It is axiomatic that greater aerobic fitness (V̇O2peak) derives from enhanced perfusive and diffusive O2 conductances across active muscles. However, it remains unknown how these conductances might be reflected by regional differences in fractional O2 extraction (i.e., deoxy [Hb+Mb] and tissue O2 saturation [StO2]) and diffusive O2 potential (i.e., total[Hb+Mb]) among muscles spatially heterogeneous in blood flow, fiber type, and recruitment (vastus lateralis, VL; rectus femoris, RF). Using quantitative time‐resolved near‐infrared spectroscopy during ramp cycling in 24 young participants (V̇2peak range: ~37.4–66.4 mL kg−1 min−1), we tested the hypotheses that (1) deoxy[Hb+Mb] and total[Hb+Mb] at V̇O2peak would be positively correlated with V̇O2peak in both VL and RF muscles; (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in V̇O2peak. Peak deoxy [Hb+Mb] and StO2 correlated with V̇O2peak for both VL (r = 0.44 and −0.51) and RF (r = 0.49 and −0.49), whereas for total[Hb+Mb] this was true only for RF (r = 0.45). Baseline deoxy[Hb+Mb] and StO2 correlated with V̇O2peak only for RF (r = −0.50 and 0.54). In addition, the deoxy[Hb+Mb] slopes were not affected by aerobic fitness. In conclusion, while the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) did not differ between fitness groups the capacity to deoxygenate [Hb+Mb] (index of maximal fractional O2 extraction) correlated significantly with V̇O2peak in both RF and VL muscles. However, only in the RF did total[Hb+Mb] (index of diffusive O2 potential) relate to fitness.
For large muscle mass exercise such as cycling or running the maximum pulmonary O2 flux (V̇O2max) is the product of whole‐body perfusive (Q̇O2 = cardiac output [Q̇] × arterial O2 concentration [CaO2]) and diffusive (muscle transcapillary) O2 conductances. The Fick relationship (V̇O2 = Q̇× [CaO2‐Cv̄O2] where v̄ is mixed venous), as measured across the lungs, provides a volume‐weighted average of fractional O2 extractions across all body compartments (Benson et al. 2013; Fick 1870); each with its own unique Q̇O2/V̇O2 ratio, and thus effluent venous blood O2 concentration. Thus, without discrete measurements within each tissue, assessments across the lungs provide little insight into Q̇O2‐to‐V̇O2 matching and the roles of perfusional and diffusional O2 transport within each tissue.
During progressive exercise from rest to V̇O2max whole‐body O2 extraction increases approximately hyperbolically from 25% to 80% or more according to the approximation (Stringer et al. 2005): (CaO2‐CvO2) = (20 × V̇O2)/(1 + V̇O2) (Whipp and Ward 1982). This relationship supports the observations that: individuals with greater V̇O2max demonstrate a greater fractional O2 extraction than their less aerobically‐fit counterparts in both health and pathophysiological conditions (Grassi et al. 2007; Porcelli et al. 2010; Salvadego et al. 2016) and endurance training increases both fractional O2 extraction and V̇O2max, although not necessarily in linear proportion (Klausen et al. 1982; Roca et al. 1992; Beere et al. 1999). To date, in human muscles, our understanding of these relationships is based overwhelmingly upon measurements made across the whole exercising limb. Within small regions of active muscle, data from both positron emission tomography imaging (Koga et al. 2014; Heinonen et al. 2015) and near‐infrared spectroscopy (NIRS) investigations (Koga et al. 2007, 2011, 2014; Okushima et al. 2015) indicated a substantial heterogeneity of the Q̇O2/V̇O2 ratio. This heterogeneity likely arises, in part, from differential motor unit recruitment (Chin et al. 2011) and fiber‐type expression (Johnson et al. 1973). In addition, the degree to which Q̇O2 and V̇O2 are well matched within muscles, appears to be greater in trained compared with untrained men (Kalliokoski et al. 2005). However, during cycling exercise from rest to V̇O2peak, whether or not regional Q̇O2/V̇O2 ratio differs among individuals differing in V̇O2peak remains unclear. In whole body and thigh muscle Q̇O2 and V̇O2 increase linearly with work rate (Knight et al. 1993; Gifford et al. 2016) and therefore the muscle deoxygenation/fractional O2 extraction will reach a greater peak in fitter individuals (Ferreira et al. 2006; Gifford et al. 2016; Roca et al. 1992). Based upon this logic, we hypothesize that the different regions of active muscle assessed using NIRS will have a similar overall profile of deoxygenation but the regional peak Q̇O2/V̇O2 values (i.e., deoxy[Hb+Mb]) will correlate with whole‐body V̇O2peak.
