Metabolic and respiratory adaptations during intense exercise following long-sprint training of short duration

This study aimed to determine metabolic and respiratory adaptations during intense exercise and improvement of long-sprint performance following six sessions of long-sprint training. Nine subjects performed before and after training (1) a 300-m test, (2) an incremental exercise up to exhaustion to determine the velocity associated with maximal oxygen uptake (v-VO_2max), (3) a 70-s constant exercise at intensity halfway between the v-VO_2max and the velocity performed during the 300-m test, followed by a 60-min passive recovery to determine an individual blood lactate recovery curve fitted to the bi-exponential time function: \textLa( t ) = \textLa( 0 ) + A ₁ ( 1- \texte ^{- g ₁ t} ) +  A ₂ ( 1- \texte ^{- g ₂ t} ) {\text{La}}\left( t \right) = {\text{La}}\left( 0 \right) + A_{ 1} ( 1- {\text{e}}^{{ - \gamma_{{ 1 } }}^{{t}}} ) +\; A_{ 2} ( 1- {\text{e}}^{{ - \gamma_{{ 2 }} }^{{t}}} ) , and blood metabolic and gas exchange responses. The training program consisted of 3–6 repetitions of 150–250 m interspersed with rest periods with a duration ratio superior or equal to 1:10, 3 days a week, for 2 weeks. After sprint training, reduced metabolic disturbances, characterized by a lower peak expired ventilation and carbon dioxide output, in addition to a reduced peak lactate (P < 0.05), was observed. Training also induced significant decrease in the net amount of lactate released at the beginning of recovery (P < 0.05), and significant decrease in the net lactate release rate (NLRR) (P < 0.05). Lastly, a significant improvement of the 300-m performance was observed after training. These results suggest that long-sprint training of short durations was effective to rapidly prevent metabolic disturbances, with alterations in lactate accumulation and gas exchange, and improvement of the NLRR. Furthermore, only six long-sprint training sessions allow long-sprint performance improvement in active subjects.     

Effect of $$ {\text{HCO}}_3^{-} $$ Ions on the ATP-Dependent GABAA Receptor-Coupled Cl– Channel in Rat Brain Plasma Membranes

We studied the effect of Cl⁻ (10–75 mM) and \textHCO₃^- {\text{HCO}}_3^{-} ions (10–25 mM) on the ATP-dependent GABA_A receptor-coupled Cl⁻ channel (Cl⁻-ATPase) in rat brain plasma membranes. The total enzyme activity was detected in the presence of both anions at a Cl⁻/ \textHCO₃^- {\text{HCO}}_3^{-} ratio of 5:1 (Cl⁻, \textHCO₃^- {\text{HCO}}_3^{-} -ATPase). Specific inhibitors of P-type transport ATPases (N-ethylmaleimide, ovanadate, and oligomycin) suppressed Cl⁻, \textHCO₃^- {\text{HCO}}_3^{-} -ATPase, while the Cl⁻- and \textHCO₃^- {\text{HCO}}_3^{-} -ATPase activities were low sensitive to these ligands. Bicuculline abolished the activating effect of Cl⁻ and \textHCO₃^- {\text{HCO}}_3^{-} ions on the enzyme. \textHCO₃^- {\text{HCO}}_3^{-} ions had no effect on the ATP-dependent Cl⁻ transport into proteoliposomes (with the involvement of reconstituted ATPase). In experiment with Cl⁻-preloaded liposomes, addition of \textHCO₃^- {\text{HCO}}_3^{-} ions to the incubation medium caused the reversion of Cl⁻ transport (ion efflux from liposomes). Our results suggest that \textHCO₃^- {\text{HCO}}_3^{-} ions play an important role in the modification of properties of the ATP-dependent GABA_A receptor-coupled Cl⁻ channel and GABAA receptor-induced Cl⁻/ \textHCO₃^- {\text{HCO}}_3^{-} exchange. These ions are probably involved in GABAA receptor-induced Cl⁻/ \textHCO₃^- {\text{HCO}}_3^{-} exchange in neuronal membranes.     

