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Purpose: To investigate the effect of voluntary hypocapnic hyperventilation or moderate hypoxia on metabolic and heart rate responses during high-intensity intermittent exercise., Methods: Ten males performed three 30-s bouts of high-intensity cycling [Ex1 and Ex2: constant-workload at 80% of the power output in the Wingate anaerobic test (WAnT), Ex3: WAnT] interspaced with 4-min recovery periods under normoxic (Control), hypocapnic or hypoxic (2500 m) conditions. Hypocapnia was developed through voluntary hyperventilation for 20 min prior to Ex1 and during each recovery period., Results: End-tidal CO 2 pressure was lower before each exercise in the hypocapnia than control trials. Oxygen uptake ([Formula: see text]) was lower in the hypocapnia than control trials (822 ± 235 vs. 1645 ± 245 mL min -1 ; mean ± SD) during Ex1, but not Ex2 or Ex3, without a between-trial difference in the power output during the exercises. Heart rates (HRs) during Ex1 (127 ± 8 vs. 142 ± 10 beats min -1 ) and subsequent post-exercise recovery periods were lower in the hypocapnia than control trials, without differences during or after Ex2, except at 4 min into the second recovery period. [Formula: see text] did not differ between the control and hypoxia trials throughout., Conclusions: These results suggest that during three 30-s bouts of high-intensity intermittent cycling, (1) hypocapnia reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate during the first but not subsequent exercises; (2) HRs during the exercise and post-exercise recovery periods are lowered by hypocapnia, but this effect is diminished with repeated exercise bouts, and (3) moderate hypoxia (2500 m) does not affect the metabolic response during exercise.

Purpose: The aim of this study is to investigate the individuality of airflow shapes during volitional hyperventilation., Methods: Ventilation was recorded on 18 healthy subjects following two protocols: (1) spontaneous breathing (SP1) followed by a volitional hyperventilation at each subject's spontaneous (HVSP) breathing rate, (2) spontaneous breathing (SP2) followed by hyperventilation at 20/min (HV20). HVSP and HV20 were performed at the same level of hypocapnia: end tidal CO2 (FETCO2) was maintained at 1% below the spontaneous level. At each breath, the tidal volume (VT), the breath (TTOT), the inspiratory (TI) and expiratory durations, the minute ventilation, VT/TI, TI/TTOT and the airflow shape were quantified by harmonic analysis. Under different conditions of breathing, we test if the airflow profiles of the same individual are more similar than airflow profiles between individuals., Results: Minute ventilation was not significantly different between SP1 (6.71 ± 1.64 l·min(-1)) and SP2 (6.57 ± 1.31 l·min(-1)) nor between HVSP (15.88 ± 4.92 l·min(-1)) and HV20 (15.87 ± 4.16 l·min(-1)). Similar results were obtained for FETCO2 between SP1 (5.06 ± 0.54 %) and SP2 (5.00 ± 0.51%), and HVSP (4.07 ± 0.51%) and HV20 (3.88 ± 0.42%). Only TI/TTOT remained unchanged in all four conditions. Airflow shapes were similar when comparing SP1-SP2, HVSP-HV20, and SP1-HVSP but not similar when comparing SP2-HV20., Conclusions: These results suggest the existence of an individuality of airflow shape during volitional hyperventilation. We conclude that volitional ventilation alike automatic breathing follows inherent properties of the ventilatory system. Registered by Pascale Calabrese on ClinicalTrials.gov, # NCT01881945.

