The ventilation, lactate and electromyographic thresholds during incremental exercise tests in normoxia, hypoxia and hyperoxia

These experiments examined the effect of hypoxia and hyperoxia on ventilation, lactate concentration and electromyographic activity during an incremental exercise test in order to determine if coincident chances in ventilation and electromyographic activity occur during an incremental exercise test, despite an enhancement or reduction of peripheral chemoreceptor activity. In addition, these experiments were completed to determine if electromyographic activity and ventilation are enhanced or reduced in response to the inspiration of oxygen-depleted and oxygen-enriched air, respectively. Seven subjects performed three incremental exercise tests, until volitional exhaustion was achieved, while inspiring air with a fractional concentration of oxygen of either 66%, 21% or 17%. In addition, another single subject completed two tests while inspiring air with a fractional concentration of either 17% or 21%. During the tests, ventilation, mixed expired oxygen and carbon dioxide, arterialized venous blood and the electromyographic activity from the vastus lateralis were sampled. From these values ventilation, electromyographic and lactate thresholds were detected during normoxia, hypoxia and hyperoxia. The results showed that although ventilation and lactate concentration were significantly less during hyperoxia as compared to normoxia or hypoxia, the carbon dioxide production values were not significantly different between the normoxic, hypoxic and hyperoxic conditions. For a particular condition, the time, carbon dioxide production and oxygen consumption values that corresponded to the ventilation and electromyographic thresholds were not significantly different, but the values corresponding to the lactate threshold were significantly less than those for the electromyographic and ventilation thresholds. Comparisons between the three conditions showed that the time, carbon dioxide production and oxyen consumption values corresponding to each of these thresholds were not significantly different. These findings have led us to conclude that the changes in lactate concentration observed during exercise may not be directly related to the fractional concentration of inspired oxygen, and that the peripheral chemoreceptors may not be the sole mediators of the first ventilatory threshold. It is suggested that this threshold may be mediated by an increase in neural activity originating from higher motor centers or the exercising limbs, induced in response to the need to progressively recruit fast twitch muscle fibers as exercise power output is increased and as individual muscle fibers begin to fatigue.     

Alterations in plasma volume, electrolytes and protein during incremental exercise at different pedal speeds

We investigated the effects of pedal speed on changes in plasma volume, electrolytes and protein during incremental exercise. Ten adult males participated in two, 30 minute incremental cycle ergometer exercise tests at room temperature (22° C, rh=56%). Exercise load was increased from 20 to 70% of peak . Five minutes were spent at each of six stages which were equally spaced in exercise intensity. Subjects pedaled at 50 (50 RPM) and 90 (90 RPM) rev · min^–1. Venous blood samples were drawn prior to exercise and during the last minute of each stage. Relative plasma volume changes showed a progressive hemoconcentration during the exercise. There were no significant differences due to pedal speed as plasma volume loss averaged –7.3% during exercise. [Na+], [Cl–], and [K+] increased significantly during exercise but were not influenced by pedal speed. Changes in plasma protein and albumin concentrations indicated that there was a loss of globulin from the vascular volume in both conditions and an addition of albumin to the plasma in 50 RPM. The difference in plasma albumin dynamics was possibly related to an effect of pedal speed on movement of fluid in the lymphatic vessels of the legs.This work was supported in part by Grants from the Theresa Monaco Endowment of the University of Houston College of Education and Nautilus Sports/Medical Industries     

Ventilatory response during incremental exercise tests in weight lifters and endurance cyclists

The effect of a progressively increasing work rate (15 W X min-1) up to exhaustion on the time course of O2 uptake (VO2), ventilation (VE) and heart rate (HR) has been studied in weight lifters (WL) in comparison to endurance cyclists (Cycl) and sedentary controls (Sed). VO2 and VE were measured as average value of 30-s intervals by a semiautomatic open circuit method. VO2max was 2.55 +/- 0.33; 4.29 +/- 0.53 and 2.86 +/- 0.19 l X min-1 in WL, Cycl and Sed respectively. With time and work rate, while VO2 and HR increased linearly, VE changed its slope at two levels. The 1st VE change occurred at a work load corresponding to a mean (+/- SD) VO2 of 1.50 +/- 0.26; 1.93 +/- 0.34; and 1.23 +/- 0.14 l X min-1 in WL, Cycl, and Sed respectively. VO2 values corresponding to the second VE change of slope were 2.18 +/- 0.32 in WL; 3.48 +/- 0.53 in Cycl and 2.17 +/- 0.28 l X min-1 in Sed. The first change of slope might be the consequence of the different readjustment of VO2 on-response and hence of early lactate in the different subjects. The second change seems to be comparable to the conventional anaerobic threshold and is achieved in all subjects when VE vs time slope is 7-10 l X min-1/min of exercise.     

