Aurélien Bringard

Reproducibility assessment of metabolic variables characterizing muscle energetics in Vivo: A 31P-MRS study

The purpose of the present study was to assess the reliability of metabolic parameters measured using 31P magnetic resonance spectroscopy (31P MRS) during two standardized rest‐exercise‐recovery protocols. Twelve healthy subjects performed the standardized protocols at two different intensities; i.e., a moderate intensity (MOD) repeated over a two‐month period and heavy intensity (HEAVY) repeated over a years time. Test‐retest reliability was analyzed using coefficient of variation (CV), limits of agreement (LOA), and intraclass correlation coefficients (ICC). During exercise and recovery periods, most of the metabolic parameters exhibited a good reliability. The CVs of individual concentration of phosphocreatine ([PCr]), concentration of adenosine diphosphate ([ADP]), and pH values recorded at end of the HEAVY exercise were lower than 15%. The CV calculated for the rate of PCr resynthesis and the maximal oxidative capacity were less than 13% during the HEAVY protocol. Inferred parameters such as oxidative and total adenosine triphosphate (ATP) production rates exhibited a good reliability (ICC ≈ 0.7; CV < 15% during the HEAVY protocol). Our results demonstrated that measurement error using 31P‐MRS during a standardized exercise was low and that biological variability accounted for the vast majority of the measurement variability. In addition, the corresponding metabolic measurements can reliably be used for longitudinal studies performed even over a long period of time. Magn Reson Med, 2009.

Effects of a prior high‐intensity knee‐extension exercise on muscle recruitment and energy cost: a combined local and global investigation in humans

The effects of a priming exercise bout on both muscle energy production and the pattern of muscle fibre recruitment during a subsequent exercise bout are poorly understood. The purpose of the present study was to determine whether a prior exercise bout which is known to increase O2 supply and to induce a residual acidosis could alter energy cost and muscle fibre recruitment during a subsequent heavy‐intensity knee‐extension exercise. Fifteen healthy subjects performed two 6 min bouts of heavy exercise separated by a 6 min resting period. Rates of oxidative and anaerobic ATP production, determined with 31P‐magnetic resonance spectroscopy, and breath‐by‐breath measurements of pulmonary oxygen uptake were obtained simultaneously. Changes in muscle oxygenation and muscle fibre recruitment occurring within the quadriceps were measured using near‐infrared spectroscopy and surface electromyography. The priming heavy‐intensity exercise increased motor unit recruitment (P < 0.05) in the early part of the subsequent exercise bout but did not alter muscle energy cost. We also observed a reduced deoxygenation time delay, whereas the deoxygenation amplitude was increased (P < 0.01). These changes were associated with an increased oxidative ATP cost after ∼50 s (P < 0.05) and a slight reduction in the overall anaerobic rate of ATP production (0.11 ± 0.04 mm min−1 W−1 for bout 1 and 0.06 ± 0.11 mm min−1 W−1 for bout 2; P < 0.05). We showed that a priming bout of heavy exercise led to an increased recruitment of motor units in the early part of the second bout of heavy exercise. Considering the increased oxidative cost and the unaltered energy cost, one could suggest that our results illustrate a reduced metabolic strain per fibre.

Comparative determination of energy production rates and mitochondrial function using different 31P MRS quantitative methods in sedentary and trained subjects.

Muscle energetics has been largely and quantitatively investigated using 31P MRS. Various methods have been used to estimate the corresponding rate of oxidative ATP synthesis (ATPox); however, potential differences among methods have not been investigated. In this study, we aimed to compare the rates of ATP production and energy cost in two groups of subjects with different training status using four different methods: indirect method (method 1), ADP control model (method 2) and phosphate potential control model (method 3). Method 4 was a modified version of method 3 with the introduction of a correction factor allowing for similar values to be obtained for the end‐exercise oxidative ATP synthesis rate inferred from exercise measurements and the initial recovery phosphocreatine resynthesis rate. Seven sedentary and seven endurance‐trained subjects performed a dynamic standardised rest–exercise–recovery protocol. We quantified the rates of ATPox and anaerobic ATP synthesis (ATPana) using 31P MRS data recorded at 1.5 T. The rates of ATPox over the entire exercise session were independent of the method used, except for method 4 which provided significantly higher values in both groups (p < 0.01). In addition, methods 1–3 were cross‐correlated, thereby confirming their statistical agreement. The rate of ATPana was significantly higher with method 1 (p < 0.01) and lower with method 4 (p < 0.01). As a result of the higher rate of ATPox, EC (method 4) calculated over the entire exercise session was higher and initial EC (method 1) was lower in both groups compared with the other methods. We showed in this study that the rate of ATPox was independent of the calculation method, as long as no corrections (method 4) were performed. In contrast, results related to the rates of ATPana were strongly affected by the calculation method and, more exactly, by the estimation of protons generated by ATPox. Although the absolute EC values differed between the methods, within‐ or between‐subject comparisons are still valid given the tight relationships between them. Copyright