Recently we employed a time‐resolved (TRS) NIRS system, with adipose tissue thickness correction, to determine muscle optical coefficients and therefore measure absolute deoxy‐ and total‐[Hb+Mb] and tissue O2 saturation (StO2) (Koga et al. 2011, 2015a; Okushima et al. 2015), which are not impacted significantly by skin blood flow changes (Koga et al. 2015b). Although TRS‐NIRS variables do not directly measure muscle V̇O2 and Q̇O2, evidence from direct measurements during muscle contractions suggest that deoxy[Hb+Mb] is an index of regional fractional O2 extraction in the face of presiding blood flow (i.e., microvascular O2 partial pressure (Koga et al. 2012)) and femoral venous O2 saturation (Vogiatzis et al. 2015; Sun et al. 2016). Moreover, the total[Hb+Mb] is an index of microvascular blood volume (Ijichi et al. 2005), which reflects local O2 diffusing capacity (Groebe and Thews 1990). The purpose of this study was to use the TRS‐NIRS technology to investigate O2 perfusive (Q̇O2/V̇O2) and diffusive profiles across the range of achievable power output in individuals ranging broadly in aerobic capacity. We addressed the following specific hypothesis during maximal ramp cycle ergometry: (1) deoxy[Hb+Mb] and total[Hb+Mb] in both VL and RF muscles at peak power output would be positively correlated with V̇O2peak, and (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in V̇O2peak.
Twenty‐four young males participated in this study (age, 22 ± 2 years; height, 174 ± 5 cm; weight, 62 ± 5 kg). All participants were nonsmokers and free of known cardiovascular, respiratory, and metabolic disease. This study was approved by the Human Subjects Committee of Kobe Design University, in compliance with the Declaration of Helsinki. Each participant signed an informed consent form after explanation of experimental procedures and the potential risks and benefits of taking part.
Participants started the experimental procedure at least 2 h postprandial and refrained from caffeine, alcohol, and intense exercise for 24 h before testing. All experiments were conducted in environmental chambers (SR‐3000, Nagano science, Osaka, Japan) maintained at the ambient temperature of 21–24°C and relative humidity of 40–60%, in order to maintain ambient conditions for the studies across Japanese seasons.
Exercise testing was completed on an electromagnetically braked cycling ergometer (XL‐75III, Combi, Tokyo, Japan) in the upright position. The exercise protocol began with 2 min of rest, followed by 4 min of 20 W baseline exercise and then a ramp‐incremental exercise test. The ramp increase was 20 W min−1. Participants were asked to maintain pedaling frequency at 60 rpm throughout the exercise test, and the test was terminated when participants could no longer maintain 60 rpm despite strong verbal encouragement. At the limit of tolerance the power output was reduced to 20 W and the participants were monitored for at least 6 min of active recovery.
Pulmonary oxygen uptake (V̇O2).
Gas exchange measurement methods were the same as in previous studies (Koga et al. 2011; Bowen et al. 2013; Spencer et al. 2014; Okushima et al. 2015). The breath‐by‐breath gas exchange system (AE‐300S, Minato‐Medical, Osaka, Japan) was calibrated according to the manufacturer's recommendation before each exercise test. Participants breathed through a low resistance mouthpiece containing a hot‐wire flowmeter for measurement of inspiratory and expiratory flows and volumes. Inspired and expired gases were continuously sampled from the mouth and O2 and CO2 fractional concentration was measured by fast‐responding paramagnetic and infrared analyzers, respectively. Gas volume and concentration signals were time‐aligned to account for the time lag between the signals to calculate V̇O2 and V̇CO2 on a breath‐by‐breath basis.
Absolute values of oxygenated (oxy[Hb+Mb]), deoxygenated (deoxy[Hb+Mb]), and total hemoglobin and myoglobin concentration (total[Hb+Mb]) were sampled from the mid‐belly of the vastus lateralis (VL) and rectus femoris (RF) on the dominant leg by two TRS‐NIRS instruments (TRS‐20, Hamamatsu photonics KK, Hamamatsu, Japan). These muscles were selected because they represent major contributors to power generation in cycle ergometry, have a somewhat different fiber‐type composition (i.e., superficial‐deep Type I %, VL 38–47 %, RF 30–42 %, Johnson et al. 1973) and are differentially recruited during maximal ramp exercise (Chin et al. 2011).