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.     

Relationship between plasma potassium and ventilation during successive periods of exercise in men

During and after two successive incremental cycle ergometer tests (tests A and B), plasma potassium concentration ([K+]p), plasma pH (pHp), plasma partial pressure of carbon dioxide, blood lactate concentration ([Lac-]b) and ventilation (VE) were measured. While there was a good correlation between the increase in [K+]p and VE or pHp, respectively, in test A, in test B a close correlation was found only between the increase in VE and [K+]p (r greater than 0.9 for nearly all single cases; r was 0.84 and 0.89 for all (pooled) cases in tests A and B, respectively; the correlation coefficients between changes in pHp and VE in tests A and B were r = 0.74 and r = 0.28, respectively, and r = 0.89 and r = 0.10 between the changes in [Lac-]b and VE in tests A and B). The close relationship for individuals between VE and [K+]p in tests A and B supported the hypothesis that the extracellular increase in [K+] may contribute to the ventilatory drive during exercise. The comparison of the results of tests A and B further indicated that the relationship between pHp and VE was dependent on the experimental design, and that pHp and VE changes are unlikely to be cause and effect.     

Breathing pattern during exercise in young black and Caucasian subjects

Lung volumes in sex-, age-, height-, and weight-matched Black subjects are 10-15% lower than those in Caucasians. To determine whether this decreased lung volume affected the ventilatory adaptation to exercise, minute ventilation (VE), its components, frequency (f) and tidal volume (VT), and breathing pattern were observed during incremental cycle-ergometer exercise. Eighteen Caucasian (age 8-30 yr) and 14 Black (age 8-25 yr) subjects were studied. Vital capacity (VC) was lower (P less than 0.001) in the Black subjects [90.6 +/- 8.6 (SD) vs. 112.9 +/- 9.9% predicted], whereas functional residual capacity/total lung capacity was higher (P less than 0.05). VE, mixed expired O2 and CO2, VT, f, and inspiratory (TI), expiratory (TE), and total respiratory cycle (TT) duration were measured during the last 30 s of each 2-min load. Statistical comparisons with increasing power output were made at rest and from 0.6 to 2.4 W/kg in 0.3-W/kg increments. VE was higher in Blacks at all work loads and reached significance (P less than 0.05) at 0.6 and 1.5 W/kg. VE/VO2 was also higher throughout exercise, reaching significance (P less than 0.01) at 1.2, 1.5, and 1.8 W/kg. The Black subjects attained any given level of VE with a higher f (P less than 0.001) and lower VT. TI and TE were shortened proportionately so that TI/TT was not different. Differences in lung volume and the ventilatory response to exercise in these Black and Caucasian subjects suggest differences in the respiratory pressure-volume relationships or that the Black subjects may breathe higher on their pressure-volume curve.     

