The effects of breathing a helium–oxygen gas mixture on maximal pulmonary ventilation and maximal oxygen consumption during exercise in acute moderate hypobaric hypoxia

To test the hypothesis that maximal exercise pulmonary ventilation ( $ \dot{V}{\text{E}}_{ \max } $ ) is a limiting factor affecting maximal oxygen uptake ( $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ ) in moderate hypobaric hypoxia (H), we examined the effect of breathing a helium–oxygen gas mixture (He–O₂; 20.9% O₂), which would reduce air density and would be expected to increase $ \dot{V}{\text{E}}_{ \max } $ . Fourteen healthy young male subjects performed incremental treadmill running tests to exhaustion in normobaric normoxia (N; sea level) and in H (atmospheric pressure equivalent to 2,500 m above sea level). These exercise tests were carried out under three conditions [H with He–O₂, H with normal air and N] in random order. $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ and arterial oxy-hemoglobin saturation (SaO₂) were, respectively, 15.2, 7.5 and 4.0% higher (all p < 0.05) with He–O₂ than with normal air ( $ \dot{V}{\text{E}}_{ \max } $ _, 171.9 ± 16.1 vs. 150.1 ± 16.9 L/min; $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ , 52.50 ± 9.13 vs. 48.72 ± 5.35 mL/kg/min; arterial oxyhemoglobin saturation (SaO₂), 79 ± 3 vs. 76 ± 3%). There was a linear relationship between the increment in $ \dot{V}{\text{E}}_{ \max } $ and the increment in $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ in H (r = 0.77; p < 0.05). When subjects were divided into two groups based on their $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ , both groups showed increased $ \dot{V}{\text{E}}_{ \max } $ and SaO₂ in H with He–O₂, but $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ was increased only in the high $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ group. These findings suggest that in acute moderate hypobaric hypoxia, air-flow resistance can be a limiting factor affecting $ \dot{V}{\text{E}}_{ \max } $ ; consequently, $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ is limited in part by $ \dot{V}{\text{E}}_{ \max } $ , especially in subjects with high $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ .     

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 verification phase and reliability of physiological parameters in peak testing of elite wheelchair athletes

The purpose of this study was (1) to examine the value of a verification phase (VER) in a peak testing protocol and (2) to assess the reliability of peak physiological variables in wheelchair athletes. On two separate days, eight tetraplegic (TETRA), eight paraplegic (PARA) and eight non-spinal cord-injured (NON-SCI) athletes performed treadmill ergometry, consisting of a graded exercise test to exhaustion (GXT) followed by a VER. Peak oxygen uptake $ \left( {\dot{V}{\text{O}}_{{ 2 {\text{peak}}}} } \right) $ was compared (1) between GXT and VER and (2) between test days. $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ did not differ between GXT and VER (P = 0.27), and coefficients of variation between GXT and VER were in the range of 2.9 and 6.4 % for all subgroups. Coefficients of variation of $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ between test days were 9.3 % (TETRA), 4.5 % (PARA) and 3.3 % (NON-SCI). It is therefore concluded that whilst a VER can be used for a more robust determination of $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ , a deviation of up to ~6 % between GXT and VER should be considered as acceptable. For between-day analyses, relatively large changes in $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ are required to confirm “true” differences, especially in TETRA athletes. This may be due to their lower aerobic capacity, which results in a larger relative variation compared with the other subgroups.     

Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

Previous studies showed that leptin-deficient (ob/ob) mice develop obesity and impaired ventilatory responses to CO₂ $ \left( {{{\dot{V}}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}}} \right) $ . In this study, we examined if leptin replacement improves chemorespiratory responses to hypercapnia (7?% CO₂) in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system (CNS). $ {\dot{V}_{{{\text{E}}\,}}}{\text{ - C}}{{\text{O}}_{{2}}} $ was measured via plethysmography in obese leptin-deficient- (ob/ob) and wild-type- (WT) mice before and after leptin (10???g/2???l?day) or vehicle (phosphate buffer solution) were microinjected into the fourth ventricle for four consecutive days. Although baseline $ {\dot{V}_{\text{E}}} $ was similar between groups, obese ob/ob mice exhibited attenuated $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ compared to WT mice (134?±?9 versus 196?±?10?ml?min^?1). Fourth ventricle leptin treatment in obese ob/ob mice significantly improved $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ (from 131 ± 15 to 197 ± 10?ml?min^?1) by increasing tidal volume (from 0.38?±?0.03 to 0.55?±?0.02?ml, vehicle and leptin, respectively). Subcutaneous leptin administration at the same dose administered centrally did not change $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in ob/ob mice. Central leptin treatment in WT had no effect on $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ . Since the fourth ventricle leptin treatment decreased body weight in ob/ob mice, we also examined $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in lean pair-weighted ob/ob mice and found it to be impaired compared to WT mice. Thus, leptin deficiency, rather than obesity, is the main cause of impaired $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in ob/ob mice and leptin appears to play an important role in regulating chemorespiratory response by its direct actions on the CNS.     

