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The immediate postexercise/physical activity period is critical for sickle cell trait (SCT) carriers and disease (SCD) patients. Exercise-related blood acidosis is known to trigger the cascade of HbS deoxygenation and polymerization, leading to red blood cell sickling and subsequent complications. Unfortunately, two facts worsen exercise-related blood acidosis during the initial postexercise period: First, blood lactate and H+ concentrations continue to increase for several minutes after exercise completion, exacerbating blood acidosis. Second, blood lactate concentration remains elevated and pH altered for 20–45 min during inactivity after intense exercise, keeping acid/base balance disturbed for a long period after exercise. Therefore, the risk of complications (including vasoocclusive crises and even sudden death) persists and even worsens several minutes after intense exercise completion in SCT carriers or SCD patients. Light physical activity following intense exercise (namely, active recovery) may, by accelerating lactate removal and acid/base balance restoration, reduce the risk of complications. Scientific evidence suggests that light exercise at or below the first lactate threshold is an appropriate strategy.

Sickle cell disease (SCD) patients display skeletal muscle hypotrophy, altered oxidative capacity, exercise intolerance and poor quality of life. We previously demonstrated that moderate-intensity endurance training is beneficial for improving muscle function and quality of life of patients. The present study evaluated the effects of this moderate-intensity endurance training program on skeletal muscle structural and metabolic properties. Of the 40 randomized SCD patients, complete data sets were obtained from 33. The training group (n = 15) followed a personalized moderate-intensity endurance training program, while the non-training (n = 18) group maintained a normal lifestyle. Biopsies of the vastus lateralis muscle and submaximal incremental cycling tests were performed before and after the training program. Endurance training increased type I muscle fiber surface area (P = .038), oxidative enzyme activity [citrate synthase, P

The main finding of the present study was that the metabolic changes associated with a moderate-intensity muscle exercise were slightly modified in stable sickle cell anemia patients and sickle cell trait carriers as compared to controls but still in the normal range. The present results strongly support the safety of a moderate-intensity exercise for stable sickle cell anemia patients and sickle cell trait carriers.

This study aimed to test if the non-oxidative energy supply (estimated by the accumulated oxygen deficit) is associated with an index of muscle lactate accumulation during exercise, muscle monocarboxylate transporter content and the lactate removal ability during recovery in well-trained rowers. Seventeen rowers completed a 3-min all-out exercise on rowing ergometer to estimate the accumulated oxygen deficit. Blood lactate samples were collected during the subsequent passive recovery to assess individual blood lactate curves, which were fitted to the bi-exponential time function: La(t)= [La](0)+A1·(1–e–γ 1 t)+A2·(1–e–γ 2 t), where the velocity constants γ1 and γ2 (min–1) denote the lactate exchange and removal abilities during recovery, respectively. The accumulated oxygen deficit was correlated with the net amount of lactate released from the previously active muscles (r =0.58, P

Introduction The understanding of fatigue in hypoxia is limited due to: lack of control in arterial saturation, different exercise intensities and hypoxia levels, lag time between exercise cessation and fatigue evaluation. We aimed at evaluating fatigue during cycling and immediately after exhaustion (EXH) in normoxia, moderate and severe hypoxia at relative and absolute intensities. Methods Thirteen subjects completed three sessions in normoxia, moderate, and severe hypoxia with intensity based on percentage of normoxic maximal power output (NOR, MODABS, SEVABS) plus two sessions where intensity was based on the corresponding environmental condition (MODREL, SEVREL). Arterial saturation was clamped at 85% and 70% in moderate and severe hypoxia, respectively. Before, during cycling, and at EXH, maximum voluntary contraction (MVC), peripheral fatigue (high-frequency doublet [Db100], twitch [Pt]), and central fatigue (cortical voluntary activation [VATMS]) were evaluated without delay using an innovative ergometer. Results Time to EXH declined not only with hypoxia level at absolute but also relative intensities compared to NOR. At isotime, MVC, Pt, and Db100 were similarly depreciated in NOR, MODREL, and SEVREL. At EXH, there was a similar reduction among conditions in MVC (-26% to -31%), Db100 (-25% to -35%) and VATMS (-9% to -13%). However, Pt was less decreased in SEVREL compared with NOR (-33% ± 17% vs -46% ± 16%). Conclusions The shorter time to EXH in relative hypoxia and yet lower peripheral fatigue and similar central fatigue compared with normoxia suggests that hypoxia per se may affect brain areas not directly implicated in quadriceps motor function.

Oxidative stress is a key feature in the pathophysiology of sickle cell disease. Endurance training has been shown to reduce oxidative stress in the heart and the liver of sickle mice. However, the effects of endurance training on skeletal muscles, which are major producers of reactive oxygen species during exercise, are currently unknown. The aim of this study was to evaluate the effect of sickle genotype on prooxidant/antioxidant response to individualized endurance training in skeletal muscles of sickle mice. Healthy and homozygous Townes sickle mice were divided into trained or sedentary groups. Maximal aerobic speed and V̇O2peak were determined using an incremental test on a treadmill. Trained mice ran at 40% to 60% of maximal aerobic speed, 1 h/day, 5 days/week for 8 weeks. Oxidative stress markers, prooxidant/antioxidant response, and citrate synthase enzyme activities were assessed in thegastrocnemius, in theplantaris, and in thesoleusmuscles. Maximal aerobic speed and V̇O2peak were significantly reduced in sickle compared to healthy mice (-57% and -17%;p<0.001). NADPH oxidase, superoxide dismutase, and catalase activities significantly increased after training in thegastrocnemiusof sickle mice only. A similar trend was observed for citrate synthase activity in sickle mice (p=0.06). In this study, we showed an adaptive response to individualized endurance training on the prooxidant/antioxidant balance in thegastrocnemius,but neither in theplantarisnor in thesoleusof trained sickle mice, suggesting an effect of sickle genotype on skeletal muscle response to endurance treadmill training.

What is the central question of this study? The aim of this study was to evaluate the potential beneficial effects of endurance training during an ischaemia-reperfusion protocol in a mouse model of sickle cell disease (SCD). What is the main finding and its importance? Endurance training did not reverse the metabolic defects induced by a simulated vaso-occlusive crisis in SCD mice, with regard to intramuscular acidosis, mitochondrial dysfunction or anatomical properties. Our results suggest that endurance training would reduce the number of vaso-occlusive crises rather than the complications related to vaso-occlusive crises.The aim of this study was to investigate whether endurance training could limit the abnormalities described in a mouse model of sickle cell disease (SCD) in response to an ischaemia-reperfusion (I/R) protocol. Ten sedentary (HbSS-SED) and nine endurance-trained (HbSS-END) SCD mice were submitted to a standardized protocol of I/R of the leg, during which ATP, phosphocreatine and inorganic phosphate concentrations and intramuscular pH were measured using magnetic resonance spectroscopy. Forty-eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured. Although the time course of protons accumulation was slightly different between trained and sedentary mice (P 0.05), the extent of acidosis was similar at the end of the ischaemic period. The initial rate of phosphocreatine resynthesis measured at blood flow restoration, illustrating mitochondrial function, was not altered in trained mice compared with sedentary mice. Although several oxidative stress markers were not different between groups (P 0.05), the I/R-related increase of uric acid concentration observed in sedentary SCD mice (P 0.05) was not present in the trained group. The spleen weight, generally used as a marker of the severity of the disease, was not different between groups (P 0.05). In conclusion, endurance training did not limit the metabolic consequences of an I/R protocol in skeletal muscle of SCD mice, suggesting that the reduction in the severity of the disease previously demonstrated in the basal state would be attributable to a reduction of the occurrence of vaso-occlusive crises rather than a decrease of the deleterious effects of vaso-occlusive crises.