Oxygen uptake and blood metabolic responses to a 400-m run

This study aimed to investigate the oxygen uptake and metabolic responses during a 400-m run reproducing the pacing strategy used in competition. A portable gas analyser was used to measure the oxygen uptake ( [(V)\dot]\textO ₂ ) \left( {\dot{V}{{{\text{O}}_{ 2} }} } \right) of ten specifically trained runners racing on an outdoor track. The tests included (1) an incremental test to determine maximal [(V)\dot]\textO ₂  ( [(V)\dot]\textO _{2 \textmax} ) \dot{V}{{{\text{O}}_{ 2} }} \,\left( {\dot{V}{{{\text{O}}_{{ 2 {\text{max}}}} }} } \right) and the velocity associated with [(V)\dot]\textO _{2 \textmax} ( \textv-[(V)\dot]\textO _{2 \textmax} ), \dot{V}{{{\text{O}}_{{ 2 {\text{max}}}} }} \left( {{\text{v}}-\dot{V}{{{\text{O}}_{{ 2 {\text{max}}}} }} } \right), (2) a maximal 400-m (400T) and 3) a 300-m running test (300T) reproducing the exact pacing pattern of the 400T. Blood lactate, bicarbonate concentrations [ \textHCO ₃ ^- ], \left[ {{\text{HCO}}_{ 3}^{ - } } \right], pH and arterial oxygen saturation were analysed at rest and 1, 4, 7, 10 min after the end of the 400 and 300T. The peak [(V)\dot]\textO ₂ \dot{V}{{{\text{O}}_{ 2} }} recorded during the 400T corresponded to 93.9 ± 3.9% of [(V)\dot]\textO_2max \dot{V}{{{\text{O}}_{2\max } }} and was reached at 24.4 ± 3.2 s (192 ± 22 m). A significant decrease in [(V)\dot]\textO ₂ \dot{V}{{{\text{O}}_{ 2} }} (P < 0.05) was observed in all subjects during the last 100 m, although the velocity did not decrease below \textv-[(V)\dot]_{\textO 2 \textmax} . {\text{v}}-\dot{V}_{{{\text{O}}_{{ 2 {\text{max}}}} }} . The [(V)\dot]\textO ₂ \dot{V}{{{\text{O}}_{ 2} }} in the last 5 s was correlated with the pH (r = 0.86, P < 0.0005) and [ \textHCO ₃ ^- ] \left[ {{\text{HCO}}_{ 3}^{ - } } \right] (r = 0.70, P < 0.05) measured at the end of 300T. Additionally, the velocity decrease observed in the last 100 m was inversely correlated with [ \textHCO ₃ ^- ] \left[ {{\text{HCO}}_{ 3}^{ - } } \right] and pH at 300T (r = −0.83, P < 0.001, r = −0.69, P < 0.05, respectively). These track running data demonstrate that acidosis at 300 m was related to both the [(V)\dot]\textO ₂ \dot{V}{{{\text{O}}_{ 2} }} response and the velocity decrease during the final 100 m of a 400-m run.     

Prediction of peak oxygen uptake from age and power output at RPE 15 in obese women

The purpose of this study was to develop a simple, convenient and indirect method for predicting peak oxygen uptake ( [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} ) from a sub-maximal graded exercise test (GXT), in obese women. Thirty obese women performed GXT to volitional exhaustion. During GXT, oxygen uptake and the power at RPE 15 ( P_{\textRPE  15} P_{{{\text{RPE}}\;15}} ) were measured, and [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} was determined. Following assessment of the relationships between [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} and P_{\textRPE  15} P_{{{\text{RPE}}\;15}} , age, height and mass were made available in a stepwise multiple regression analysis with [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} as the dependent variable. The equation to predict [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} was:

HCO<Subscript>3</Subscript><Superscript>−</Superscript>-dependent transient acidification induced by ionomycin in rat submandibular acinar cells

Ionomycin (IM, 5 μM), which exchanges 1 Ca²⁺ for 1 H⁺, changed intracellular pH (pH_i) with Ca²⁺ entry into rat submandibular acinar cells. IM-induced changes in pH_i consisted of two components: the first is an HCO₃ ⁻-dependent transient pH_i decrease, and the second is an HCO₃ ⁻-independent gradual pH_i increase. IM (1 μM), which activates store-operated Ca²⁺ channels, induced an HCO₃ ⁻-dependent and transient pH_i decrease without any HCO₃ ⁻-independent pH_i increase. Thus, a gradual pH_i increase was induced by the Ca²⁺/H⁺ exchange. The HCO₃ ⁻-dependent and transient pH_i decrease induced by IM was abolished by acetazolamide, but not by methyl isobutyl amiloride (MIA) or diisothiocyanatostilbene disulfonate (DIDS), suggesting that the Na⁺/H⁺ exchange, the Cl⁻/HCO₃ ⁻ exchange, or the Na⁺-HCO₃ ⁻ cotransport induces no transient pH_i decrease. Thapsigargin induced no transient pH_i decrease. Thus, IM, not Ca²⁺ entry, reduced pH_i transiently. IM reacts with Ca²⁺ to produce H⁺ in the presence of \textCO ₂ /\textHCO ₃ ^- :  [ \textH - \textIM ] ^- + \text Ca ²⁺  + \textCO ₂ \rightleftarrows [ \textH-\textCa - \textIM ] ⁺ ·\textHCO ₃ ^- + \textH ⁺ {\text{CO}}_{ 2} /{\text{HCO}}_{ 3}{^{ - }} : \, \left[ {{\text{H}} - {\text{IM}}} \right]^{ - } + {\text{ Ca}}^{ 2+ } \,+ {\text{CO}}_{ 2} \rightleftarrows \left[ {{\text{H}}-{\text{Ca}} - {\text{IM}}} \right]^{ + } \cdot {\text{HCO}}_{ 3}{^{ - } }+ {\text{H}}^{ + } . In this reaction, a monoprotonated IM reacts with Ca²⁺ and CO₂ to produce an electroneutral IM complex and H⁺, and then H⁺ is removed from the cells via CO₂ production. Thus, IM transiently decreased pH_i. In conclusion, in rat submandibular acinar cells IM (5 μM) transiently reduces pH_i because of its chemical characteristics, with HCO₃ ⁻ dependence, and increases pH_i by exchanging Ca²⁺ for H⁺, which is independent of HCO₃ ⁻.     

