Speeding of V̇o2 kinetics during moderate-intensity exercise subsequent to heavy-intensity exercise is associated with improved local O2 distribution

2011 ◽  
Vol 111 (5) ◽  
pp. 1410-1415 ◽  
Author(s):  
Juan M. Murias ◽  
Matthew D. Spencer ◽  
Darren S. DeLorey ◽  
Brendon J. Gurd ◽  
John M. Kowalchuk ◽  
...  

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.

2003 ◽  
Vol 95 (1) ◽  
pp. 113-120 ◽  
Author(s):  
Darren S. DeLorey ◽  
John M. Kowalchuk ◽  
Donald H. Paterson

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (V̇o2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 ± 3 yr; mean ± SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath V̇o2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 V̇o2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for V̇o2p (30 ± 8 s) was slower ( P < 0.01) than that for HHb (10 ± 3 s). The TDHHb before an increase in HHb was 13 ± 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 V̇o2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.


2010 ◽  
Vol 108 (6) ◽  
pp. 1641-1650 ◽  
Author(s):  
Lisa M. K. Chin ◽  
George J. F. Heigenhauser ◽  
Donald H. Paterson ◽  
John M. Kowalchuk

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (V̇o2p) and leg femoral conduit artery (“bulk”) blood flow (LBF) during moderate-intensity exercise (Mod) was examined in eight young male adults. Subjects completed four to six repetitions of alternate-leg knee-extension exercise during normal breathing [Con; end-tidal partial pressure of CO2 (PetCO2) ∼40 mmHg] and sustained hyperventilation (Hypo; PetCO2 ∼20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold). V̇o2p was measured breath by breath by mass spectrometry and volume turbine, and LBF (calculated from mean femoral artery blood velocity and femoral artery diameter) was measured simultaneously by Doppler ultrasound. Concentration changes of deoxy (Δ[HHb])-, oxy (Δ[O2Hb])-, and total hemoglobin-myoglobin (Δ[HbTot]) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). The kinetics of V̇o2p, LBF, and Δ[HHb] were modeled using a monoexponential equation by nonlinear regression. The time constants for the phase 2 V̇o2p (Hypo, 49 ± 26 s; Con, 28 ± 8 s) and LBF (Hypo, 46 ± 16 s; Con, 23 ± 6 s) were greater ( P < 0.05) in Hypo compared with Con. However, the mean response time for the overall Δ[HHb] response was not different between conditions (Hypo, 23 ± 5 s; Con, 24 ± 3 s), whereas the Δ[HHb] amplitude was greater ( P < 0.05) in Hypo (8.05 ± 7.47 a.u.) compared with Con (6.69 ± 6.31 a.u.). Combined, these results suggest that hyperventilation-induced hypocapnic alkalosis is associated with slower convective (i.e., slowed femoral artery and microvascular blood flow) and diffusive (i.e., greater fractional O2 extraction for a given ΔV̇o2p) O2 delivery, which may contribute to the hyperventilation-induced slowing of V̇o2p (and muscle O2 utilization) kinetics.


Author(s):  
Norita Gildea ◽  
Adam McDermott ◽  
Joel Rocha ◽  
Donal O'Shea ◽  
Simon Green ◽  
...  

We assessed the time course of changes in oxygen uptake (V̇O2) and muscle deoxygenation (i.e., deoxygenated haemoglobin and myoglobin, [HHb+Mb]) kinetics during transitions to moderate-intensity cycling following 12-weeks of low-volume high-intensity interval training (HIIT) vs. moderate-intensity continuous training (MICT) in adults with type 2 diabetes (T2D). Participants were randomly assigned to MICT (n=10, 50 min of moderate-intensity cycling), HIIT (n=9, 10x1 min at ~90% maximal heart rate) or non-exercising control (n=9) groups. Exercising groups trained 3 times per week and measurements were taken every 3 weeks. [HHb+Mb] kinetics were measured by near-infrared spectroscopy at the vastus lateralis muscle. The local matching of O2 delivery to O2 utilization was assessed by the Δ[HHb+Mb]/ΔV̇O2ratio. The pretraining time constant of the primary phase of V̇O2 (τV̇O2p ) decreased (P<0.05) at wk 3 of training in both MICT (from 44±12 to 32±5 s) and HIIT (from 42±8 to 32 ± 4 s) with no further changes thereafter; while no changes were reported in controls. The pretraining overall dynamic response of muscle deoxygenation (τ'[HHb+Mb]) was faster than τV̇O2p in all groups, resulting in Δ[HHb+Mb]/V̇O2p showing a transient "overshoot" relative to the subsequent steady-state level. After 3 wks, the Δ[HHb+Mb]/V̇O2p overshoot was eliminated only in the training groups, so that τ'[HHb+Mb] was not different to τV̇O2p in MICT and HIIT. The enhanced V̇O2 kinetics response consequent to both MICT and HIIT in T2D was likely attributed to a training-induced improvement in matching of O2 delivery to utilization.