Introduction: Evidence has long suggested that mammalian ventilatory and locomotor rhythms are linked, yet determinants and implications of locomotor-respiratory coupling (LRC) continue to be investigated. Anecdotally, respiratory muscle fatigue seen at the end of heavy exercise may result in an uncoupling of movement-ventilation rhythms; however, there is no scientific evidence to substantiate this claim., Purpose: We sought to determine whether or not fatigue of the respiratory muscles alters locomotor-respiratory coupling patterns typically observed in highly trained individuals while running. A related query was to examine the relationship between the potential changes in LRC and measures of running economy., Method: Twelve male distance runners ran at four submaximal workloads (68-89 % VO2peak) on two separate days while LRC was quantified. One LRC trial served as a control (CON), while the other was performed following an isocapnic voluntary hyperpnea to task failure to induce respiratory muscle fatigue (FT+). LRC was assessed as stride-to-breathing frequency ratios (SF/fB) and degree of LRC (percentage of breaths occurring during the same decile of the step cycle)., Result: Hyperpnea resulted in significant declines in maximal voluntary inspiratory (MIP) and expiratory (MEP) mouth pressures (ΔMIP = -10 ± 12 cm H2O; ΔMEP = -6 ± 9 cm H2O). There were no differences in minute ventilation between CON and FT+ (CON, all speeds pooled = 104 ± 25 L min(-1); FT+ pooled = 106 ± 23 L min(-1)). Stride frequency was not different between trials; however, breathing frequency was significantly greater during FT+ compared to CON at all speeds (CON pooled = 47 ± 10 br min(-1); FT+ pooled = 52 ± 9 br min(-1)), resulting in smaller corresponding SF/fB. Yet, the degree of LRC was the same during CON and FT+ (CON pooled = 63 ± 15 %; FT+ pooled = 64 ± 18 %)., Conclusion: The results indicate that trained runners are able to continue entraining breath and step cycles, despite marked changes in exercise breathing frequency, after a fatiguing hyperpnea challenge.

Purpose: We evaluated whether hypocapnia achieved through voluntary hyperventilation diminishes the increases in oxygen uptake elicited by short-term (e.g., ~30 s) all-out exercise without affecting exercise performance., Methods: Nine subjects performed 30-s Wingate anaerobic tests (WAnT) in control and hypocapnia trials on separate days in a counterbalanced manner. During the 20-min rest prior to the 30-s WAnT, the subjects in the hypocapnia trial performed voluntary hyperventilation (minute ventilation = 31 L min(-1)), while the subjects in the control trial continued breathing spontaneously (minute ventilation = 14 L min(-1))., Results: The hyperventilation in the hypocapnia trial reduced end-tidal CO2 pressure from 34.8 ± 2.5 mmHg at baseline rest to 19.3 ± 1.0 mmHg immediately before the 30-s WAnT. In the control trial, end-tidal CO2 pressure at baseline rest (35.9 ± 2.5 mmHg) did not differ from that measured immediately before the 30-s WAnT (35.9 ± 3.3 mmHg). Oxygen uptake during the 30-s WAnT was lower in the hypocapnia than the control trial (1.55 ± 0.52 vs. 1.95 ± 0.44 L min(-1)), while the postexercise peak blood lactate concentration was higher in the hypocapnia than control trial (10.4 ± 1.9 vs. 9.6 ± 1.9 mmol L(-1)). In contrast, there was no difference in the 5-s peak (842 ± 111 vs. 850 ± 107 W) or mean (626 ± 74 vs. 639 ± 80 W) power achieved during the 30-s WAnT between the control and hypocapnia trials., Conclusions: These results suggest that during short-period all-out exercise (e.g., 30-s WAnT), hypocapnia induced by voluntary hyperventilation reduces the aerobic metabolic rate without affecting exercise performance. This implies a compensatory elevation in the anaerobic metabolic rate.

