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Purpose: This study determined the effects of pre-exercise sodium bicarbonate ingestion (ALK) on changes in oxygen uptake (VO2) at the end of a supramaximal exercise test (SXT)., Methods: Eleven well-trained cyclists completed a 70-s all-out cycling effort, in double-blind trials, after oral ingestion of either 0.3 g kg(-1) of sodium bicarbonate (NaHCO3) or 0.2 g kg(-1) body mass of calcium carbonate (PLA). Blood samples were taken to assess changes in acid-base balance before the start of the supramaximal exercise, and 0, 5 and 8 min after the exercise; ventilatory parameters were also measured at rest and during the SXT., Results: At the end of the PLA trial, which induced mild acidosis (blood pH = 7.20), subjects presented a significant decrease in VO2 (P < 0.05), which was related to the amplitude of the decrease in minute ventilation (VE) during the SXT (r = 0.70, P < 0.01, n = 11). Pre-exercise metabolic alkalosis significantly prevented the exercise-induced decrease in VO2 in eleven well-trained participants (PLA:12.5 ± 2.1 % and ALK: 4.9 ± 0.9 %, P < 0.05) and the decrease in mean power output was significantly less pronounced in ALK (P < 0.05). Changes in the VO2 decrease between PLA and ALK trials were positively related to changes in the VE decrease (r = 0.74, P < 0.001), but not to changes in power output (P > 0.05)., Conclusions: Pre-exercise alkalosis counteracted the VO2 decrease related to mild acidosis, potentially as a result of changes in VE and in muscle acid-base status during the all-out supramaximal exercise.

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.

This study aimed to reveal the neural and muscular adjustments following a repeated-sprint (RS) running exercise. Sixteen subjects performed a series of neuromuscular tests before, immediately after and 30 min (passive recovery) post-RS exercise (12 x 40 m sprints interspaced by 30 s of passive recovery). Sprint times significantly lengthened over repetitions (+17% from the first to the last sprint; P < 0.05). After RS running exercise, maximal voluntary contraction torque of the plantar flexors (-11 +/- 7.3%), muscle activation (twitch interpolation) (-2.7 +/- 3.4%) and soleus maximal M-wave amplitude (-20 +/- 17%) were significantly (P < 0.05) reduced but returned close to baseline after 30 min. Both soleus EMG activity and maximal Hoffmann reflex normalized with respect to M-wave amplitude did not change during the whole experiment. From pre- to post-RS exercise, evoked twitch response was characterized by lower peak torque and maximal rate of torque development (-13 and -11%, respectively, P < 0.05), but was not different from baseline after recovery. Peak tetanus at 20 and 80 Hz were 17 and 8% lower (P < 0.05) in the fatigued state, respectively. Acute muscle fatigue induced by RS running exercise is mainly peripheral as the short-term (30 min) recovery pattern of plantar flexors contractile properties follows that of the voluntary force-generating capacity.

Investigations of training effects on exercise energy cost have yielded conflicting results. The purpose of the present study was to compare quadriceps energy cost and oxidative capacity between endurance-trained and sedentary subjects during a heavy dynamic knee extension exercise. We quantified the rates of ATP turnover from oxidative and anaerobic pathways with (31)P-MRS, and we measured simultaneously pulmonary oxygen uptake in order to assess both total ATP production [i.e., energy cost (EC)] and O(2) consumption (O(2) cost) scaled to power output. Seven sedentary (SED) and seven endurance-trained (TRA) subjects performed a dynamic standardized rest-exercise-recovery protocol at an exercise intensity corresponding to 35% of maximal voluntary contraction. We showed that during a dynamic heavy exercise, the O(2) cost and EC were similar in the SED and endurance-trained groups. For a given EC, endurance-trained subjects exhibited a higher relative mitochondrial contribution to ATP production at the muscle level (84 +/- 12% in TRA and 57 +/- 12% in SED; P < 0.01) whereas the anaerobic contribution was reduced (18 +/- 12% in TRA and 44 +/- 11% in SED; P < 0.01). Our results obtained in vivo illustrate that on the one hand the beneficial effects of endurance training are not related to any reduction in EC or O(2) cost and on the other hand that this similar EC was linked to a change regarding the contribution of anaerobic and oxidative processes to energy production, i.e., a greater aerobic energy contribution associated with a concomitant reduction of the anaerobic energy supply.

The aim of this study was to investigate whether (1) spinal modulation would change after non-exhausting eccentric exercise of the plantar flexor muscles that produced muscle soreness and (2) central modulation of the motor command would be linked to the development of muscle soreness. Ten healthy subjects volunteered to perform a single bout of backward downhill walking exercise (duration 30 min, velocity 1 ms(-1), negative grade -25%, load 12% of body weight). Neuromuscular test sessions [H-reflex, M-wave, maximal voluntary torque (MVT)] were performed before, immediately after, as well as 1-3 days after the exercise bout. Immediately after exercise there was a -15% decrease in MVT of the plantar flexors partly attributable to an alteration in contractile properties (-23% in electrically evoked mechanical twitch). However, MVT failed to recover before the third day whereas the contractile properties had significantly recovered within the first day. This delayed recovery of MVT was likely related to a decrement in voluntary muscle drive. The decrease in voluntary activation occurred in the absence of any variation in spinal modulation estimated from the H-reflex. Our findings suggest the development of a supraspinal modulation perhaps linked to the presence of muscle soreness.