Before applying the probes, the skin under the probes was shaved. The NIRS optodes were housed in black rubber holders and fixed to the skin with adhesive tape to minimize incidental movement and intrusion of ambient light on the NIRS detectors. The interoptode spacing between irradiation and detection probes was 3 cm for all measurement sites. The sample rate was set to 1 Hz.
Adipose tissue thickness (ATT) at each NIRS site was measured using B‐mode Doppler ultrasound (Logiq 400, GE‐Yokogawa Medical Systems, Tokyo, Japan). Ultrasound images were collected with care to prevent pressure and distortion of the thickness of the skin and adipose tissues under the probe.
Peak pulmonary V̇O2 (V̇O2peak) was determined as the mean value of the last 30 sec during the ramp exercise test. Participants were grouped into those with low aerobic capacity (LO: n = 8, ≤45 mL kg−1 min−1), mid‐range (MID, n = 9, 46–55 mL kg−1 min−1) and those with high aerobic capacity (HI, n = 7, ≥56 mL kg−1 min−1) using similar reference ranges as in a previous study (Gifford et al. 2016). Analysis of deoxy‐ and total[Hb+Mb] was performed after correction for ATT to a thickness of 0 mm using linear regression of the relationship between total[Hb+Mb] and ATT at rest (Bowen et al. 2013; Okushima et al. 2015) (total [Hb+Mb] = 15.7 × [ATT] + 201, r2 = 0.801, P < 0.001). For NIRS measurements (deoxy‐ and total[Hb+Mb] and StO2), 1 Hz optical measurements were averaged over 6 data points, resulting in one NIRS datum calculation every 6 sec. The baseline of each NIRS measurement was calculated as the mean value of 60 sec prior to the start of ramp exercise. The absolute value of each NIRS measurement during ramp exercise was calculated at 20 W, 50 W and each 50 W increment thereafter, as well as for each 10 % of peak power (Wpeak) increment between 10 and 100 %Wpeak. NIRS variable amplitudes were derived from the difference between baseline and the mean value of the final 18 sec of ramp exercise. The slope of NIRS variables across absolute power (i.e., watt) was determined from linear regression in two regions of the response: below 50 %Wpeak and above 70 %Wpeak (Okushima et al. 2015).
All values were expressed as mean ± standard deviation. Pearson product moment correlation was calculated to quantify the relationship between NIRS variables and V̇O2peak. Comparisons of V̇O2peak and Wpeak were analyzed by one‐way ANOVA with the main effect of fitness (LO, MID, HI). Comparisons of baseline and amplitude in each NIRS variable and ATT were analyzed by two‐way repeated‐measures ANOVA, with main effects of aerobic fitness and muscle site (VL, RF). Comparison of the temporal profile for NIRS variables was analyzed by two‐way repeated‐measures ANOVA, with main effects of aerobic fitness and exercise intensity (normalized power output: every 10 %Wpeak from 10 to 100 %Wpeak; absolute power output: 20 W, peak power and every 50 W from 50 to 200 W). Comparison of the slopes of each NIRS variable was made by two‐way repeated‐measures ANOVA, with main effects of aerobic fitness and exercise intensity (<50 %Wpeak, >70 %Wpeak). A significant F ratio was analyzed using Bonferroni's post‐hoc test. Effect size (ES: using Cohen's d) and statistical power (1‐β) were also calculated for the comparison of each NIRS variable. Significance was accepted at P < 0.05.
By design, participants achieved a wide range of peak power (Wpeak), ranging from 204 to 385 W, and a V̇O2peak, ranging from 37.4 to 66.4 mL kg−1 min−1 (Table 1). ATT averaged 4.0 ± 1.2 mm and 5.5 ± 1.8 mm for the VL and RF, respectively, and was significantly less for the VL than the RF muscle (Table 1). However, ATT was not significantly different across participants differing in V̇O2peak.
