Similar pattern of change in V̇o2 kinetics, vascular function, and tissue oxygen provision following an endurance training stimulus in older and young adults.

The purpose of this study was to examine the time course of changes in the oxygen uptake (V̇o2) kinetics response subsequent to short-term exercise training (i.e., 24, 48, 72, and 120 h posttraining) and examine the relationship with the time course of changes in microvascular [deoxygenated hemoglobin concentration ([HHb])-to-V̇o2 ratio ([HHb])/V̇o2)] and macrovascular [flow-mediated dilation (FMD)] O2 delivery to the active tissues/limbs. Seven healthy older [OA; 74 ± 6 (SD) yr] and young men (YA; 25 ± 3 yr) completed three endurance cycling exercise training sessions at 70% V̇o2peak Moderate-intensity exercise on-transient V̇o2 (measured breath by breath) and [HHb] (measured by near-infrared spectroscopy) were modeled with a monoexponential and normalized (0-100% of response), and the [HHb])/V̇o2 was calculated. Ultrasound-derived FMD of the popliteal artery was assessed after 5 min of cuff occlusion. %FMD was calculated as the greatest percent change in diameter from baseline. Time constant of V̇o2 (τV̇o2) was significantly reduced in both OA (~18%) and YA (~23%) at 24 h (P < 0.001) posttraining and remained decreased at 48 h before returning toward pretraining (PRE) values. Both groups showed a significant decrease in the [HHb])/V̇o2 at 24, 48, and 72 h (P = 0.001, 0.01, and 0.03, respectively) posttraining before returning toward PRE values at 120 h. %FMD followed a similar time course to that of changes in the [HHb])/V̇o2, being significantly greater in both OA (by ~64%) and YA (by ~26%) at 24 h (P < 0.001), remaining increased at 48 and 72 h (P = 0.02 and 0.03, respectively), and returning toward PRE values at 120 h. These data suggest the rate of adjustment of V̇o2 may be constrained by O2 availability in the active tissues.

Formulation of evidence-based messages to promote the use of physical activity to prevent and manage Alzheimer's disease.

BACKGROUND: The impending public health impact of Alzheimer's disease is tremendous. Physical activity is a promising intervention for preventing and managing Alzheimer's disease. However, there is a lack of evidence-based public health messaging to support this position. This paper describes the application of the Appraisal of Guidelines Research and Evaluation II (AGREE-II) principles to formulate an evidence-based message to promote physical activity for the purposes of preventing and managing Alzheimer's disease. METHODS: A messaging statement was developed using the AGREE-II instrument as guidance. Methods included (a) conducting a systematic review of reviews summarizing research on physical activity to prevent and manage Alzheimer's disease, and (b) engaging stakeholders to deliberate the evidence and formulate the messaging statement. RESULTS: The evidence base consisted of seven systematic reviews focused on Alzheimer's disease prevention and 20 reviews focused on symptom management. Virtually all of the reviews of symptom management conflated patients with Alzheimer's disease and patients with other dementias, and this limitation was reflected in the second part of the messaging statement. After deliberating the evidence base, an expert panel achieved consensus on the following statement: "Regular participation in physical activity is associated with a reduced risk of developing Alzheimer's disease. Among older adults with Alzheimer's disease and other dementias, regular physical activity can improve performance of activities of daily living and mobility, and may improve general cognition and balance." The statement was rated favourably by a sample of older adults and physicians who treat Alzheimer's disease patients in terms of its appropriateness, utility, and clarity. CONCLUSION: Public health and other organizations that promote physical activity, health and well-being to older adults are encouraged to use the evidence-based statement in their programs and resources. Researchers, clinicians, people with Alzheimer's disease and caregivers are encouraged to adopt the messaging statement and the recommendations in the companion informational resource.

Vascular responsiveness measured by tissue oxygen saturation reperfusion slope is sensitive to different occlusion durations and training status.