Epub ahead of print; Sickle cell disease (SCD) is a genetic hemoglobinopathy leading to two major clinical manifestations: severe chronic hemolytic anemia and iterative vaso-occlusive crises. SCD is also accompanied by profound muscle microvascular remodeling. The beneficial effects of endurance training on microvasculature are widely known. The aim of this study was to evaluate the effects of an endurance training program on microvasculature of skeletal muscle in SCD patients. A biopsy of the vastus lateralis muscle and submaximal incremental exercise were performed before and after the training period. Of the forty randomized SCD patients, complete data sets from 32 were obtained. The training group (n=15) followed a personalized moderate-intensity endurance training program, while the non-training (n=17) group maintained a normal lifestyle. Training consisted of three 40-minute cycle ergometer exercise sessions per week for 8 weeks. Histological analysis highlighted microvascular benefits in the training SCD patients compared to non-training patients, including increases in capillary density (CD) (P = .003), number of capillaries around a fiber (CAF) (P = .015) and functional exchange surface (LC/PF) (P < .0001). Conversely, no significant between-group difference was found in the morphology of capillaries. Indexes of physical ability also improved in the training patients. The moderate-intensity endurance exercise training program improved the muscle capillary network and partly reversed the microvascular defects commonly observed in skeletal muscle of SCD patients. This trial was registered at www.clinicaltrials.gov as #NCT02571088.

Although strenuous exercise may expose sickle cell disease (SCD) patients to risks of vaso-occlusive crisis, evidence suggests that regular endurance exercise may be beneficial. This study aimed to test (i) the safety and usefulness of a submaximal incremental exercise in evaluating physical ability of SCD patients and identify a marker for the management of endurance exercise and (ii) the feasibility of endurance exercise sessions in SCD patients.Twenty adults with SCD (12 men and 8 women) performed a submaximal incremental exercise used to determine the first lactate threshold (LT1) and stopped as soon as blood lactate concentration ([lactate]b) reached ≥4 mmol·L. Fifteen of those patients (8 men and 7 women) also performed three 30-min endurance exercise sessions at ~2.5 mmol·L of [lactate]b on separate occasions.LT1 occurred at 47 ± 3 and 33 ± 3 W for men and women, respectively, demonstrating the extreme deconditioning and, thus, low physical ability of adult SCD patients. During endurance exercise, peripheral oxygen saturation and [lactate]b most often remained stable and within acceptable ranges.The proposed strategy of submaximal incremental exercise allowed safe determination of LT1, an important parameter of patients' physical ability. The study also demonstrated the feasibility and safety of individually tailored endurance exercises at ~2.5 mmol·L of [lactate]b. These latter results suggest that endurance training programs may be considered for adult SCD patients and that the method proposed here may be helpful in that regard.

The aim of this study was to investigate lactate recovery kinetics after high-intensity exercises. Six competitive middle-distance runners performed 500-, 1000-, and 1500-m trials at 90 % of their current maximal speed over 1500 m. Each event was followed by a passive recovery to obtain blood lactate recovery curves (BLRC). BLRC were fitted by the bi-exponential time function: La(t) = La(0) + A 1(1–e −γ1t ) + A 2(1–e −γ2t ), where La(0) is the blood lactate concentration at exercise completion, and γ 1 and γ 2 enlighten the lactate exchange ability between the previously active muscles and the blood and the overall lactate removal ability, respectively. Applications of the model provided parameters related to lactate release, removal and accumulation rates at exercise completion, and net amount of lactate released during recovery. The increase of running distance was accompanied by (1) a continuous decrease in γ 1 (p

Summary Background Exercise could be a triggering factor for vaso-occlusive crises in patients with sickle-cell disease. We aimed to investigate whether a patient-adapted training programme of moderate endurance exercise could be safe and beneficial for patients with sickle-cell disease. Methods We did a multicentre, prospective, open-label, randomised controlled trial at four university hospitals in France. Eligible patients were older than 18 years, with an HbSS or S/β0-thalassaemia genotype, and with no severe chronic complications. All patients underwent cardiopulmonary exercise tests (CPETs) on a stationary bicycle with cardiac, pulmonary, laboratory, and muscle parameter evaluations at the start and end of the study period. We randomly assigned patients (1:1) to the training group (three 45-min exercise sessions per week, for 8 weeks) or the control group (no lifestyle changes) using a central computer-generated randomisation list. During baseline evaluation, patients and researchers were masked to group assignment; randomisation was done after completion of the baseline evaluation to minimise bias. The primary outcome was difference in power output at a blood lactate concentration of 4 mmol/L during CPET between baseline and the end of the 8-week training period. Patients were analysed on a per-protocol basis, excluding those who missed more than 20% of the training sessions or had other major protocol violations. This trial is registered with ClinicalTrials.gov, number NCT02571088, and is completed. Findings Between Sept 8, 2014, and Dec 11, 2015, 40 patients were enrolled (20 to each group). After exclusion of seven patients (one pregnancy, one appendicitis, one protocol violation, two lost to follow-up, and two incompatibilities with work schedule), 33 patients were analysed (15 in the training group, 18 in the control group). At the 8-week follow-up, the absolute change from baseline in mean power output at 4 mmol/L blood lactate was 7·2 W (SD 8·7) in trained patients (from 70·4 W [SD 16·2] at baseline to 77·6 W [15·1] at end of intervention) compared with −0·3 W (9·4) in controls (from 66·2 W [13·8] to 65·9 W [15·6]; mean difference between groups 7·3 W [95% CI 0·7–13·8], p=0·031). No adverse events requiring hospital admission occurred in the training group, whereas five occurred in the control group: four (20%) vaso-occlusive crises (one complicated by an acute chest syndrome), and one (6%) viral infection with isolated chest pain (hazard ratio 0·143 [95% CI 0·024–0·827; p=0·029). Interpretation Moderate-intensity endurance-exercise training seems to be safe for adults with sickle-cell disease without severe chronic complications and significantly improved their functional capacity, especially for exercise levels close to those needed for daily activities. Our findings support consideration of endurance-exercise training as a novel therapeutic strategy for patients with sickle-cell disease. Funding Societe Francaise de Cardiologie and Institut National du Sport, de l'Expertise et de la Performance (INSEP).

Sickle cell disease (SCD) is characterized by painful vaso-occlusive crisis. While there are several metabolic abnormalities potentially associated with muscular ischemia–reperfusion cycles that could be harmful in the context of SCD, the metabolic consequences of such events are still unknown. Ten controls (HbAA), thirteen heterozygous (HbAS), and ten homozygous (HbSS) SCD mice were submitted to a standardized protocol of rest–ischemia–reperfusion of the left leg during which adenosine triphosphate, phosphocreatine, and inorganic phosphate concentrations as well as intramuscular pH were measured using phosphorous magnetic resonance spectroscopy (MRS). Forty-eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured on the tibialis anterior. At the end of the ischemic period, HbSS mice had a lower pH value as compared with the HbAA and HbAS groups (P

This study aimed to compare the effect of a 40-min submaximal rowing exercise performed on ergometers with fixed and free-floating designs. Heart rate, blood lactate concentration, force and rate of force development (RFD) at the handle, stroke rate, duty factor, movement kinematics of upper and lower limbs, and muscle activity of lumbar spine muscles iliocostalis and erector spinae (IC and ESL) were measured at the beginning and at the end of a 40-min rowing exercise at ~60% of peak power output, in eleven competitive rowers. Force of lumbar extension decreased, and blood lactate increased following submaximal exercise on both ergometers. No changes in RFD, duty factor, and muscle activity of IC occurred in response to submaximal exercise. Rowing on DYN elicited higher heart rate and modified rowing kinematics (stroke rate, acceleration of the lower limbs) without changes in temporal or force application patterns compared to rowing on STAT at the same power output. Rowing on DYN was also associated with increased activity of the lumbar spine muscle ESL, which could originate from a greater range of motion, or from an increased lumbar spine muscle activity, at the same overall power.