Breathing pattern and metabolic behavior during anticipation of exercise

The mechanisms responsible for the marked increase in ventilation at the onset of exercise are incompletely defined. A conditioned response to exercise anticipation has been suggested as an influencing factor, but systematic measurements have not been made during the transition from rest to the time when exercise is anticipated but has not yet commenced. We tested the hypothesis that cortical activity associated with the anticipation of exercise causes hyperpnea, which is at least partly responsible for the increased ventilation at the onset of exercise. To assess the influence of continuous cortical activity in the absence of exercise anticipation the subjects performed mental arithmetic tasks. Fifteen subjects performed the two experiments in a random order. Ventilation was measured noninvasively using a calibrated respiratory inductive plethysmograph and end-tidal CO2 concentration (FETCO2) was monitored at the nasal vestibule. Both exercise anticipation and mental arithmetic caused an increase in minute ventilation (VI) (P less than 0.01) and mean inspiratory flow (VT/TI, P less than 0.01), which reflects respiratory center drive, although the derivation differed in that the former was volume based, whereas the latter was due to alteration in timing. Despite the increase in VI, FETCO2 remained constant in both instances. In a complementary study the constant FETCO2 in the face of increased VI was shown to be due to increased CO2 output. The results show that the mere anticipation of exercise causes an increase in ventilation. The mechanism responsible for this hyperpnea cannot be due solely to respiratory center activation because of the constancy of FETCO2 and the associated alterations in cardiac and metabolic behavior.     

Breathing pattern during and after exercise of different intensities

We recently observed rapid shallow breathing during recovery from maximal exercise in some normal subjects. We wondered whether this phenomenon is randomly related to level of exercise or is limited to recovery from very high levels of exercise. We monitored ventilation, tidal volume, and respiratory frequency in seven normal subjects during and after exercise. Each subject exercised on several occasions on separate days. At least two of the tests were maximal (i.e., subject terminated). In the other tests exercise was terminated by the experimenter at different fractions of the highest level attained by the subject. There was no systematic difference between breathing pattern during exercise and recovery in tests where final O2 consumption (VO2) was 45-92% of the subjects' highest VO2. By contrast 13 of 19 studies in which final VO2 was 92-100% of highest VO2 were followed by relative rapid shallow breathing. We conclude that rapid shallow breathing during recovery from exercise is a phenomenon that is limited to very high exercise levels. On consideration of the various mechanisms that may be entertained to explain this phenomenon, we believe that development of pulmonary congestion-interstitial edema at very high levels of exercise is the most consistent with our findings.     

Electromyogram as an indicator of neuromuscular fatigue during incremental exercise

This study analysed the changes in the electromyographic activity (EMG) of the vastus lateralis muscle (VL) during an incremental maximal oxygen uptake test on a treadmill. A breakpoint in the integrated electromyogram (iEMG)-velocity relationship has already been interpreted in two ways: either as a sign of neuromuscular fatigue or as an expression of the iEMG-velocity relationship characteristics. The aim of this study was to test a method of distinguishing fatigue effects from those due to increases in exercise power. Eight well-trained male runners took part in the study. They completed a running protocol consisting of 4-min stages of increments in power output. Between each stage (about 15 s after the start of a minute at rest), the subjects had to maintain a standard effort: a 10-s isometric leg extension contraction [50% isometric maximal voluntary contraction (IMVC)]. The EMG was recorded during the running and isometric protocols, a change in the EMG signal during the isometric exercise being considered as the sign of fatigue. The iEMG-velocity relationships were strongly fitted by a second-order polynomial function for data taken at both the start (r = 0.98) and the end (r = 0.98) of the stage. Based on the stability of the 50%IMVC-iEMG relationship noted between stages, the start-iEMG has been identified as expressing the iEMG-velocity relationship without fatigue. The stage after which end-iEMG increased significantly more steeply than start-iEMG was considered as the iEMG threshold and was simultaneous with the ventilatory equivalent for carbon dioxide threshold. The parallel changes of minute ventilation and iEMG would suggest the existence of common regulation stimuli linked either to effort intensity and/or to metabolic conditions. The fall in intracellular [K⁺] has been discussed as being one of the main factors in regulating ventilation. Accepted: 16 December 1997     

Comparing the lactate and EMG thresholds of recreational cyclists during incremental pedaling exercise

