Neuromuscular fatigability during repeated sprints assessed with an innovative cycle ergometer.

PURPOSE: Repeated sprint ability is an integral component of team sports. This study aimed to evaluate fatigability development and its aetiology during and immediately after a cycle repeated sprint exercise performed until a given fatigability threshold. METHODS: On an innovative cycle ergometer, 16 healthy males completed an RSE (10-s sprint/28-s recovery) until task failure (TF): a 30% decrease in sprint mean power (Pmean). Isometric maximum voluntary contraction of the quadriceps (IMVC), central alterations [voluntary activation (VA)], and peripheral alterations [twitch (Pt)] were evaluated before (pre), immediately after each sprint (post), at TF and 3 min after. Sprints were expressed as a percentage of the total number of sprints to TF (TSTF). Individual data were extrapolated at 20, 40, 60, and 80% TSTF. RESULTS: Participants completed 9.7 ± 4.2 sprints before reaching a 30% decrease in Pmean. Post-sprint IMVCs were decreased from pre to 60% TSTF and then plateaued (pre: 345 ± 56 N, 60% 247 ± 55 N, TF: 233 ± 57 N, p < 0.001). Pt decreased from 20% and plateaued after 40% TSTF (p < 0.001, pre-TF = - 45 ± 13%). VA was not significantly affected by repeated sprints until 60% TSTF (pre-TF = - 6.5 ± 8.2%, p = 0.036). Unlike peripheral parameters, VA recovered within 3 min (p = 0.042). CONCLUSION: During an RSE, Pmean and IMVC decreases were first concomitant to peripheral alterations up to 40% TSTF and central alterations was only observed in the second part of the test, while peripheral alterations plateaued. The distinct recovery kinetics in central versus peripheral components of fatigability further confirm the necessity to reduce traditional delays in neuromuscular fatigue assessment post-exercise.

Left ventricular dyssynchrony and post-systolic shortening in young bodybuilders using anabolic-androgenic steroids.

Left ventricular (LV) remodeling, characterized by increased LV hypertrophy and depressed systolic and diastolic function, is observed in strength-trained athletes who use anabolic-androgenic steroids (AAS). Previous studies suggested a pathological remodeling with an increase in cardiac fibrosis in these athletes, which could promote intraventricular dyssynchrony. In this context, this study evaluated LV dyssynchrony in strength-trained athletes using AAS, hypothesizing that the use of AAS would lead to an increase in post-systolic shortening. Forty-four male subjects (aged 20-40 yr) were divided into three age-matched groups: strength-trained athletes using (users, n = 14) or not (nonusers, n = 15) AAS and healthy sedentary men (controls, n = 15). After completing a survey, each participant was assessed with two-dimensional (2D)-strain echocardiography. LV dyssynchrony was quantified using the standard deviation (SD) of the time to peak for longitudinal strain of the 18 LV-segments (from the apical 4, 3, and 2 chambers views), the longitudinal strain delay index (LSDI), and the segmental post-systolic index (PSI). Users showed mean AAS dosages of 564 ± 288 mg[Formula: see text]wk-1 with a mean protocol duration of 12 ± 6 wk and a history of use of 4.7 ± 1.8 yr. They exhibited a greater LV mass index and depressed systolic and diastolic function when compared with both nonusers and controls. The decrease in LV strain in users was predominantly observed at the interventricular septum level (-16.9% ± 2.5% vs. -19.2% ± 1.8% and -19.0% ± 1.6% in users, nonusers, and controls, respectively, P < 0.01). Users showed higher SD than controls (43 ± 8 ms vs. 32 ± 5 ms, respectively, P < 0.01). The LSDI was significantly higher in users compared with both nonusers and controls (-23.4 ± 9.5 vs. -15.9 ± 9.3 and -9.8 ± 3.9, respectively, P < 0.01). PSI, calculated on the basal inferoseptal, basal anteroseptal, and basal inferolateral segments, were also greater in users compared with the two other groups. Our results reported an increase in LV dyssynchrony in young AAS users that brought new evidences of a pathologic cardiac remodeling in this specific population.NEW & NOTEWORTHY Illicit androgenic anabolic steroids (AAS) use is widespread, but data on LV dyssynchrony are lacking, although it could be increased by a higher prevalence of myocardial fibrosis reported in this population. In AAS users, the decrease in LV strain was predominantly observed in interventricular segments. All dyssynchrony indices were higher in AAS users and several segments exhibited post-systolic shortening. These results showed an association between AAS consumption, LV remodeling, and dyssynchrony.