Sickle cell disease (SCD) is the most frequent life-threatening genetic hemoglobinopathy in the world and occurs due to the synthesis of abnormal hemoglobin S (HbS). hemoglobin S-containing red blood cells (RBC) are fragile, leading to hemolysis and anemia, and adhere to the endothelium, leading to hemorheological and hemodynamical disturbances. In its deoxygenated form, HbS may polymerize, leading to sickling of red blood cells and potentially to vasoocclusive crises. Recent findings observed that SCD patients demonstrate significant skeletal muscle remodeling and display reduced muscle functional capacities, contributing to exercise intolerance and poor quality of life. Although acute high-intensity exercise is not recommended for SCD patients because it may increase the risk of sickling, regular moderate-intensity physical activity could have beneficial effects on skeletal muscle and more generally on the well-being of SCD patients. This article reviews the literature regarding the impact of the disease on muscular tissue characteristics and function, as well as the corresponding implications for SCD patients' quality of life.

New findings What is the topic of this review? The aim of this review is to discuss the potential involvement of exercise-induced acidosis in the commonly reported complications in sickle cell disease. What advances does it highlight? Blood acidosis appears clearly to be a risk factor for HbS polymerization, red blood cell sickling and the occurrence of vaso-occlusive crisis and could induce hyperkalaemia-related complications. It could be of great interest to try to avoid blood acidosis during exercise, which could be done using some alkalinizing solutions or adapted endurance training interventions. Abstract Sickle cell disease (SCD) is an inherited haemoglobin (Hb) disorder and the most common monogenic disease in the world. The root cause of this pathology is the synthesis of an abnormal Hb (HbS) that polymerizes in deoxygenated conditions, leading to the sickling of red blood cells. Acidosis is well recognized as a promoter of HbS polymerization and therefore red blood cell sickling. Indeed, it has been shown in vitro that the relative amount of sickled red blood cells increases markedly from 1% at pH 7.4 to >90% at pH 7.0. Nevertheless, no study has directly tested whether exercise-induced acidosis could favour SCD complications. Greater knowledge of the effects of metabolic acidosis during exercise could be of importance given the conclusions reached in several studies that proposed regular physical exercise as a therapeutic strategy in the management of SCD. In this review, we discuss the potential consequences of exercise-induced acidosis for the pathophysiology of SCD. We also propose some potential therapeutic interventions with the aim of reducing the metabolic acidosis related to exercise.

International audience; The aim of this study was to compare the physiological responses and rowing efficiency on two different rowing ergometers: the Concept2 stationary versus dynamic ergometers. Eleven oarswomen and oarsmen rowed four minutes at 60% and 70% of peak power output on both ergometers (randomized order). Power output, stroke rate, heart rate, oxygen uptake, carbon dioxyde production, lactate accumulation and rating of perceived exertion were recorded at each stage on the two ergometers. Gross and net efficiencies were computed. Exercise intensity was associated with increases in all parameters. Rowing on dynamic ergometer was associated with higher heart rate, oxygen uptake, carbon dioxyde production and stroke rate, concomitantly to lower blood lactate accumulation but also lower gross and net efficiencies. The present study showed that rowing efficiency and blood lactate accumulation were lower on the Concept2 dynamic ergometer than on its stationary counterpart. If the use of the Concept2 dynamic ergometer may provide some advantages (reduced risk of injuries), its utilisation requires specific evaluation of physiological responses during an incremental exercise for an adapted management of training.

The present study investigated morphological and physiological factors of rowing ergometer performance over 2000 m (P2000, W) in 70 national and international level [27 lightweight (LW) and 43 heavyweight (HW)] female rowers. Maximal oxygen uptake (V̇O2max, L.min−1), maximal aerobic power (Pamax, W), power output corresponding to 4 mmol.L−1 blood lactate concentration expressed in absolute (PLa4, W) and relative to Pamax (PLa4%, %) values, peak power output (Ppeak, W), and rowing gross efficiency (RGE, %) were determined during an incremental rowing test. In the whole group, Ppeak was the best predictor of P2000 (r=0.89, p

Sickle cell disease (SCD) mice (Townes model of SCD) presented exacerbated exercise-induced acidosis and fatigability as compared to control animals. We hypothesize that endurance training could represent a valuable approach to reverse these muscle defects. Endurance-trained HbAA (HbAA-END, n=10), HbAS (HbAS-END, n=11) and HbSS (HbSS-END, n=8) mice were compared to their sedentary counterparts (10 HbAA-SED, 10 HbAS-SED and 9 HbSS-SED mice) during two rest - exercise - recovery protocols during which muscle energetics and function were measured. In vitro analyses of some proteins involved in muscle energetics, pH regulation and oxidative stress were also performed. Exercise-induced acidosis was lower in HbSS-END mice as compared to their sedentary counterparts during both moderate (p0.001) and intense (p0.1) protocols. The total force production measured during both protocols was higher in trained mice compared to sedentary animals. In vitro analyses revealed that enolase/citrate synthase ratio was reduced in HbSS-END (p0.001) and HbAS-END (p0.01) mice compared to their sedentary counterparts. In addition, malondialdehyde concentration was reduced in trained mice (p0.05). In conclusion, endurance training would reverse the more pronounced exercise-induced acidosis, reduce oxidative stress and ameliorate some of the muscle function parameters in SCD mice.

Currently, cortical voluntary activation (VATMS) is assessed by superimposing transcranial magnetic stimulation (TMS) on a maximal voluntary contraction (MVC), 75% MVC and 50% MVC, each contraction being interspersed with 5–10 s of relaxation. Here, we assessed whether this traditional approach (TRADI) underestimates central fatigue due to this short recovery compared to a continuous method (CONTI). VATMS, motor-evoked potential (MEP), and cortical silent period (CSP) of the vastus lateralis were determined in 12 young healthy adults before and after a 2-min sustained MVC of knee extensors in two randomly assigned sessions. In TRADI, evaluations comprised a 7-s rest between the three contractions (100, 75, and 50% MVC) and evaluation following the 2-min sustained MVC started after a minimal rest (3–4 s). In CONTI, evaluations were performed with no rest allowed between the three levels of contraction, and evaluation after the 2-min sustained MVC commenced without any rest. MVC was equally depressed at the end of the 2 min in both conditions. Post 2-min sustained MVC, VATMS change was greater in CONTI than in TRADI (−29 (15)% [−42, −17] vs. −9 (4)% [−13, −5], respectively, P

International audience; While sickle cell disease (SCD) is characterized by frequent vaso-occlusive crisis (VOC), no direct observation of such an event in skeletal muscle has been performed in vivo. The present study reported exacerbated in vivo metabolic changes suggestive of a spontaneous muscular VOC in exercising muscle of a sickle cell mouse. Using magnetic resonance spectroscopy of phosphorus 31, phosphocreatine and inorganic phosphate concentrations and intramuscular pH were measured throughout two standardized protocols of rest – exercise – recovery at two different intensities in ten SCD mice. Among these mice, one single mouse presented divergent responses. A statistical analysis (based on confidence intervals) revealed that this single mouse presented slower phosphocreatine resynthesis and inorganic phosphate disappearance during the post-stimulation recovery of one of the protocols, what could suggest an ischemia. This study described, for the first time in a sickle cell mouse in vivo, exacerbated metabolic changes triggered by an exercise session that would be suggestive of a live observation of a muscular VOC. However, no evidence of a direct cause-effect relationship between exercise and VOC has been put forth.