Performance and physiological responses during a sprint interval training session: relationships with muscle oxygenation and pulmonary oxygen uptake kinetics

The purpose of this study was to examine the cardiorespiratory and muscle oxygenation responses to a sprint interval training (SIT) session, and to assess their relationships with maximal pulmonary O₂ uptake ([(V)\dot]\textO _{2 \textp} \textmax) (\dot{V}{\text{O}}_{{ 2 {\text{p}}}} {\text{max)}} , on- and off- [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} kinetics and muscle reoxygenation rate (Reoxy rate). Ten male cyclists performed two 6-min moderate-intensity exercises (≈90–95% of lactate threshold power output, Mod), followed 10 min later by a SIT session consisting of 6 × 30-s all out cycling sprints interspersed with 2 min of passive recovery. [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} kinetics at Mod onset ( [(V)\dot]\textO _{2 \textp} t_\texton \dot{V}{\text{O}}_{{ 2 {\text{p}}}} \tau_{\text{on}} ) and cessation ( [(V)\dot]\textO _{2 \textp} t_\textoff \dot{V}{\text{O}}_{{ 2 {\text{p}}}} \tau_{\text{off}} ) were calculated. Cardiorespiratory variables, blood lactate ([La]_b) and muscle oxygenation level of the vastus lateralis (tissue oxygenation index, TOI) were recorded during SIT. Percentage of the decline in power output (%Dec), time spent above 90% of [(V)\dot]\textO _{2 \textp} max \dot{V}{\text{O}}_{{ 2 {\text{p}}}} { \max } (t > 90% [(V)\dot]\textO _{2 \textp} max \dot{V}{\text{O}}_{{ 2 {\text{p}}}} { \max } ) and Reoxy rate after each sprint were also recorded. Despite a low mean [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} (48.0 ± 4.1% of [(V)\dot]\textO _{2 \textp} max \dot{V}{\text{O}}_{{ 2 {\text{p}}}} { \max } ), SIT performance was associated with high peak [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} (90.4 ± 2.8% of [(V)\dot]\textO _{2 \textp} max \dot{V}{\text{O}}_{{ 2 {\text{p}}}} { \max } ), muscle deoxygenation (sprint ΔTOI = −27%) and [La]_b (15.3 ± 0.7 mmol l⁻¹) levels. Muscle deoxygenation and Reoxy rate increased throughout sprint repetitions (P < 0.001 for both). Except for t > 90% [(V)\dot]\textO _{2 \textp} max \dot{V}{\text{O}}_{{ 2 {\text{p}}}} { \max } versus [(V)\dot]\textO _{2 \textp} t_\textoff \dot{V}{\text{O}}_{{ 2 {\text{p}}}} \tau_{\text{off}} [r = 0.68 (90% CL, 0.20; 0.90); P = 0.03], there were no significant correlations between any index of aerobic function and either SIT performance or physiological responses [e.g., %Dec vs. [(V)\dot]\textO _{2 \textp} t_\textoff \dot{V}{\text{O}}_{{ 2 {\text{p}}}} \tau_{\text{off}} : r = −0.41 (−0.78; 0.18); P = 0.24]. Present results show that SIT elicits a greater muscle O₂ extraction with successive sprint repetitions, despite the decrease in external power production (%Dec = 21%). Further, our findings obtained in a small and homogenous group indicate that performance and physiological responses to SIT are only slightly influenced by aerobic fitness level in this population.     

Experimental and numerical characterization of magnetophoretic separation for MEMS-based biosensor applications

Magnetophoretic isolation of biochemical and organic entities in a microfluidic environment is a popular tool for a wide range of bioMEMS applications, including biosensors. An experimental and numerical analysis of magnetophoretic capture of magnetic microspheres in a microfluidic channel under the influence of an external field is investigated. For a given microfluidic geometry, the operating conditions for marginal capture is found to be interrelated in such a manner that a unique critical capture parameter P_\textcrit = ( I_\textcrit \texta )² \mathord

Kinematic Modeling-based Left Ventricular Diastatic (Passive) Chamber Stiffness Determination with <Emphasis Type="Italic">In-Vivo</Emphasis> Validation