The validity of the Moxus Modular metabolic system during incremental exercise tests: impacts on detection of small changes in oxygen consumption

Purpose

We investigated the accuracy of the Moxus Modular Metabolic System (MOXUS) against the Douglas Bag Method (DBM) during high-intensity exercise, and whether the two methods agreed when detecting small changes in $\dot{V}{\text{O}}_{2}$ between two consecutive workloads ( $\Delta {\dot{{V}}\text{O}}_{ 2}$ ).

Methods

Twelve trained male runners performed two maximal incremental running tests while gas exchange was analyzed simultaneously by the two systems using a serial setup for four consecutive intervals of 30 s on each test. Comparisons between methods were performed for $\dot{V}{\text{O}}_{2}$ , ${\dot{{V}}}_{\text{E}}$ , fractions of expired O₂ (FeO₂) and CO₂ (FeCO₂) and $\Delta {\dot{{V}}\text{O}}_{ 2}$ .

Results

The MOXUS produced significant higher (mean ± SD, n = 54) readings for $\dot{V}{\text{O}}_{2}$ (80 ± 200 mL min^?1, p = 0.005) and ${\dot{{V}}}_{\text{E}}$ (2.9 ± 4.2 L min^?1, p < 0.0001), but not FeO₂ (?0.01 ± 0.09). Log-transformed 95 % limits of agreement for readings between methods were 94–110 % for $\dot{V}{\text{O}}_{2}$ , 97–108 % for $\dot{V}_{\text{E}}$ and 99–101 % for FeO₂. $\Delta \dot{V}{\text{O}}_{2}$ for two consecutive measurements was not different between systems (120 ± 110 vs. 90 ± 190 mL min^?1 for MOXUS and DBM, respectively, p = 0.26), but agreement between methods was very low (r = 0.25, p = 0.12).

Discussion

Although it was tested during high-intensity exercise and short sampling intervals, the MOXUS performed within the acceptable range of accuracy reported for automated analyzers. Most of the differences between equipments were due to differences in $\dot{V}_{\text{E}}$ . Detecting small changes in $\dot{V}{\text{O}}_{2}$ during an incremental test with small changes in workload, however, might be beyond the equipment’s accuracy.     

Effects of recovery mode (active vs. passive) on performance during a short high-intensity interval training program: a longitudinal study

The aim of this longitudinal study was to compare two recovery modes (active vs. passive) during a seven-week high-intensity interval training program (SWHITP) aimed to improve maximal oxygen uptake ( $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ ), maximal aerobic velocity (MAV), time to exhaustion (t _lim) and time spent at a high percentage of $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ , i.e., above 90 % (t90 $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ ) and 95 % (t95 $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ ) of $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ . Twenty-four adults were randomly assigned to a control group that did not train (CG, n = 6) and two training groups: intermittent exercise (30 s exercise/30 s recovery) with active (IE_A, n = 9) or passive recovery (IE_P, n = 9). Before and after seven weeks with (IE_A and IE_P) or without (CG) high-intensity interval training (HIT) program, all subjects performed a maximal graded test to determine their $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ and MAV. Subsequently only the subjects of IE_A and IE_P groups carried out an intermittent exercise test consisting of repeating as long as possible 30 s intensive runs at 105 % of MAV alternating with 30 s active recovery at 50 % of MAV (IE_A) or 30 s passive recovery (IE_P). Within IE_A and IE_P, mean t _lim and MAV significantly increased between the onset and the end of the SWHITP and no significant difference was found in t90 VO_2max and t95 VO_2max. Furthermore, before and after the SWHITP, passive recovery allowed a longer t _lim for a similar time spent at a high percentage of VO_2max. Finally, within IE_A, but not in IE_P, mean VO_2max increased significantly between the onset and the end of the SWHITP both in absolute (p < 0.01) and relative values (p < 0.05). In conclusion, our results showed a significant increase in VO_2max after a SWHITP with active recovery in spite of the fact that t _lim was significantly longer (more than twice longer) with respect to passive recovery.     