Cardiovascular determinants of maximal oxygen consumption in upright and supine posture at the end of prolonged bed rest in humans

We tested the hypothesis that, after bed rest, maximal oxygen consumption ( VO₂max ) decreases more upright than supine, because of adequate cardiovascular response supine, but not upright. On 9 subjects, we determined VO₂max and maximal cardiac output (Q ) upright and supine, before and after (reambulation day upright, the following day supine) 35-day bed rest, by classical steady state protocol. Oxygen consumption, heart rate (f(H)) and stroke volume (Q(st)) were measured by a metabolic cart, electrocardiography and Modelflow from pulse pressure profiles, respectively. We computed Q as f(H) times Q(st), and systemic oxygen flow ( QaO₂) as Q. times arterial oxygen concentration, obtained after haemoglobin and arterial oxygen saturation measurements. Before bed rest, all parameters at maximal exercise were similar upright and supine. After bed rest, VO₂max was lower (p<0.05) than before, both upright (-38.6%) and supine (-17.0%), being 30.8% higher supine than upright. Maximal Q(st) decreased upright (-44.3%), but not supine (+3.7%), being 98.9% higher supine than upright. Maximal Q decreased upright (-45.1%), but not supine (+9.0%), being higher supine than upright (+98.4%). Maximal QaO₂ decreased upright (-37.8%), but not supine (+14.8%), being higher (+74.8%) upright than supine. After bed rest, the cardiovascular response (i) did not affect VO₂max supine, (ii) partially explained the VO₂max decrease upright, and (iii) caused the VO₂max differences between postures. We speculate that impaired peripheral oxygen transfer and/or utilisation may explain the VO₂max decrease supine and the fraction of VO₂max decrease upright unexplained by cardiovascular responses.

An analysis of performance in human locomotion

This paper reports an analysis of the principles underlying human performances on the basis of the work initiated by Pietro Enrico di Prampero. Starting from the concept that the maximal speed that can be attained over a given distance with a given locomotion mode is directly proportional to the maximal sustainable power and inversely proportional to the energy cost of locomotion, we discuss the maximal powers (and capacities) of anaerobic (lactic and alactic) and aerobic metabolisms and the factors that limit them, and the factors affecting the energy cost of various locomotion modes. Special attention is given to the role of air resistance and frictional forces. Finally, computation of performance speed is discussed along the approach originally developed by di Prampero.

Influence of repeated isometric contractions on muscle deoxygenation and pulmonary oxygen uptake kinetics in humans

The purpose of the present study was to compare simultaneously vastus lateralis (VL) deoxygenation and pulmonary O2 uptake (O2) kinetics during fatiguing knee extension exercise with minimal cardiac load. Eight healthy subjects realized an intermittent bilateral knee‐extension exercise (3‐s contraction/3‐s relaxation) at 40% of maximum voluntary contraction for 10 min. VL deoxygenation was recorded by near infrared spectroscopy at 2 Hz (NIRO‐300, Hamamatsu Photonics, Japan) and O2 was determined breath‐by‐breath (K4b2, Cosmed, Italy). After a time delay of 16 ± 5 s, deoxygenation kinetics at the onset of exercise followed an exponential time course at a significant faster rate than O2 (time constant of 5·4 ± 4·0 s vs. 31·6 ± 10·4 s, P<0·01) reflecting a mismatch between local O2 consumption and perfusion. Thereafter, a rise in O2 of 223 ± 123 ml min−1 (consistent with the mathematical model, 259 ± 126 ml min−1) was observed between minutes 2 and 10. During the same exercise time, changes in tissue oxygenation index decreased significantly and were individually correlated with the corresponding increased O2 (P<0·05), suggesting that the majority of the slow rise of O2 arose from the exercising limbs. Averaged heart rate increased from 67 ± 11 to 116 ± 20 beats min−1 during exercise. Knee extension exercise may be relevant to estimate the cardiopulmonary and deoxygenation of working skeletal muscle responses for assessment of exercise limiting factors in clinical settings or in the exercise physiology.