The slope of the diastatic pressure–volume relationship (D-PVR) defines passive left ventricular (LV) stiffness K. \mathcal{K}. Although K \mathcal{K} is a relative measure, cardiac catheterization, which is an absolute measurement method, is used to obtain the former. Echocardiography, including transmitral flow velocity (Doppler E-wave) analysis, is the preferred quantitative diastolic function (DF) assessment method. However, E-wave analysis can provide only relative, rather than absolute pressure information. We hypothesized that physiologic mechanism-based modeling of E-waves allows derivation of the D-PVR_E-wave whose slope, K_{\textE-\textwave} \mathcal{K}_{{\text{E-}}{\text{wave}}} , provides E-wave-derived diastatic, passive chamber stiffness. Our kinematic model of filling and Bernoulli’s equation were used to derive expressions for diastatic pressure and volume on a beat-by-beat basis, thereby generating D-PVR_E-wave, and K_{\textE-\textwave} \mathcal{K}_{{\text{E-}}{\text{wave}}} . For validation, simultaneous (conductance catheter) P–V and echocardiographic E-wave data from 30 subjects (444 total cardiac cycles) having normal LV ejection fraction (LVEF) were analyzed. For each subject (15 beats average) model-predicted K_{\textE-\textwave} \mathcal{K}_{{\text{E-}}{\text{wave}}} was compared to experimentally measured K_\textCATH \mathcal{K}_{\text{CATH}} via linear regression yielding as follows: K_{\textE-\textwave} = aK_\textCATH + b  (R² = 0.92), \mathcal{K}_{{\text{E-}}{\text{wave}}} = \alpha {\mathcal{K}}_{\text{CATH}} + b\;(R^{2} = 0.92), where, α = 0.995 and b = 0.02. We conclude that echocardiographically determined diastatic passive chamber stiffness, K_{\textE-\textwave} \mathcal{K}_{{\text{E-}}{\text{wave}}} , provides an excellent estimate of simultaneous, gold standard (P–V)-defined diastatic stiffness, K_\textCATH \mathcal{K}_{\text{CATH}} . Hence, in chambers at diastasis, passive LV stiffness can be accurately determined by means of suitable analysis of Doppler E-waves (transmitral flow).     

Adaptation of the respiratory controller contributes to the attenuation of exercise hyperpnea in endurance-trained athletes

We have reported that minute ventilation [ [(V)\dot]_\textE \dot{V}_{\text{E}} ] and end-tidal CO₂ tension [ P_{\textETCO 2} P_{{{\text{ETCO}}_{ 2} }} ] are determined by the interaction between central controller and peripheral plant properties. During exercise, the controller curve shifts upward with unchanged central chemoreflex threshold to compensate for the plant curve shift accompanying increased metabolism. This effectively stabilizes P_{\textETCO 2} P_{{{\text{ETCO}}_{ 2} }} within the normal range at the expense of exercise hyperpnea. In the present study, we investigated how endurance-trained athletes reduce this exercise hyperpnea. Nine exercise-trained and seven untrained healthy males were studied. To characterize the controller, we induced hypercapnia by changing the inspiratory CO₂ fraction with a background of hyperoxia and measured the linear P_{\textETCO 2} - [(V)\dot]_\textE P_{{{\text{ETCO}}_{ 2} }} - \dot{V}_{\text{E}} relation [ [(V)\dot]_\textE = S (P_\textETCO2 - B) \dot{V}_{\text{E}} = S\, (P_{{{\text{ETCO}}_{2} }} - {\rm B}) ]. To characterize the plant, we instructed the subjects to alter [(V)\dot]_\textE \dot{V}_{\text{E}} voluntarily and measured the hyperbolic [(V)\dot]_\textE - P_{\textETCO 2} \dot{V}_{\text{E}} - P_{{{\text{ETCO}}_{ 2} }} relation ( P_{\textETCO 2} = A/[(V)\dot]_\textE + C P_{{{\text{ETCO}}_{ 2} }} = A/\dot{V}_{\text{E}} + C ). We characterized these relations both at rest and during light exercise. Regular exercise training did not affect the characteristics of either controller or plant at rest. Exercise stimulus increased the controller gain (S) both in untrained and trained subjects. On the other hand, the P_{\textETCO 2} P_{{{\text{ETCO}}_{ 2} }} -intercept (B) during exercise was greater in trained than in untrained subjects, indicating that exercise-induced upward shift of the controller property was less in trained than in untrained subjects. The results suggest that the additive exercise drive to breathe was less in trained subjects, without necessarily a change in central chemoreflex threshold. The hyperbolic plant property shifted rightward and upward during exercise as predicted by increased metabolism, with little difference between two groups. The [(V)\dot]_\textE \dot{V}_{\text{E}} during exercise in trained subjects was 21% lower than that in untrained subjects (P < 0.01). These results indicate that an adaptation of the controller, but not that of plant, contributes to the attenuation of exercise hyperpnea at an iso-metabolic rate in trained subjects. However, whether training induces changes in neural drive originating from the central nervous system, afferents from the working limbs, or afferents from the heart, which is additive to the chemoreflex drive to breathe, cannot be determined from these results.     

