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]/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 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]/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). 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]/VO₂ 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 O₂ delivery limitation; and (3) that increasing Mod WR increments elicits an increased functional G, regardless of the τVO_2p response.     

Cerebral oxygenation during the Richalet hypoxia sensitivity test and cycling time-trial performance in severe hypoxia

Background

The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to acute hypoxia during exercise at an intensity corresponding to a heart rate of ~130 bpm in normoxia, can predict susceptibility of altitude sickness. Its ability to predict exercise performance in hypoxia is unknown.

Objectives

Investigate: (1) whether cerebral blood flow (CBF) and cerebral tissue oxygenation (O₂Hb; oxygenated hemoglobin, HHb; deoxygenated hemoglobin) responses during RT predict time-trial cycling (TT) performance in severe hypoxia; (2) if subjects with blunted cardiorespiratory responses during RT show greater impairment of TT performance in severe hypoxia.

Study design

Thirteen men [27 ± 7 years (mean ± SD), Wmax: 385 ± 30 W] were evaluated with RT and the results related to two 15 km TT, in normoxia and severe hypoxia (FIO₂ = 0.11).

Results

During RT, mean middle cerebral artery blood velocity (MCAv: index of CBF) was unaltered with hypoxia at rest (p > 0.05), while it was increased during normoxic (+22 ± 12 %, p < 0.05) and hypoxic exercise (+33 ± 17 %, p < 0.05). Resting hypoxia lowered cerebral O₂Hb by 2.2 ± 1.2 μmol (p < 0.05 vs. resting normoxia); hypoxic exercise further lowered it to ?7.6 ± 3.1 μmol below baseline (p < 0.05). Cerebral HHb, increased by 3.5 ± 1.8 μmol in resting hypoxia (p < 0.05), and further to 8.5 ± 2.9 μmol in hypoxic exercise (p < 0.05). Changes in CBF and cerebral tissue oxygenation during RT did not correlate with TT performance loss (R = 0.4, p > 0.05 and R = 0.5, p > 0.05, respectively), while tissue oxygenation and SaO₂ changes during TT did (R = ?0.76, p < 0.05). Significant correlations were observed between SaO₂, MCAv and HHb during RT (R = ?0.77, ?0.76 and 0.84 respectively, p < 0.05 in all cases).

Conclusions

CBF and cerebral tissue oxygenation changes during RT do not predict performance impairment in hypoxia. Since the changes in SaO₂ and brain HHb during the TT correlated with performance impairment, the hypothesis that brain oxygenation plays a limiting role for global exercise in conditions of severe hypoxia remains to be tested further.     

Speeding of VO2 kinetics in response to endurance-training in older and young women

The goal of this study was to examine the time-course of changes in oxygen uptake kinetics (??VO_2p) during step-transitions from 20?W to moderate-intensity cycling in response to endurance-training in older (O) and young (Y) women. Six O (69?±?7?years) and 8 Y (25?±?5?years) were tested pre-training, and at 3, 6, 9, and 12?weeks of training. VO_2p was measured breath-by-breath using a mass spectrometer. Changes in deoxygenated-hemoglobin concentration of the vastus lateralis (?[HHb]) were measured by near-infrared spectroscopy in Y (but this was not possible in O). VO_2p and ?[HHb] were modeled with a mono-exponential. Training was performed on a cycle-ergometer three times per week for 45?min at ~70% of VO_2peak. Pre-training ??VO_2p was greater (p?<?0.05) in O (55?±?16?s) than Y (31?±?8?s). After 3?weeks training, ??VO_2p decreased (p?<?0.05) in both O (35?±?12?s) and Y (22?±?4?s). A pre-training ??overshoot?? in the normalized ?[HHb]/VO_2p ratio relative to the subsequent steady-state level (interpreted as a mismatch of local O₂ delivery to muscle VO₂) was observed in Y. Three weeks of training resulted in that ??overshoot?? being abolished. Thus there was a training-induced speeding of VO₂ kinetics in O and Y. In the Y this appeared to be the result of improved matching of local O₂ delivery to muscle VO₂. In O, inadequate systemic O₂ distribution (as indirectly expressed by the arterial-venous O₂ difference/VO_2p ratio) seemed to play a role for the initial slower rate of adjustment in VO_2p.     