Beneficial effects of endurance exercise training on skeletal muscle microvasculature in sickle cell disease patients.

Sickle cell disease (SCD) is a genetic hemoglobinopathy leading to 2 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 was performed before and after the training period. Of the 40 randomized SCD patients, complete data sets from 32 patients were obtained. The training group (n = 15) followed a personalized moderate-intensity endurance training program, while the nontraining (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 with nontraining patients, including increases in capillary density (P = .003), number of capillaries around a fiber (P = .015), and functional exchange surface (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.

Cerebral haemodynamics and oxygenation during whole-body exercise over 5 days at high altitude.

NEW FINDINGS: What is the central question of this study? Impairment and subsequent improvement in cerebral oxygenation during acute and prolonged exposure to high altitude affect exercise performance. This study innovates by investigating the effect of acute and prolonged high-altitude exposure on cerebral haemodynamics during submaximal endurance exercise performed at the same relative intensity. What is the main finding and its importance? Despite exercising at the same relative intensity at sea level and high altitude, participants showed a sustained impairment in cerebral oxygenation after prolonged exposure to high altitude, which might contribute to the absence of improvement in exercise tolerance. ABSTRACT: Deterioration and subsequent improvement in cerebral oxygenation during acute and prolonged hypoxic exposure may affect whole-body exercise performance at high altitude. In this study, we investigated the effect of hypoxic exposure on cerebral haemodynamics at different cortical locations during exercise at the same relative intensity after 1 (D1) and 5 days (D5) at 4350 m. Eleven male subjects performed a submaximal bout of cycling exercise (6 min at 35% + 6 min at 55% + time-to-exhaustion at 75% of peak work rate achieved in the same conditions, i.e. normoxia or hypoxia at sea level) on D1 and D5. Transcranial Doppler and near-infrared spectroscopy were used to assess middle cerebral artery blood velocity and prefrontal and motor cortex oxygenation, respectively. Despite using the same relative intensity, the duration of exercise was reduced on D1 (22.7 ± 5.1 min) compared with sea level (32.2 ± 9.0 min; P < 0.001), with no improvement on D5 (20.9 ± 6.3 min; P > 0.05). Middle cerebral artery blood velocity during exercise was elevated on D1 (+18.2%) and D5 (+15.0%) compared with sea level (P < 0.001). However, prefrontal and motor cortex oxygenation was reduced on D1 and D5 compared with sea level (P < 0.001). This pattern was of similar magnitude between cortical locations, whereas the total haemoglobin concentration increased to a greater extent in the prefrontal versus motor cortex at exhaustion on D1 and D5. In contrast to our primary hypothesis, prefrontal and motor cortex oxygenation and exercise performance did not improve over 5 days at 4350 m. The sustained impairment in cerebral oxygenation might contribute to the absence of improvement in exercise performance after partial acclimatization to high altitude.

Task failure during sustained low-intensity contraction is not associated with a critical amount of central fatigue.

Fatigue-related mechanisms induced by low-intensity prolonged contraction in lower limb muscles are currently unknown. This study investigated central fatigue kinetics in the knee extensors during a low-intensity sustained isometric contraction. Eleven subjects sustained a 10% maximal voluntary contraction (MVC) until task failure (TF) with neuromuscular evaluation every 3 minutes. Testing encompassed transcranial magnetic stimulation to evaluate maximal voluntary activation (VATMS ), motor evoked potential (MEP), and silent period (SP), and peripheral nerve stimulation to assess M-wave. Rating of perceived exertion (RPE) was also recorded. MVC progressively decreased up to 50% of the time to TF (ie, 50%TTF ) and then plateaued, reaching ~50% at TF (P < .001). VATMS progressively decreased up to 90%TTF and then plateaued, the decrease reaching ~20% at TF (P < .001). SP was lengthened early (ie, from 20%TTF ) during the exercise and then plateaued (P < .01). No changes were reported for MEP evoked during MVC (P = .87), while MEP evoked during submaximal contractions decreased early (ie, from 20%TTF ) during the exercise and then plateaued (P < .01). RPE increased linearly during the exercise to be almost maximal at TF. M-waves were not altered (P = .88). These findings confirm that TF is due to the subjects reaching their maximal perceived effort rather than any particular central event or neuromuscular limitations since MVC at TF was far from 10% of its original value. It is suggested that strategies minimizing RPE (eg, motivational self-talk) should be employed to enhance endurance performance.