Across absolute submaximal power outputs up to 200 W, deoxy[Hb+Mb] was greater in LO than MID at 150 and 200 W (P < 0.05) for RF muscle, whereas total[Hb+Mb] and StO2 were greater in HI than MID (P < 0.05, except 200 W) and LO (P < 0.05, except 100 W) for only the RF muscle (Fig. 1). At peak power output, deoxy[Hb+Mb] in VL and total[Hb+Mb] in RF were greater in HI than LO and MID (P < 0.05), while StO2 in VL tended to be less in HI compared to LO (P = 0.05). When exercise intensity was normalized (Fig. 2), deoxy[Hb+Mb] was greater in HI than LO at 100 %Wpeak and MID at 80–100 %Wpeak in the VL (P < 0.05, Fig. 2). In addition, StO2 was less in HI than LO at 100 %Wpeak and MID at 90 %Wpeak in the VL (P < 0.05). In the RF muscle, total[Hb+Mb] was greater in HI than LO at 100 %Wpeak and greater than MID at all intensities (P < 0.05).
The VL muscle evinced a lower baseline deoxy[Hb+Mb] (P < 0.001, ES = 0.89, 1‐β = 0.99, Table 2) and greater baseline StO2 (P < 0.001, ES = 1.05, 1‐β = 0.97) compared to the RF muscle, in all V̇O2peak groups. Baseline total[Hb+Mb] was greater in HI than MID for both RF and VL muscles (P = 0.019, ES = 1.04, 1‐β = 0.81). The exercise‐induced increase in deoxy[Hb+Mb] (P = 0.041, ES = 1.08, 1‐β = 0.81) and decrease in StO2 (P = 0.035, ES = 1.14, 1‐β = 0.92) were greater in HI than LO in both VL and RF muscles. The deoxy[Hb+Mb] and StO2 amplitudes were significantly correlated with V̇O2peak (Fig. 3) in both VL and RF muscles. At each muscle site, the deoxy[Hb+Mb] and StO2 baselines (negative correlation) and the amplitude of total[Hb+Mb] (positive correlation) were significantly correlated with V̇O2peak in RF (Figs. 3 and 4) but not VL.
In each aerobic fitness group, deoxy[Hb+Mb] increased systematically during exercise up to V̇O2peak in the RF muscle, but in the VL muscle deoxy[Hb+Mb] plateaued above 70 %Wpeak (Figs. 1 and 2, Table 3). Thus, in the VL muscle, deoxy[Hb+Mb] increased far more slowly above 70 %Wpeak than below 50 %Wpeak irrespective of V̇O2peak (P = 0.033, ES = 0.54, 1‐β = 0.72). In contrast, in the RF muscle deoxy[Hb+Mb] increased more rapidly above 70 %Wpeak than below 50 %Wpeak (P < 0.001, ES = 1.26, 1‐β = 0.99). The total[Hb+Mb] increased systematically to V̇O2peak in the RF muscle but decreased above 70 %Wpeak in the VL muscle independent of aerobic capacity group (P < 0.001, ES = 1.55, 1‐β = 1.00). The StO2 in the VL decreased systematically up to V̇O2peak, whereas the StO2 in RF muscle decreased more rapidly above 70 %Wpeak than below 50 %Wpeak irrespective of aerobic capacity group (P < 0.001, ES = 1.21, 1‐β = 0.99).
This investigation resolved the magnitude and pattern of Q̇O2/V̇O2 matching and O2 diffusive potential in the VL and RF muscles across groups of individuals ranging broadly in aerobic capacity using quantitative TRS‐NIRS during ramp‐incremental cycling exercise. The principal original findings are: (1) the magnitude of absolute deoxy[Hb+Mb] increase (i.e., the amplitude of the exercise‐induced reduction in Q̇O2/V̇O2) and StO2 decrease were correlated with V̇O2peak in both VL and RF muscles; (2) a high baseline deoxygenation and StO2 in the RF muscle (i.e., low preexercise Q̇O2/V̇O2) was negatively associated with V̇O2peak; (3) the magnitude of increase in the total[Hb+Mb] (i.e., the exercise‐induced increase in O2 diffusive potential) was positively correlated with V̇O2peak in the RF muscle only; (4) the rate of change in each NIRS variable across absolute work rates was not related to aerobic fitness (i.e., V̇O2peak).