Kinetics of VO2 limb blood flow and regional muscle deoxygenation in young adults during moderate intensity, knee-extension exercise

The kinetics of pulmonary O₂ uptake ( [(V)\dot]\textO _2 \textp ), \left( {\dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} } \right), limb blood flow (LBF) and deoxygenation (ΔHHb) of the vastus lateralis (VL) and vastus medialis (VM) muscles during the transition to moderate-intensity knee-extension exercise (MOD) was examined. Seven males (27 ± 5 years; mean ± SD) performed repeated step transitions (n = 4) from passive exercise to MOD. Breath by breath [(V)\dot]\textO _2 \textp , \dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} , femoral artery LBF, and VL and VM muscle ∆HHb were measured, respectively, by mass spectrometer and volume turbine, Doppler ultrasound and near-infrared spectroscopy. Phase 2 [(V)\dot]\textO _2 \textp , \dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} , LBF, and ∆HHb data were fit with a mono-exponential model. The time constant (τ) of the [(V)\dot]\textO _2 \textp \dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} and LBF response were not different ( t[(V)\dot]\textO _2 \textp , \tau \dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} , 24 ± 6 s; τLBF, 23 ± 8 s). The ∆HHb response did not differ between VL and VM in amplitude (VL 6.97 ± 4.22 a.u.; VM 7.24 ± 3.99 a.u.), time delay (∆HHb_TD: VL 17 ± 2 s; VM 15 ± 1 s), time constant (τ∆HHb: VL 11 ± 6 s; VM 13 ± 4 s), or effective time constant [τ′∆HHb (= ∆HHb_TD + τ∆HHb): VL 28 ± 7 s; VM 28 ± 4 s]. Adjustments in ∆HHb in VL and VM depict a similar balance of regional O₂ delivery and utilization within the quadriceps muscle group. The τ′∆HHb and t[(V)\dot]\textO _2 \textp \tau \dot{V}{{{\text{O}}_{{ 2\,{\text{p}}}} }} were similar, however, the ∆HHb displayed an “overshoot” relative to the steady-state levels reflecting a slower alteration of microvascular blood flow (O₂ delivery) relative to O₂ utilization, necessitating a greater reliance on O₂ extraction.     

Are the parameters of VO2, heart rate and muscle deoxygenation kinetics affected by serial moderate-intensity exercise transitions in a single day?

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 (CI₉₅) 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 CI₉₅ 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 CI₉₅, was appreciably improved by averaging of at least three MODs.     

Muscle deoxygenation to VO₂ relationship differs in young subjects with varying τVO₂

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 O₂ distribution to O₂ 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 τVO₂ 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 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.     

Influence of cerebral and muscle oxygenation on repeated-sprint ability

The study examined the influence of cerebral (prefrontal cortex) and muscle (vastus lateralis) oxygenation on the ability to perform repeated, cycling sprints. Thirteen team-sport athletes performed ten, 10-s sprints (with 30 s of rest) under normoxic (F_IO₂ 0.21) and acute hypoxic (F_IO₂ 0.13) conditions in a randomised, single-blind fashion and crossover design. Mechanical work was calculated and arterial O₂ saturation (S_pO₂) was estimated via pulse oximetry for every sprint. Cerebral and muscle oxy-(O₂Hb), deoxy-(HHb), and total haemoglobin (THb) were monitored continuously by near-infrared spectroscopy. Compared with normoxia, hypoxia induced larger decrements in S_pO₂ and work (11.6 and 7.6%, respectively; P < 0.05). In the muscle, we observed a fairly constant level of deoxygenation across sprints, with no effect of the condition. In normoxia, regional cerebral oxygenation increased during the first two sprints and slightly fluctuated thereafter. In contrast, this initial cerebral hyper-oxygenation was attenuated in hypoxia. Changes in [O₂Hb] and [HHb] occurred earlier and were larger in hypoxia compared with normoxia (P < 0.05), while regional blood volume (Δ[THb]) remained unaffected by the condition. Changes in cerebral [HHb] and mechanical work were strongly correlated in normoxia and hypoxia (R ² = 0.81 and R ² = 0.85, respectively; P < 0.05), although the slope of this relationship differed (normoxia, −351.3 ± 183.3 vs. hypoxia, −442.4 ± 227.2; P < 0.05). The results of this NIRS study show that O₂ availability influences prefrontal cortex, but not muscle, oxygenation during repeated, short sprints. By using a hypoxia paradigm, the study suggests that cerebral oxygenation contributes to the impairment of repeated-sprint ability.     