Optimal load for a torque-velocity relationship test during cycling.

PURPOSE: Lower limbs' neuromuscular force capabilities can only be determined during single sprints if the test provides a good fit of the data in the torque-velocity (T-V) and power-velocity (P-V) relationships. This study compared the goodness of fit of single sprints performed against traditional (7.5% of the body mass) vs. optimal load (calculated based on the force production capacity and ergometer specificities), and examined if reducing the load in fatigued state enhances T-V and P-V relationship goodness of fit. METHODS: Thirteen individuals performed sprints before (PRE) and after (POST) a fatiguing task against different loads: (1) TRAD: traditional, (2) OPT: optimal, and (3) LOW-OPT: optimal load reduced according to fatigue levels. RESULTS: At PRE, OPT sprints presented a higher R2 of the T-V relationship (0.92 ± 0.06) and lower time to reach maximal power (Pmax) (48 ± 9%) when compared with TRAD sprints (0.89 ± 0.06 and 66 ± 22%, respectively, p < 0.01). At POST, the range of velocity spectrum was greater in the LOW-OPT (33 ± 4%) vs. TRAD (24 ± 3%) and OPT (26 ± 8%, p < 0.007). Similarly, the time to reach Pmax was lower in the LOW-OPT (46 ± 12%) vs. TRAD (76 ± 24%) and OPT (70 ± 24%, p < 0.006). CONCLUSION: Sprints performed against an OPT load and reducing the OPT load after fatigue improve the fit of data in the T-V and P-V curves. Sprints load assignment should consider force production capacities rather than body mass.

Positive expiratory pressure improves arterial and cerebral oxygenation in acute normobaric and hypobaric hypoxia.

Positive expiratory pressure (PEP) has been shown to limit hypoxia-induced reduction in arterial oxygen saturation, but its effectiveness on systemic and cerebral adaptations, depending on the type of hypoxic exposure [normobaric (NH) versus hypobaric (HH)], remains unknown. Thirteen healthy volunteers completed three randomized sessions consisting of 24-h exposure to either normobaric normoxia (NN), NH (inspiratory oxygen fraction, FiO2 = 13.6%; barometric pressure, BP = 716 mmHg; inspired oxygen partial pressure, PiO2 = 90.9 ± 1.0 mmHg), or HH (3,450 m, FiO2 = 20.9%, BP = 482 mmHg, PiO2 = 91.0 ± 0.6 mmHg). After the 6th and the 22nd hours, participants breathed quietly through a facemask with a 10-cmH2O PEP for 2 × 5 min interspaced with 5 min of free breathing. Arterial (SpO2, pulse oximetry), quadriceps, and cerebral (near-infrared spectroscopy) oxygenation, middle cerebral artery blood velocity (MCAv; transcranial Doppler), ventilation, and cardiovascular responses were recorded continuously. SpO2without PEP was significantly lower in HH (87 ± 4% on average for both time points, P < 0.001) compared with NH (91 ± 3%) and NN (97 ± 1%). PEP breathing did not change SpO2 in NN but increased it similarly in NH and HH (+4.3 ± 2.5 and +4.7 ± 4.1% after 6h; +3.5 ± 2.2 and +4.1 ± 2.9% after 22h, both P < 0.001). Although MCAv was reduced by PEP (in all sessions and at all time points, -6.0 ± 4.2 cm/s on average, P < 0.001), the cerebral oxygenation was significantly improved (P < 0.05) with PEP in both NH and HH, with no difference between conditions. These data indicate that PEP could be an attractive nonpharmacological means to improve arterial and cerebral oxygenation under both normobaric and hypobaric mild hypoxic conditions in healthy participants.

Medex 2015: The key role of cardiac mechanics to maintain biventricular function at high altitude.