The purpose of this study was to determine the validity of using the electromyography (EMG) signal as a noninvasive method of estimating the lactate threshold (LT) power output in recreational cyclists. Using an electromagnetic bicycle ergometer and constant pedaling cadence of 80 rpm, 24 recreational cyclists performed an incremental exercise protocol that consisted of stepwise increases in power output of 25 W every 3 min until exhaustion. The EMG signal was recorded from the right vastus lateralis (VL) and right rectus femoris (RF) throughout the test. Blood samples were taken from the fingertip every 3 min. The LT was determined by examining the relation between the lactate concentration and the power output using a log-log transformation model. The root mean square (RMS) value from the EMG signal was calculated for every 1-second non-superimposing window. Sets of pairs of straight regression lines were plotted and the corresponding determination coefficients (R(2)) were calculated. The intersection point of the pair of lines with the highest R(2) product was chosen to represent the EMG threshold (EMGT). The results showed that the correlation coefficients (r) between EMGT and LT were significant (p < 0.01) and high for the VL (r = 0.826) and RF (r = 0.872). The RF and VL muscles showed similar behavior during the maximal incremental test and the EMGT and LT power output were equivalent for both muscles. The validity of using EMG to estimate the LT power output in recreational cyclists was confirmed.     

Influence of cold exposure on blood lactate response during incremental exercise

This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24 degrees C (MT) or at -2 degrees C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption (VO2) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1st, 4th, 7th, and the 10th min following exercise for the determination of blood lactate (LA) concentration. The VO2 was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute VO2, and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase off FFA was found only during CT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maximal power and torque-velocity relationship on a cycle ergometer during the acceleration phase of a single all-out exercise

Seven subjects pedalled on a Monark cycle ergometer as fast as possible for approximately 7 s against four different resistances which corresponded to braking torques (T _B) equal to 19, 38, 57 and 76 N · m at the crank level. Exercise periods were separated by 5-min recovery periods. Pedal velocity was recorded every 50 ms by means of a disc with 360 slots fixed on the flywheel, passing in front of a photo-electric cell linked to a microcomputer which processed the data. Every 50 ms, the time necessary to perform half a pedal revolution (t _1/2) was computed by adding the 50-ms periods necessary to reach 669 slots (the number of slots corresponding to half a pedal revolution). To measuret _1/2 to an accuracy better than 50 ms, this time was computed by a linear interpolation of the time-slot number relationship. Power (P) was averaged duringt ₁₂ by adding the power dissipated against braking torque and the power necessary to accelerate the flywheel. The torque-velocity (T-) relationship was studied during the acceleration phase of a sprint against a single TB by computing every 50 ms the relationship between and T (N · m), equal to the sum ofT _B and the torque necessary to accelerate the flywheel at the same time. The T- relationships calculated from the acceleration phase of a single all-out exercise were linear and similar to the previously described relationships between peak velocity and braking force. These relationships can be expressed as follows: = _0,acc (1 –T/T _0,acc) where is pedal velocity,T the torque exerted on the crank andT _0,acc and _0,acc have the dimensions of maximal torque and maximal velocity respectively. Based on this model, maximal power (P _max,acc) is calculated as 0.257_{0, acc} T _{0, acc}. Maximal powerP _max,acc measured with the acceleration method was independent of braking torqueT _B and slightly higher thanP _max calculated from the relationship between peak velocity andT _B.     

Patterns of leg muscle recruitment vary between novice and highly trained cyclists

This study compared patterns of leg muscle recruitment and coactivation, and the relationship between muscle recruitment, coactivation and cadence, in novice and highly trained cyclists. Electromyographic (EMG) activity of tibialis anterior (TA), tibialis posterior (TP), peroneus longus (PL), gastrocnemius lateralis (GL) and soleus (SOL) was recorded using intramuscular fine-wire electrodes. Four experimental conditions of varying cadence were investigated. Differences were evident between novice and highly trained cyclists in the recruitment of all muscles. Novice cyclists were characterized by greater individual variance, greater population variance, more extensive and more variable muscle coactivation, and greater EMG amplitude in periods between primary EMG bursts. Peak EMG amplitude increased linearly with cadence and was not different at individual preferred cadence in either novice or highly trained cyclists. However, EMG amplitude in periods between primary EMG bursts, as well as the duration of primary EMG bursts, increased with increasing cadence in novice cyclists but were not influenced by cadence in highly trained cyclists. Our findings suggest that muscle recruitment is highly skilled in highly trained cyclists and less refined in novice cyclists. More skilled muscle recruitment in highly trained cyclists is likely a result of neuromuscular adaptations due to repeated performance of the cycling movement in training and competition.     

Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia.