Effects of hypoxia on cerebral and muscle haemodynamics during knee extensions in healthy subjects

A hypoxic model was used to investigate changes in localized cerebral and muscle haemodynamics during knee extension (KE) in healthy individuals. Thirty-one young healthy volunteers performed one set of KE until failure under hypoxia (14 % O₂) or normoxia (21 % O₂) at 50, 75 or 100 % of 1 repetition maximum, in random order, on three occasions. Prefrontal cerebral and vastus lateralis muscle oxygenation and blood volume (Cox, Mox, Cbv and Mbv, respectively) were recorded simultaneously by near-infrared spectroscopy. Hypoxia induced significant declines in Cox [?0.017 ± 0.016 optical density (OD) units] and Mox (?0.014 ± 0.026 OD units) and increases in Cbv (0.017 ± 0.027 OD units) and Mbv (0.016 ± 0.023 OD units) at rest. Hypoxia significantly reduced total work (TW) performed during KE at each exercise intensity. Cox, Cbv, Mox, and Mbv changes during KE did not differ between normoxia and hypoxia. Correlations between TW done and Cox changes under normoxia (r = 0.04, p = 0.182) and hypoxia (r = 0.05, p = 0.122) were not significant. However, TW was significantly correlated with Mox under both normoxia (R ² = 0.24, p = 0.000) and hypoxia (R ² = 0.15, p = 0.004). Since changes in Cox and Mox reflect alterations in the balance between oxygen delivery and extraction in these tissues, which, in the brain, is an index of neuronal activation, we conclude that: (1) limitation of KE performance was mediated peripherally under both normoxia and hypoxia, with no additional effect of hypoxia, and (2) because of the low common variance with Mox additional intramuscular factors likely play a role in limiting KE performance.     

The effects of recreational sport on VO2peak, VO2 kinetics and submaximal exercise performance in males and females

The purpose of the present study was to examine changes in VO_2peak, VO₂ kinetics and steady-state exercise performance following 4 weeks of participation in recreational sport. Subjects (male n = 8, female n = 9) participated in recreational sport (basketball, floor hockey and soccer) four times per week for 4 weeks. Both before and after training, VO_2peak was measured on a cycle ergometer, VO₂ kinetics was determined as the average of three transitions to 80 W, and heart rate (HR) and respiratory exchange ratio (RER) were measured during 60 min at a work rate corresponding to 50 % of pre-training VO_2peak. HR was also monitored during all training sessions. After training, VO_2peak was increased in females, but not males, while VO₂ kinetics (τVO₂) were sped in both males and females. HR during constant load exercise was reduced in both males and females, but exercise RER was only reduced in females. Mean HR during participation in sport was higher in males than females and higher during basketball than both floor hockey and soccer. These results demonstrate that training adaptations traditionally associated with endurance exercise can also be obtained through regular participation in recreational sport.     

Haemodynamic responses to dehydration in the resting and exercising human leg

Dehydration and hyperthermia reduces leg blood flow (LBF), cardiac output ( $ \dot{Q} $ ) and arterial pressure during whole-body exercise. It is unknown whether the reductions in blood flow are associated with dehydration-induced alterations in arterial blood oxygen content (C _aO₂) and O₂-dependent signalling. This study investigated the impact of dehydration and concomitant alterations in C _aO₂ upon LBF and $ \dot{Q} $ . Haemodynamics, arterial and femoral venous blood parameters and plasma [ATP] were measured at rest and during one-legged knee-extensor exercise in 7 males in four conditions: (1) control, (2) mild dehydration, (3) moderate dehydration, and (4) rehydration. Relative to control, C _aO₂ and LBF increased with dehydration at rest and during exercise (C _aO₂: from 199 ± 1 to 208 ± 2, and 202 ± 2 to 210 ± 2 ml L^?1 and LBF: from 0.38 ± 0.04 to 0.77 ± 0.09, and 1.64 ± 0.09 to 1.88 ± 0.1 L min^?1, respectively). Similarly, $ \dot{Q} $ was unchanged or increased with dehydration at rest and during exercise, whereas arterial and leg perfusion pressures declined. Following rehydration, C _aO₂ declined (to 193 ± 2 mL L^?1) but LBF remained elevated. Alterations in LBF were unrelated to C _aO₂ (r ² = 0.13–0.27, P = 0.48–0.64) and plasma [ATP]. These findings suggest dehydration and concomitant alterations in C _aO₂ do not compromise LBF despite reductions in plasma [ATP]. While an additive or synergistic effect cannot be excluded, reductions in LBF during exercise with dehydration may not necessarily be associated with alterations in C _aO₂ and/or intravascular [ATP].     