NEW FINDINGS: What is the central question of this study? This study is the first to investigate the effects of high-altitude trekking on biventricular mechanics, including measurements of left ventricular subendocardial and subepicardial function. What is the main finding and its importance? We provide new evidence that an increased contractility and untwisting efficiency, a key element of diastolic function, probably plays a key role in preservation of cardiac function during high-altitude trekking. Persistent increased loading conditions during several weeks at high altitude might have a key role in the appearance of left or right ventricular dysfunction. ABSTRACT: Cardiac responses to acute hypoxic exposure have been thoroughly investigated. We analysed the effects of high-altitude trekking (i.e. prolonged hypoxic exposure) on biventricular function, including the evaluation of subendocardial and subepicardial function in the left ventricle (LV). Resting evaluations of LV and right ventricular (RV) function and mechanics were assessed by speckle tracking echocardiography on 20 subjects at sea level and at high altitude (5085 m, after a 10 day ascent). Pulmonary artery systolic pressure was increased at high altitude (sea level, 13.1 ± 5.9 mmHg; high altitude, 26.6 ± 10.8 mmHg; P < 0.001). Left ventricular volumes were decreased, whereas RV volumes were increased at high altitude. Alterations in pulmonary artery systolic pressure and cardiac volumes were correlated with hypoxaemia. We observed neither RV nor LV systolic dysfunction, including analysis of LV subendocardial and subepicardial function. Left ventricular systolic strain rates were enhanced at high altitude. Transmitral and transtricuspid diastolic filling ratios were decreased at high altitude. Diastolic apical rotational rate, untwisting rate and untwisting rate/peak twist ratio (i.e. untwisting efficiency) were enhanced at high altitude. We observed no echocardiographic signs of LV and RV pathological dysfunction at rest at high altitude. In contrast, our data highlighted major changes in the LV mechanics, with an increased LV contractility and a higher untwisting efficiency at high altitude. Biventricular interaction, alterations in loading conditions and an increase in plasma catecholamine concentration might partly explain these modifications. Thus, we demonstrated that LV mechanics (i.e. increased strain rates and untwisting efficiency) have a key role in preservation of cardiac function during high-altitude trekking.

Neuromuscular evaluation of arm-cycling repeated sprints under hypoxia and/or blood flow restriction.

PURPOSE: This study aimed to determine the effects of hypoxia and/or blood flow restriction (BFR) on an arm-cycling repeated sprint ability test (aRSA) and its impact on elbow flexor neuromuscular function. METHODS: Fourteen volunteers performed an aRSA (10 s sprint/20 s recovery) to exhaustion in four randomized conditions: normoxia (NOR), normoxia plus BFR (NBFR), hypoxia (FiO2 = 0.13, HYP) and hypoxia plus BFR (HBFR). Maximal voluntary contraction (MVC), resting twitch force (Db10), and electromyographic responses from the elbow flexors [biceps brachii (BB)] to electrical and transcranial magnetic stimulation were obtained to assess neuromuscular function. Main effects of hypoxia, BFR, and interaction were analyzed on delta values from pre- to post-exercise. RESULTS: BFR and hypoxia decreased the number of sprints during aRSA with no significant cumulative effect (NOR 16 ± 8; NBFR 12 ± 4; HYP 10 ± 3 and HBFR 8 ± 3; P < 0.01). MVC decrease from pre- to post-exercise was comparable whatever the condition. M-wave amplitude (- 9.4 ± 1.9% vs. + 0.8 ± 2.0%, P < 0.01) and Db10 force (- 41.8 ± 4.7% vs. - 27.9 ± 4.5%, P < 0.01) were more altered after aRSA with BFR compared to without BFR. The exercise-induced increase in corticospinal excitability was significantly lower in hypoxic vs. normoxic conditions (e.g., BB motor evoked potential at 75% of MVC: - 2.4 ± 4.2% vs. + 16.0 ± 5.9%, respectively, P = 0.03). CONCLUSION: BFR and hypoxia led to comparable aRSA performance impairments but with distinct fatigue etiology. BFR impaired the muscle excitation-contraction coupling whereas hypoxia predominantly affected corticospinal excitability indicating incapacity of the corticospinal pathway to adapt to fatigue as in normoxia.

Cortical voluntary activation testing methodology impacts central fatigue.