Near-infrared spectroscopy (NIRS) allows non-invasive monitoring of central and peripheral changes in oxygenation during exercise and may provide valuable insight into the factors affecting fatigue. This study aimed to explore the changes in oxygenation of prefrontal cortex and active muscle tissue as limiting factors of incremental exercise performance in trained cyclists. Thirteen trained healthy subjects (mean +/- SE: age 24.9 +/- 1.5 years, body mass 70.1 +/- 1.2 kg, training 6.1 +/- 0.9 h week(-1)) performed a progressive maximal exercise to exhaustion on a cycling ergometer. Prefrontal cortex (Cox) and vastus lateralis muscle (Mox) oxygenation were measured simultaneously by NIRS throughout the exercise. Maximal voluntary isometric knee torques and quadriceps neuromuscular fatigue (M-wave properties and voluntary activation ratio) were evaluated before and after exercise. Maximal power output and oxygen consumption were 380.8 +/- 7.9 W and 75.0 +/- 2.2 ml min(-1) kg(-1), respectively. Mox decreased significantly throughout exercise while Cox increased in the first minutes of exercise but decreased markedly from the workload corresponding to the second ventilatory threshold up to exhaustion (P < 0.05). No significant difference was noted 6 min after maximal exercise in either the voluntary activation ratio or the M-wave properties. These findings are compatible with the notion that supraspinal modulation of motor output precedes exhaustion.

The primary aim of our study was to examine supra-maximal cycling performance and related mechanical variables in trained cyclists using a new prototype chainring (PC) designed to produce a higher mean net torque (T (N mean)) than a standard chainring (SC). The main feature of the PC is that crank-arm alignment and lever-arm length change as a function of the crank angle during the pedaling cycle. The PC presents two features theorized to effect cycling performance: (1) out of line of pedal cranks resulting in an decrease in the dead points, and (2) a change in crank arm length inducing a torque different from that of SC during the down- and up-stroke of the pedaling cycle. To investigate this theory, we examined eight male cyclists who performed a 1-km "all-out" cycling test in the following order: SC, PC, and SC. Performance was measured as the time (s) to complete the 1-km test. Mechanical variables included torque (N m(-1)), crank velocity (rad s(-1)), and power output (W). We performed our statistical analysis using a two-way ANOVA for repeated measurements and Newman-Keuls post hoc assessment. Our results showed that performance was similar for SC (69.41 +/- 6.69 s) and PC (73.33 +/- 4.58 s). Torque, crank velocity, and power output were also similar throughout (P > 0.05). We conclude that despite the theoretically benefits proposed by the inventors the new PC investigated in our study failed to improve cycling performance or mechanical variables during a supramaximal test when compared with SC.

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.

The aim of the study was to evaluate the effectiveness of the Poincaré plot analysis of heart rate variability (HRV) in observing endurance training-induced changes. Four 10-min manoeuvres were performed (supine lying, standing, steady state exercising and subsequent recovery) by eight control subjects before and after a short-term endurance training and by eight subjects trained for at least 3 years. HRV was assessed by traditional time- and frequency-domain indexes, in parallel with the Poincaré plot analysis. In the latter each R-R interval is plotted as a function of the previous one, and the standard deviations of the instantaneous and long-term R-R interval variability are calculated. In our subjects, the Poincaré scatter grams became gradually narrower from supine to exercising, with progressive parasympathetic withdrawal. Short- and long-term endurance training led to higher aerobic power ( p<0.05) and ventilatory threshold shifted towards higher power output ( p<0.05). All HRV evaluation methods showed that HRV values were higher after training both during supine lying and standing ( p<0.05). The Poincaré scatter grams were wider in the trained state. Standard deviations of the Poincaré plot were significantly correlated with the main parameters of the time- and frequency-domain analyses, especially concerning the parasympathetic indicators. These results suggested that Poincaré plot parameters as well as the "width" of the scatter gram could be considered as surrogates of time- and frequency-domain analysis to assess training-induced changes in HRV.

This study compared ventilation, gas exchange (oxygen uptake, VO(2)) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% VO(2peak). The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [VO(2peak)=60.2 (1.7) ml.kg(-1).min(-1)] completed two identical 6-min bouts of cycling performed at high intensity [approximately 90% VO(2peak); 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). VO(2) at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml.min(-1), respectively, P<0.05) than in Pre-Ex but there was a approximately 25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml.min(-1), respectively, P<0.05]. The greater whole-body VO(2) after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (approximately 12-16 l.min(-1) and approximately 10 beats.min(-1), respectively, P<0.05) as were the ratios V(E)/O(2) and V(E)/VCO(2) in the Post-Ex tests. It was concluded that the VO(2) and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.