Perceived exertion as a tool to self-regulate exercise in individuals with tetraplegia

The purpose of this investigation was to examine the use of subjective rating of perceived exertion (RPE) as a tool to self-regulate the intensity of wheelchair propulsive exercise in individuals with tetraplegia. Eight motor complete tetraplegic (C5/6 and below; ASIA Impairment Scale = A) participants completed a submaximal incremental exercise test followed by a graded exercise test to exhaustion to determine peak oxygen uptake ( $ \dot{V}O_{{ 2 {\text{peak}}}} $ ) on a wheelchair ergometer. On a separate day, a 20-min exercise bout was completed at an individualised imposed power output (PO) equating to 70 % of $ \dot{V}O_{{ 2 {\text{peak}}}} $ . On a third occasion, participants were instructed to maintain a workload equivalent to the average RPE for the 20-min imposed condition. $ \dot{V}O_{2} $ , heart rate (HR) and PO were measured at 1-min intervals and blood lactate concentration [BLa^?] was measured at 0, 10 and 20 min. No differences (P > 0.17) were found between mean $ \dot{V}O_{2} $ , %  $ \dot{V}O_{{ 2 {\text{peak}}}} $ , HR, % HR_peak, [BLa^?], velocity or PO between the imposed and RPE-regulated trials. No significant (P > 0.05) time-by-trial interaction was present for $ \dot{V}O_{2} $ data. A significant interaction (P < 0.001) for the PO data represented a trend for an increase in PO from 10 min to the end of exercise during the RPE-regulated condition. However, post hoc analysis revealed none of the differences in PO across time were significant (P > 0.05). In conclusion, these findings suggest that RPE can be an effective tool for self-regulating 20 min of wheelchair propulsion in a group of trained participants with tetraplegia who are experienced in wheelchair propulsion.     

Adaptations in muscle metabolic regulation require only a small dose of aerobic-based exercise

This study investigated the hypothesis that the duration of aerobic-based cycle exercise would affect the adaptations in substrate and metabolic regulation that occur in vastus lateralis in response to a short-term (10 day) training program. Healthy active but untrained males (n = 7) with a peak aerobic power ( $ \dot{V}{\text{O}}_{{ 2 {\text{ peak}}}} $ ) of 44.4 ± 1.4 ml kg^?1 min^?1 participated in two different training programs with order randomly assigned (separated by ≥2 weeks). The training programs included exercising at a single intensity designated as light (L) corresponding to 60 % $ \dot{V}{\text{O}}_{{ 2 {\text{ peak}}}} $ , for either 30 or 60 min. In response to a standardized task (60 % $ \dot{V}{\text{O}}_{{ 2 {\text{ peak}}}} $ ), administered prior to and following each training program, L attenuated the decrease (P < 0.05) in phosphocreatine and the increase (P < 0.05) in free adenosine diphosphate and free adenosine monophosphate but not lactate. These effects were not altered by daily training duration. In the case of muscle glycogen, training for 60 versus 30 min exaggerated the increase (P < 0.05) that occurred, an effect that extended to both rest and exercise concentrations. No changes were observed in $ \dot{V}{\text{O}}_{{ 2 {\text{ peak}}}} $ measured during progressive exercise to fatigue or in $ \dot{V}{\text{O}}_{ 2} $ and RER during submaximal exercise with either training duration. These findings indicate that reductions in metabolic strain, as indicated by a more protected phosphorylation potential, and higher glycogen reserves, can be induced with a training stimulus of light intensity applied for as little as 30 min over 10 days. Our results also indicate that doubling the duration of daily exercise at L although inducing increased muscle glycogen reserves did not result in a greater metabolic adaptation.     

Faster \dot{V}{\text{O}}_{ 2} kinetics after eccentric contractions is explained by better matching of O2 delivery to O2 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 ( \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) kinetics during moderate exercise.

Methods

Fourteen males (25 ± 3 year; mean ± SD) completed three step transitions to 90 % θ_L 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 \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) time constant (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) ≤ 25 s (fast group; n = 7) or τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\)  > 25 s (slow group; n = 7). \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) 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). τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was designed to be different (p < 0.05) at Pre between the Fast (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ; 19 ± 4 s) and Slow (32 ± 6 s) groups. There were no differences among time points (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) : 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 τ \(\dot{V}{\text{O}}_{{2{\text{p}}}} \,\) was concomitant with the abolishment (p < 0.05) of an overshoot in the [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio.