PURPOSE: 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). METHODS: 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. RESULTS: 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 < 0.001). Differences were also observed between TRADI and CONTI for MEP and CSP immediately after the fatiguing exercise. All differences between the two methods disappeared after 2 min of recovery. CONCLUSION: After a 2-min sustained MVC, a few seconds of recovery change the amount of measured VATMS and associated parameters of central fatigue. The continuous method should be preferred to determine deficits in voluntary activation.

Acute and chronic changes in baroreflex sensitivity in hypobaric vs. normobaric hypoxia.

Normobaric hypoxia (NH) is used as a surrogate for hypobaric hypoxia (HH). Recent studies reported physiological differences between NH and HH. Baroreflex sensitivity (BRS) decreases at altitude or following intense training. However, until now no study compared the acute and chronic changes of BRS in NH vs. HH. First, BRS was assessed in 13 healthy male subjects prior and after 20 h of exposure at 3450 m (study 1), and second in 15 well-trained athletes prior and after 18 days of "live-high train-low" (LHTL) at 2250 m (study 2) in NH vs. HH. BRS decreased (p < 0.05) to the same extent in NH and HH after 20 h of hypoxia and after LHTL. These results confirm that altitude decreases BRS but the decrease is similar between HH and NH. The persistence of this decrease after the cessation of a chronic exposure is new and does not differ between HH and NH. The previously reported physiological differences between NH and HH do not appear strong enough to induce different BRS responses.

Effects of high-altitude exposure on supraspinal fatigue and corticospinal excitability and inhibition.

PURPOSE: While acute hypoxic exposure enhances exercise-induced central fatigue and can alter corticospinal excitability and inhibition, the effect of prolonged hypoxic exposure on these parameters remains to be clarified. We hypothesized that 5 days of altitude exposure would (i) normalize exercise-induced supraspinal fatigue during isolated muscle exercise to sea level (SL) values and (ii) increase corticospinal excitability and inhibition. METHODS: Eleven male subjects performed intermittent isometric elbow flexions at 50% of maximal voluntary contraction to task failure at SL and after 1 (D1) and 5 (D5) days at 4350 m. Transcranial magnetic stimulation and peripheral electrical stimulation were used to assess supraspinal and peripheral fatigues. Pre-frontal cortex and biceps brachii oxygenation was monitored by near-infrared spectroscopy. RESULTS: Exercise duration was not statistically different between SL (1095 ± 562 s), D1 (1132 ± 516 s), and D5 (1440 ± 689 s). No significant differences were found between the three experimental conditions in maximal voluntary activation declines at task failure (SL -16.8 ± 9.5%; D1 -25.5 ± 11.2%; D5 -21.8 ± 7.0%; p > 0.05). Exercise-induced peripheral fatigue was larger at D5 versus SL (100 Hz doublet at task failure: -58.8 ± 16.6 versus -41.8 ± 20.1%; p < 0.05). Corticospinal excitability at 50% maximal voluntary contraction was lower at D5 versus SL (brachioradialis p < 0.05, biceps brachii p = 0.055). Cortical silent periods were shorter at SL versus D1 and D5 (p < 0.05). CONCLUSIONS: The present results show similar patterns of supraspinal fatigue development during isometric elbow flexions at SL and after 1 and 5 days at high altitude, despite larger amount of peripheral fatigue at D5, lowered corticospinal excitability and enhanced corticospinal inhibition at altitude.

Progressive and biphasic cardiac responses during extreme mountain ultramarathon.

