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Temporal responses of ratings of perceived breathlessness (RBP) during constant-load and incremental exercise, and during voluntary hyperpnea (EVH) were examined in women with obesity. Following 6 min of constant-load (60W) cycling, 34 women rated RPB≥4 (+DOE) and 22 women rated RPB≤2 (–DOE). Both groups completed an incremental cycling test and an EVH test at 40 and 60L/min; RPB was assessed each minute of incremental cycling and at the end of each EVH trial. RPB increased with ventilation during constant-load (+DOE: R2=0.86; –DOE: R2=0.82) and incremental (+DOE: R2=0.91; –DOE: R2=0.92) exercise, but + DOE had a greater y-intercept than –DOE (60W: -0.16±1.53 vs. -0.73±0.55; incremental: -0.50±1.40 vs. -1.71±0.84). Despite matching ventilation, RPB was greater in + DOE at baseline (0.97±1.14 vs. 0.14±0.28), 40L/min (2.50±1.43 vs. 0.98±0.91), and 60L/min (3.94±2.19 vs. 2.07±1.32) during EVH. These findings show that despite linear associations between RPB and ventilation during exercise and voluntary hyperpnea, breathlessness perception at a given ventilatory demand is heightened in +DOE compared with –DOE.

The present study compared peak muscle deoxygenation ([HHb]peak) responses at three quadriceps sites during occlusion (OCC), ramp incremental (RI), severe- (SVR) and moderate-intensity (MOD) exercise. Seven healthy men (25 ± 4 yr) each completed a stationary cycling RI (20 W/min) test to determine [HHb]peak [at distal and proximal vastus lateralis (VLD and VLP) and rectus femoris (RF)], peak V̇o2 (V̇o2peak), gas exchange threshold (GET), and peak work rate (WRpeak). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇o2peak) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇o2p) monitored continuously. Additionally, [HHb] and total hemoglobin ([Hb]tot) were monitored at rest and during subsequent OCC (250 mmHg). Site-specific adipose tissue thickness was assessed (B-mode ultrasound), and its relationship with resting [Hb]tot was used to correct absolute [HHb]. For VLD and RF, [HHb]peak was higher ( P < 0.05) during OCC (VLD = 111 ± 38, RF = 114 ± 26 μM) than RI (VLD 64 ± 14, RF = 85 ± 20) and SVR (VLD = 63 ± 13, RF = 81 ± 18). [HHb]peak was similar ( P > 0.05) across these conditions at the VLP (OCC = 67 ± 17, RI = 69 ± 17, SVR = 63 ± 17 μM). [HHb] peaked and then decreased prior to exercise cessation during SVR at all three muscle sites. [HHb]peak during MOD was consistently lower than other conditions at all sites. A “[HHb] reserve” exists during intense cycling at the VLD and RF, likely implying either sufficient blood flow to meet oxidative demands or insufficient diffusion time for complete equilibration. In VLP this [HHb] reserve was absent, suggesting that a critical Po2 may be challenged during intense cycling.

Sex-specific differences in the temporal profiles of fractional O2 extraction during incremental cycling were examined using changes in near-infrared spectroscopy (NIRS)-derived muscle deoxygenated hemoglobin concentration (Δ[HHb]) and breath-by-breath pulmonary O2 uptake (V˙O2p) measurements. Subject's (men: n = 10; women: n = 10) Δ[HHb] data were normalized to 100% of the response, plotted as a function V˙O2p, %V˙O2p, power output (PO), and % PO, and fit with a piecewise double-linear regression model. The slope of the first segment of the double linear model was significantly greater in women compared to men when %Δ[HHb] was plotted as a function of V˙O2p, %V˙O2p and PO (p < 0.05). Both sexes displayed a near-plateau in the %Δ[HHb] which occurred at an exercise intensity near the respiratory compensation point. Thus, young women display a poorer ability to deliver O2 to the exercising tissue compared to men and oxidative demands must be supplemented by a greater fractional O2 extraction.

During ramp incremental cycling exercise increases in pulmonary O2 uptake (V̇o2p) are matched by a linear increase in systemic cardiac output ( Q). However, it has been suggested that blood flow in the active muscle microvasculature does not display similar linearity in blood flow relative to metabolic demand. This study simultaneously examined both systemic and regional (microvascular) blood flow and O2 extraction during incremental cycling exercise. Ten young men (V̇o2 peak = 4.2 ± 0.5 l/min) and 10 young women (V̇o2 peak = 3.2 ± 0.5 l/min) were recruited to perform two maximal incremental cycling tests on separate days. The acetylene open-circuit technique and mass spectrometry and volume turbine were used to measure Q (every minute) and breath-by-breath V̇o2p, respectively; systemic arterio-venous O2 difference (a-vO2diff) was calculated as V̇o2p/ Q on a minute-by-minute basis. Changes in near-infrared spectroscopy-derived muscle deoxygenation (Δ[HHb]) were used (in combination with V̇o2p data) to estimate the profiles of peripheral O2 extraction and blood flow of the active muscle microvasculature. The systemic Q-to-V̇o2p relationship was linear (∼5.8 l/min increase in Q for a 1 l/min increase in V̇o2p) with a-vO2diff displaying a hyperbolic response as exercise intensity increased toward V̇o2 peak. The peripheral blood flow response profile was described by an inverted sigmoid curve, indicating nonlinear responses relative to metabolic demand. The Δ[HHb] profile increased linearly with absolute V̇o2p until high-intensity exercise, thereafter displaying a “near-plateau”. Results indicate that systemic blood flow and thus O2 delivery does not reflect the profile of blood flow changes at the level of the microvasculature.