Conclusion

We propose that the sped \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) kinetics observed in the Slow group coupled with an improved [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio suggest a better matching of local muscle O₂ delivery to O₂ utilization following eccentric contractions.     

Influence of blood donation on the incidence of plateau at \dot{V}{\text{O}} 2max

Purpose

The purpose of this study was to examine the effects of reductions in blood volume and associated oxygen-carrying capacity on the incidence of plateau at $\dot{V}{\text{O}}$ _2max.

Methods

Fifteen well-trained athletes (age 23.3 ± 4.5; mass 77.4 ± 13.1 kg, height 180.1 ± 6.0 cm) completed three incremental cycle tests to volitional exhaustion, of which the first was defined as familiarisation, with the remaining two trials forming the experimental conditions of pre- (UBL) and post-(BLE) blood donation (~450 cm³). The work rate for the incremental tests commenced at 100 W for 60 s followed by a ramp of 0.42 W s^?1, with cadence being held constant at 80 rpm. Throughout all trials, $\dot{V}{\text{O}}$ ₂ was determined on a breath-by-breath basis using a pre-calibrated metabolic cart. The criteria for plateau determination was a ? $\dot{V}{\text{O}}$ ₂ ≤ 50 ml min^?1 over the final two consecutive 30 s sampling periods.

Results

Despite a significant (P = 0.0028) 9.4 % reduction in haemoglobin concentration and 10.8 % (P = 0.016) reduction in erythrocyte count between UBL and BLE, there was no change in plateau incidence. However, significant differences were observed for both $\dot{V}{\text{O}}$ _2max (P = 0.0059) 51.3 ± 7.6 (UBL) 48.4 ± 7.9 ml kg^?1 min^?1 (BLE) and gas exchange threshold arrival time 383.4 ± 85.2 s (UBL) 349.2 ± 71.4 s (BLE) (P = 0.0028).

Conclusion

These data suggest that plateau at $\dot{V}{\text{O}}$ _2max is unaffected by O₂ availability lending support to the notion of the plateau being dependent on the anaerobic capacity and the classically orientated concept of $\dot{V}{\text{O}}$ _2max.     

Algorithms,modelling and $$ \dot{V}{\text{O}}_{ 2} $$ kinetics

This article summarises the pros and cons of different algorithms developed for estimating breath-by-breath (B-by-B) alveolar O₂ transfer (\( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \)) in humans. \( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \) is the difference between O₂ uptake at the mouth and changes in alveolar O₂ stores (?VO_2s), which for any given breath, are equal to the alveolar volume change at constant \( F_{{{\text{AO}}_{ 2} }} [ (F_{{{\text{A}}i{\text{O}}_{ 2} }} \Updelta {\text{V}}_{{{\text{A}}i}} ) ] \) plus the O₂ alveolar fraction change at constant volume \( [V_{{{\text{A}}i - 1}} (F_{{{\text{A}}i}} -F_{{{\text{A}}i - 1}} )_{{{\text{O}}_{ 2} }} ] \), where V _Ai?1 is the alveolar volume at the beginning of a breath. Therefore, \( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \) can be determined B-by-B provided that V _Ai?1 is: (a) set equal to the subject’s functional residual capacity (algorithm of Auchincloss, A) or to zero; (b) measured (optoelectronic plethysmography, OEP); (c) selected according to a procedure that minimises B-by-B variability (algorithm of Busso and Robbins, BR). Alternatively, the respiratory cycle can be redefined as the time between equal FO₂ in two subsequent breaths (algorithm of Grønlund, G), making any assumption of V _Ai?1 unnecessary. All the above methods allow an unbiased estimate of \( \dot{V}{\text{O}}_{ 2} \) at steady state, albeit with different precision. Yet the algorithms “per se” affect the parameters describing the B-by-B kinetics during exercise transitions. Among these approaches, BR and G, by increasing the signal-to-noise ratio of the measurements, reduce the number of exercise repetitions necessary to study \( \dot{V}{\text{O}}_{ 2} \) kinetics, compared to A approach. OEP and G (though technically challenging and conceptually still debated), thanks to their ability to track ?VO_2s changes during the early phase of exercise transitions, appear rather promising for investigating B-by-B gas exchange.     