Investigations on the cardiac function consequences of mountain ultramarathon (MUM) >100 h are lacking. The present study assessed the progressive cardiac responses during the world's most challenging MUM (Tor des Géants; Italy; 330 km; 24,000 m of cumulative elevation gain). Resting echocardiographic evaluation of morphology, function, and mechanics of left and right ventricle (LV and RV) including speckle tracking echocardiography was conducted in 15 male participants (46 ± 13 yr) before (pre), during (mid; 148 km), and after (post) the race. Runners completed the race in 126 ± 15 h. From pre to post, the increase in stroke volume (SV) (103 ± 19 vs. 110 ± 23 vs. 116 ± 21 ml; P < 0.001 at pre, mid, and post) was concomitant to the increase in LV early filling (peak E; 72.9 ± 15.7 vs. 74.6 ± 13.1 vs. 82.1 ± 11.5 cm/s; P < 0.05). Left and right atrial end-diastolic areas, RV end-diastolic area, and LV end-diastolic volume were 12-19% higher at post compared with pre (P < 0.05). Resting heart rate and LV systolic strain rates demonstrated a biphasic adaptation with an increase from pre to mid (55 ± 8 vs. 72 ± 11 beats/min, P < 0.001) and a return to baseline values from mid to post (59 ± 8 beats/min). Significant correlations were found between pre-to-post percent changes in peak E and LV end-diastolic volume (r = 0.63, P < 0.05) or RV (r = 0.82, P < 0.001) or atrial end-diastolic areas (r = 0.83, P < 0.001). An extreme MUM induced a biphasic pattern of heart rate in parallel with specific cardiac responses characterized by a progressive increase in diastolic filling, biventricular volumes, and SV. The underlying mechanisms and their clinical implications remain challenging for the future.

Ozone Differentially Affects Perception of Plant Volatiles in Western Honey Bees.

Floral scents play a key role in mediating plant-pollinator interactions. Volatile organic compounds (VOCs) emitted by flowers are used by flower visitors as olfactory cues to locate flowers, both from a distance and at close range. More recently it has been demonstrated that reactive molecules such as ozone can modify or degrade VOCs, and this may impair the communication between plants and their pollinators. However, it is not known whether such reactive molecules also may affect the olfactory system of pollinators, and thus not only influence signal transmission but perception of the signal. In this study, we used electroantennographic measurements to determine the effect of increased levels of ozone on antennal responses in western honey bees (Apis mellifera L.). Linalool and 2-phenylethanol, both known to be involved in location of flowers by the bees, and (Z)-3-hexenyl acetate, a widespread green leaf volatile also detected by bees, were used. The results showed that ozone affected antennal responses to the different substances differently. Ozone decreased antennal responses to (Z)-3-hexenyl acetate, whereas responses to linalool and 2-phenylethanol were not influenced by ozone. Overall, the study does not provide evidence that pollination by honey bees is impaired by damage in the olfactory system of the bees caused by increased levels of ozone, at least when linalool and 2-phenylethanol are the attractive signals. However, the results also suggest that ozone can change the overall perception of an odor blend. This might have negative effects in pollination systems and other organismic interactions mediated by specific ratios of compounds.

Modulation of exercise-induced spinal loop properties in response to oxygen availability.

This study investigated the effects of acute hypoxia on spinal reflexes and soleus muscle function after a sustained contraction of the plantar flexors at 40% of maximal voluntary isometric contraction (MVC). Fifteen males (age 25.3 ± 0.9 year) performed the fatigue task at two different inspired O2 fractions (FiO2 = 0.21/0.11) in a randomized and single-blind fashion. Before, at task failure and after 6, 12 and 18 min of passive recovery, the Hoffman-reflex (H max) and M-wave (M max) were recorded at rest and voluntary activation (VA), surface electromyogram (RMSmax), M-wave (M sup) and V-wave (V sup) were recorded during MVC. Normalized H-reflex (H max/M max) was significantly depressed pre-exercise in hypoxia compared with normoxia (0.31 ± 0.08 and 0.36 ± 0.08, respectively, P < 0.05). Hypoxia did not affect time to task failure (mean time of 453.9 ± 32.0 s) and MVC decrease at task failure (-18% in normoxia vs. -16% in hypoxia). At task failure, VA (-8%), RMSmax/M sup (-11%), H max/M max (-27%) and V sup/M sup (-37%) decreased (P < 0.05), but with no FiO2 effect. H max/M max restored significantly throughout recovery in hypoxia but not in normoxia, while V sup/M sup restored significantly during recovery in normoxia but not in hypoxia (P < 0.05). Collectively, these findings indicate that central adaptations resulting from sustained submaximal fatiguing contraction were not different in hypoxia and normoxia at task failure. However, the FiO2-induced differences in spinal loop properties pre-exercise and throughout recovery suggest possible specific mediation by the hypoxic-sensitive group III and IV muscle afferents, supraspinal regulation mechanisms being mainly involved in hypoxia while spinal ones may be predominant in normoxia.

Dynamics of corticospinal changes during and after high-intensity quadriceps exercise.