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial PO(2) (Pa(O(2)); 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa(O(2)) (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O(2)). During normoxia at 90% peak O(2) consumption, Pa(O(2)) was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O(2) tension difference (A-aDO(2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0. 001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aDO(2) (P < 0.01). There were no significant differences between groups in arterial PCO(2) (Pa(CO(2))) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O(2) diffusing capacity (DL(O(2))), logSD(Q), and Pa(CO(2)) each accounted for approximately 30% of the variance in Pa(O(2)) (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DL(O(2)), VA/Q inequality, and ventilation.     

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease

To determine if decreased systemic oxygen (O₂) extraction contributes to the exercise limit in severe chronic obstructive pulmonary disease (COPD), 40 consecutive incremental cycle ergometer exercise tests performed by such patients, from which a “log-log” lactate threshold (LT) was identified, were compared to those of 8 patients with left ventricular failure (LVF) and 10 normal controls. Pulmonary gas exchange and minute ventilation were measured continuously and arterial blood gas tensions, pH, and lactate concentrations were sampled each minute. Cardiac output (Q˙ _c) was measured by first-pass radionuclide ventriculography. The systemic O₂ extraction ratio (O₂ER) was calculated as arterial − mixed venous O₂ content difference (C _aO₂ − C _vO₂)/C _aO₂. Peak exercise O₂ uptake (V˙O_2peak) was markedly reduced in both COPD and LVF [41 (3) and 42 (3)% predicted, respectively], compared to controls [89 (2)% predicted, P < 0.0001 for each]. Similarly, the LT occurred at a low percentage of predicted maximal oxygen consumption in both COPD and LVF [25 (2) and 27 (3)%] compared to normals [46 (3)%, P < 0.0001 for each]. The systemic O₂ER at peak exercise was severely reduced in COPD [0.36 (0.02)] compared to the other groups [P < 0.0001 for each], for whom it was nearly identical [0.58 (0.03) vs 0.63 (0.04), LVF vs control, P > 0.05]. In the COPD group, an early LT correlated with reduced systemic O₂ER at peak exercise (r = 0.64, P < 0.0001), but not with any index of systemic O₂ delivery. These data suggest that lactic acidemia during exercise in patients with severe COPD is better related to abnormal systemic O₂ extraction than to its delivery and contributes to the exercise limit. Accepted: 10 March 1998     

The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man

The influence of a pattern of exercise and dietary manipulation, intended to alter carbohydrate (CHO) availability, on pre-exercise acid-base status and plasma ammonia and blood lactate accumulation during incremental exercise was investigated. On three separate occasions, five healthy male subjects underwent a pre-determined incremental exercise test (IET) on an electrically braked cycle ergometer. Each IET involved subjects exercising for 5 min at 30%, 50%, 70% and 95% of their maximal oxygen uptake (VO2max) and workloads were separated by 5 min rest. The first IET took place after 3 days of normal dietary CHO intake. The second and third tests followed 3 days of low or high CHO intake, which was preceded by prolonged exercise to exhaustion in an attempt to deplete muscle and liver glycogen stores. Acid-base status and plasma ammonia and blood lactate levels were measured on arterialised venous blood samples immediately prior to and during the final 15 s of exercise at each workload and for 40 min following the completion of each IET. Three days of low CHO intake resulted in the development of a mild metabolic acidosis in all subjects. Plasma ammonia (NH3) accumulation on the low-CHO diet tended to be greater than normal at each exercise workload. Values returned towards resting levels during each recovery period. After the normal and high-CHO diets plasma NH3 levels did not markedly increase above resting values until after exercise at 95% VO2max. Plasma NH3 levels after the high-CHO diet were similar to those after the normal CHO diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Recovery of the torque-velocity relationship after short exhausting cycling exercise

The effects of fatigue upon the torque-velocity (T-omega) relationship in cycling were studied in 11 subjects. Fatigue was induced by short exhausting exercise, on a cycle ergometer, consisting of 4 all-out sprints without recovery. The linear (T-omega) relationship was determined during each all-out sprint, before, during and after the exhausting exercise. The kinetics of the T-omega relationship had permitted the study of the recovery of optimal torque, optimal velocity and their corresponding maximal power outputs (Pmax), 30 s or 1 min after the short exhausting exercise. Fatigue induced a parallel shift to the left of the T-omega relationship which was partly reversed by a parallel shift to the right during recovery. After 30 s recovery optimal velocity, optimal torque and Pmax were slightly lower than the corresponding values before the exhausting exercise; after 1-min optimal velocity and optimal torque had recovered 99% and 97% of their initial values. These mechanical data suggested that the causes of exhaustion were processes that allowed fast recovery of both optimal velocity and optimal torque.     

