Dyspnea during exercise and voluntary hyperpnea in women with obesity.

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.

Cerebrovascular Responsiveness to Hypercapnia Is Stable over Six Months in Older Adults.

The primary purpose of this Brain in Motion (BIM) sub-study was to determine the 6-month stability of resting blood flow velocity and cerebrovascular responsiveness to a euoxic hypercapnic challenge in a group of physically inactive community dwelling men and men aged ≥55 yrs (range 55-92 yrs). At baseline and 6 months later 88 women (65±6 yr) and 78 men (67±7 yr) completed a hypercapnic challenge (step changes from resting end-tidal PCO2 ((PETCO2) to +1, +5 and +8 mmHg above rest) while cerebral blood flow velocity was assessed using transcranial Doppler ultrasound. Peak velocity of the middle cerebral artery (MCAv) was increased (p<0.05) at the second visit during rest (51±2 vs. 52±4); however, these differences were abolished (p>0.05) when MCAv was normalized to PETCO2. During hypercapnia, MCAv tended to be increased at follow-up, but this finding was absent when MCAv/PETCO2 was compared across time. Cerebrovascular reactivity (i.e., ΔMCAv/ΔPETCO2) was similar (p>0.05) between testing occasions regardless of the approach taken (i.e., considering only the lower step [from +1 to +5 mmHg]; the upper step [+5 to +8 mmHg]; or the complete test taken together). In conclusion, this study has shown that cerebral blood flow and cerebrovascular responsiveness to acute euoxic hypercapnia are stable in older, healthy adults over a 6-month period. Modest changes in MCAv over time must be viewed in the context of underlying differences in PETCO2, an important finding with implications for future studies considering cerebral blood flow velocity.

Effects of age and long-term endurance training on VO2 kinetics.

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 deoxygenation ([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 (τVO2p) was larger in OuT (42.0 ± 11.3 s) compared with that in YT (17.0 ± 7.5 s), MT (18.1 ± 5.3 s), OT (19.8 ± 5.4 s), YuT (25.7 ± 6.6 s), and MuT (24.4 ± 7.4 s) (P < 0.05). Similarly, the [HHb]/VO2 ratio was larger than 1.0 in OuT (1.30 ± 0.13, P < 0.05) and this value was larger than that observed in YT (1.01 ± 0.07), MT (1.04 ± 0.05), OT (1.04 ± 0.04), YuT (1.05 ± 0.03), and MuT (1.02 ± 0.09) (P < 0.05). CONCLUSIONS: This study showed that the slower VO2kinetics 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.

Heart rate recovery after maximal exercise is blunted in hypertensive seniors.

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.

Muscle O2 extraction reserve during intense cycling is site-specific.

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 (V̇O(2peak)), gas exchange threshold (GET), and peak work rate (WR(peak)). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇O(2peak)) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇O(2p)) 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.

The critical role of O2 provision in the dynamic adjustment of oxidative phosphorylation.

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.

Sex-related differences in muscle deoxygenation during ramp incremental exercise.

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 ( .VO2p ) measurements. Subject's (men: n=10; women: n=10) Δ[HHb] data were normalized to 100% of the response, plotted as a function ( .VO2p, % .VO2p), 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 .VO2p, % .VO2p 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.

Prolonged moderate-intensity exercise oxygen uptake response following heavy-intensity priming exercise with short- and longer-term recovery.

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.

Systemic and vastus lateralis muscle blood flow and O2 extraction during ramp incremental cycle exercise.

During ramp incremental cycling exercise increases in pulmonary O2 uptake (Vo2p) 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 (Vo2 peak = 4.2 ± 0.5 l/min) and 10 young women (Vo2 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 Vo2p, respectively; systemic arterio-venous O2 difference (a-vO2diff) was calculated as Vo2p/Q on a minute-by-minute basis. Changes in near-infrared spectroscopy-derived muscle deoxygenation (Δ[HHb]) were used (in combination with Vo2p data) to estimate the profiles of peripheral O2 extraction and blood flow of the active muscle microvasculature. The systemic Q-to-Vo2p relationship was linear (~5.8 l/min increase in Q for a 1 l/min increase in Vo2p) with a-vO2diff displaying a hyperbolic response as exercise intensity increased toward Vo2 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 Vo2p 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.

Oxygen uptake kinetics in endurance-trained and untrained postmenopausal women.

The rate of adjustment for pulmonary oxygen uptake (τV̇O(2p)) 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 τV̇O(2p) 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 (V̇O(2)) 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. τV̇O(2p) was faster in trained (35.1 ± 5.5 s) than in untrained (57.0 ± 8.1 s) women. The normalized [HHb] to V̇O(2) ratio, an indicator of muscle O(2) delivery to O(2) 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 V̇O(2p) data with NIRS-derived [HHb] data indicates that endurance-trained older women likely have better matching of O(2) delivery to O(2) utilization than older untrained women during moderate-intensity exercise, leading to a more rapid adjustment of V̇O(2p).

Effect of acute hypoxia on muscle blood flow, VO2p, and [HHb] kinetics during leg extension exercise in older men.

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.

Effect of moderate-intensity work rate increment on phase II τVO2, functional gain and Δ[HHb].