This study tested the hypothesis that during fatiguing quadriceps exercise, supraspinal fatigue develops late, is associated with both increased corticospinal excitability and inhibition and recovers quickly. Eight subjects performed 20 s contractions [15 s at 50% maximal voluntary contraction (MVC) followed by 5 s MVC] separated by a 10 s rest period until task failure. Transcranial magnetic stimulation (TMS) and electrical femoral nerve stimulation (PNS) were delivered ∼ 2 s apart during 50% MVC, during MVC and after MVC in relaxed muscle. Voluntary activation was assessed by TMS (VATMS) immediately before and after exercise and then three times over a 6 min recovery period. During exercise, MVC and twitch force evoked by PNS in relaxed muscle decreased progressively to 48 ± 8 and 36 ± 16% of control values, respectively (both P < 0.01). Significant changes in voluntary activation assessed by PNS and twitch evoked by TMS during MVC were observed during the last quarter of exercise only (from 96.4 ± 1.7 to 86 ± 13%, P = 0.03 and from 0.76 ± 0.8 to 4.9 ± 4.7% MVC, P = 0.02, from baseline to task failure, respectively). The TMS-induced silent period increased linearly during both MVC (by ∼ 79 ms) and 50% MVC (by ∼ 63 ms; both P < 0.01). Motor-evoked potential amplitude did not change during the protocol at any force levels. Both silent period and VATMS recovered within 2 min postexercise, whereas MVC and twitch force evoked by PNS in relaxed muscle recovered to only 84 ± 9 and 73 ± 17% of control values 6 min after exercise, respectively. In conclusion, high-intensity single-joint quadriceps exercise induces supraspinal fatigue near task failure, with increased intracortical inhibition and, in contrast to previous upper-limb results, unchanged corticospinal excitability. These changes recover rapidly after task failure, emphasizing the need to measure corticospinal adaptations immediately at task failure to avoid underestimation of exercise-induced corticospinal changes.

Resting and active motor thresholds versus stimulus-response curves to determine transcranial magnetic stimulation intensity in quadriceps femoris.

BACKGROUND: Transcranial magnetic stimulation (TMS) is a widely-used investigative technique in motor cortical evaluation. Recently, there has been a surge in TMS studies evaluating lower-limb fatigue. TMS intensity of 120-130% resting motor threshold (RMT) and 120% active motor threshold (AMT) and TMS intensity determined using stimulus-response curves during muscular contraction have been used in these studies. With the expansion of fatigue research in locomotion, the quadriceps femoris is increasingly of interest. It is important to select a stimulus intensity appropriate to evaluate the variables, including voluntary activation, being measured in this functionally important muscle group. This study assessed whether selected quadriceps TMS stimulus intensity determined by frequently employed methods is similar between methods and muscles. METHODS: Stimulus intensity in vastus lateralis, rectus femoris and vastus medialis muscles was determined by RMT, AMT (i.e. during brief voluntary contractions at 10% maximal voluntary force, MVC) and maximal motor-evoked potential (MEP) amplitude from stimulus-response curves during brief voluntary contractions at 10, 20 and 50% MVC at different stimulus intensities. RESULTS: Stimulus intensity determined from a 10% MVC stimulus-response curve and at 120 and 130% RMT was higher than stimulus intensity at 120% AMT (lowest) and from a 50% MVC stimulus-response curve (p < 0.05). Stimulus intensity from a 20% MVC stimulus-response curve was similar to 120% RMT and 50% MVC stimulus-response curve. Mean stimulus intensity for stimulus-response curves at 10, 20 and 50% MVC corresponded to approximately 135, 115 and 100% RMT and 180, 155 and 130% AMT, respectively. Selected stimulus intensity was similar between muscles for all methods (p > 0.05). CONCLUSIONS: Similar optimal stimulus intensity and maximal MEP amplitudes at 20 and 50% MVC and the minimal risk of residual fatigue at 20% MVC suggest that a 20% MVC stimulus-response curve is appropriate for determining TMS stimulus intensity in the quadriceps femoris. The higher selected stimulus intensities at 120-130% RMT have the potential to cause increased coactivation and discomfort and the lower stimulus intensity at 120% AMT may underestimate evoked responses. One muscle may also act as a surrogate in determining optimal quadriceps femoris stimulation intensity.