Two methods for estimating changes in microvascular O2 delivery during the on-transient of exercise were evaluated. They were tested to assess the role of the adjustment of the estimated microvascular O2 delivery in the speeding of V̇o2 kinetics during a Mod1-Hvy-Mod2 protocol (Mod, moderate-intensity exercise; Hvy, heavy-intensity “priming” exercise), in which Mod2 is preceded by a bout of Hvy. Mod pulmonary V̇o2 (V̇o2p) and deoxy-hemoglobin [HHb] data were collected in 12 males (23 ± 3 yr); response profiles were fit with a monoexponential. Signals were also 1) scaled to a relative % of the response (0–100%) to calculate the [HHb]/V̇o2 ratio for each individual and 2) rearranged in the Fick equation for estimation of capillary blood flow (Qcap). A transient [HHb]/V̇o2 “overshoot” observed in Mod1 (1.06 ± 0.05; P < 0.05) was absent during Mod2 (1.01 ± 0.06; P > 0.05); reductions in the [HHb]/V̇o2 ratio (Mod1 − Mod2) were related to reductions in phase II τV̇o2p ( r = 0.82; P < 0.05). For Qcap, a near-exponential response was observed in 8/12 subjects in Mod1 and only in 4/12 subjects in Mod2. The Qcap profile was shown to be highly dependent on the [HHb] baseline-to-amplitude ratio. Thus, accurate and physiologically consistent estimations of Qcap were not possible in most cases. This study confirmed that priming exercise results in an improved O2 delivery as shown by the decreased [HHb]/V̇o2 ratio that was related to the smaller τV̇o2 in Mod2. Additionally, this study suggested that Qcap analysis may not be valid and should be interpreted with caution when assessing microvascular delivery of O2.

This study systematically examined the role of work rate (WR) increment on the kinetics of pulmonary oxygen uptake (VO2p) and near-infrared spectroscopy (NIRS)-derived muscle deoxygenation (Δ[HHb]) during moderate-intensity (Mod) cycling. Fourteen males (24 ± 5 years) each completed four to eight repetitions of Mod transitions from 20 to 50, 70, 90, 110 and 130 W. VO2p and Δ[HHb] responses were modelled as a mono-exponential; responses were then scaled to a relative % of the respective response (0–100 %). The Δ[HHb]/VO2 ratio was calculated as the average Δ[HHb]/VO2 during the 20–120 s period of the on-transient. When considered as a single group, neither the phase II VO2p time constant (τVO2p; 27 ± 9, 26 ± 11, 25 ± 10, 27 ± 14, 29 ± 13 s for 50–130 W transitions, respectively) nor the Δ[HHb]/VO2 ratio (1.04 ± 0.13, 1.10 ± 0.13, 1.08 ± 0.07, 1.09 ± 0.11, 1.09 ± 0.09, respectively) was affected by WR (p > 0.05); yet, the VO2 functional gain (G; ΔVO2/ΔWR) increased with increasing WR transitions (8.6 ± 1.3, 9.1 ± 1.2, 9.5 ± 1.0, 9.5 ± 1.0, 9.9 ± 1.0 mL min−1 W−1; p 0.05). The Δ[HHb]/VO2 ratio was smaller (p

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity “priming” exercise (Hvy) on pulmonary O2 uptake (V̇o2p) kinetics during moderate-intensity exercise (Mod). Breath-by-breath V̇o2p and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O2 (FiO2) = 15%, Mod 2 + Hypo] or “sham” (FiO2 = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient V̇o2p and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0–100%), the signals were time-aligned, and the individual [HHb]-to-V̇o2 ratio was calculated. Compared with control (Mod 1), τV̇o2p and the O2 deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced ( P < 0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased ( P < 0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τV̇o2p was increased (30 ± 8 s, P < 0.05), yet O2 deficit was unaffected (643 ± 193 ml, P > 0.05). The modest “overshoot” in the [HHb]-to-V̇o2 ratio (reflecting an O2 delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P = 0.13). The present data do not support an “O2 delivery-independent” speeding of τV̇o2p following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O2 delivery likely governs the rate of adjustment of V̇o2 at τV̇o2p greater than ∼20 s.