This study systematically examined the role of work rate (WR) increment on the kinetics of pulmonary oxygen uptake (VO(2p)) 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. VO(2p) 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]/VO(2) ratio was calculated as the average Δ[HHb]/VO(2) during the 20-120 s period of the on-transient. When considered as a single group, neither the phase II VO(2p) time constant (τVO(2p); 27 ± 9, 26 ± 11, 25 ± 10, 27 ± 14, 29 ± 13 s for 50-130 W transitions, respectively) nor the Δ[HHb]/VO(2) 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 VO(2) functional gain (G; ΔVO(2)/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). When subjects were stratified into two groups [Fast (n = 6), τVO(2p130W) < 25 s < τVO(2p130W), Slower (n = 8)], a group by WR interaction was observed for τVO(2p). The increasing functional G persisted (p < 0.05) and did not differ between groups (p > 0.05). The Δ[HHb]/VO(2) ratio was smaller (p < 0.05) in the Fast than Slower group, but was unaffected by WR. In conclusion, the present study demonstrated (1) a non-uniform effect of Mod WR increment on τVO(2p); (2) that τVO(2p) in the Slower group is likely determined by an O(2) delivery limitation; and (3) that increasing Mod WR increments elicits an increased functional G, regardless of the τVO(2p) response.

Duration of "Phase I" VO2p: a comparison of methods used in its estimation and the effects of varying moderate-intensity work rate.

The present study was designed to investigate whether absolute work rate (WR) affects Phase I pulmonary oxygen uptake (Vo(2)(p)) duration during moderate-intensity (Mod) exercise and to compare two methods for estimating Phase I Vo(2)(p) duration (P(I-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. P(I-Dur) was identified by 1) a marked decrease in both respiratory exchange ratio and end-tidal partial pressure of O(2) 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 Vo(2)(p) response from exercise onset. P(I-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 P(I-Dur). A nonsignificant correlation coefficient (r = 0.13) and broad limits of agreement suggest disparity between individual Avg and TD estimates of P(I-Dur). The present data do not support a role for Mod WR in determining P(I-Dur) per se. Furthermore, this study illustrated a poor agreement of P(I-Dur) estimates derived from two different, but accepted methods.

Adjustments of pulmonary O2 uptake and muscle deoxygenation during ramp incremental exercise and constant-load moderate-intensity exercise in young and older adults.

The matching of muscle O(2) delivery to O(2) utilization can be inferred from the adjustments in muscle deoxygenation (Δ[HHb]) and pulmonary O(2) uptake (Vo(2p)). This study examined the adjustments of Vo(2p) 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). Vo(2p) 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. Vo(2p) 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 Vo(2p) kinetics in both groups. The greater reliance on O(2) extraction displayed in OA during RI exercise suggests a lower O(2) delivery-to-O(2) utilization relationship at a given absolute WR compared with YA.

Noninvasive estimation of microvascular O2 provision during exercise on-transients in healthy young males.

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 Vo2 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 Vo2 (Vo(2p)) 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]/Vo2 ratio for each individual and 2) rearranged in the Fick equation for estimation of capillary blood flow (Q(cap)). A transient [HHb]/Vo2 "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]/Vo2 ratio (Mod1 - Mod2) were related to reductions in phase II τVo(2p) (r = 0.82; P < 0.05). For Q(cap), a near-exponential response was observed in 8/12 subjects in Mod1 and only in 4/12 subjects in Mod2. The Q(cap) profile was shown to be highly dependent on the [HHb] baseline-to-amplitude ratio. Thus, accurate and physiologically consistent estimations of Q(cap) were not possible in most cases. This study confirmed that priming exercise results in an improved O2 delivery as shown by the decreased [HHb]/Vo2) ratio that was related to the smaller τVo2 in Mod2. Additionally, this study suggested that Q(cap) analysis may not be valid and should be interpreted with caution when assessing microvascular delivery of O2.

Characterizing the profile of muscle deoxygenation during ramp incremental exercise in young men.

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.

Regulation of VO2 kinetics by O2 delivery: insights from acute hypoxia and heavy-intensity priming exercise in young men.

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 (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, τVo(2p) was increased (30 ± 8 s, P < 0.05), yet O(2) deficit was unaffected (643 ± 193 ml, P > 0.05). 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.

Higher Cardiorespiratory Fitness in Older Trained Women is Due to Preserved Stroke Volume.

UNLABELLED: 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.

Speeding of VO2 kinetics during moderate-intensity exercise subsequent to heavy-intensity exercise is associated with improved local O2 distribution.

The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II V(O(2p)) during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity "priming" exercise. Moderate intensity V(O(2p)) and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). V(O(2p)) was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. V(O(2p)) and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0-100%). The Δ[HHb]/Vo(2) ratio for each individual (reflecting the local matching of O(2) delivery to O(2) utilization) was calculated as the average Δ[HHb]/Vo(2) response from 20 s to 120 s during the exercise on-transient. Phase II τV(O(2p)) 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]/Vo(2) 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]/Vo(2) ratio and the smaller τV(O(2p)) from Mod 1 to Mod 2 (r = 0.78; P < 0.05). This study showed that a smaller τV(O(2p)) during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O(2) delivery during the on-transient of exercise, as suggested by a smaller Δ[HHb]/Vo(2) ratio.