The absolute peak amplitude and baseline of muscle deoxygenation
The peak absolute amplitude of deoxy[Hb+Mb] increase (positively) and StO2 decrease (negatively) were correlated with V̇O2peak for both muscle sites (Table 2, Figs. 1, 2, 3) and this represents the first demonstration of this relationship with technology capable of measuring absolute deoxy[Hb+Mb] together with ATT correction. This is consistent with the notion that the capacity for O2 extraction between the capillary and myocyte relates to the aerobic capacity of active muscle. Previous studies have reported that the systemic arteriovenous O2 difference and O2 extraction capacity (Murias et al. 2010) and leg O2 extraction capacity (Roca et al. 1992; Sala et al. 1999; Proctor et al. 2001) are associated with V̇O2max. These data extend that notion to the level of individual muscles. Blomstrand et al. (1997) and Robinson et al. (1994) reported that a greater V̇O2max in human and rat muscle is attributed to a greater O2 flux capacity, consequent to a greater muscle mitochondrial enzyme activity. The present results suggest that the increase in the peak amplitude of muscle deoxygenation reflects the peripheral adaptation of fractional O2 extraction to exercise at each muscle site. In addition, this was not different between VL and RF muscles, irrespective of V̇O2peak (Table 2). Thus, the amplitude of muscle deoxygenation at V̇O2peak may be limited to a similar magnitude among active muscle sites.
Baseline deoxy[Hb+Mb] were greater in RF compared with VL independent of V̇O2peak (Table 2), and was associated with V̇O2peak in RF but not in VL (Fig. 4), extending our previous findings (Chin et al. 2011; Okushima et al. 2015). This suggests that less aerobically‐fit individuals may have a lower Q̇O2/V̇O2 of leg muscles at rest or during very low exercise intensities. A low Q̇O2/V̇O2 at baseline is consistent with a small intercept for the Q̇O2/V̇O2 relationship, which predisposes capillary‐myocyte O2 flux to be highly sensitive to the adjustment in convective O2 delivery: only a small “underperfusion” would rapidly limit capillary PO2 (Ferreira et al. 2006; Benson et al. 2013). However, the mechanistic bases for this effect, be they structural (e.g., muscle fiber composition and vascular bed) and/or functional (e.g., regulation of O2 distribution and muscle recruitment), remain unclear at present.
The absolute peak amplitude and baseline of total[Hb+Mb]
The peak absolute amplitude of total[Hb+Mb] for RF, but not for VL, was significantly related to V̇O2peak (Fig. 3). Our previous study reported that RF activation increased slower than that of the VL and was subsequently speeded further from high submaximal exercise intensities up to V̇O2peak (Chin et al. 2011). Another study reported that in the VL muscle there was a relationship between the total[Hb+Mb] plateau onset and the steep reduction in the EMG mean power frequency (MPF) (Boone et al. 2016), where the MPF reduction is thought to reflect a reduction in fast twitch fiber activity related to muscle fatigue (Komi and Tesch 1979) (although this interpretation of MPF is controversial). These findings support that the RF muscle increases capillary O2 diffusional capacity by longitudinal capillary recruitment (Poole et al. 2013), whereas the VL muscle is limited in this regard. Thus in the RF muscle the relationship of the absolute total[Hb+Mb] amplitude with V̇O2peak may reflect a higher capacity of hematocrit regulation than for VL. Accordingly, the capacity for diffusive O2 conductance may be more important for aerobic exercise performance in some muscles (i.e., RF) compared to others (i.e., VL).
The total[Hb+Mb] concentration at submaximal exercise intensities is greater for HI compared with MID in RF muscle (Figs. 1, 2). It is quite possible that this may also reflect differences in muscle capillarity among individual participants.
Kinetics of regional muscle deoxygenation pattern
The slope of NIRS variables measured as a function of absolute work (watts) did not differ among participants varying in V̇O2peak per se (Table 3). Although in the VL muscle each NIRS variable, except StO2, plateaued above 70 %Wpeak, in the RF muscle these NIRS variables increased up to V̇O2peak systematically or at least more rapidly above 70 %Wpeak than below 50 %Wpeak, except total[Hb+Mb] (Table 3). This suggests that the balance of Q̇O2/V̇O2 in active muscle is adjusted according to the metabolic requirements of the myocytes as the exercise intensity increases irrespective of the differential V̇O2peak. In previous studies, a controversy has arisen over whether or not the increase in the deoxy[Hb+Mb] slope across normalized power is actually delayed (Boone et al. 2009; Gravelle et al. 2012). In this respect, it is true that, for the whole body, the regression line between V̇O2 and Q̇O2 is largely independent of training status, age and, perhaps, sex differences (Ogawa et al. 1992; Roca et al. 1992; Proctor et al. 1998). Moreover, in rat muscle the slope of the blood flow to V̇O2 is similar between slow and fast twitch muscle fibers (Ferreira et al. 2006). Thus, it may not be requisite to increase the Q̇O2/V̇O2 ratio within active muscles to elevate V̇O2peak.