This study characterized the profile of near-infrared spectroscopy (NIRS)-derived muscle deoxygenation (Δ[HHb]) and the tissue oxygenation index (TOI) as a function of absolute (PO(ABS)) and normalized power output (%PO) or oxygen consumption (%VO(2)) during incremental cycling exercise. Eight men (24 ± 5 year) each performed two fatigue-limited ramp incremental cycling tests (20 W min(-1)), during which pulmonary VO(2), Δ[HHb] and TOI were measured continuously. Responses from the two tests were averaged and the TOI (%) and normalized Δ[HHb] (%Δ[HHb]) were plotted against %VO(2), %PO and PO(ABS). The overall responses were modelled using a sigmoid regression (y = f ( 0 ) + A/(1 + e(-(-c+dx)))) and piecewise 'double-linear' function of the predominant adjustment of %Δ[HHb] or TOI observed throughout the middle portion of exercise and the 'plateau' that followed. In ~85% of cases, the corrected Akaike Information Criterion (AIC(C)) was smaller (suggesting one model favoured) for the 'double-linear' compared with the sigmoid regression for both %Δ[HHb] and TOI. Furthermore, the f ( 0 ) and A estimates from the sigmoid regressions of %Δ[HHb] yielded unrealistically large projected peak (f ( 0 ) + A) values (%VO(2p) 114.3 ± 17.5; %PO 113.3 ± 9.5; PO(ABS) 113.5 ± 9.8), suggesting that the sigmoid model does not accurately describe the underlying physiological responses in all subjects and thus may not be appropriate for comparative purposes. Alternatively, the present study proposes that the profile of %Δ[HHb] and TOI during ramp incremental exercise may be more accurately described as consisting of three distinct phases in which there is little adjustment early in the ramp, the predominant increase in %Δ[HHb] (decrease in TOI) is approximately linear and an approximately linear 'plateau' follows.

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary VO(2) uptake (τ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV(O(2)) using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O(2) uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and τV(O(2)) lung was assessed by computer simulations. The τV(O(2)) in R2 (32 ± 9 s) was not different (P > 0.05) from S2 (30 ± 10 s), but both were greater (P < 0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowed V(O(2)) kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV(O(2)) predicted by simulations: S1 = R2 < S2). These data therefore suggest that the dynamics of muscle O(2) consumption are slowed when exercise is initiated from a less favourable energetic state.

The relationship between the adjustment of muscle deoxygenation (∆[HHb]) and phase II VO2p was examined in subjects presenting with a range of slow to fast VO2p kinetics. Moderate intensity VO2p and ∆[HHb] kinetics were examined in 37 young males (24 ± 4 years). VO2p was measured breath-by-breath. Changes in ∆[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. VO2p and ∆[HHb] response profiles were fit using a mono-exponential model, and scaled to a relative % of the response (0–100%). The ∆[HHb]/∆VO2p ratio for each individual (reflecting the matching of O2 distribution to O2 utilization) was calculated as the average ∆[HHb]/∆VO2p response from 20 to 120 s during the exercise on-transient. Subjects were grouped based on individual phase II VO2p time-constant (τVO2p): 41 s [slow (S)]. The corresponding ∆[HHb]/∆VO2p were 0.98 (VF), 1.05 (F), 1.09 (M), and 1.22 (S). The larger ∆[HHb]/∆VO2p in the groups with slower VO2p kinetics resulted in the ∆[HHb]/∆VO2p displaying a transient “overshoot” relative to the subsequent steady state level, which was progressively reduced as τVO2 became smaller (r = 0.91). When τVO2p > ~20 s, the rate of adjustment of phase II VO2p appears to be mainly constrained by the matching of local O2 distribution to muscle VO2. These data suggest that in subjects with “slower” VO2 kinetics, the rate of adjustment of VO2 may be constrained by O2 availability within the active tissues related to the matching of microvascular O2 distribution to muscle O2 utilization.

This study sought to determine the effect of the pre-transition work rate (WR) and WR transition magnitude on the adjustment of pulmonary oxygen uptake (VO2p kinetics) in older men. Seven men (69 ± 5 years; mean ± SD) each performed 4–6 cycling transitions from 20 W to either a WR corresponding to 90% estimated lactate threshold (full step, FS) or 2 equal-step transitions (lower step, LS; upper step, US) to the same end-exercise WR as in FS. Gas exchange was analysed breath-by-breath and muscle deoxygenation (∆[HHb]) was measured with NIRS. The time constant (τ) for VO2p was greater in US (53 ± 17 s) and FS (44 ± 11 s) compared to LS (37 ± 9 s); τVO2p for US also trended (p = 0.05) towards being greater than FS. The VO2p gain in US (9.97 ± 0.41 mL/min/W) was greater than LS (9.06 ± 1.17; p = 0.06) and FS (9.13 ± 0.54; p