Sickle cell disease (SCD) is associated with an impaired oxygen delivery to skeletal muscle that could alter ATP production processes. The present study aimed to determine the effects of sickle hemoglobin (HbS) on muscle pH homeostasis in response to exercise in homozygous (HbSS, n = 9) and heterozygous (HbAS, n = 10) SCD (Townes) mice in comparison to control (HbAA, n = 10) littermates. Magnetic resonance spectroscopy of phosphorus 31 enabled to measure intramuscular pH and phosphocreatine (PCr) concentration during rest-stimulation-recovery protocols at two different intensities. Maximal activity of some enzymes involved in muscle energetics and content of proteins involved in pH regulation were also investigated. HbSS mice presented a more pronounced exercise-induced intramuscular acidosis, whatever the intensity of exercise. Moreover, the depletion of PCr was also exacerbated in HbSS mice in response to intense exercise as compared with both HbAA and HbAS mice ( P < 0.01). While no difference was observed concerning proteins involved in muscle pH regulation, the activity of enolase (a glycolytic enzyme) was higher in both HbSS and HbAS mice as compared with controls ( P < 0.05). Interestingly, HbAS mice presented also metabolic impairments as compared with their control counterparts. This study has identified for the first time an exacerbated exercise-induced intramuscular acidosis in SCD mice.NEW & NOTEWORTHY The main finding of the present study was that the exercise-induced intramuscular acidosis was systematically more pronounced in sickle cell disease (SCD) mice as compared with their control counterparts. This result is important since it has been demonstrated in vitro that acidosis can trigger hemoglobin polymerization. From that point of view, our results tend to support the idea that high-intensity exercise may increase the risk of hemoglobin polymerization in SCD.

Although fatigue generally increases the energy cost of running (Cr), the changes of Cr and associated variables during an ultramarathon are not known. This study aimed to determine the changes of metabolic and cardiovascular adjustments during an ultraendurance exercise.Twelve healthy males ran 24 h on a motorized treadmill (24TR). Overall oxygen consumption (V˙O2 mL·min·kg), net energy cost (Cr J·kg·m), and respiratory exchange ratio (RER) were determined before, every 2 h, and after the 24TR at 8 km·h. Running speed and heart rate (HR) were continuously measured during the 24TR.V˙O2 increased (+7.6%, P0.001) during the 24TR, principally in the first 8 h of exercise. The RER mirrored changes in V˙O2, that is, decreased significantly until the eighth hour and remained constant thereafter. As a consequence of RER decrease, the increased Cr was markedly attenuated but was still significantly higher at the 8th and 12th hour compared with pre-24TR. Speed was constant over the first 6 h then significantly decreased during the 24TR. HR increased until the sixth hour (i.e., HR drift), then decreased until post-24TR. Furthermore, a significant positive correlation (R = 0.75, P0.01) was observed between the velocity sustained during the 24TR (expressed in percentage of the velocity attained at V˙O2max: %VV˙O2max) and the pre- to postchanges in Cr.The present study characterized accurately the changes of energy cost and substrate use during an extreme run, showing a plateau after 8 h of exercise. It is also concluded that the participants who maintained the highest %VV˙O2max were also those having most deteriorated their Cr over the 24TR, supporting the notion of a trade-off between running speed (relative to VV˙O2max) and Cr.

This experiment investigated the fatigue induced by a 24-h running exercise (24TR) and particularly aimed at testing the hypothesis that the central component would be the main mechanism responsible for neuromuscular fatigue. Neuromuscular function evaluation was performed before, every 4 h during, and at the end of the 24TR on 12 experienced ultramarathon runners. It consisted of a determination of the maximal voluntary contractions (MVC) of the knee extensors (KE) and plantar flexors (PF), the maximal voluntary activation (%VA) of the KE and PF, and the maximal compound muscle action potential amplitude (Mmax) on the soleus and vastus lateralis. Tetanic stimulations also were delivered to evaluate the presence of low-frequency fatigue and the KE maximal muscle force production ability. Strength loss occurred throughout the exercise, with large changes observed after 24TR in MVC for both the KE and PF muscles (−40.9 ± 17.0 and −30.3 ± 12.5%, respectively; P < 0.001) together with marked reductions of %VA (−33.0 ± 21.8 and −14.8 ± 18.9%, respectively; P < 0.001). A reduction of Mmax amplitude was observed only on soleus, and no low-frequency fatigue was observed for any muscle group. Finally, KE maximal force production ability was reduced to a moderate extent at the end of the 24TR (−10.2%; P < 0.001), but these alterations were highly variable ( ± 15.7%). These results suggest that central factors are mainly responsible for the large maximal muscle torque reduction after ultraendurance running, especially on the KE muscles. Neural drive reduction may have contributed to the relative preservation of peripheral function and also affected the evolution of the running speed during the 24TR.

B Gellen and L Messonnier, and L Feasson and P Bartolucci equally contributed to this work Introduction Sickle cell disease (SCD) is the most common inherited disease worldwide. Because favoring the risk of vaso-occlusive crises (VOC), SCD patients are banned from strenuous exercise. We hypothesized that a well-controlled moderate-intensity endurance exercise training (EET) program could improve SCD patients without provoking VOC. Patients and Methods: Weconducted aprospective, multicenter, controlled study with individually tailored Blood lactate-guided (BL) endurance training on a cycloergometer for 8 weeks in adult SCD patients. The primary end point was the submaximal incremental cardio-pulmonary exercise testing (CPET) at a BL concentration of 4 mmol.L-1. Secondary endpoints were: CPET at a BL 2.5 mmol/L and at the first lactic threshold (LT1), BL levels at given workload level (Female: 40W and Male: 60W), safety (pain, VOC and acute chest syndrome), biological and echocardiography parameters, pulmonary function test (PFT), 6-minute walk test (6MWT), quality of life (QoL) and muscle properties and vascularization (biopsy of vastus lateralis muscle). Results: Forty homozygous SCD patients (33±10 years, 23 male) were included. Four patients (3 EET and 1 control) were lost to follow-up. Data of 33 patients (15 EET and 18 controls) were analyzed. EET and control patients were comparable at baseline with regard to CPET, clinical, biological, and resting cardiorespiratory parameters. EET patients presented a significant increase of CPET workload at BL4 (p=0.031), BL2.5 (p=0.003) and LT1 (p Conclusion In SCD patients, EET based on Blood lactate guidance is safe and yields a significant functional benefit. This benefit is linked essentially to improved oxidative function of the peripheral skeletal musculature. Disclosures Galactéros: Addmedica: Membership on an entity's Board of Directors or advisory committees. Bartolucci: GBT: Membership on an entity's Board of Directors or advisory committees; Addmedica: Research Funding; Fondation Fabre: Research Funding; Novartis US: Membership on an entity's Board of Directors or advisory committees.