The marked increase in deoxy[Hb+Mb] in RF muscle close to V̇O2peak suggests that the ability to activate the RF muscle during severe intensity exercise is related to the capacity for high V̇O2′s during cycling exercise (Table 3). Using magnetic resonance T2 imaging, Reid et al. (2001) reported that trained subjects had a greater activation of their RF muscle during severe compared with moderate intensity exercise. Moreover, Cannon et al. (2013) showed during incremental knee‐extension exercise that rates of PCr and pH decline varied by muscle region, with one quadriceps muscle often “leading” others. Thus, supplemental activation of other skeletal muscles (e.g., deeper RF and possibly VM, Okushima et al. 2015) may be requisite if the severe intensity exercise is to be continued.
In our preliminary analyses, we fitted NIRS variables with both sigmoidal (Boone et al. 2009; Chin et al. 2011; Spencer et al. 2014) and double linear models (Spencer et al. 2012, 2014; Boone et al. 2016). We found several patterns in the deoxy‐ and total‐[Hb+Mb] responses, for example, a systematic increase, a plateau after reaching the apex, and a decrease after reaching that apex. Therefore we concluded that it was inappropriate to fit a single model to all deoxy‐ and total[Hb+Mb] data. This suggests that other factors besides aerobic capacity also exert an influence over muscle deoxygenation and capillary hematocrit responses, for example, muscle fiber distribution, capillarity, and muscle recruitment patterns. Thus, rather than presuming that one (i.e., sigmoidal) model fits all, future investigations should clarify the disparate patterns of muscle deoxygenation extant during ramp exercise.
The VL and RF muscles measured in this study are two of the dominant locomotor muscles during cycling exercise. These muscles have different EMG activation patterns during incremental cycling (Chin et al. 2011) and their timing of activation is different during a single crank revolution (Heinonen et al. 2015). In addition, there are individual differences in these characteristics due to handle and saddle position, foot position on the pedal, and experience of cycling (Ericson et al. 1985; Takaishi et al. 1998). In our study, we did not measure muscle EMG activity during cycling exercise, and therefore it is not known whether or not the temporal profile of VL and RF activation across the incremental exercise is different among aerobic fitness groups. In addition, we did not assess arterial O2 saturation, so we do not know whether exercise‐induced arterial hypoxemia was greater in the HI group compared with MID and LO (Powers et al. 1989; Harms et al. 2000). Should arterial desaturation occur, it could impact the muscle deoxy[Hb+Mb] and StO2 responses, potentially contributing to the observed greater muscle deoxygenation in the HI group. The sample size was small for the analysis by two‐way repeated‐measures ANOVA of some (but not all) variables presented in Figures 1, 2. This increases the potential for type II error; therefore the main effect and interaction in each test of Figures 1, 2 may be an underestimate.
During ramp‐incremental cycling exercise the amplitude of absolute deoxy[Hb+Mb] and StO2 for both VL and RF muscles was significantly related to V̇O2peak (i.e., higher and lower, respectively, in individuals with a greater V̇O2peak). This implies that the capacity for muscle O2 extraction, down to the individual active muscles, is correlated with whole‐body aerobic capacity. A high baseline deoxygenation in the RF muscle was negatively associated with V̇O2peak, which implies a greater reliance on increased regional muscle O2 delivery during exercise rather than enhanced O2 extraction in low‐V̇O2peak individuals (see Ferreira et al. 2006). In addition, the increase in absolute total[Hb+Mb] (an estimate of diffusive O2 conductance) within the RF muscle was significantly correlated with V̇O2peak. These data suggest that the capacity for diffusive O2 conductance may be more important for aerobic exercise performance in some muscles (RF) than others (VL). Overall, however, the pattern of muscle Q̇O2‐to‐V̇O2 balance (i.e., the relative slopes of deoxygenation) and diffusive O2 potential (total[Hb+Mb]) were less strongly associated with aerobic capacity, while peak deoxy[Hb+Mb] and StO2 (reflecting maximal O2 extraction) were more strongly related to V̇O2peak.
Conflict of Interest
The authors express our gratitude to the subjects in this study. We also express our gratitude to Drs. M. D. Spencer and N. Gerrett for very helpful insights during the preparation of the manuscript.
D. Okushima was supported by grants from Japan Society for the Promotion of Science (KAKENHI‐ 15K16476). S. Koga was supported by grants from Japan Society for the Promotion of Science (KAKENHI‐ 24247046, 26560362).
- Manuscript Received: October 25, 2016.
- Manuscript Accepted: November 3, 2016.
- © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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