GREY, T. M., M. D. SPENCER, G. R. BELFRY, J. M. KOWALCHUK, D. H. PATERSON, and J. M. MURIAS. Effects of Age and Long-Term Endurance Training on VO2 Kinetics. Med. Sci. Sports Exerc., Vol. 47, No. 2, pp. 289-298, 2015. Purpose: This study examined the effects of age and training status on the pulmonary oxygen uptake (VO2p) kinetics of untrained and chronically trained young, middle-age, and older groups of men. Methods: Breath-by-breath VO2p and near-infrared spectroscopy-derived muscle deoxy- genation ((HHb)) were monitored continuously in young (20-39 yr) trained (YT, n = 8) and untrained (YuT, n = 8), middle-age (40-59 yr) trained (MT, n = 9) and untrained (MuT, n = 9), and older (60-85 yr) trained (OT, n = 9) and untrained (OuT, n = 8) men. On-transient VO2p and (HHb) responses to cycling exercise at 80% of the estimated lactate threshold (three repeats) were modeled as monoexponential. Data were scaled to a relative percentage of the response (0%-100%), the signals time aligned, and the individual (HHb)-to-VO2p ratio was calculated as the average (HHb)/VO2 during the 20- to 120-s period after exercise onset. Results: The time constant for the adjustment of phase II pulmonary VO2 (TVO2p) was larger in OuT (42.0 T 11.3 s) compared with that in YT (17.0 T 7.5 s), MT (18.1 T 5.3 s), OT (19.8 T 5.4 s), YuT (25.7 T 6.6 s), and MuT (24.4 T 7.4 s) (P G 0.05). Similarly, the (HHb)/VO2 ratio was larger than 1.0 in OuT (1.30 T 0.13, P G 0.05) and this value was larger than that observed in YT (1.01 T 0.07), MT (1.04 T 0.05), OT (1.04 T 0.04), YuT (1.05 T 0.03), and MuT (1.02 T 0.09) (P G 0.05). Conclusions: This study showed that the slower VO2 kinetics typically observed in older individuals can be prevented by long- term endurance training interventions. Although the role of O2 delivery relative to peripheral use cannot be elucidated from the current measures, the absence of age-related slowing of VO2 kinetics seems to be partly related to a preservation of the matching of O2 delivery to O2 utilization in chronically trained older individuals, as suggested by the reduction in the (HHb)/VO2 ratio. Key Words: EXERCISE, AGING, MUSCLE DEOXYGENATION, O2 DELIVERY

Abnormal heart rate recovery (HRR) after maximal exercise may indicate autonomic dysfunction and is a predictor for cardiovascular mortality. HRR is attenuated with aging and in middle-age hypertensive patients, but it is unknown whether HRR is attenuated in older-age adults with hypertension. This study compared HRR among 16 unmedicated stage 1 hypertensive (HTN) participants [nine men/seven women; 68 ± 5 (SD) yr; awake ambulatory blood pressure (BP) 149 ± 10/87 ± 7 mmHg] and 16 normotensive [control (CON)] participants (nine men/seven women; 67 ± 5 yr; 122 ± 4/72 ± 5 mmHg). HR, BP, oxygen uptake (V̇o2), cardiac output (Qc), and stroke volume (SV) were measured at rest, at two steady-state work rates, and graded exercise to peak during maximal treadmill exercise. During 6 min of seated recovery, the change in HR (ΔHR) was obtained every minute and BP every 2 min. In addition, HRR and R-R interval (RRI) recovery kinetics were analyzed using a monoexponential function, and the indexes (HRRI and RRII) were calculated. Maximum V̇o2, HR, Qc, and SV responses during exercise were not different between groups. ΔHR was significantly different ( P < 0.001) between the HTN group (26 ± 8) and the CON group (36 ± 12 beats/min) after 1 min of recovery but less convincing at 2 min ( P = 0.055). BP recovery was similar between groups. HRRI was significantly lower ( P = 0.016), and there was a trend of lower RRII ( P = 0.066) in the HTN group compared with the CON group. These results show that in older-age adults, HRR is attenuated further with the presence of hypertension, which may be attributable to an impairment of autonomic function.

It has been proposed that the adjustment of oxygen uptake (V˙O2) during the exercise on-transient is controlled intracellularly in young healthy individuals and that insufficient local O2 delivery plays a rate-limiting role in aging and disease only. This review shows that adequate O2 provision to the active tissues is critical in the dynamic adjustment of oxidative phosphorylation even in young healthy individuals.