This report describes the changes in physiological capacity of a heavy-weight rower who obtained seven medals in World Championships and Olympic Games. The investigation was carried out over the last 6 years of the rower’s international competition career in comparison with peer champions, and the following 4 years. Over the first period, maximal oxygen uptake ( $$ \dot{V}{\text{O}}_{2\max } $$ ) remained above 6 l min−1 which is an outstanding value. The training load measured over the last 18 months of the period increased from 119 to 142 km wk−1 of rowing. Four years after the international competition period, $$ \dot{V}{\text{O}}_{2\max } $$ had only declined by 3.6% although the training load had declined by 35%. These data suggest that the ability of this rower to compete at top level for years was related to ability to maintain an outstanding $$ \dot{V}{\text{O}}_{2\max } $$ . Gross efficiency and ability to rely on anaerobic glycolysis did not emerge as relevant factors.

To assess whether the ability to demonstrate a plateau in oxygen consumption VO2 could be related to adaptation to exercise, the data obtained over a period of 10 years on 94 elite oarsmen who had participated in annual testing were re-evaluated. The test consisted in an incremental step protocol until volitional exhaustion. VO2, heart rate (HR), blood lactate ([La]b) and respiratory exchange ratio (RER) were measured at each step. The maximal oxygen consumption (VO2max), the power corresponding to VO2maxPamax and the maximal power achieved (Ppeak) were recorded. Thirty-eight oarsmen achieved a VO2 plateau and were designated as Pla; 56 did not and were designed as N-Pla. The Pla and N-Pla VO2max, Pamax and maximal HR values were similar. In comparison with N-Pla, the Pla group displayed a rightward shift of the [La]b versus power curve, accounted for by both the increased percentage of VO2max corresponding to 4 mmol l(-1) and the decreased value of [La]b corresponding to Pamax (P

We examine the influence of the cytosolic and membrane-bound contents of carbonic anhydrase (CA; CAII, CAIII, CAIV, and CAXIV) and the muscle content of proteins involved in lactate and proton transport [monocarboxylate transporter (MCT) 1, MCT4, and Na+/H+exchanger 1 (NHE1)] on work capacity during supramaximal exercise. Eight healthy, sedentary subjects performed exercises at 120% of the work rate corresponding to maximal oxygen uptake (Ẇmax) until exhaustion in placebo (Con) and metabolic alkalosis (Alk) conditions. The total (Wtot) and supramaximal work performed (Wsup) was measured. Muscle biopsies were obtained before and immediately after standardized exercises (se) at 120% Ẇmaxin both conditions to determine the content of the targeted proteins, the decrease in muscle pH (ΔpHm), and the muscle lactate accumulation ([Lac]m) per joule of Wsup(ΔpHm/Wsup-seand Δ[Lac]m/Wsup-se, respectively) and the dynamic buffer capacity. In Con, Wsupwas negatively correlated with ΔpHm/Wsup-se, positively correlated with Δ[Lac]m/Wsup-seand MCT1, and tended to be positively correlated with MCT4 and NHE1. CAII + CAIII were correlated positively with ΔpHm/Wsup-seand negatively with Δ[Lac]m/Wsup-se, while CAIV was positively related to Wtot. The changes in Wsupwith Alk were correlated positively with those in dynamic buffer capacity and negatively with Wsupin Con. Performance improvement with Alk was greater in subjects having a low content of proteins involved in pH regulation and lactate/proton transport. These results show the importance of pH regulating mechanisms and lactate/proton transport on work capacity and the role of the CA to delay decrease in pHmand accumulation in [Lac]mduring supramaximal exercise in humans.

Sickle cell anemia (SCA) is a hemoglobinopathy leading to major hematologic, hemorheologic, and hemodynamic disorders that induce various complications, including organ failure, and ultimately lead to death. Here, we assessed for the first time repercussions of SCA on skeletal muscle and its microvasculature. Twenty-seven sedentary Cameroonian volunteer men participated in the study. They were assigned to one of three groups according to their hemoglobin status (healthy control subjects, n = 10; sickle cell trait carriers, n = 10; and SCA patients, n = 7) and underwent muscle biopsy of the vastus lateralis. SCA was associated with microvessel rarefaction, decrease in capillary tortuosity, and widening of microvessel diameter. The absence of capillary wall reinforcement was shown by lack of wall thickening and lack of fibrous tissue or smooth muscle in their constitution. We also observed changes in fiber type distribution, muscle atrophy, an increase in satellite cell number, and a decrease in activity of creatine kinase and several oxidative enzymes. No signs of tissue necrosis, inflammatory stress, fibrosis, or segmented fibers were observed. The present study highlighted marked effects of SCA on microvascular, structural, and energetic characteristics of skeletal muscle.

The purpose of the present study was to relate the training-induced alterations in lactate kinetics parameters to the concomitant changes in time to exhaustion (T(lim)) at a work rate corresponding to maximal oxygen uptake (Pa(peak)). Eight subjects performed before and after training i) an incremental exercise up to exhaustion to determine Pa(peak), ii) a 5-min 90 % Pa(peak) exercise followed by a 90-min passive recovery to determine an individual blood lactate recovery curve fitted to the bi-exponential time function: La(t) = La(0) + A1(1 - e -gamma1 x t) + A2(1 - e -gamma2 x t), and iii) a time to exhaustion at Pa peak to determine T lim. A biopsy of the vastus lateralis muscle was made before and after training. The training programme consisted in pedalling on a cycle ergometer 2 h a day, 6 days a week, for 4 weeks. Training-induced increases (p < 0.05) in Pa(peak), muscle capillary density, citrate synthase activity, gamma2 that denotes the lactate removal ability (from 0.0547 +/- 0.0038 to 0.0822 +/- 0.0071 min (-1)) and T(lim) (from 299 +/- 23 to 486 +/- 63 s), decreases (p < 0.05) in activities of lactate dehydrogenase (LDH) and muscle type of LDH, the phosphofructokinase/citrate synthase activities ratio and the estimated net amount of lactate released (NALR) during exercise recovery (from 66.5 +/- 8.6 to 47.2 +/- 11.1 mmol) were also observed. The improvement of T (lim) with training was related to the increase in gamma2 (r = 0.74, p = 0.0367) and to the decrease in NALR (r = 0.77, p = 0.0250). These results suggest that the post-training greater ability to remove lactate from the organism and reduced muscle lactate accumulation during exercise account for the concomitant improvement of the time to exhaustion during high-intensity exercise performed at the same relative work rate.

We related the rowing performance and the associated physiological parameters to the training load as estimated by a questionnaire addressing the mean habitual weekly energy expenditure (MHWEE) of twenty-one international and national level oarsmen. The questionnaire also addressed the energy expenditure during training (EET) sessions classified as low- (EE1), moderate- (EE2), and high-intensity (EE3). To evaluate the physiological capability of the oarsmen, they performed incremental exercise to determine their maximal oxygen uptake (V.O(2max)) and the V.O(2) relative to V.O(2max) corresponding to the 4 mmol.l(-1) blood lactate concentration (V.O(2)4 %). The mean work rate sustained during a 2000-m all-out event on a rowing ergometer was considered as the rowing performance. On average, the rowers spent 16.4 +/- 1.0 h.wk(-1) in training with 56 +/- 3 % of the time spent on the water. EET represented 43.5 +/- 1.7 % of MHWEE. Rowing performance and V.O(2max) were both related to MHWEE and EET. Also, rowing performance was related to EE1, EE2, and EE3. In contrast, V.O(2)4 % was not related to the estimated energy expenditures. These results suggest that rowing performance and V.O(2max) are related to training load while V.O(2)4 % was not in the present group of highly trained oarsmen.