Influence of exercise intensity on respiratory muscle fatigue and brachial artery blood flow during cycling exercise

Purpose

During high intensity exercise, both respiratory muscle fatigue and cardiovascular reflexes occur; however, it is not known how inactive limb blood flow is influenced. The purpose of this study was to determine the influence of moderate and high exercise intensity on respiratory muscle fatigue and inactive limb muscle and cutaneous blood flow during exercise.

Methods

Twelve men cycled at 70 and 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) for 20 min. Subjects also performed a second 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test after ingesting 1,800 mg of N-acetylcysteine (NAC), which has been shown to reduce respiratory muscle fatigue (RMF). Maximum inspiratory pressures (P _Imax), brachial artery blood flow (BABF), cutaneous vascular conductance (CVC), and mean arterial pressure were measured at rest and during exercise.

Results

Significant RMF occurred with 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (P _Imax, ?12.8 ± 9.8 %), but not with 70 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (P _Imax, ?5.0 ± 5.9 %). BABF and BA vascular conductance were significantly lower at end exercise of the 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test compared to the 70 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test. CVC during exercise was not different (p > 0.05) between trials. With NAC, RMF was reduced (p < 0.05) and BABF was significantly higher (~30 %) compared to 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (p < 0.05).

Conclusions

These data suggest that heavy whole-body exercise at 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) leads to RMF, decreases in inactive arm blood flow, and vascular conductance, but not cutaneous blood flow.     

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 ( \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) 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 τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) .

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 \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) associated with 90 rpm cycling (40_MATCH); transitions lasted 6 min. \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was measured breath-by-breath using mass spectrometry and turbinometry; vastus lateralis muscle deoxygenation [HHb] was measured using near-infrared spectroscopy. \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) and HHb responses were modeled using nonlinear least squares regression analysis.

Results

\(\dot{V}{\text{O}}_{{2{\text{p}}}}\) at BSL, LS and US was similar for 90 rpm and 40_MATCH, but greater than in 40 rpm. Compared to 90 rpm, τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) 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 40_MATCH, τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) 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 \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) 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) \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) .     

How long does it take to achieve steady state for an accurate assessment of resting \dot{\text{V}}{\text{O}}_{2} in healthy men?

The time necessary to obtain a steady state for an accurate and reliable assessment of resting $ \dot{V}{\text{O}}_{2} $ remains unclear and was the purpose of this study. Thirty healthy men, aged 17–28 years, visited the laboratory twice for the assessment of resting $ \dot{V}{\text{O}}_{2} $ , which was assessed as follows: (a) 24 h abstention from physical exercise, alcohol, soft drinks and caffeine, (b) fasting for at least 8 h, (c) an acclimation period of 10 min, and (d) 60 min assessment in a supine position. Resting $ \dot{V}{\text{O}}_{2} $ significantly changed during the 60 min (F = 37.4, P < 0.001), exhibiting a monoexponential decrease before reaching an asymptote. Post hoc pairwise comparisons showed that significant differences existed between consecutive means until the 30 min time point, after which there were no significant differences. The $ \dot{V}{\text{O}}_{2} $ response across trials exhibited high test–retest reliability, with within-subject coefficients of variations at each time point ranging from 2.8 to 7.0 % and intraclass correlation coefficients ranging from 0.90 to 0.99. The reliability was higher from the 25 min time point onwards. Based on these findings, the following recommendations are made to promote accurate assessment of resting $ \dot{V}{\text{O}}_{2} $ : (a) initiate the resting $ \dot{V}{\text{O}}_{2} $ measurement with 10 min of acclimation to the assessment apparatus, (b) determine resting $ \dot{V}{\text{O}}_{2} $ for a minimum of 30 min, until an apparent $ \dot{V}{\text{O}}_{2} $ steady state has been achieved; and (c) determine resting $ \dot{V}{\text{O}}_{2} $ for a further 5 min, with the average of this last 5 min of data being regarding as the resting $ \dot{V}{\text{O}}_{2} $ .     