What is the central question of this study? Is the near-infrared spectroscopy-derived measure of tissue oxygen saturation (StO2) reperfusion slope sensitive to a range of ischaemic conditions, and do differences exist between trained and untrained individuals? What is the main finding and its importance? The StO2 reperfusion rate is sensitive to different occlusion durations, and changes in the reperfusion slope in response to a variety of ischaemic challenges can be used to detect differences between two groups. These data indicate that near-infrared spectroscopy-derived measures of StO2, specifically the reperfusion slope following a vascular occlusion, can be used as a sensitive measure of vascular responsiveness. The reperfusion rate of near-infrared spectroscopy-derived measures of tissue oxygen saturation (StO2) represents vascular responsiveness. This study examined whether the reperfusion slope of StO2 is sensitive to different ischaemic conditions (i.e. a dose-response relationship) and whether differences exist between two groups of different fitness levels. Nine healthy trained (T; age 25 ± 3 years; maximal oxygen uptake 63.4 ± 6.7 ml kg-1  min-1 ) and nine healthy untrained men (UT; age 21 ± 1 years; maximal oxygen uptake 46.6 ± 2.5 ml kg-1  min-1 ) performed a series of vascular occlusion tests of different durations (30 s, 1, 2, 3 and 5 min), each separated by 30 min. The StO2 was measured over the tibialis anterior using near-infrared spectroscopy, with the StO2 reperfusion slope calculated as the upslope during 10 s following cuff release. The reperfusion slope was steeper in T compared with UT at all occlusion durations (P < 0.05). For the T group, the reperfusion slopes for 30 s and 1 min occlusions were less than for all longer durations (P < 0.05). The reperfusion slope following 2 min occlusion was similar to that for 3 min (P > 0.05), but both were less steep than for 5 min of occlusion. In UT, the reperfusion slope at 30 s was smaller than for all longer occlusion durations (P < 0.05), and 1 min occlusion resulted in a reperfusion slope that was less steep than following 2 and 3 min (P < 0.05), albeit not different from 5 min (P > 0.05). The present study demonstrated that the reperfusion rate of StO2 is sensitive to different occlusion durations, and that changes in the reperfusion rate in response to a variety of ischaemic challenges can be used to detect differences in vascular responsiveness between trained and untrained groups.

Vascular responsiveness determined by near-infrared spectroscopy measures of oxygen saturation.

Vascular impairments at the macro- and microcirculatory levels are associated with increased risk for cardiovascular disease. Flow-mediated dilation (FMD) is currently the most widely used method for non-invasive assessment of vascular endothelial function. Recently, near-infrared spectroscopy (NIRS)-derived measures of tissue oxygen saturation (StO2) have been used to characterize the dynamic response of local tissue perfusion to a brief period of ischaemia. The purpose of the present study was to establish correlations between the reperfusion rate of StO2 and FMD. Ultrasound-derived FMD was quantified after 5 min of distal cuff occlusion of the popliteal artery in 20 healthy young men (26 ± 3 years old). Triplicate measurements of end-diastolic arterial diameter were made every 15 s after cuff release, and FMD response was calculated as the greatest percentage change in diameter from baseline (%FMD). The StO2 was measured using NIRS throughout the duration of each test. Two consecutive FMD tests were performed, separated by 30 min of rest, and were averaged for %FMD and StO2. The %FMD was significantly correlated with the reperfusion slope of StO2 after cuff release (slope 2 StO2; r = 0.63, P = 0.003). In conclusion, the present study established a correlation between slope 2 StO2 and %FMD in healthy young men. These data suggest that NIRS-derived slope 2 StO2 can be used as a measure of vascular endothelial function.

Breath-by-breath pulmonary O2 uptake kinetics: effect of data processing on confidence in estimating model parameters.

To improve the signal-to-noise ratio of breath-by-breath pulmonary O2 uptake (V̇O2p) data, it is common practice to perform multiple step transitions, which are subsequently processed to yield an ensemble-averaged profile. The effect of different data-processing techniques on phase II V̇O2p kinetic parameter estimates (V̇O2p amplitude, time delay and phase II time constant (τV̇O2p)] and model confidence [95% confidence interval (CI95)] was examined. Young (n = 9) and older men (n = 9) performed four step transitions from a 20 W baseline to a work rate corresponding to 90% of their estimated lactate threshold on a cycle ergometer. Breath-by-breath V̇O2p was measured using mass spectrometry and volume turbine. Mono-exponential kinetic modelling of phase II V̇O2p data was performed on data processed using the following techniques: (A) raw data (trials time aligned, breaths of all trials combined and sorted in time); (B) raw data plus interpolation (trials time aligned, combined, sorted and linearly interpolated to second by second); (C) raw data plus interpolation plus 5 s bin averaged; (D) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 1; points joined by straight-line segments), ensemble averaged]; (E) 'D' plus 5 s bin averaged; (F) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 2; points copied until subsequent point appears), ensemble averaged]; and (G) 'F' plus 5 s bin averaged. All of the model parameters were unaffected by data-processing technique; however, the CI95 for τV̇O2p in condition 'D' (4 s) was lower (P < 0.05) than the CI95 reported for all other conditions (5-10 s). Data-processing technique had no effect on parameter estimates of the phase II V̇O2p response. However, the narrowest interval for CI95 occurred when individual trials were linearly interpolated and ensemble averaged.