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O_2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O_2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg ^–1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg ^–1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min^–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.     

Performance indicators and functional adaptive windows in competitive cyclists: effect of one-year strength and conditioning training programme

Changes and relationships between cycling performance indicators following a one-year strength and conditioning training have not been totally clarified. The aims of this study are to investigate (i) the effect of a combined one-year strength and conditioning training programme on performance indicators and the possible relationships between these indicators, and (ii) the existence of possible endurance-functional-adaptive windows (EFAWs) linked to changes in muscular strength and body composition markers. Functional and lactate threshold power (FTP and LTP), maximal strength (1RM) and body composition (body mass index [BMI], body cell mass [BCM] and phase angle [PA]) were measured at the beginning and the end of a one-year strength and conditioning training programme of thirty cyclists. Correlations, differences, and predictive analysis were performed among parameters. Significant differences were found between pre- and post-conditioning programme results for FTP, LTP, 1RM (p < 0.0001) and BCM (p = 0.038). When expressed as power output (W), FTP and LTP were significantly correlated with 1RM (r = 0.36, p = 0.005 and r = 0.37, p = 0.004, respectively), body mass (r = 0.30 and p = 0.02), BCM (r = 0.68, p < 0.001) and PA (r = 0.42 and 0.39, respectively and p < 0.001). When expressed as W·kg-¹, these power thresholds were strongly correlated with body mass (r = -0.56 and -0.61, respectively) and BMI (r = -0.57 and -0.61 respectively) with p < 0.001. Predictive polynomial regressions revealed possible endurance and strength adaptation zones. The present findings indicated beneficial impacts of one-year strength and conditioning training on cycling performance indicators, confirmed the correlation between performance indicators, and suggested the existence of different EFAWs. Strategies aiming to improve performance should consider cyclist characteristics and performance goals to achieve EFAWs and thereby enhance cycling performance.     

The role of pulmonary CO2 flow in the control of the phase i ventilatory response to exercise in humans

To gain an insight into the origin of the phase I ventilatory response to exercise (ph I) in humans, pulmonary ventilation WE) and end-tidal partial pressures of oxygen and carbon dioxide (P _ETO₂ and P _ETCO₂, respectively) were measured breath-by-breath in six male subjects during constant-intensity exercise on the cycle ergometer at 50, 100 and 150 W, with eupnoeic normocapnia (N) or hyperpnoeic hypocapnia (H) established prior to the exercise test. Cardiac output (Q₂) was also determined beat-by-beat by impedance cardiography on eight subjects during moderate exercise (50 W), and the C0₂ flow to the lungs (Q₂·C_vCO₂ where C_vCO₂ is concentration of CO₂ in mixed veneous blood) was estimated with a time resolution of one breathing cycle. In N, the initial abrupt increase of PE during ph I (V_E approximately 18 l · min^–1 above rest) was followed by a transient fall. When P _ETCO₂ started to increase (and P _ETO₂ decreased) V_E increased again (phase II ventilatory response, ph II). In H, during ph I V_E was similar to that of N. By contrast, during ph II V_E kept gradually decreasing and started to increase only when P _ETCO₂ had returned to approximately 40 mmHg (5.3 kPa). Thus, as a result of the prevailing initial conditions (N or H) a temporal shift of the time-course of V_E during ph II became apparent. No correlation was found between C0₂ flow to the lungs and V_E during ph I. These results are interpreted as suggesting that an increased C0₂ flow to the lungs does not constitute an important factor for the initial hyperventilatory response to exercise. They are rather compatible with a neural origin of ph I, and would support the neurohumoral theory of ventilatory control during exercise.