This study examines the effects of recovery duration following heavy-intensity “priming” exercise (Hvy) on pulmonary oxygen (O2) uptake (V̇O2p) during subsequent prolonged moderate-intensity exercise (Mod). Nine participants (6 men and 3 women) (27 ± 7 years) each completed 3 repetitions of 2 continuous Mod 1-Hvy-Mod 2 leg-cycling protocols in which Mod 2 lasted 30 min, but was preceded by a recovery duration of either 6 (R6) or 20 (R20) min at 20 W following Hvy; in each case, Mod 1 and Hvy lasted 6 min and were preceded by 6 min at 20 W. V̇O2p, heart rate (HR), and near-infrared spectroscopy (NIRS)–derived muscle deoxygenation ([HHb]) responses were modeled as a monoexponential; additionally, 60-s averages were computed every 6 min in Mod 1 and Mod 2. V̇O2p was elevated (p < 0.05) throughout Mod 2 compared with Mod 1 in both R6 and R20 (by −82 mL·min−1 or ∼5.0%); this occurred despite a complete recovery of baseline V̇O2p (V̇O2pBsln) following R20. HR and minute ventilation (V̇E), but not [HHb], were also elevated throughout Mod 2. The phase II time constant for V̇O2p (τV̇O2p) was reduced in Mod 2 (22 s (Mod 1), 19 s (Mod 2); p < 0.05), as was the “overshoot” in the normalized [HHb]/O2 uptake ratio (p < 0.05). This study shows that V̇O2p was elevated during Mod following Hvy, regardless of recovery duration; however, a determining role for V̇O2pBsln is precluded. Furthermore, neither V̇O2p, HR, nor V̇E showed any evidence of a readjustment back to no-Hvy conditions during prolonged Mod (p > 0.05). Lastly, regardless of recovery duration, τV̇O2p was reduced to a similar extent with Hvy, likely resulting from an improved matching of local muscle O2 delivery to O2 utilization.

The rate of adjustment for pulmonary oxygen uptake (τV̇O2p) is slower in untrained and in older adults. Near-infrared spectroscopy (NIRS) has shed light on potential mechanisms underlying this in young men and women and in older men; however, there is no such data available in older women. The purpose of this study was to gain a better understanding of the mechanisms of slower τV̇O2p in older women who were either endurance-trained or untrained. Endurance-trained (n = 10; age, 62.6 ± 1.0 years) and untrained (n = 9; age, 69.1 ± 2.2 years) older women attended 2 maximal and 2 submaximal (90% of ventilatory threshold) exercise sessions. Oxygen uptake (V̇O2) was measured breath by breath, using a mass spectrometer, and changes in deoxygenated hemoglobin concentration of the vastus lateralis ([HHb]) were measured using NIRS. Heart rate was measured continuously with a 3-lead electrocardiogram. τV̇O2p was faster in trained (35.1 ± 5.5 s) than in untrained (57.0 ± 8.1 s) women. The normalized [HHb] to V̇O2 ratio, an indicator of muscle O2 delivery to O2 utilization, indicated a smaller overshoot in trained (1.09 ± 0.1) than in untrained (1.39 ± 0.1) women. Heart rate data indicated a faster adjustment of heart rate in trained (33.0 ± 13.0) than in untrained (68.7 ± 14.1) women. The pairing of V̇O2p data with NIRS-derived [HHb] data indicates that endurance-trained older women likely have better matching of O2 delivery to O2 utilization than older untrained women during moderate-intensity exercise, leading to a more rapid adjustment of V̇O2p.

The adjustment of pulmonary oxygen uptake (VO2p), heart rate (HR), limb blood flow (LBF), and muscle deoxygenation [HHb] was examined during the transition to moderate-intensity, knee-extension exercise in six older adults (70 ± 4 years) under two conditions: normoxia (FIO₂ = 20.9 %) and hypoxia (FIO₂ = 15 %). The subjects performed repeated step transitions from an active baseline (3 W) to an absolute work rate (21 W) in both conditions. Phase 2 VO₂p, HR, LBF, and [HHb] data were fit with an exponential model. Under hypoxic conditions, no change was observed in HR kinetics, on the other hand, LBF kinetics was faster (normoxia 34 ± 3 s; hypoxia 28 ± 2), whereas the overall [HHb] adjustment (τ' = TD + τ) was slower (normoxia 28 ± 2; hypoxia 33 ± 4 s). Phase 2 VO₂p kinetics were unchanged (p < 0.05). The faster LBF kinetics and slower [HHb] kinetics reflect an improved matching between O₂ delivery and O₂ utilization at the microvascular level, preventing the phase 2 VO₂p kinetics from become slower in hypoxia. Moreover, the absolute blood flow values were higher in hypoxia (1.17 ± 0.2 L min(-1)) compared to normoxia (0.96 ± 0.2 L min(-1)) during the steady-state exercise at 21 W. These findings support the idea that, for older adults exercising at a low work rate, an increase of limb blood flow offsets the drop in arterial oxygen content (CaO₂) caused by breathing an hypoxic mixture.

The present study was designed to investigate whether absolute work rate (WR) affects Phase I pulmonary oxygen uptake (V̇o2p) duration during moderate-intensity (Mod) exercise and to compare two methods for estimating Phase I V̇o2p duration (PI-Dur). Fourteen males (24 ± 5 yr) each completed 4–8 repetitions of Mod transitions from 20 W to 50, 70, 90, 110, and 130 W. PI-Dur was identified by 1) a marked decrease in both respiratory exchange ratio and end-tidal partial pressure of O2 following exercise onset [i.e., visual inspection of three independent reviewers, and the average (Avg) of the two most similar values]; or 2) the intersection (time delay, TD) of the first and second components in a biexponential nonlinear regression of the entire V̇o2p response from exercise onset. PI-Dur did not differ among WRs ( P > 0.05), regardless of the estimation method used. No differences were detected between Avg and TD (time in s) at any of the five WRs (50 W, 21 ± 6 vs. 23 ± 10 s; 70 W, 23 ± 9 vs. 23 ± 7 s; 90 W, 24 ± 3 vs. 22 ± 5 s; 110 W, 23 ± 6 vs. 22 ± 6 s; 130 W, 21 ± 6 vs. 21 ± 7 s; P > 0.05 for Avg and TD, respectively). Broad limits of agreement within Bland-Altman plots revealed relatively weak agreement among reviewers for individual estimation of PI-Dur. A nonsignificant correlation coefficient ( r = 0.13) and broad limits of agreement suggest disparity between individual Avg and TD estimates of PI-Dur. The present data do not support a role for Mod WR in determining PI-Dur per se. Furthermore, this study illustrated a poor agreement of PI-Dur estimates derived from two different, but accepted methods.