Effects of membrane depolarization and changes in extracellular [K<Superscript>+</Superscript>] on the Ca<Superscript>2+</Superscript> transients of fast skeletal muscle fibers. Implications for muscle fatigue

Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K⁺ gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K⁺ ( \textK_\texto ⁺ {\text{K}}_{\text{o}}^{ + } ) concentration ( [ \textK ⁺ ]_\texto [ {\text{K}}^{ + } ]_{\text{o}} ) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca²⁺ transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various [ \textK ⁺ ]_\texto [ {\text{K}}^{ + } ]_{\text{o}} and membrane potentials. Depolarization resulting from current injection or raised [ \textK ⁺ ]_\texto [ {\text{K}}^{ + } ]_{\text{o}} produced an increase in the resting [Ca²⁺]. Ca²⁺ transients elicited by single stimulation were potentiated by depolarization from −80 to −60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca²⁺ transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca²⁺ transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca²⁺ transients along the trains were associated with impaired or abortive APs. Raising [ \textK ⁺ ]_\texto [ {\text{K}}^{ + } ]_{\text{o}} to 10 mM potentiated Ca²⁺ transients elicited by single and tetanic stimulation, while raising [ \textK ⁺ ]_\texto [ {\text{K}}^{ + } ]_{\text{o}} to 15 mM markedly depressed both responses. The effects of 10 mM \textK_\texto ⁺ {\text{K}}_{\text{o}}^{ + } on Ca²⁺ transients, but not those of 15 mM \textK_\texto ⁺ {\text{K}}_{\text{o}}^{ + } , could be fully reversed by hyperpolarization. The results suggests that the force potentiating effects of 10 mM \textK_\texto ⁺ {\text{K}}_{\text{o}}^{ + } might be mediated by depolarization dependent changes in resting [Ca²⁺] and Ca²⁺ release, and that additional mechanisms might be involved in the effects of 15 mM \textK_\texto ⁺ {\text{K}}_{\text{o}}^{ + } on force generation.     

Prediction of maximal oxygen uptake from submaximal ratings of perceived exertion and heart rate during a continuous exercise test: the efficacy of RPE 13

This study assessed the utility of a single, continuous exercise protocol in facilitating accurate estimates of maximal oxygen uptake ( [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max) from submaximal heart rate (HR) and the ratings of perceived exertion (RPE) in healthy, low-fit women, during cycle ergometry. Eleven women estimated their RPE during a continuous test (1 W 4 s⁻¹) to volitional exhaustion (measured [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max). Individual gaseous exchange thresholds (GETs) were determined retrospectively. The RPE and HR values prior to and including an RPE 13 and GET were extrapolated against corresponding oxygen uptake to a theoretical maximal RPE (20) and peak RPE (19), and age-predicted HRmax, respectively, to predict [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max. There were no significant differences (P > 0.05) between measured (30.9 ± 6.5 ml kg⁻¹ min⁻¹) and predicted [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max from all six methods. Limits of agreement were narrowest and intraclass correlations were highest for predictions of [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max from an RPE 13 to peak RPE (19). Prediction of [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max from a regression equation using submaximal HR and work rate at an RPE 13 was also not significantly different to actual [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max (R ²  = 0.78, SEE = 3.42 ml kg⁻¹ min⁻¹, P > 0.05). Accurate predictions of [(V)\dot] \textO ₂ \dot{V} {\text{O}}_{ 2} max may be obtained from a single, continuous, estimation exercise test to a moderate intensity (RPE 13) in low-fit women, particularly when extrapolated to peak terminal RPE (RPE₁₉). The RPE is a valuable tool that can be easily employed as an adjunct to HR, and provides supplementary clinical information that is superior to using HR alone.     

The validity and reliability of predicting maximal oxygen uptake from a treadmill-based sub-maximal perceptually regulated exercise test

The purpose of this study was to determine for the first time whether [(V)\dot]\textO _2max {\dot{V}}{\text{O}}_{ 2\hbox{max}} could be predicted accurately and reliably from a treadmill-based perceptually regulated exercise test (PRET) incorporating a safer and more practical upper limit of RPE 15 (“Hard”) than used in previous investigations. Eighteen volunteers (21.7 ± 2.8 years) completed three treadmill PRETs (each separated by 48 h) and one maximal graded exercise test. Participants self-regulated their exercise at RPE levels 9, 11, 13 and 15 in a continuous and incremental fashion. Oxygen uptake ( [(V)\dot]\textO ₂ ) \left( {{\dot{V}}{\text{O}}_{ 2} } \right) was recorded continuously during each 3 min bout. [(V)\dot]\textO₂ {\dot{V}}{\text{O}}_{2} values for the RPE range 9–15 were extrapolated to RPE₁₉ and RPE₂₀ using regression analysis to predict individual [(V)\dot]\textO_2max {\dot{V}}{\text{O}}_{2\hbox{max}} scores. The optimal limits of agreement (LoA) between actual (48.0 ± 6.2 ml kg⁻¹ min⁻¹) and predicted scores were −0.6 ± 7.1 and −2.5 ± 9.4 ml^.kg⁻¹ min⁻¹ for the RPE₂₀ and RPE₁₉ models, respectively. Reliability analysis for the [(V)\dot]\textO_2max {\dot{V}}{\text{O}}_{2\hbox{max}} predictions yielded LoAs of 1.6 ± 8.5 (RPE₂₀) and 2.7 ± 9.4 (RPE₁₉) ml kg⁻¹ min⁻¹ between trials 2 and 3. These findings demonstrate that (with practice) a novel treadmill-based PRET can yield predictions of [(V)\dot]\textO_2max {\dot{V}}{\text{O}}_{2\hbox{max}} that are acceptably reliable and valid amongst young, healthy, and active adults.     