Cardiovascular re-adjustments and baroreflex response during clinical reambulation procedure at the end of 35-day bed rest in humans

During the reambulation procedure after 35-day head-down tilt bed rest (HDTBR) for 9 men, we recorded for the first time heart rate (HR; with electrocardiogram) and arterial pressure profiles (fingertip plethysmography) for 5 min in HDTBR and horizontal (SUP) positions, followed by 12 min in standing position, during which 4 subjects fainted (intolerant, INT) and were laid horizontal again (Recovery). We computed: mean arterial pressure (P̄; pressure profiles integral mean), stroke volume (SV; obtained with Modelflow method), and cardiac output (Q̇; SV × HR). All cardiovascular data remained stable in HDTBR and SUP for both groups (EXP). Taking the upright posture, EXP showed a decrease in SV and an increase in HR, becoming significantly different from SUP within 1 min. Further evolution of these parameters kept Q̇ stable in both groups until the second minute of standing. Afterward, in INT, P̄ precipitated without further HR increases: SV stopped being corrected and Q̇ reached 2.9 ± 0.4 L·min(-1) at the last 15 s of standing. Sudden drop in P̄ allowed identification of a low-pressure threshold in INT (70.7 ± 12.9 mm Hg), after which syncope occurred within 80 s. During Recovery, baroreflex curves showed a flat phase (P̄ increase, HR stable), followed by a steep phase (P̄ increased, HR decreased, starting when P̄ was 84.5 ± 12.5 mm Hg and Q̇ was 9.6 ± 1.5 L·min(-1)). INT, in contrast with tolerant subjects, did not sustain standing because HR was unable to correct for the P̄ drop. These results indicate a major role for impaired arterial baroreflexes in the onset of orthostatic intolerance.

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

PURPOSE We hypothesized that the third dynamic phase (ϕ3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase (ϕ2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. METHODS Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (fH), stroke volume (SV), cardiac output (Q˙). RESULTS The fH, SV and Q˙ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady ϕ2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p<0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. CONCLUSIONS The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine ϕ3, the increase in CO2 stores might play a central role in eliciting their activation.

Vastus lateralis oxygenation dynamics during maximal fatiguing concentric and eccentric isokinetic muscle actions

The present study aimed to assess whether high intensity exhaustive eccentric (ECC) exercise was associated with a greater decrease in muscle oxygenation compared to high intensity exhaustive concentric (CON) exercise during maximal isokinetic knee extensions. On two separate days, ten recreationally active participants performed maximal isokinetic concentric (KE(CON)) and eccentric (KE(ECC)) knee extension exercises at 60°s(-1) until exhaustion. Muscle oxygenation profile and activity were acquired continuously from the vastus lateralis (VL) muscle using near-infrared spectroscopy, along with surface electromyography (sEMG). The torque output was significantly greater during KE(ECC) (P<0.01). Total time to exhaustion was longer in ECC condition (P<0.01). The decrease in tissue oxygenation index observed between the beginning and end-exercise values was significantly greater during KE(ECC) than during KE(CON) (P<0.05) while total haemoglobin volume did not differ significantly. KE(ECC) resulted in a significant increase in end-exercise integrated sEMG (P<0.05). We propose that the associated higher intramuscular pressure may have compressed blood vessels and led to a greater decrease in tissue oxygenation index. The observed end-exercise increase in neural drive during KE(ECC) may have occurred to prevent from muscle performance decrease. These results suggest that, over time, repeated maximal ECC actions induce a greater O(2) extraction compared to maximal CON actions.

Cardiac output, O2 delivery and V˙O2 kinetics during step exercise in acute normobaric hypoxia

We hypothesised that phase II time constant (τ2) of alveolar O2 uptake ( [Formula: see text] ) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery ( [Formula: see text] ). To test this hypothesis, breath-by-breath [Formula: see text] and beat-by-beat [Formula: see text] were measured in eight male subjects (25.4±3.4yy, 1.81±0.05m, 78.8±5.7kg) at the onset of cycling exercise (100W) in normoxia and acute hypoxia ( [Formula: see text] ). Blood lactate ([La]b) accumulation during the exercise transient was also measured. The τ2 for [Formula: see text] was shorter than that for [Formula: see text] in normoxia (8.3±6.8s versus 17.8±3.1s), but not in hypoxia (31.5±21.7s versus 28.4 5.4±5.4s). [La]b was increased in the exercise transient in hypoxia (3.0±0.5mM at exercise versus 1.7±0.2mM at rest), but not in normoxia. We conclude that the slowing down of the [Formula: see text] kinetics generated the longer τ2 for [Formula: see text] in hypoxia, with consequent contribution of anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in [La]b.