Previous literature has shown that sedentary older women rely on peripheral adaptations to improve cardiorespiratory fitness with endurance training i.e. they show minimal increases in central parameters (cardiac output, Q) in response to endurance training. The purpose of this study therefore was to determine whether endurance trained older women were able to preserve maximal exercise Q and were characterized by a high stroke volume (SV) when compared to physically inactive older women. Trained (n = 7) and untrained (n = 1 0) women attended two maximal and one submaximal laboratory session. Breath-by-breath analysis was conducted using mass spectrometry and Q was assessed using acetylene open circuit inert gas wash-in. Multivariate analysis of variance and paired samples t-tests were used to determine between and within group differences. Trained women had a significantly higher VO2max (37.5 vs. 24.1 ml-1·kg·min-1) compared to untrained women. There were no differences for peripheral oxygen extraction (VO2/Q) at either submaximal or maximal work rates; however trained women had a significantly higher SV at maximal (119.3 vs. 94.6 ml) exercise compared to untrained women. In both trained and untrained women, SV did not rise significantly between submaximal and maximal exercise. Conclusion: Highly fit, endurance trained older women are able to preserve central parameters of VO2max. Peripheral oxygen extraction is similar between older trained and untrained women.

The matching of muscle O2 delivery to O2 utilization can be inferred from the adjustments in muscle deoxygenation (Δ[HHb]) and pulmonary O2 uptake (V̇o2p). This study examined the adjustments of V̇o2p and Δ[HHb] during ramp incremental (RI) and constant-load (CL) exercise in adult males. Ten young adults (YA; age: 25 ± 5 yr) and nine older adults (OA; age: 70 ± 3 yr) completed two RI tests and six CL step transitions to a work rate (WR) corresponding to 1) 80% of the estimated lactate threshold (same relative WR) and 2) 50 W (same absolute WR). V̇o2p was measured breath by breath, and Δ[HHb] of the vastus lateralis was measured using near-infrared spectroscopy. Δ[HHb]-WR profiles were normalized from baseline (0%) to peak Δ[HHb] (100%) and fit using a sigmoid function. The sigmoid slope ( d) was greater ( P < 0.05) in OA (0.027 ± 0.01%/W) compared with YA (0.017 ± 0.01%/W), and the c/ d value (a value corresponding to 50% of the amplitude) was smaller ( P < 0.05) for OA (133 ± 40 W) than for YA (195 ± 51 W). No age-related differences in the sigmoid parameters were reported when WR was expressed as a percentage of peak WR. V̇o2p kinetics compared with Δ[HHb] kinetics for the 50-W transition were similar between YA and OA; however, Δ[HHb] kinetics during the transition to 80% of the lactate threshold were faster than V̇o2p kinetics in both groups. The greater reliance on O2 extraction displayed in OA during RI exercise suggests a lower O2 delivery-to-O2 utilization relationship at a given absolute WR compared with YA.

The adjustment of pulmonary oxygen uptake (VO2p), heart rate (HR), limb blood flow (LBF), and muscle deoxygenation [HHb] was examined during the transition to moderate-intensity, knee-extension exercise in six older adults (70 ± 4 years) under two conditions: normoxia (FIO₂ = 20.9 %) and hypoxia (FIO₂ = 15 %). The subjects performed repeated step transitions from an active baseline (3 W) to an absolute work rate (21 W) in both conditions. Phase 2 VO₂p, HR, LBF, and [HHb] data were fit with an exponential model. Under hypoxic conditions, no change was observed in HR kinetics, on the other hand, LBF kinetics was faster (normoxia 34 ± 3 s; hypoxia 28 ± 2), whereas the overall [HHb] adjustment (τ' = TD + τ) was slower (normoxia 28 ± 2; hypoxia 33 ± 4 s). Phase 2 VO₂p kinetics were unchanged (p0.05). The faster LBF kinetics and slower [HHb] kinetics reflect an improved matching between O₂ delivery and O₂ utilization at the microvascular level, preventing the phase 2 VO₂p kinetics from become slower in hypoxia. Moreover, the absolute blood flow values were higher in hypoxia (1.17 ± 0.2 L min(-1)) compared to normoxia (0.96 ± 0.2 L min(-1)) during the steady-state exercise at 21 W. These findings support the idea that, for older adults exercising at a low work rate, an increase of limb blood flow offsets the drop in arterial oxygen content (CaO₂) caused by breathing an hypoxic mixture.