1999 ◽  
Vol 86 (2) ◽  
pp. 687-693 ◽  
Author(s):  
Maureen J. MacDonald ◽  
Mark A. Tarnopolsky ◽  
Howard J. Green ◽  
Richard L. Hughson

We hypothesized that near-infrared spectroscopy (NIRS) measures of hemoglobin and/or myoglobin O2 saturation (IR-So 2) in the vascular bed of exercising muscle would parallel changes in femoral venous O2 saturation (S[Formula: see text]) at the onset of leg-kicking exercise in humans. Six healthy subjects performed transitions from rest to 48 ± 3 (SE)-W two-legged kicking exercise while breathing 14, 21, or 70% inspired O2. IR-So 2 was measured over the vastus lateralis muscle continuously during all tests, and femoral venous and radial artery blood samples were drawn simultaneously during rest and during 5 min of exercise. In all gas-breathing conditions, there was a rapid decrease in both IR-So 2 and SfvO2 at the onset of moderate-intensity leg-kicking exercise. Although SfvO2 remained at low levels throughout exercise, IR-So 2increased significantly after the first minute of exercise in both normoxia and hyperoxia. Contrary to the hypothesis, these data show that NIRS does not provide a reliable estimate of hemoglobin and/or O2 saturation as reflected by direct femoral vein sampling.


2016 ◽  
Vol 311 (6) ◽  
pp. H1530-H1539 ◽  
Author(s):  
Victor M. Niemeijer ◽  
Ruud F. Spee ◽  
Thijs Schoots ◽  
Pieter F. F. Wijn ◽  
Hareld M. C. Kemps

The extent and speed of transient skeletal muscle deoxygenation during exercise onset in patients with chronic heart failure (CHF) are related to impairments of local O2 delivery and utilization. This study examined the physiological background of submaximal exercise performance in 19 moderately impaired patients with CHF (Weber class A, B, and C) compared with 19 matched healthy control (HC) subjects by measuring skeletal muscle oxygenation (SmO2) changes during cycling exercise. All subjects performed two subsequent moderate-intensity 6-min exercise tests (bouts 1 and 2) with measurements of pulmonary oxygen uptake kinetics and SmO2 using near-infrared spatially resolved spectroscopy at the vastus lateralis for determination of absolute oxygenation values, amplitudes, kinetics (mean response time for onset), and deoxygenation overshoot characteristics. In CHF, deoxygenation kinetics were slower compared with HC (21.3 ± 5.3 s vs. 16.7 ± 4.4 s, P < 0.05, respectively). After priming exercise (i.e., during bout 2), deoxygenation kinetics were accelerated in CHF to values no longer different from HC (16.9 ± 4.6 s vs. 15.4 ± 4.2 s, P = 0.35). However, priming did not speed deoxygenation kinetics in CHF subjects with a deoxygenation overshoot, whereas it did reduce the incidence of the overshoot in this specific group ( P < 0.05). These results provide evidence for heterogeneity with respect to limitations of O2 delivery and utilization during moderate-intensity exercise in patients with CHF, with slowed deoxygenation kinetics indicating a predominant O2 utilization impairment and the presence of a deoxygenation overshoot, with a reduction after priming in a subgroup, indicating an initial O2 delivery to utilization mismatch.


2012 ◽  
Vol 303 (8) ◽  
pp. R815-R823 ◽  
Author(s):  
Juan M. Murias ◽  
Matthew D. Spencer ◽  
Silvia Pogliaghi ◽  
Donald H. Paterson

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.


2013 ◽  
Vol 38 (2) ◽  
pp. 154-160 ◽  
Author(s):  
Shilpa Dogra ◽  
Matthew D. Spencer ◽  
Juan M. Murias ◽  
Donald H. Paterson

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.


2001 ◽  
Vol 280 (4) ◽  
pp. E669-E675 ◽  
Author(s):  
Mark Bruce ◽  
Dumitru Constantin-Teodosiu ◽  
Paul L. Greenhaff ◽  
Leslie H. Boobis ◽  
Clyde Williams ◽  
...  

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine α-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ∼70% maximal O2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wtl-(+)-ornithine α-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt l-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (ΣTCAI; citrate, malate, fumarate, and succinate, ∼85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, ΣTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 ± 0.61) than in the CON condition (3.74 ± 0.38, P < 0.05) and the OKG condition (3.85 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced ( P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of α-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.


2012 ◽  
Vol 113 (9) ◽  
pp. 1466-1475 ◽  
Author(s):  
Braden M. R. Gravelle ◽  
Juan M. Murias ◽  
Matthew D. Spencer ◽  
Donald H. Paterson ◽  
John M. Kowalchuk

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.


2012 ◽  
Vol 112 (6) ◽  
pp. 1023-1032 ◽  
Author(s):  
Matthew D. Spencer ◽  
Juan M. Murias ◽  
Tyler M. Grey ◽  
Donald H. Paterson

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.


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