Pulmonary O₂ uptake and muscle deoxygenation kinetics are slowed in the upper compared with lower region of the moderate-intensity exercise domain in older men

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; p < 0.05). The O₂ deficit was greater in US (0.25 ± 0.08 L) than LS (0.19 ± 0.06 L); yet the ‘accumulated O₂ deficit’ (0.44 ± 0.13 L; O₂ 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; p < 0.05), suggesting that the slowed adjustment of muscle O₂ extraction was associated with the slowed VO₂ 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 O₂ deficit. This slowing in US compared to LS does not appear to be related to local O₂ availability.     

Differences in exercise limb blood flow and muscle deoxygenation with age: contributions to O2 uptake kinetics

The adjustments of pulmonary oxygen uptake $ \left( {\mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} } \right), $ limb blood flow (LBF) and muscle deoxygenation (ΔHHb) were examined during transitions to moderate-intensity, knee-extension exercise in seven older (OA; 71 ± 7 year) and seven young (YA; 26 ± 3 year) men. YA and OA performed repeated step transitions from an active baseline (3 W; 100 g) to a similar relative intensity of ~80% estimated lactate threshold (θ_L), and YA also performed the same absolute work rate as the OA (24 W, 800 g). Breath-by-breath $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} , $ femoral artery LBF (Doppler ultrasound) and muscle HHb (near-infrared spectroscopy) were measured. Phase 2 $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} , $ LBF, and ΔHHb data were fit with a mono-exponential model. $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ was greater in OA (58 ± 21 s) than YA_80% (31 ± 9 s) and YA_24W (29 ± 11 s). The increase in LBF per increase in $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ was not different between groups (5.3–5.8 L min^?1/L min^?1); however, the τLBF was greater in OA (44 ± 19 s) than YA_24W (18 ± 7 s). The overall adjustment in ΔHHb (τ′ΔHHb) was not different between OA and YA, but was faster than $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ in OA. This faster τ′ΔHHb than $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ resulted in an “overshoot” of the normalized $ \Updelta {\text{HHb}}/\Updelta\mathop{{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ response relative to the steady state level that was significantly greater in OA compared with YA suggesting that the adjustment of microvascular blood flow is slowed in OA thereby requiring a greater reliance on O₂ extraction during the transition to exercise.     

The sustainability of VO2max: effect of decreasing the workload

The study examined the maintenance of VO_2max using VO_2max as the controlling variable instead of power. Therefore, ten subjects performed three exhaustive cycling exercise bouts: (1) an incremental test to determine VO_2max and the minimal power at VO_2max (PVO_max), (2) a constant-power test at PVO_max and (3) a variable-power test (VPT) during which power was varied to control VO₂ at VO_2max. Stroke volume (SV) was measured by impedance in each test and the stroke volume reserve was calculated as the difference between the maximal and the average 5-s SV. Average power during VPT was significantly lower than PVO_max (238 ± 79 vs. 305 ± 86 W; p < 0.0001). All subjects, regardless of their VO_2max values and/or their ability to achieve a VO_2max plateau during incremental test, were able to sustain VO_2max for a significantly longer time during VPT compared to constant-power test (CPT) (958 ± 368 s vs. 136 ± 81 s; p < 0.0001). Time to exhaustion at VO_2max during VPT was correlated with the power drop in the first quarter of the time to exhaustion at VO_2max (r = 0.71; p < 0.02) and with the stroke volume reserve (r = 0.70, p = 0.02) but was not correlated with VO_2max. This protocol, using VO_2max rather than power as the controlling variable, demonstrates that the maintenance of exercise at VO_2max can exceed 15 min independent of the VO_2max value, suggesting that the ability to sustain exercise at VO_2max has different limiting factors than those related to the VO_2max value.     