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity "priming" exercise (Hvy) on pulmonary O(2) uptake (Vo(2p)) kinetics during moderate-intensity exercise (Mod). Breath-by-breath Vo(2p) and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O(2) (Fi(O(2))) = 15%, Mod 2 + Hypo] or "sham" (Fi(O(2)) = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient Vo(2p) and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0-100%), the signals were time-aligned, and the individual [HHb]-to-Vo(2) ratio was calculated. Compared with control (Mod 1), τVo(2p) and the O(2) deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced (P0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased (P0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τVo(2p) was increased (30 ± 8 s, P0.05), yet O(2) deficit was unaffected (643 ± 193 ml, P0.05). The modest "overshoot" in the [HHb]-to-Vo(2) ratio (reflecting an O(2) delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P = 0.13). The present data do not support an "O(2) delivery-independent" speeding of τVo(2p) following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O(2) delivery likely governs the rate of adjustment of Vo(2) at τVo(2p) greater than ∼20 s.

The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II VO2p during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity “priming” exercise. Moderate intensity VO2p and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). VO2p was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. VO2p and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0–100%). The Δ[HHb]/V̇o2 ratio for each individual (reflecting the local matching of O2 delivery to O2 utilization) was calculated as the average Δ[HHb]/V̇o2 response from 20 s to 120 s during the exercise on-transient. Phase II τVO2p was reduced in Mod 2 compared with Mod 1 ( P < 0.05). The effective τ′Δ[HHb] remained the same in Mod 1 and Mod 2 ( P > 0.05). During Mod 1, there was an “overshoot” in the Δ[HHb]/V̇o2 ratio (1.08; P < 0.05) that was not present during Mod 2 (1.01; P > 0.05). There was a positive correlation between the reduction in the Δ[HHb]/V̇o2 ratio and the smaller τVO2p from Mod 1 to Mod 2 ( r = 0.78; P < 0.05). This study showed that a smaller τVO2p during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O2 delivery during the on-transient of exercise, as suggested by a smaller Δ[HHb]/V̇o2 ratio.

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary VO(2) uptake (τ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV(O(2)) using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O(2) uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and τV(O(2)) lung was assessed by computer simulations. The τV(O(2)) in R2 (32 ± 9 s) was not different (P0.05) from S2 (30 ± 10 s), but both were greater (P0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowed V(O(2)) kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV(O(2)) predicted by simulations: S1 = R2S2). These data therefore suggest that the dynamics of muscle O(2) consumption are slowed when exercise is initiated from a less favourable energetic state.

Older adults (O) may have a longer phase I pulmonary O2 uptake kinetics (V̇o2p) than young adults (Y); this may affect parameter estimates of phase II V̇o2p. Therefore, we sought to: 1) experimentally estimate the duration of phase I V̇o2p (EE phase I) in O and Y subjects during moderate-intensity exercise transitions; 2) examine the effects of selected phase I durations (i.e., different start times for modeling phase II) on parameter estimates of the phase II V̇o2p response; and 3) thereby determine whether slower phase II kinetics in O subjects represent a physiological difference or a by-product of fitting strategy. V̇o2p was measured breath-by-breath in 19 O (68 ± 6 yr; mean ± SD) and 19 Y (24 ± 5 yr) using a volume turbine and mass spectrometer. Phase I V̇o2p was longer in O (31 ± 4 s) than Y (20 ± 7 s) ( P < 0.05). In O, phase II τV̇o2p was larger ( P < 0.05) when fitting started at 15 s (49 ± 12 s) compared with fits starting at the individual EE phase I (43 ± 12 s), 25 s (42 ± 10 s), 35 s (42 ± 12 s), and 45 s (45 ± 15 s). In Y, τV̇o2p was not affected by the time at which phase II V̇o2p fitting started (τV̇o2p = 31 ± 7 s, 29 ± 9 s, 30 ± 10 s, 32 ± 11 s, and 30 ± 8 s for fittings starting at 15 s, 25 s, 35 s, 45 s, and EE phase I, respectively). Fitting from EE phase I, 25 s, or 35 s resulted in the smallest CI τV̇o2p in both O and Y. Thus, fitting phase II V̇o2p from (but not constrained to) 25 s or 35 s provides consistent estimates of V̇o2p kinetics parameters in Y and O, despite the longer phase I V̇o2p in O.