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.

Faster VO(2) kinetics after eccentric contractions is explained by better matching of O(2) delivery to O(2) utilization.

PURPOSE: This study examined the impact of eccentric exercise-induced muscle damage on the rate of adjustment in muscle deoxygenation and pulmonary O2 uptake (VO(2p)) kinetics during moderate exercise. METHODS: Fourteen males (25 ± 3 year; mean ± SD) completed three step transitions to 90 % θL before (Pre), 24 h (Post24) and 48 h after (Post48) eccentric exercise (100 eccentric leg-press repetitions with a load corresponding to 110 % of the participant's concentric 1RM). Participants were separated into two groups: phase II VO(2p) time constant (τVO(2p)) ≤ 25 s (fast group; n = 7) or τVO(2p) > 25 s (slow group; n = 7). VO(2p) and [HHb] responses were modeled as a mono-exponential. RESULTS: In both groups, isometric peak torque (0°/s) at Post24 was decreased compared to Pre (p < 0.05) and remained depressed at Post48 (p < 0.05). τVO(2p) was designed to be different (p < 0.05) at Pre between the Fast (τVO(2p); 19 ± 4 s) and Slow (32 ± 6 s) groups. There were no differences among time points (τVO(2p): Pre, 19 ± 4 s; Post24, 22 ± 3 s; Post48, 20 ± 4 s) in the Fast group. In Slow, there was a speeding (p < 0.05) from the Pre (32 ± 6 s) to the Post24 (25 ± 6) but not Post48 (31 ± 6), resulting in no difference (p > 0.05) between groups at Post24. This reduction of τVO(2p) was concomitant with the abolishment (p < 0.05) of an overshoot in the [HHb]/VO(2p) ratio. CONCLUSION: We propose that the sped VO(2p) kinetics observed in the Slow group coupled with an improved [HHb]/VO(2p) ratio suggest a better matching of local muscle O2 delivery to O2 utilization following eccentric contractions.

Pulmonary O2 uptake kinetics during moderate-intensity exercise transitions initiated from low versus elevated metabolic rates: insights from manipulations in cadence.

INTRODUCTION: The rate of adjustment (τ) of phase II pulmonary O2 uptake (VO2p) is slower when exercise transitions are initiated from an elevated baseline work rate (WR) and metabolic rate (MR). In this study, combinations of cycling cadence (40 vs. 90 rpm) and external WR were used to examine the effect of prior MR on τVO2p. METHODS: Eleven young men completed transitions from 20 W (BSL) to 90% lactate threshold, with transitions performed as two steps of equal ∆WR (LS, lower step; US, upper step), while maintaining a cadence of (1) 40 rpm, (2) 90 rpm, and (3) 40 rpm but with the WRs elevated to match the higher VO2p associated with 90 rpm cycling (40MATCH); transitions lasted 6 min. VO2p was measured breath-by-breath using mass spectrometry and turbinometry; vastus lateralis muscle deoxygenation [HHb] was measured using near-infrared spectroscopy. VO2p and HHb responses were modeled using nonlinear least squares regression analysis. RESULTS: VO2p at BSL, LS and US was similar for 90 rpm and 40MATCH, but greater than in 40 rpm. Compared to 90 rpm, τVO2p at 40 rpm was shorter (p < 0.05) in LS (18 ± 5 vs. 28 ± 8 s) but not in US (26 ± 8 vs. 33 ± 9 s), and at 40MATCH, τVO2p was lower (p < 0.05) (19 ± 6 s) in LS but not in US (34 ± 13 s) despite differing external WR and ∆WR. CONCLUSIONS: A similar overall adjustment of [HHb] and VO2p in LS and US across conditions suggested dynamic matching between microvascular blood flow and O2 utilization. Prior MR (rather than external WR per se) plays a role in the dynamic adjustment of pulmonary (and muscle) VO2p.