Skeletal muscle \dot{V} {\text{O}_2} kinetics from cardio-pulmonary measurements: assessing distortions through O2 transport by means of stochastic work-rate signals and circulatory modelling

During non-steady-state exercise, dynamic changes in pulmonary oxygen uptake ( $\dot{V} {\text{O}_{\text{2pulm}}}$ ) are dissociated from skeletal muscle $ \dot{V} {\text{O}_2}$ ( $\dot{V} {\text{O}_{\text{2musc}}}$ ) by changes in lung and venous O₂ concentrations (CvO₂), and the dynamics and distribution of cardiac output (CO) between active muscle and remaining tissues ( $ \dot{Q}_{\text{rem}}$ ). Algorithms can compensate for fluctuations in lung O₂ stores, but the influences of CO and CvO₂ kinetics complicate estimation of $\dot{V} {\text{O}_{\text{2musc}}}$ from cardio-pulmonary measurements. We developed an algorithm to estimate $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics from $\dot{V} {\text{O}_{\text{2pulm}}}$ and heart rate (HR) during exercise. 17 healthy volunteers (28 ± 7 years; 71 ± 12 kg; 7 females) performed incremental exercise using recumbent cycle ergometry ( $\dot{V} {\text{O}_{\text{2peak}}}$ 52 ± 8 ml min^?1 kg^?1). Participants completed a pseudo-random binary sequence (PRBS) test between 30 and 80 W. $\dot{V} {\text{O}_{\text{2pulm}}}$ and HR were measured, and CO was estimated from HR changes and steady-state stroke volume. $\dot{V} {\text{O}_{\text{2musc}}}$ was derived from a circulatory model and time series analyses, by solving for the unique combination of venous volume and the perfusion of non-exercising tissues that provided close to mono-exponential $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics. Independent simulations showed that this approach recovered the $\dot{V} {\text{O}_{\text{2musc}}}$ time constant (τ) to within 7 % (R ² = 0.976). Estimates during PRBS were venous volume 2.96 ± 0.54 L; $ \dot{Q}_{\text{rem}}$ 3.63 ± 1.61 L min^?1; τHR 27 ± 11 s; τ $\dot{V} {\text{O}_{\text{2musc}}}$ 33 ± 8 s; τ $\dot{V} {\text{O}_{\text{2pulm}}}$ 43 ± 14 s; $\dot{V} {\text{O}_{\text{2pulm}}}$ time delay 19 ± 8 s. The combination of stochastic test signals, time series analyses, and a circulatory model permitted non-invasive estimates of $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics. Large kinetic dissociations exist between muscular and pulmonary $\dot{V} {\text{O}_{\text{2}}}$ during rapid exercise transients.     

The influence of acute and 23 days of intermittent hypoxic exposures on the exercise-induced forehead sweating response

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high–train low regimen). Peak oxygen uptake and peak work rate (WR_peak) were determined under normoxic (20.9%O₂) and hypoxic (13.5%O₂) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WR_peak attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WR_peak attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease (P < 0.001) in pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially (P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead was greater (P < 0.01) in the HAT (2.60 (0.80) mg cm⁻² min⁻¹) compared to the other two trials (CT = 1.87 (1.09) mg cm⁻² min⁻¹; HRT = 1.57 (0.82) mg cm⁻² min⁻¹) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented (P < 0.01) gain of the sweating response The augmented and during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures.     

Prediction of peak oxygen uptake from differentiated ratings of perceived exertion during wheelchair propulsion in trained wheelchair sportspersons

Purpose

To assess the validity of predicting peak oxygen uptake ( $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ ) from differentiated ratings of perceived exertion (RPE) obtained during submaximal wheelchair propulsion.

Methods

Three subgroups of elite male wheelchair athletes [nine tetraplegics (TETRA), nine paraplegics (PARA), eight athletes without spinal cord injury (NON-SCI)] performed an incremental speed exercise test followed by graded exercise to exhaustion ( $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ test). Oxygen uptake ( $ {\dot{\text{V}}}{\text{O}}_2$ ), heart rate (HR) and differentiated RPE (Central RPE_C, Peripheral RPE_P and Overall RPE_O) were obtained for each stage. The regression lines for the perceptual ranges 9–15 on the Borg 6–20 scale ratings were performed to predict $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ .

Results

There were no significant within-group mean differences between measured $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ (mean 1.50 ± 0.39, 2.74 ± 0.48, 3.75 ± 0.33 L min^?1 for TETRA, PARA and NON-SCI, respectively) and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ determined using HR or differentiated RPEs for any group (P > 0.05). However, the coefficients of variation (CV %) between measured and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ using HR showed high variability for all groups (14.3, 15.9 and 9.7 %, respectively). The typical error ranged from 0.14 to 0.68 L min^?1 and the CV % between measured and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ using differentiated RPE was ≤11.1 % for TETRA, ≤7.5 % for PARA and ≤20.2 % for NON-SCI.

