a transition from a variety of physical activity pursuits of their youth.
Is the age-related slowing of V·O2 kinetics attributable to lack of physical activity or to decrease in cardiorespiratory fitness with age or rather aging itself? In this study, relative V·O2max declined at similar rates in both trained and untrained groups, with each age group having significantly lower V·O2max than that of the preceding training-matched group and with endurance trained group values consistently greater than those in the untrained group. The young-to-old rate of decline in V·O2max was similar in trained and untrained groups (8%–9% per decade), which was consistent with values previously reported in the literature (approximately 6%–10%) (17,36,45,46) and occurred despite the endurance-trained individuals being chronically active at all ages; thus, the decline in V·O2max does not necessarily indicate a decline in physical activity but, rather, a natural decline in HRmax and cardiac output (18,22,38). However, in individuals with chronically high levels of physical training, the age-related increase in [tau]V·O2p was absent, thus maintaining a V·O2 kinetic profile similar to that of the young endurance-trained individuals. Therefore, individuals who are regularly active for a long term are able to avoid the change in [tau]V·O2p with age. Thus, it seems that mechanisms determining V·O2max and V·O2 kinetics with aging might be different or, at least, have a different contribution during maximal and submaximal activities. During moderate-intensity exercise, the matching of O2 delivery to O2 utilization plays a critical role in determining the rate of adjustment of oxidative phosphorylation and a virtually perfect matching seems to be feasible when the vasculature is “trained” to support adequate distribution of blood flow to the active sites. However, at higher intensities of exercises, even if local distribution of blood flow is improved to sustain the metabolic needs, central delivery of blood flow (cardiac output) imposes a limit to exercise (3).
It is possible that factors that were not evaluated in this investigation such as changes in body composition (i.e., an increase in body fat percentage or a reduction in fat-free mass) may have contributed in some way to the slower adjustment of V·O2 in the older untrained individuals. Even though our data preclude us from making any further assumptions in this regard, this missing element should be acknowledged as a limitation of the study. However, it should also be noted that although the older untrained individuals in this study were community-dwelling men, physical activity level might be reduced in this population relative to middle-age men, which could have a detrimental effect on different components of the O2 transport pathway (e.g., vascular responsiveness, capillarization, etc.), so that a slower V·O2 kinetics response is observed. In other words, the results from this study could reflect both the positive aspects of exercise training and the detrimental effects of detraining.
In conclusion, this study demonstrated that the age-related slowing of V·O2 kinetics can be prevented when long-term endurance training interventions are in place. This abolishment of the usual age-related slowing of the dynamic adjustment of V·O2 was related to a preserved matching of O2 delivery to O2 utilization in the chronically trained older group, as suggested by the absence of an “overshoot” in the normalized [HHb]/V·O2 ratio as compared with untrained older individuals. The data demonstrate that it is not aging per se that determines the V·O2 kinetic response and emphasize that exercise training can maintain the V·O2 kinetics of youth and thereby prevent the early fatigue experienced during the on-transient energy requirements of daily physical activities.
We would like to express our gratitude to the subjects in this study.
This study was supported by the Natural Sciences and Engineering Research Council of Canada research and equipment grants. T. M. G. was supported by a Masters-level research scholarship from the Natural Sciences and Engineering Research Council of Canada.
None of the authors has any conflicts of interest to declare.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:© 2015 American College of Sports Medicine
EXERCISE; AGING; MUSCLE DEOXYGENATION; O2 DELIVERY