The aim of the present study was to test the hypothesis that peak power output (Ppeak) sustained during maximal incremental testing would be an overall index of rowing ergometer performance over 2000 m (P2000), and to study the influence of selected physiological variables on Ppeak. A group of 54 highly trained rowers (31 heavyweight [HW] and 23 lightweight [LW] rowers) was studied. Body mass, maximal oxygen uptake ((.-)VO(2max)), oxygen consumption corresponding to a blood lactate of 4 mmol. l (-1) expressed in percentage of (.-)VO(2max) (V.O (2)La4 %), and rowing gross efficiency (RGE) were also determined during the incremental test. In the whole group Ppeak was the best predictor of P2000 (r = 0.92, p < 0.0001). Body mass (r = 0.65, p < 0.0001), V.O (2max) (r = 0.84, p < 0.0001), (.-)VO 2)La4 % (r = 0.49, p < 0.0001) and RGE (r = 0.35, p < 0.01) were significantly correlated with P2000 as well. To take the influence of body mass into account, (.-)VO(2max) was related to kg (0.57). Ppeak was significantly related to body mass (r = 0.56, p < 0.0001), (.-)VO(2max) x kg (-0.57) (r = 0.63, p < 0.0001), (.-)VO(2)La4 % (r = 0.45, p < 0.001) and RGE (r = 0.34, p < 0.05). Multiple regression analysis indicated that the above parameters taken together explained 82.8 % of Ppeak variation in the whole group. It was also demonstrated that Ppeak was the best predictor of P2000 when LW and HW groups were considered separately. It was concluded that, by integrating the main physiological factors of performance, Ppeak is an overall index of physiological rowing capacity and rowing efficiency in heterogeneous as well as in homogeneous groups. It presents the further advantage of being easily measured in the field.

Mentally imaged but unexecuted physical activity has been reported to induce a cardiorespiratory change. In order to test whether the previous experience of the performed exercise was a prerequisite to observe these changes, ventilation and heart rate were recorded during mental imagination of a rowing race in four groups of volunteers: 12 competitive rowers, 10 non-rower athletes, 12 students (22-30 years old) and 12 senior subjects (50-60 years old). Recordings were performed at rest, during the viewing of a rowing race and during mental imagination of this race. Analysis of variance revealed significant condition effect for all cardiorespiratory variables. All subjects increased their breathing rate (mean increase: 16 breaths.min(-1) in rowers, 8 breaths.min(-1) in athletes, 8 breaths.min(-1) in students, and 6 breaths.min(-1) in seniors), 29 decreased their tidal volume (mean decrease: 100 ml in rowers, 102 ml in athletes, 120 ml in students and 26 ml in seniors), with an increase in the resulting ventilation in 38 subjects (mean increase: 14 l.min(-1) in rowers, 3.6 l.min(-1) in athletes, 2.8 l.min(-1) in students, 2.6 l.min(-1) in seniors). Heart rate was increased in 34 subjects (mean increase: 12 beats.min(-1) in rowers, 5 beats.min(-1) in athletes, 6 beats.min(-1) in students and 5 beats.min(-1) in seniors). The number of subjects who exhibited changes was evenly distributed among the four groups. However, mean values of the changes were higher in rowers than in the three other groups, mainly due to three rowers who exhibited extremely large increases in cardioventilatory variables. Analysis of variance showed no significant group effect for heart rate and breathing rate. These results suggest that rowing experience may not be necessary for changes in heart rate and ventilation to be elicited by mentally imagining a rowing race.

The purpose of this study was to investigate whether track running specialisation could be associated with differences in the ability to exchange and remove lactate. Thirty-four male high-level runners were divided into two groups according to their specialty (100 - 400 m/800 - 1500 m). All performed a 1-min 25.2 km x h -1 event, followed by a 90-min passive recovery to obtain individual blood lactate recovery curves which were fitted to a bi-exponential time function: [La](t) = [La](0) + A 1 (1-e -gamma1t) + A 2 (1-e -gamma2t). The velocity constant gamma 1 which denotes the ability to exchange lactate between the previously worked muscles and blood was higher (p < 0.001) in middle-distance runners than in sprint runners. The velocity constant gamma 2 which reflects the overall ability to remove lactate did not differ significantly between the two groups. gamma 1 was positively correlated with the best performance over 800 m achieved by 16 athletes during the outdoor track season following the protocol (r = 0.55, p < 0.05). In conclusion, the lactate exchange ability seems to play a role on the athlete's capacity to sustain exercise close to 2-min-duration and specifically to run 800 m.

The effects of 4 weeks of endurance training in conditions of normoxia or hypoxia on muscle characteristics and blood lactate responses after a 5-min constant-load exercise (CLE) at 90% of the power corresponding to the maximal oxygen uptake were examined at sea-level in 13 sedentary subjects. Five subjects trained in normobaric hypoxia (HT group, fraction of oxygen in inspired gas = 13.2%), and eight subjects trained in normoxia at the same relative work rates (NT group). The blood lactate recovery curves from the CLE were fitted to a biexponential time function: La(t) = La(0) + A1(1 - e- gamma 1.t) + A2(1 - e- gamma 2.t), where the velocity constants gamma 1 and gamma 2 denote the lactate exchange and removal abilities, respectively, A1 and A2 are concentration parameters that describe the amplitudes of concentration variations in the space represented by the arterial blood, La(t) is the lactate concentration at time t, and La(0) is the lactate concentration at the beginning of recovery from CLE. Before training, the two groups displayed the same muscle characteristics, blood lactate kinetics after CLE, and gamma 1 and gamma 2 values. Training modified their muscle characteristics, blood lactate kinetics and the parameters of the fits in the same direction, and proportions among the HT and the NT subjects. Endurance training increased significantly the capillary density (by 31%), citrate synthase activity (by 48%) and H isozyme proportion of lactate dehydrogenase (by 24%), and gamma 1 (by 68%) and gamma 2 (by 47%) values. It was concluded that (1) endurance training improves the lactate exchange and removal abilities estimated during recovery from exercises performed at the same relative work rate, and (2) training in normobaric hypoxia results in similar effects on lactate exchange and removal abilities to training in normoxia performed at the same relative work rates. These results, which were obtained non-invasively in vivo in humans during recovery from CLE, are comparable to those obtained in vitro or by invasive methods during exercise and subsequent recovery.

The relationships between individual performance and lactate exchange and removal abilities were studies in 12 male rowers all subjected to three measurements on a rowing ergometer. An incremental exercise carried out to determine the maximal oxygen uptake (VO2max) and the corresponding maximal aerobic power (Pamax), a 2500-m all-out test where the mean work rate (P2500) represented the individual performance, and a 6-min 90% Pamax exercise designed to assess the lactate kinetics during the following 90 min passive recovery were performed. The lactate recovery curves were fitted to the bi-exponential time function: La(t) = La(O) + A1(1-e-gamma 1.t) + A2(1-e-gamma 2.t). The velocity constants gamma 1 and gamma 2 denote the lactate exchange and removal abilities, respectively. The mean value of P2500 sustained by the rowers was 376 +/- 41W (106 +/- 5% of Pamax (P2500%). P2500 was positively correlated with gamma 2 (P < 0.05). gamma 1 and gamma 2 explained 67% of the P2500 variance. P2500% was also correlated with gamma 2 (P < 0.01). These results suggest that a better performance on the rowing ergometer is associated with improved lactate exchange and removal abilities. Furthermore, the ability to row at high relative work rates was correlated with an increased lactate removal ability. Training-induced adaptations could explain the high gamma 1 and gamma 2 displayed by the present rowers.