"Tailored" submaximal step test for VO2max prediction in healthy older adults.

The authors developed and validated a "tailored" version of the Astrand-Rhyming step test (tA-R) and a new equation for VO2max prediction in older adults (OA). Sixty subjects (age 68 ± 4 yr, 30 male, 30 female) performed their tA-R step test (5-min, 30-cm step, tailored stepping rate) and an incremental cycling test to exhaustion. VO2max was (a) predicted using the standard A-R equation (predicted VO2max), (b) predicted based on the authors' new multiple linear equation (equation VO2max), and (c) directly measured by incremental cycling test (direct VO2max). Agreement among values of VO2max was evaluated by Bland-Altman analysis. The predicted VO2max was not significantly different from the direct VO2max, yet with relatively large imprecision. The equation VO2max allowed more precise as well as accurate predictions of VO2max compared with standard A-R prediction. The "tailored" version of the Astrand-Rhyming step test and the new prediction equation appear suitable for a rapid (5-min), safe (submaximal), accurate, and precise VO2max prediction in healthy OA.

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.

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.

Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate-intensity exercise.

Pulmonary O2 uptake (V(O2p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO2)) ~40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P(ET, CO2) ~20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P(ET, CO2) ~40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (~5%). The V(O2p) was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 V(O2p) kinetics (τV(O2p)) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower V(O2p) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P(CO2) (NORMO) restored LBF kinetics, but not V(O2p) kinetics, which remained 'slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower V(O2p) kinetics observed during HYPO.

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.

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.

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.

The effects of short recovery duration on VO2 and muscle deoxygenation during intermittent exercise.

This study compared the oxygen uptake (VO(2)) and muscle deoxygenation (∆HHb) of two intermittent protocols to responses during continuous constant load cycle exercise in males (24 year ± 2, n = 7). Subjects performed three protocols: (1) 10 s work/5 s active recovery (R), R at 20 W (INT1): (2) 10 s work/5 s R, R at moderate intensity (INT2); and (3) continuous exercise (CONT), all for 10 min, on separate days. The work rate of CONT and the 10 s work of INT1 and INT2 were set within the heavy intensity domain. VO(2) and ∆HHb data were filtered and averaged to 5 s bins. Average VO(2) (80-420 s) was highest during CONT (3.77 L/min), lower in INT2 (3.04 L/min), and lowest during INT1 (2.81 L/min), all (p < 0.05). Average ∆HHb (80-420 s) was higher during CONT (p < 0.05) than both INT exercise protocols (CONT; 25.7 ± 0.9 a.u. INT1; 16.4 ± 0.8 a.u., and INT2; 15.8 ± 0.8 a.u.). The repeated changes in metabolic rate elicited oscillations in ΔHHb in both intermittent protocols, whereas oscillations in VO(2) were only observed during INT1. The greater ΔHHb during CONT suggests a reduction in oxygen delivery compared to oxygen consumption relative to INT. The higher VO(2) for INT 2 versus INT 1 and similar ΔHHb during INT suggests an increase in oxygen delivery during INT 2. Thus the different demands of INT1, INT2, and CONT protocols elicited differing physiological responses to a similar heavy intensity power output. These intermittent exercise models seem to elicit an elevated O(2) delivery condition compared to CONT.

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.

Influence of phase I duration on phase II VO2 kinetics parameter estimates in older and young adults.

Older adults (O) may have a longer phase I pulmonary O(2) uptake kinetics (Vo(2)(p)) than young adults (Y); this may affect parameter estimates of phase II Vo(2)(p). Therefore, we sought to: 1) experimentally estimate the duration of phase I Vo(2)(p) (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 Vo(2)(p) response; and 3) thereby determine whether slower phase II kinetics in O subjects represent a physiological difference or a by-product of fitting strategy. Vo(2)(p) 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 Vo(2)(p) was longer in O (31 ± 4 s) than Y (20 ± 7 s) (P < 0.05). In O, phase II τVo(2)(p) 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, τVo(2)(p) was not affected by the time at which phase II Vo(2)(p) fitting started (τVo(2)(p) = 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 τVo(2)(p) in both O and Y. Thus, fitting phase II Vo(2)(p) from (but not constrained to) 25 s or 35 s provides consistent estimates of Vo(2)(p) kinetics parameters in Y and O, despite the longer phase I Vo(2)(p) in O.