The effect of acute exercise in hypoxia on flow-mediated vasodilation

The purpose of this study was to clarify the effect of acute exercise in hypoxia on flow-mediated vasodilation (FMD). Eight males participated in this study. Two maximal exercise tests were performed using arm cycle ergometry to estimate peak oxygen uptake $ \left( {\dot{V}{\text{O}}_{{ 2 {\text{peak}}}} } \right) $ while breathing normoxic [inspired O₂ fraction (FIO₂) = 0.21] or hypoxic (FIO₂ = 0.12) gas mixtures. Next, subjects performed submaximal exercise at the same relative exercise intensity $ \left( {30\,\% \;\dot{V}{\text{O}}_{{ 2 {\text{peak}}}} } \right) $ in normoxia or hypoxia for 30 min. Before (Pre) and after exercise (Post 5, 30, and 60 min), brachial artery FMD was measured during reactive hyperemia by ultrasound under normoxic conditions. FMD was estimated as the percent (%) rise in the peak diameter from the baseline value at prior occlusion at each FMD measurement (%FMD). The area under the curve for the shear rate stimulus (SR_AUC) was calculated in each measurement, and each %FMD value was normalized to SR_AUC (normalized FMD). %FMD and normalized FMD decreased significantly (P < 0.05) immediately after exercise in both condition (mean ± SE, FMD, normoxic trial, Pre: 8.85 ± 0.58 %, Post 5: ?0.01 ± 1.30 %, hypoxic trial, Pre: 8.84 ± 0.63 %, Post 5: 2.56 ± 0.83 %). At Post 30 and 60, %FMD and normalized FMD returned gradually to pre-exercise levels in both trials (FMD, normoxic trial, Post 30: 1.51 ± 0.68 %, Post 60: 2.99 ± 0.79 %; hypoxic trial, Post 30: 4.57 ± 0.78 %, Post 60: 6.15 ± 1.20 %). %FMD and normalized FMD following hypoxic exercise (at Post 5, 30, and 60) were significantly (P < 0.05) higher than after normoxic exercise. These results suggest that aerobic exercise in hypoxia has a significant impact on endothelial-mediated vasodilation.     

Heterogeneity of muscle deoxygenation kinetics during two bouts of repeated heavy exercises

This study examines the effect of prior heavy exercise on the spatial distribution of muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Young untrained male adults (n = 16) performed two consecutive bouts of 6 min of high intensity cycle exercise separated by 6 min at 35 W. Muscle deoxygenation (HHb) was monitored continuously by near-infrared spectroscopy at eight sites in the quadriceps. Prior heavy exercise reduced the delay before the increase in HHb (9 ± 2 vs. 5 ± 2 s; P < 0.001). The standard deviation of TD HHb of the eight sites was decreased by the performance of prior exercise (1.1 ± 0.5 vs. 0.8 ± 0.4 s; P < 0.05). The transient decrease in HHb during the first 10 s of exercise was less during the second bout than during the first bout (0.6 ± 0.6 vs. 0.3 ± 0.3 A.U.; P < 0.01). The standard deviation of this decrease was also reduced by prior exercise (0.5 ± 0.3 vs. 0.3 ± 0.2 A.U.; P < 0.01). Lastly, prior exercise decreased significantly the standard deviation of the HHb rise during the time period corresponding to the pulmonary [(V)\dot] \dot{V} O₂ slow component. These results indicate that prior heavy exercise reduced the spatial heterogeneity of muscle deoxygenation kinetics at the early onset of heavy exercise and during the development of the pulmonary [(V)\dot] \dot{V} O₂ slow component. It indicates that the distribution of the [(V)\dot] \dot{V} O₂/O₂ delivery ratio within muscle was improved by the performance of a prior exercise.     