The present study aimed to investigate (1) whether high-level 400-m track runners of different ethnic origin displayed divergent post-run blood lactate concentrations (p400m[La]) and (2) if this discrepancy was based on differences in lactate exchange and removal abilities. Twenty male African (n = 12) and Caucasian (n = 8) runners, paired in terms of personal record, performed (1) an all-out 400-m run to measure p400m[La] at 3, 5 and 7 min into recovery and (2) a 1-min 25.2 km h−1 running (not maximal but standardized) exercise followed by 90-min passive recovery to determine individual blood lactate recovery curves (IBLRC). IBLRCs were fitted to a bi-exponential time function: \( {\text{La(}}t )= {\text{La(}}0 )+ {{\text{A}}_1}( 1-{{\text{e}}^{ - {\gamma_ 1}t}}) + {{\text{A}}_ 2}( 1-{{\text{e}}^{ - {\gamma_ 2}t}}) \) where γ1 and γ2 denote lactate exchange ability between the previously worked muscles and blood, and overall ability for lactate removal, respectively. The quantity of lactate accumulated at the end of the 1-min exercise (QLaA) was also estimated. Our study showed that after the all-out 400-m run, p400m[La] was lower in African than in Caucasian runners at 3 and 5 min but not at 7 min into recovery. After the standardized exercise, γ1 and γ2 were lower (p < 0.01) and QLaA was higher (p < 0.05) in African than in Caucasian runners. These data suggest that for similar performance levels, ethnicity involves differences in lactate accumulation, exchange and removal.

To assess the effects of regular physical activity on muscle functional characteristics of carriers of sickle cell trait (SCT), 39 untrained (U) and trained (T) hemoglobin (Hb)AA (CON) and SCT subjects (U-CON, n = 12; U-SCT, n = 8; T-CON, n = 10; and T-SCT, n = 9) performed a graded exercise and a time to exhaustion (Tex) test, and were subjected to a muscle biopsy. Maximal power, total work performed during Tex, citrate synthase and cytochrome c oxidase (COX) activities, respiratory chain complexes I and IV content, and capillary density (CD), diameter (COD), and surface area (CSA) were upregulated by the same proportion in T-CON and T-SCT compared with their untrained counterparts. These proportionally similar differences imply that the observed discrepancies between U-SCT and U-CON remained in the trained subjects. Specifically, both CD and COX remained and tended to remain lower, and both COD and CSA remained and tended to remain higher in T-SCT than in T-CON. Besides, carriers of SCT displayed specific adaptations with regular physical activity: creatine kinase activity; complexes II, III, and V content; and type I fiber surface area and capillary tortuosity were lower or unchanged in T-SCT than in U-SCT. In summary, our results show that 1) carriers of SCT adapted almost similarly to CON to regular physical activity for most of the studied muscle characteristics, 2) oxidative potential remains altered in physically active carriers of SCT compared with HbAA counterparts, and 3) the specific remodeling of muscle microvascular network persists in the trained state.

Aim Alpha-thalassaemia is known to reduce intra-erythrocyte HbS (sickle haemoglobin) concentration in sickle cell trait (SCT) subjects. Because HbS was shown to increase oxidative stress, the purpose of this study was to assess the effects of the coexistence of α-thalassaemia and SCT on oxidative stress markers and nitric oxide (NO) metabolism after an acute physical exercise. Methods Forty subjects (age: 23.5 ± 2.21 years), SCT carriers (HbAS) or healthy subjects (HbAA), with (-αT) or without (-NαT) an associated α-thalassaemia took part in the study. Plasma markers of oxidative stress [advanced oxidation protein products (AOPP), protein carbonyl, malondialdehyde (MDA) and nitrotyrosine], anti-oxidant defences and NO metabolism (NOx) were measured at rest (Trest), immediately following an incremental maximal exercise test (Tex) and during recovery (T1h, T2h and T24h). Results Malondialdehyde expressed as the percentage of changes from baseline was significantly higher in the HbAS-NαT compared with HbAS-αT during recovery (+36.3 ± 14.1% vs. −1.8 ± 13.2% at T1h, P = 0.02; +36.6 ± 13.4% vs. −11.4 ± 12.5% at T2h, P = 0.004 and +24.1 ± 12.3% vs. −14.4 ± 11.5% at T24h, P = 0.02 in HbAS-NαT vs. HbAS-αT). Compared with HbAS-NαT, HbAS-αT had a higher NOx change from baseline at Tex (−23.4 ± 20.6% vs. +57.7 ± 19.3%, respectively; P = 0.005) and lower nitrotyrosine change from baseline at T1h (+7.2 ± 22.2% vs. +93.5%±29.3%, respectively; P = 0.04). Conclusion All these data suggest that the presence of α-thalassaemia may blunt the higher level of oxidative stress and the impaired bioavailability of NO observed in the SCT carriers.

The aim of this study was to analyze the effects of exercise training on oxidative stress in sickle cell trait carriers. Plasma levels of oxidative stress [advanced oxidation protein products (AOPP), protein carbonyl, malondialdehyde (MDA), and nitrotyrosine], antioxidant markers [catalase, glutathione peroxidase (GPX), and superoxide dismutase (SOD)], and nitrite and nitrate (NOx) were assessed at baseline, immediately following a maximal exercise test (Tex), and during recovery (T1h, T2h, T24h) in trained (T: 8 h/wk minimum) and untrained (U: no regular physical activity) sickle cell trait (SCT) carriers or control (CON) subjects (T-SCT, n = 10; U-SCT, n = 8; T-CON, n = 11; and U-CON, n = 11; age: 23.5 ± 2.2 yr). The trained subjects had higher SOD activities (7.6 ± 5.4 vs. 5.2 ± 2.1 U/ml, P = 0.016) and lower levels of AOPP (142 ± 102 vs. 177 ± 102 μM, P = 0.028) and protein carbonyl (82.1 ± 26.0 vs. 107.3 ± 30.6 nm/ml, P = 0.010) than the untrained subjects in response to exercise. In response to exercise, U-SCT had a higher level of AOPP (224 ± 130 vs. 174 ± 121 μM, P = 0.012), nitrotyrosine (127 ± 29.1 vs.70.6 ± 46.6 nM, P = 0.003), and protein carbonyl (114 ± 34.0 vs. 86.9 ± 26.8 nm/ml, P = 0.006) compared with T-SCT. T-SCT had a higher SOD activity (8.50 ± 7.2 vs. 4.30 ± 2.5 U/ml, P = 0.002) and NOx (28.8 ± 11.4 vs. 14.6 ± 7.0 μmol·l−1·min−1, P = 0.003) in response to exercise than U-SCT. Our data indicate that the overall oxidative stress and nitric oxide response is improved in exercise-trained SCT carriers compared with their untrained counterparts. These results suggest that physical activity could be a viable method of controlling the oxidative stress. This could have a beneficial impact because of its involvement in endothelial dysfunction and subsequent vascular impairment in hemoglobin S carriers.