Physiological determinants of Yo-Yo intermittent recovery tests in male soccer players

The physiological determinants of performance in two Yo-Yo intermittent recovery tests (Yo-YoIR1 and Yo-YoIR2) were examined in 25 professional (n = 13) and amateur (n = 12) soccer players. The aims of the study were (1) to examine the differences in physiological responses to Yo-YoIR1 and Yo-YoIR2, (2) to determine the relationship between the aerobic and physiological responses to standardized high-intensity intermittent exercise (HIT) and Yo-Yo performance, and (3) to investigate the differences between professional and amateur players in performance and responses to these tests. All players performed six tests: two versions of the Yo-Yo tests, a test for the determination of maximum oxygen uptake ( [(\textV)\dot]\textO_{2  max} {\dot{\text{V}}}{\text{O}}_{{2\,{ \max }}} ), a double test to determine [(\textV)\dot]\textO₂ {\dot{\text{V}}}{\text{O}}_{2} kinetics and a HIT evaluation during which several physiological responses were measured. The anaerobic contribution was greatest during Yo-YoIR2. [(\textV)\dot]\textO_{2  max} {\dot{\text{V}}}{\text{O}}_{{2\,{ \max }}} was strongly correlated with Yo-YoIR1 (r = 0.74) but only moderately related to Yo-YoIR2 (r = 0.47). The time constant (τ) of [(\textV)\dot]\textO₂ {\dot{\text{V}}}{\text{O}}_{2} kinetics was largely related to both Yo-Yo tests (Yo-YoIR1: r = 0.60 and Yo-YoIR2: r = 0.65). The relationships between physiological variables measured during HIT (blood La⁻, H⁺, HCO₃ ⁻ and the rate of La⁻ accumulation) and Yo-Yo performance (in both versions) were very large (r > 0.70). The physiological responses to HIT and the τ of the [(\textV)\dot]\textO₂ {\dot{\text{V}}}{\text{O}}_{2} kinetics were significantly different between professional and amateur soccer players, whilst [(\textV)\dot]\textO_{2  max} {\dot{\text{V}}}{\text{O}}_{{2\,{ \max }}} was not significantly different between the two groups. In conclusion, [(\textV)\dot]\textO_{2  max} {\dot{\text{V}}}{\text{O}}_{{2\,{ \max }}} is more important for Yo-YoIR1 performance, whilst τ of the [(\textV)\dot]\textO₂ {\dot{\text{V}}}{\text{O}}_{2} kinetics and the ability to maintain acid–base balance are important physiological factors for both Yo-Yo tests.     

Effect of ramp bicycle exercise on exhaled carbon monoxide in humans

The effect of exercise on the increase of exhaled CO in smokers compared to non-smokers has not been clarified yet. In this study we compared the dynamics of exhaled CO before, during and after exercise between smokers and non-smokers. A group of 8 smokers and a group of 8 non-smokers underwent a bicycle exercise in a ramp fashion to near maximum intensity. Ventilation and gas exchange, and CO exhalation were continuously measured every 30-s before, during and after the exercise. The fraction of CO (F _CO) in the exhaled air decreased gradually, but the total amount of exhaled CO ([(V)\dot]_\textCO ) (\dot{V}_{{{\text{CO}}}} ) increased in a linear manner during the ramp exercise, and F _CO and [(V)\dot]_\textCO \dot{V}_{\text{CO}} returned to the pre-exercise level within several minutes after exercise in all subjects. A linear relationship was observed between [(V)\dot]_{\textO 2} \dot{V}_{{{\text{O}}_{ 2} }} and [(V)\dot]_\textCO , \dot{V}_{\text{CO}} , and between [(V)\dot]_\textE \dot{V}_{\text{E}} and [(V)\dot]_\textCO \dot{V}_{\text{CO}} in both the whole period of measurement and during the ramp exercise period in all subjects. However, the [(V)\dot]_\textCO \dot{V}_{\text{CO}} at 0 W, the peak [(V)\dot]_\textCO \dot{V}_{\text{CO}} and the slope coefficients in the regression equation between [(V)\dot]_\textCO \dot{V}_{\text{CO}} and [(V)\dot]_{\textO 2} , \dot{V}_{{{\text{O}}_{ 2} }} , and between [(V)\dot]_\textCO \dot{V}_{\text{CO}} and [(V)\dot]_\textE \dot{V}_{\text{E}} in the ramp exercise as well as the entire periods of measurement were significantly higher in smokers compared with those in non-smokers, and these were correlated with the number of cigarettes smoked per day. It was concluded that CO exhalation increases linearly with the increase of [(V)\dot]_{\textO 2} \dot{V}_{{{\text{O}}_{ 2} }} and [(V)\dot]_\textE \dot{V}_{\text{E}} during exercise, and habitual smoking shifts these relationships upward depending on the number of cigarettes smoked daily.     