Conclusions

Results suggest that differentiated RPE may be used cautiously for TETRA and PARA athletes when predicting $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ across the perceptual range of 9–15. However, predicting $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ is not recommended for the NON-SCI athletes due to the large CV %s (16.8, 20.2 and 18.0 %; RPE_C, RPE_P and RPE_O, respectively).     

Effects of high vs. moderate exercise intensity during interval training on lipids and adiponectin levels in obese young females

Purpose

We investigate the effects of 12-week interval training of moderate- or high-intensity exercise on blood lipids and plasma levels of adiponectin.

Methods

Thirty-four obese adolescent females [age = 15.9 ± 0.3 years; BMI and BMI-Z-score = 30.8 ± 1.6 kg/m² and 3 ± 0.3, respectively], were randomized to high-intensity interval training (HIIT, n = 11), moderate-intensity interval training (MIIT, n = 11), or a control group (CG, n = 12). Maximal oxygen uptake ( $\mathop V\limits^{.} {\text{O}}_{{2{\text{peak}}}}$ V . O 2 peak ), maximal aerobic speed (MAS), plasma lipids and adiponectin levels were measured in all subjects before and after training.

Results

Following the training program, in both training groups, body mass, BMI-Z-score, and percentage body fat (% BF) decreased, while $\mathop V\limits^{.} {\text{O}}_{{2{\text{peak}}}}$ V . O 2 peak and MAS increased. Low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and adiponectin levels were positively altered (?12.6 and ?7.4 %; 6.3 and 8.0 %; 35.8 and 16.2 %; high to moderate training program, respectively). Waist circumference, triglyceride and total cholesterol decreased only in HIIT group (?3.5; ?5.3 and ?7.0 %, respectively, in all P < 0.05). Significant decrease in the usual index of insulin resistance (HOMA-IR) occurred in HIIT and MIIT groups (?29.2 ± 5.3 and ?18.4 ± 8.6 %, respectively; P < 0.01).

Conclusion

The results show that HIIT positively changes blood lipids and adiponectin variables in obese adolescent girls, resulting in improved insulin sensitivity, as attested by a lower HOMA-IR, and achieving better results compared to moderate-intensity exercise.     

Physical activity intensity and surrogate markers for cardiovascular health in adolescents

We examined the impact of physical activity (PA) on surrogate markers of cardiovascular health in adolescents. 52 healthy students (28 females, mean age 14.5 ± 0.7 years) were investigated. Microvascular endothelial function was assessed by peripheral arterial tonometry to determine reactive hyperemic index (RHI). Vagal activity was measured using 24 h analysis of heart rate variability [root mean square of successive normal-to-normal intervals (rMSSD)]. Exercise testing was performed to determine peak oxygen uptake ( $ \dot{V}{\text{O}}_{{2{\text{ peak}}}} $ ) and maximum power output. PA was assessed by accelerometry. Linear regression models were performed and adjusted for age, sex, skinfolds, and pubertal status. The cohort was dichotomized into two equally sized activity groups (low vs. high) based on the daily time spent in moderate-to-vigorous PA (MVPA, 3,000–5,200 counts^.min^?1, model 1) and vigorous PA (VPA, >5,200 counts^.min^?1, model 2). MVPA was an independent predictor for rMSSD (β = 0.448, P = 0.010), and VPA was associated with maximum power output (β = 0.248, P = 0.016). In model 1, the high MVPA group exhibited a higher vagal tone (rMSSD 49.2 ± 13.6 vs. 38.1 ± 11.7 ms, P = 0.006) and a lower systolic blood pressure (107.3 ± 9.9 vs. 112.9 ± 8.1 mmHg, P = 0.046). In model 2, the high VPA group had higher maximum power output values (3.9 ± 0.5 vs. 3.4 ± 0.5 W kg^?1, P = 0.012). In both models, no significant differences were observed for RHI and $ \dot{V}{\text{O}}_{{ 2 {\text{ peak}}}} $ . In conclusion, in healthy adolescents, PA was associated with beneficial intensity-dependent effects on vagal tone, systolic blood pressure, and exercise capacity, but not on microvascular endothelial function.