The aim of this study was to test (a) three methods to estimate the quantity of lactate accumulated (QLaA ) in response to supramaximal exercise and (b) correlations between QLaA and the nonoxidative energy supply assessed by the accumulated oxygen deficit (AOD). Nine rowers performed a 3-min all-out test on a rowing ergometer to estimate AOD and lactate accumulation in response to exercise. Peak blood lactate concentration [(La)peak ] during recovery was assessed, allowing QLaA(m1) to be estimated by the method of Margaria et al. Application of a bicompartmental model of lactate distribution space to the blood lactate recovery curves allowed estimation of (a) the net amount of lactate released during recovery from the active muscles (NALR max ), and (b) QLaA according to two methods (QLaA(m2) and QLaA(m3)). (La)peak did not correlate with AOD. QLaA(m1), QLaA(m2) and QLaA(m3) correlated with AOD (r = 0.70, r = 0.85 and r = 0.92, respectively). These results confirm that (La)peak does not provide reliable information on nonoxidative energy supply during supramaximal exercise. The correlations between AOD and QLaA(m2) and QLaA(m3) support the concept of studying blood lactate recovery curves to estimate lactate accumulation and thus the contribution of nonoxidative pathway to energy supply during supramaximal exercise.

This study tested the hypothesis that trained sickle cell trait (SCT) carriers are not subjected to greater risk of rhabdomyolysis or renal failure in response to moderate submaximal exercise than subjects with normal hemoglobin (CONT). Blood markers in 11 trained SCT carriers and 12 control counterparts were measured before and after 40 min of exercise at 55% of peak power output (Ppeak) conducted in thermoneutral environment. Body weights decreased with exercise in the same proportion in the two groups (from 65.1 ± 7.0 kg to 64.1 ± 7.0 kg and from 70.2 ± 6.6 to 68.6 ± 6.6 kg at the end of exercise in SCT and CONT, respectively). Heart rate and rectal temperature increased in the two groups in response to exercise, but the groups remained closely matched. Serum urea, CRP, CK and LDH were similar in the two groups and remained unchanged in response to exercise. Creatinine, Na(+), K(+), Cl(-) and myoglobin concentrations increased above baseline in response to exercise, with changes of the same magnitude in the two groups. In summary, the results of the present study suggest that moderate submaximal exercise is not unsafe from a biochemical point of view for sportsmen carrying SCT.

International audience; In the military context, soldiers carry equipments of total mass often exceeding 30%-40% of their body mass (BM) and complexly distributed around their body (backpack, weapons, electronics, protections, etc.), which represents severe load carrying conditions. Purpose: This study aimed to better understand the effects of load carriage on walking energetics and mechanics during military-type walking. Methods: Ten male infantrymen recently retired from the French Foreign Legion performed 3-min walking trials at a constant speed of 4 km[middle dot]h-1 on an instrumented treadmill, during which walking pattern spatiotemporal parameters, energy cost (CW), external mechanical work (Wext), and the work done by one leg against the other during the double-contact period (Wint,dc) were specifically assessed. Three conditions were tested: (i) light sportswear (SP, reference condition considered as unloaded), (ii) battle equipment (BT, ~22 kg, ~27% of subjects' BM, corresponding to a military intermediate load), and (iii) road march equipment (RM, ~38 kg, ~46% of subjects' BM, corresponding to a military high load). Results: Repeated-measures ANOVA showed that military equipment carriage significantly (i) altered the spatiotemporal pattern of walking (all P \textless 0.01), (ii) increased absolute gross and net CW (P \textless 0.0001), and (iii) increased both absolute and mass-relative Wext (P \textless 0.01) and Wint,dc (P \textless 0.0001) but did not alter the inverted pendulum recovery or locomotor efficiency. Conclusions: Military equipments carriage induced significant changes in walking mechanics and energetics, but these effects appeared not greater than those reported with loads carried around the waist and close to the center of mass. This result was not expected because the latter has been hypothesized to be the optimal method of load carriage from a metabolic standpoint.

International audience; Trekking and military missions generally consist of carrying heavy loads for extreme durations. These factors have been separately shown to be sources of neuromuscular (NM) fatigue and locomotor alterations. However, the question of their combined effects remains unresolved, and addressing this issue required a representative context. PURPOSE: The aim was to investigate the effects of extreme-duration heavy load carriage on NM function and walking characteristics.METHODS: Ten experienced infantrymen performed a 21-h simulated military mission (SMM) in a middle-mountain environment with equipment weighing ∼27 kg during battles and ∼43 kg during marches. NM function was evaluated for knee extensors (KE) and plantar flexors (PF) pre- and immediately post-SMM using isometric maximal voluntary contraction (MVC) measurement, neural electrical stimulation and surface EMG. The twitch-interpolation method was used to assess central fatigue. Peripheral changes were examined by stimulating the muscle in the relaxed state. The energy cost, mechanical work and spatio-temporal pattern of walking were also evaluated pre-/post-SMM on an instrumented treadmill in three equipment conditions: Sportswear, Battle and March.RESULTS: After the SMM, MVC declined by -10.2±3.6% for KE (P\textless0.01) and -10.7±16.1% for PF (P = 0.06). The origin of fatigue was essentially peripheral for both muscle groups. A trend toward low-frequency fatigue was detected for KE (5.5%, P = 0.08). These moderate NM alterations were concomitant with a large increase in perceived fatigue from pre- (rating of 8.3±2.2) to post-SMM (15.9±2.1, P\textless0.01). The SMM-related fatigue did not alter walking energetics or mechanics, and the different equipment carried on the treadmill did not interact with this fatigue either.CONCLUSION: this study reports the first data on physiological and biomechanical consequences of extreme-duration heavy load carriage. Unexpectedly, NM function alterations due to the 21-h SMM were moderate and did not alter walking characteristics.CLINICAL TRIAL REGISTRATION: Name: Effect of prolonged military exercises with high load carriage on neuromuscular fatigue and physiological/biomechanical responses. Number: NCT01127191.

This study aimed to investigate if wearing compression stockings (CS) during exercise and recovery could affect lactate profile in sportsmen. Eight young healthy trained male subjects performed two maximal exercise tests on a cycle ergometer on two different occasions performed randomly: CS during both exercise and recovery, and no CS. Blood lactate concentration was taken during exercise and at 0, 3, 5, 10, 15, 30 and 60 min post-exercise. The individual blood lactate recovery curves were fitted to a biexponential time function: La(t) = La(0) + A1(1 - e(-gamma1t)) + A2(1 - e(-gamma2t)), where gamma(1) and gamma(2) denote the abilities to exchange lactate between the previously active muscles and the blood and to remove lactate from the organism, respectively. A significantly higher blood lactate value at the end of the maximal exercise was found (12.1 +/- 0.5 vs. 10.8 +/- 0.5 mmol l(-1)) wearing CS as compared to no CS (P < 0.05). Lower gamma(1) and higher gamma(2) values were observed with CS during recovery, as compared to no CS. It was concluded that CS during graded exercise leads to a significant higher blood lactate value at exhaustion. Since lactate exchanges were expected to be decreased during exercise due to CS, this result was likely attributable to a higher lactate accumulation related to a greater overall contribution of anaerobic glycolysis. Although the lactate removal ability was significantly improved when wearing CS during recovery, its efficacy in promoting blood lactate clearance after high-intensity exercise is limited.