Pulmonary oxygen uptake and muscle deoxygenation kinetics during recovery in trained and untrained male adolescents

Previous studies have demonstrated faster pulmonary oxygen uptake ( [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} ) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max} 54.9 ± 6.4 mL kg⁻¹ min⁻¹) and 8 untrained (15 ± 0.5 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max } 44.0 ± 4.6 mL kg⁻¹ min⁻¹) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding “baseline” of exercise at a workload equivalent to 80% lactate threshold; [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P < 0.01) and mean response time (trained 24.2 ± 9.2 s vs. untrained 34 ± 13 s, P = 0.05) of muscle deoxyhaemoglobin off-kinetics was faster in the trained subjects compared to the untrained subjects. [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics was unaffected by training status; the faster muscle deoxyhaemoglobin kinetics in the trained subjects thus indicates slower blood flow kinetics during recovery from exercise compared to the untrained subjects.     

Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T _es), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ( [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} ) during exercise. The training lowered the T _es threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T _es and the peak FVC during exercise. It also lowered minute ventilation ( [(V)\dot]_\textE \dot{V}_{\text{E}} ) during exercise, but this effect disappeared after removing the influence of [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} on [(V)\dot]_\textE \dot{V}_{\text{E}} . The training did not change the slope relating ventilatory variables to T _es. We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.     

Inter-individual variability in adaptation of the leg muscles following a standardised endurance training programme in young women

There is considerable inter-individual variability in adaptations to endurance training. We hypothesised that those individuals with a low local leg-muscle peak aerobic capacity ([(V)\dot] \textO_2\textpeak) (\dot{V} {\text{O}}_{{2{\text{peak}}}}) relative to their whole-body maximal aerobic capacity ( [(V)\dot] \textO_2max) ( \dot{V} {\text{O}}_{2\max}) would experience greater muscle training adaptations compared to those with a relatively high [(V)\dot] \textO_2\textpeak \dot{V} {\text{O}}_{{2{\text{peak}}}} . 53 untrained young women completed one-leg cycling to measure [(V)\dot] \textO_2\textpeak \dot{V} {\text{O}}_{{2{\text{peak}}}} and two-leg cycling to measure [(V)\dot] \textO_2max \dot{V} {\text{O}}_{2\max} . The one-leg [(V)\dot] \textO_2\textpeak \dot{V} {\text{O}}_{{2{\text{peak}}}} was expressed as a ratio of the two-leg [(V)\dot] \textO_2max \dot{V} {\text{O}}_{2\max} (Ratio _1:2). Magnetic resonance imaging was used to indicate quadriceps muscle volume. Measurements were taken before and after completion of 6 weeks of supervised endurance training. There was large inter-individual variability in the pre-training Ratio _1:2 and large variability in the magnitude of training adaptations. The pre-training Ratio _1:2 was not related to training-induced changes in [(V)\dot] \textO_2max \dot{V} {\text{O}}_{2\max} (P = 0.441) but was inversely correlated with changes in one-leg [(V)\dot] \textO_2\textpeak \dot{V} {\text{O}}_{{2{\text{peak}}}} and muscle volume (P < 0.05). No relationship was found between the training-induced changes in two-leg [(V)\dot] \textO_2max \dot{V} {\text{O}}_{2\max} and one-leg [(V)\dot] \textO_2\textpeak \dot{V} {\text{O}}_{{2{\text{peak}}}} (r = 0.21; P = 0.129). It is concluded that the local leg-muscle aerobic capacity and Ratio _1:2 vary from person to person and this influences the extent of muscle adaptations following standardised endurance training. These results help to explain why muscle adaptations vary between people and suggest that setting the training stimulus at a fixed percentage of [(V)\dot] \textO_2max \dot{V} {\text{O}}_{2\max} might not be a good way to standardise the training stimulus to the leg muscles of different people.     

Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise

The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O₂ uptake ([(V)\dot]\textO _{2 \textp}) (\dot{V}{\text{O}}_{{ 2 {\text{p}}}}) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P_ETCO₂ ~ 40 mmHg) and (2) controlled hyperventilation (HYPO, P_ETCO₂ ~ 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Δ50%); each transition lasted 6 min and was preceded by 20 W cycling. [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} was measured breath-by-breath and concentration changes in oxy- and deoxy-hemoglobin/myoglobin (Δ[HHb]) of the vastus lateralis muscle were measured by near-infrared spectroscopy. Adjustment of [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} and Δ[HHb] were modeled using a mono-exponential equation by non-linear regression. During MOD1, the phase 2 time constant (τ) for [(V)\dot]\textO _{2 \textp}  (t[(V)\dot]\textO _{2 \textp} ) \dot{V}{\text{O}}_{{ 2 {\text{p}}}} \,(\tau \dot{V}{\text{O}}_{{ 2 {\text{p}}}} ) was greater (P < 0.05) in HYPO (45 ± 24 s) than CON (28 ± 17 s). During MOD2, t[(V)\dot]\textO _{2 \textp} \tau \dot{V}{\text{O}}_{{ 2 {\text{p}}}} was reduced (P < 0.05) in both conditions (HYPO: 24 ± 7 s, CON: 20 ± 8 s). The Δ[Hb_TOT] and Δ[O₂Hb] were greater (P < 0.05) prior to and throughout MOD2. The Δ[HHb] mean response time was similar in MOD1 and MOD2, and between conditions, however, the MOD1 Δ[HHb] amplitude was greater (P < 0.05) in HYPO compared to CON, with no differences between conditions in MOD2. These findings suggest that the speeding of [(V)\dot]\textO _{2 \textp} \dot{V}{\text{O}}_{{ 2 {\text{p}}}} kinetics after prior HVY in HYPO was related, in part, to an increase in microvascular perfusion.     

Muscle metabolic, enzymatic and transporter responses to a session of prolonged cycling

A single session of prolonged work was employed to investigate changes in selected metabolic, transporter and enzymatic properties in muscle. Ten active but untrained volunteers (weight = 73.9 ± 4.2 kg) with a peak aerobic power ( [(V)\dot]\textO_2\textpeak ) \left( {\dot{V}{\text{O}}_{{2{\text{peak}}}} } \right) of 2.95 ± 0.27 l min⁻¹, cycled for 2 h at 62 ± 1.3% ( [(V)\dot]\textO_2\textpeak ) \left( {\dot{V}{\text{O}}_{{2{\text{peak}}}} } \right) Tissue extraction from the vastus lateralis occurred prior to (E1-Pre) and following (E1-Post) exercise and on 3 consecutive days of recovery (R1, R2, R3). The exercise resulted in decreases (P < 0.05) in ATP (−9.3%) and creatine phosphate (−49%) and increases in lactate (+100%), calculated free ADP (+253%) and free AMP (+1,207%), all of which recovered to E1-Pre by R1. Glycogen concentration, which was depressed (P < 0.05) by 75% at E1-Post, did not recover until R3. Compared to E1-Pre, the cycling also resulted in decreases (P < 0.05) in the activities of cytochrome c oxidase, phosphorylase, and hexokinase but not in citrate synthase (CS) or 3-hydroxy-CoA dehydrogenase at E1-Post. With the exception of CS, which was elevated (P < 0.05) at R3, all enzyme activities were not different from E1-Pre during recovery. For the glucose (GLUT1, GLUT4) and monocarboxylate (MCT1, MCT4) transporters, changes in expression levels (P < 0.05) were only observed for GLUT1 at R1 (+42%) and R3 (+33%). It is concluded that the metabolic stress produced by prolonged exercise is reversed by 1 day of recovery. One day of exercise also resulted in a potential upregulation in the citric acid cycle and glucose transport capabilities, adaptations which are expressed at variable recovery durations.     

Energetics of karate (<Emphasis Type="Italic">kata</Emphasis> and <Emphasis Type="Italic">kumite</Emphasis> techniques) in top-level athletes

Breath-by-breath O₂ uptake ( [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} , L min⁻¹) and blood lactate concentration were measured before, during exercise, and recovery in six kata and six kumite karate Word Champions performing a simulated competition. [(V)\dot]_{\textO 2 \textmax} , \dot{V}_{{{\text{O}}_{{ 2 {\text{max}}}} }} , maximal anaerobic alactic, and lactic power were also assessed. The total energy cost ( V_{\textO 2 \textTOT} , V_{{{\text{O}}_{{ 2 {\text{TOT}}}} }} , mL kg⁻¹ above resting) of each simulated competition was calculated and subdivided into aerobic, lactic, and alactic fractions. Results showed that (a) no differences between kata and kumite groups in [(V)\dot]_{\textO 2 \textmax} , \dot{V}_{{{\text{O}}_{{ 2 {\text{max}}}} }} , height of vertical jump, and Wingate test were found; (b) V_{\textO 2 \textTOT} V_{{{\text{O}}_{{ 2 {\text{TOT}}}} }} were 87.8 ± 6.6 and 82.3 ± 12.3 mL kg⁻¹ in kata male and female with a performance time of 138 ± 4 and 158 ± 14 s, respectively; 189.0 ± 14.6 mL kg⁻¹ in kumite male and 155.8 ± 38.4 mL kg⁻¹ in kumite female with a predetermined performance time of 240 ± 0 and 180 ± 0 s, respectively; (c) the metabolic power was significantly higher in kumite than in kata athletes (p ≤ 0.05 in both gender); (d) aerobic and anaerobic alactic sources, in percentage of the total, were significantly different between gender and disciplines (p < 0.05), while the lactic source was similar; (e) HR ranged between 174 and 187 b min⁻¹ during simulated competition. In conclusion, kumite appears to require a much higher metabolic power than kata, being the energy source with the aerobic contribution predominant.