The relationship between the adjustment of muscle deoxygenation (∆[HHb]) and phase II VO(2p) was examined in subjects presenting with a range of slow to fast VO(2p) kinetics. Moderate intensity VO(2p) and ∆[HHb] kinetics were examined in 37 young males (24 ± 4 years). VO(2p) was measured breath-by-breath. Changes in ∆[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. VO(2p) and ∆[HHb] response profiles were fit using a mono-exponential model, and scaled to a relative % of the response (0-100%). The ∆[HHb]/∆VO(2p) ratio for each individual (reflecting the matching of O(2) distribution to O(2) utilization) was calculated as the average ∆[HHb]/∆VO(2p) response from 20 to 120 s during the exercise on-transient. Subjects were grouped based on individual phase II VO(2p) time-constant (τVO(2p)):21 s [very fast (VF)]; 21-30 s [fast (F)]; 31-40 s [moderate (M)];41 s [slow (S)]. The corresponding ∆[HHb]/∆VO(2p) were 0.98 (VF), 1.05 (F), 1.09 (M), and 1.22 (S). The larger ∆[HHb]/∆VO(2p) in the groups with slower VO(2p) kinetics resulted in the ∆[HHb]/∆VO(2p) displaying a transient "overshoot" relative to the subsequent steady state level, which was progressively reduced as τVO(2) became smaller (r = 0.91). When τVO(2p)~20 s, the rate of adjustment of phase II VO(2p) appears to be mainly constrained by the matching of local O(2) distribution to muscle VO(2). These data suggest that in subjects with "slower" VO(2) kinetics, the rate of adjustment of VO(2) may be constrained by O(2) availability within the active tissues related to the matching of microvascular O(2) distribution to muscle O(2) utilization.

This study sought to determine the effect of the pre-transition work rate (WR) and WR transition magnitude on the adjustment of pulmonary oxygen uptake (VO(2p) kinetics) in older men. Seven men (69 ± 5 years; mean ± SD) each performed 4-6 cycling transitions from 20 W to either a WR corresponding to 90% estimated lactate threshold (full step, FS) or 2 equal-step transitions (lower step, LS; upper step, US) to the same end-exercise WR as in FS. Gas exchange was analysed breath-by-breath and muscle deoxygenation (∆[HHb]) was measured with NIRS. The time constant (τ) for VO(2p) was greater in US (53 ± 17 s) and FS (44 ± 11 s) compared to LS (37 ± 9 s); τVO(2p) for US also trended (p = 0.05) towards being greater than FS. The VO(2p) gain in US (9.97 ± 0.41 mL/min/W) was greater than LS (9.06 ± 1.17; p = 0.06) and FS (9.13 ± 0.54; p0.05). The O(2) deficit was greater in US (0.25 ± 0.08 L) than LS (0.19 ± 0.06 L); yet the 'accumulated O(2) deficit' (0.44 ± 0.13 L; O(2) deficit from LS + US) was similar to that of FS (0.42 ± 0.13 L; p = 0.38). The effective Δ[HHb] response time (τ'∆[HHb]) for US (36 ± 12 s) was greater than LS (27 ± 6 s; p = 0.07) and FS (26 ± 4 s; p0.05), suggesting that the slowed adjustment of muscle O(2) extraction was associated with the slowed VO(2) kinetics of the US. Despite already slowed VO(2p) kinetics, older men exhibit further slowing when small WR transitions are initiated from an elevated pre-transition WR, yet this results in no cumulative impact on O(2) deficit. This slowing in US compared to LS does not appear to be related to local O(2) availability.

This study compared the parameter estimates of pulmonary oxygen uptake (VO(2p)), heart rate (HR) and muscle deoxygenation (Δ[HHb]) kinetics when several moderate-intensity exercise transitions (MODs) were performed during a single visit versus several MODs performed during separate visits. Nine subjects (24 ± 5 years, mean ± SD) each completed two successive cycling MODs on six occasions (1-6A and 1-6B) from 20 W to a work rate corresponding to 80% estimated lactate threshold with 6 min recovery at 20 W. During one visit, subjects completed two series of three MODs (6A-F), separated by 20 min rest. VO(2p) time constants (τVO(2p); 27 ± 10 s, 25 ± 12 s, 25 ± 11 s) were similar (p > 0.05) for MODs 1-6A, 1-6B and 6A-F, respectively. τVO(2p) had reproducibility 95% confidence intervals (CI(95)) of 8.3, 8.2, 4.7, 4.9 and 4.7 s when comparing single (1A vs. 2A), the average of two (1-2A vs. 3-4A), three (1-3A vs. 4-6A), four (1-2AB vs. 3-4AB) and six (1-3AB vs. 4-6AB) MODs, respectively. The effective Δ[HHb] response time (τ'Δ[HHb]) was unaffected across conditions (1-6A: 19 ± 2 s, 1-6B: 19 ± 3 s, 6A-F: 17 ± 4 s) with reproducibility CI(95) of 5.3, 4.5, 3.1, 2.9 and 3.3 s when a single, two, three, four and six MODs were compared, respectively. τHR was reduced in MODs 6A-F compared to 1-6A and 1-6B (23 ± 5 s, 25 ± 5 s, 27 ± 6 s, respectively). This study showed that parameter estimates of VO(2p), HR and Δ[HHb] kinetics are largely unaffected by data collection sequence, and the day-to-day reproducibility of τVO(2p) and τ'Δ[HHb] estimates, as determined by the CI(95), was appreciably improved by averaging of at least three MODs.