Low total haemoglobin mass, blood volume and aerobic capacity in men with type 1 diabetes

Blood O₂ carrying capacity affects aerobic capacity (VO_2max). Patients with type 1 diabetes have a risk for anaemia along with renal impairment, and they often have low VO_2max. We investigated whether total haemoglobin mass (tHb-mass) and blood volume (BV) differ in men with type 1 diabetes (T1D, n = 12) presently without complications and in healthy men (CON, n = 23) (age-, anthropometry-, physical activity-matched), to seek an explanation for low VO_2max. We determined tHb-mass, BV, haemoglobin concentration ([Hb]), and VO_2max in T1D and CON. With similar (mean ± SD) [Hb] (144 vs. 145 g l^?1), T1D had lower tHb-mass (10.1 ± 1.4 vs. 11.0 ± 1.1 g kg^?1, P < 0.05), BV (76.8 ± 9.5 vs. 83.5 ± 8.3 ml kg^?1, P < 0.05) and VO_2max (35.4 ± 4.8 vs. 44.9 ± 7.5 ml kg^?1 min^?1, P < 0.001) than CON. VO_2max correlated with tHb-mass and BV both in T1D (r = 0.71, P < 0.01 and 0.67, P < 0.05, respectively) and CON (r = 0.54, P < 0.01 and 0.66, P < 0.001, respectively), but not with [Hb]. Linear regression slopes were shallower in T1D than CON both between VO_2max and tHb-mass (2.4 and 3.6 ml kg^?1 min^?1 vs. g kg^?1, respectively) and VO_2max and BV (0.3 and 0.6 ml kg^?1 min^?1 vs. g kg^?1, respectively), indicating that T1D were unable to reach similar VO_2max than CON at a given tHb-mass and BV. In conclusion, low tHb-mass and BV partly explained low VO_2max in T1D and may provide early and more sensitive markers of blood O₂ carrying capacity than [Hb] alone.     

Oxygen uptake, cardiac output and muscle deoxygenation at the onset of moderate and supramaximal exercise in humans

[(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} , [(Q)\dot] \dot{Q} and muscular deoxyhaemoglobin (HHb) kinetics were determined in 14 healthy male subjects at the onset of constant-load cycling exercise performed at 80% of the ventilatory threshold (80%_VT) and at 120% of [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max } (120%_Wmax). An innovative approach was applied to calculate the time constant (τ₂) of the primary phase of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} and [(Q)\dot] \dot{Q} kinetics at 120%_Wmax. Data were linearly interpolated after a semilogarithmic transformation of the difference between required/steady state and measured values. Furthermore, [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} , \mathop Q ^· \mathop Q\limits^{ \cdot } and HHb data were fitted with traditional exponential models. τ₂ of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics was longer (62.5 ± 20.9 s) at 120%_Wmax than at 80%_VT (27.8 ± 10.4 s). The τ₂ of [(Q)\dot] \dot{Q} kinetics was unaffected by exercise intensity and, at 120% of [(V)\dot]\textO_2max , \dot{V}{\text{O}}_{2\max } , it was significantly faster (τ₂ = 35.7 ± 28.4 s) than that of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} response. The time delay of HHb kinetics was shorter (4.3 ± 1.7 s) at 120%_Wmax than at 80%_VT (8.5 ± 2.6 s) suggesting a larger mismatch between O₂ uptake and delivery at 120%_Wmax. These results suggest that [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} at the onset of exercise is not regulated/limited by muscle’s O₂ utilisation and that a slower adaptation of capillary perfusion may cause the deceleration of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics observed during supramaximal exercise.     

Warm-up effects on muscle oxygenation, metabolism and sprint cycling performance

To investigate the effects of warm-up intensity on all-out sprint cycling performance, muscle oxygenation and metabolism, 8 trained male cyclists/triathletes undertook a 30-s sprint cycling test preceded by moderate, heavy or severe warm up and 10-min recovery. Muscle oxygenation was measured by near-infrared spectroscopy, with deoxyhaemoglobin ([HHb]) during the sprint analysed with monoexponential models with time delay. Aerobic, anaerobic-glycolytic and phosphocreatine energy provision to the sprint were estimated from oxygen uptake and lactate production. Immediately prior to the sprint, blood [lactate] was different for each warm up and higher than resting for the heavy and severe warm ups (mod. 0.94 ± 0.36, heavy 1.92 ± 0.64, severe 4.37 ± 0.93 mmol l^?1 P < 0.05), although muscle oxygenation was equally raised above rest. Mean power during the sprint was lower following severe compared to moderate warm up (mod. 672 ± 54, heavy 666 ± 56, severe 655 ± 59 W, P < 0.05). The [HHb] kinetics during the sprint were not different among conditions, although the time delay before [HHb] increased was shorter for severe versus moderate warm up (mod. 5.8 ± 0.6, heavy 5.6 ± 0.9, severe 5.2 ± 0.7 s, P < 0.05). The severe warm up was without effect on estimated aerobic metabolism, but increased estimated phosphocreatine hydrolysis, the latter unable to compensate for the reduction in estimated anaerobic-glycolytic metabolism. It appears that despite all warm ups equally increasing muscle oxygenation, and indicators of marginally faster oxygen utilisation at the start of exercise following a severe-intensity warm up, other energy sources may not be able to fully compensate for a reduced glycolytic rate in sprint exercise with potential detrimental effects on performance.     