Chemical imitation of yeast fermentation by the drosophilid-pollinated deceptive trap-flower Aristolochia baetica (Aristolochiaceae).

Deceptive flowers, unlike in mutualistic pollination systems, mislead their pollinators by advertising rewards which ultimately are not provided. Although our understanding of deceptive pollination systems increased in recent years, the attractive signals and deceptive strategies in the majority of species remain unknown. This is also true for the genus Aristolochia, famous for its deceptive and fly-pollinated trap flowers. Representatives of this genus were generally assumed to be oviposition-site mimics, imitating vertebrate carrion or mushrooms. However, recent studies found a broader spectrum of strategies, including kleptomyiophily and imitation of invertebrate carrion. A different deceptive strategy is presented here for the western Mediterranean Aristolochia baetica L. We found that this species is mostly pollinated by drosophilid flies (Drosophilidae, mostly Drosophila spp.), which typically feed on fermenting fruit infested by yeasts. The flowers of A. baetica emitted mostly typical yeast volatiles, predominantly the aliphatic compounds acetoin and 2,3-butandiol, and derived acetates, as well as the aromatic compound 2-phenylethanol. Analyses of the absolute configurations of the chiral volatiles revealed weakly (acetoin, 2,3-butanediol) to strongly (mono- and diacetates) biased stereoisomer-ratios. Electrophysiological (GC-EAD) experiments and lab bioassays demonstrated that most of the floral volatiles, although not all stereoisomers of chiral compounds, were physiologically active and attractive in drosophilid pollinators; a synthetic mixture thereof successfully attracted them in field and lab bioassays. We conclude that A. baetica chemically mimics yeast fermentation to deceive its pollinators. This deceptive strategy (scent chemistry, pollinators, trapping function) is also known from more distantly related plants, such as Arum palaestinum Boiss. (Araceae) and Ceropegia spp. (Apocynaceae), suggesting convergent evolution. In contrast to other studies working on floral scents in plants imitating breeding sites, the present study considered the absolute configuration of chiral compounds.

Changes in cerebral blood flow and vasoreactivity to CO2 measured by arterial spin labeling after 6days at 4350m.

Changes in cerebral perfusion and CO2 cerebrovascular reactivity during and immediately after a sojourn at high altitude remain unclear but may be critical for acclimatization. The aim of the present study was to assess the effects of 6days at 4350m on cerebral perfusion and cerebrovascular reactivity (CVR) to CO2 by arterial spin labeling (ASL) magnetic resonance imaging at sea level and to compare it with transcranial Doppler (TCD) results at altitude. Eleven healthy male subjects, non-acclimatized to altitude, stayed for 6days at 4350m (Observatoire Vallot, massif du Mont-Blanc). Prior to the stay and within 6h after returning to sea level, subjects were investigated using pseudo-continuous ASL at 3T during a block-design inhalation paradigm to measure basal cerebral blood flow (CBF) and CO2 CVR. End-tidal CO2 (PetCO2), respiratory rate, heart rate and oxygen saturation were recorded during the exam. Subjects were also examined using TCD prior to and on day 5 of the stay at altitude to measure blood velocity in the middle cerebral artery (MCAv) and CO2 CVR. CO2 CVR was expressed as percent change in ASL CBF or TCD MCAv per mmHg change in PetCO2. PetCO2 was significantly decreased during and after altitude. Significant increases in TCD MCAv compared to before altitude measurements were observed on day 5 at altitude (+20.5±15.5%). Interestingly, ASL CBF remained increased in the MCA and anterior vascular territories (+22.0±24.1% and 20.5±20.3%, respectively) after altitude under normoxic conditions. TCD CVR tended to decrease on day 5 at 4350m (-12.3±54.5% in the MCA) while the ASL CVR was significantly decreased after altitude (-29.5±19.8% in the MCA). No correlation was observed between cerebral hemodynamic changes and symptoms of acute mountain sickness at high altitude. In conclusion, prolonged exposure to high altitude significantly increases blood flow during the altitude stay and within 6h after returning to sea level. Decreased CO2 CVR after prolonged altitude exposure was also observed using ASL. Changes in cerebral hemodynamics with altitude exposure probably involve other mechanisms than the vasodilatory effect of hypoxia only, since it persists under normoxia several hours following the descent.