Maximal strength,power, and aerobic endurance adaptations to concurrent strength and sprint interval training

Purpose

This study was designed to examine whether concurrent sprint interval and strength training (CT) would result in compromised strength development when compared to strength training (ST) alone. In addition, maximal oxygen consumption (VO₂max) and time to exhaustion (TTE) were measured to determine if sprint interval training (SIT) would augment aerobic performance.

Methods

Fourteen recreationally active men completed the study. ST (n = 7) was performed 2 days/week and CT (n = 7) was performed 4 days/week for 12 weeks. CT was separated by 24 h to reduce the influence of acute fatigue. Body composition was analyzed pre- and post-intervention. Anaerobic power, one-repetition maximum (1RM) lower- and upper-body strength, VO₂max and TTE were analyzed pre-, mid-, and post-training. Training intensity for ST was set at 85 % 1RM and SIT trained using a modified Wingate protocol, adjusted to 20 s.

Results

Upper- and lower-body strength improved significantly after training (p < 0.001) with no difference between the groups (p > 0.05). VO₂max increased 40.9 ± 8.4 to 42.3 ± 7.1 ml/kg/min (p < 0.05) for CT, whereas ST remained unchanged. A significant difference in VO₂max (p < 0.05) was observed between groups post-intervention (CT: 42.3 ± 7.1 vs. ST: 36.0 ± 3.0 ml/kg/min). A main effect for time and group was observed in TTE (p < 0.05). A significant main effect for time was observed in average power (p < 0.05).

Conclusion

Preliminary findings suggest that performing concurrent sprint interval and strength training does not attenuate the strength response when compared to ST alone, while also improves aerobic performance measures, such as VO₂max at the same time.     

Retrograde blood flow in the inactive limb is enhanced during constant-load leg cycling in hypoxia

Purpose

This study aimed to elucidate the effects of hypoxia on the pattern of oscillatory blood flow in the inactive limb during constant-load dynamic exercise. We hypothesised that retrograde blood flow in the brachial artery of the inactive limb would increase during constant-load leg cycling under hypoxic conditions.

Methods

Three maximal exercise tests were conducted in eight healthy males on a semi-recumbent cycle ergometer while the subjects breathed a normoxic [inspired oxygen fraction (FIO₂) = 0.209] or two hypoxic gas mixtures (FIO₂ = 0.155 and 0.120). Subjects then performed submaximal exercise at the same relative exercise intensity of 60 % peak oxygen uptake under normoxic or the two hypoxic conditions for 30 min. Brachial artery blood velocity and diameter were recorded simultaneously during submaximal exercise using Doppler ultrasonography.

Results

Antegrade blood flow gradually increased during exercise, with no significant differences among the three trials. Retrograde blood flow showed a biphasic response, with an initial increase followed by a gradual decrease during normoxic exercise. In contrast, retrograde blood flow significantly increased during moderate and severe hypoxic exercise, and remained elevated above normoxic conditions during exercise. At 30 min of exercise, the magnitude of the change in retrograde blood flow during exercise was greater as the level of hypoxia increased (normoxia: ?18.7 ± 23.5 ml min^?1; moderate hypoxia: ?39.3 ± 21.4 ml min^?1; severe hypoxia: ?64.0 ± 36.3 ml min^?1).

Conclusion

These results indicate that moderate and severe hypoxia augment retrograde blood flow in the inactive limb during constant-load dynamic leg exercise.