Purpose: Hyperventilation, implemented during recovery of repeated maximal sprints, has been shown to attenuate performance decrement. This study evaluated the effects of hyperventilation, using strength exercises, on muscle torque output and EMG amplitude., Methods: Fifteen power-trained athletes underwent maximal isokinetic knee extensions consisting of 12 repetitions × 8 sets at 60°/s and 25 repetitions × 8 sets at 300°/s. The inter-set interval was 40 s for both speeds. For the control condition, subjects breathed spontaneously during the interval period. For the hyperventilation condition, subjects hyperventilated for 30 s before each exercise set (50 breaths/min, PETCO2: 20-25 mmHg). EMG was recorded from the vastus medialis and lateralis muscles to calculate the mean amplitude for each contraction., Results: Hyperventilation increased blood pH by 0.065-0.081 and lowered PCO2 by 8.3-10.3 mmHg from the control values (P < 0.001). Peak torque declined with repetition and set numbers for both speeds (P < 0.001), but the declining patterns were similar between conditions. A significant, but small enhancement in peak torque was observed with hyperventilation at 60°/s during the initial repetition phase of the first (P = 0.032) and fourth sets (P = 0.040). EMG amplitude also declined with set number (P < 0.001) for both speeds and muscles, which was, however, not attenuated by hyperventilation., Conclusion: Despite a minor ergogenic effect in peak torque at 60°/s, hyperventilation was not effective in attenuating the decrement in torque output at 300°/s and decrement in EMG amplitude at both speeds during repeated sets of maximal isokinetic knee extensions.

The arterial blood pressure and ventilatory responses to severe passive heating at rest varies greatly among individuals. We tested the hypothesis that the increase in ventilation seen during severe passive heating of resting humans is associated with a decrease in arterial blood pressure. Passive heating was performed on 18 healthy males using hot water immersion to the level of the iliac crest and a water-perfused suit. We then divided the subjects into two groups: MAP(NOTINC) (n = 8), whose mean arterial blood pressure (MAP) at the end of heating had increased by ≤3 mmHg, and MAP(INC) (n = 10), whose MAP increased by >3 mmHg. Increases in esophageal temperature (T (es)) elicited by the heating were similar in the two groups (+2.3 ± 0.3 vs. +2.4 ± 0.4 °C). Early during heating (increase in T (es) was <1.5 °C), MAP, minute ventilation ([Formula: see text]), and end-tidal CO(2) pressure ([Formula: see text]) were similar between the groups. However, during the latter part of heating (increase in T (es) was ≥1.5 °C), the increase in [Formula: see text] and decrease in [Formula: see text] were significantly greater or tended to be greater, while the increase in MAP was significantly smaller in MAP(NOTINC) than MAP(INC). Among all subjects, heating-induced changes in [Formula: see text] significantly and negatively correlated with heating-induced changes in MAP during the latter part of heating (r = -0.52 to -0.74, P < 0.05). These results suggest that, in resting humans, 25-50 % of the variation in the magnitude of the arterial blood pressure response to severe passive heating can be explained by the magnitude of hyperthermia-induced hyperventilation.

We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac(-)](B)) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation ([Formula: see text]). Prior to the intervention, the MLSS [lac(-)](B) was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L(-1) in the IMT and control groups, respectively. During volitional hyperpnoea, [Formula: see text] increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min(-1) at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min(-1) in IMT and control groups, respectively; [lac(-)](B) concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L(-1) (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.

The present study sought to establish links between hyperventilation and postural stability. Eight university students were asked to stand upright under two hyperventilation conditions applied randomly: (1) a metabolic hyperventilation induced by 5 min of hypercapnic-hyperoxic rebreathing (CO(2)-R); and, (2) a voluntary hyperventilation (VH) of 3 min imposed by a metronome set at 25 cycles per min. Recordings were obtained with eyes open, with the subjects standing on a force plate over 20-s periods. Ventilatory response, displacements in the centre of pressure in both the frontal and sagittal planes and fluctuations in the three planes of the ground reaction force were monitored in the time and frequency domains. Postural changes related to respiratory variations were quantified by coherence analysis. Myoelectric activities of the calf muscles were recorded using surface electromyography. Force plate measurements revealed a reduction in postural stability during both CO(2)-R and VH conditions, mainly in the sagittal plane. Coherence analysis provided evidence of a ventilatory origin in the vertical ground reaction force fluctuations during VH. Electromyographic analyses showed different leg muscles strategies, assuming the existence of links between the control of respiration and the control of posture. Our results suggest that the greater disturbing effects caused by voluntary hyperventilation on body balance are more compensated when respiration is under automatic control. These findings may have implications for understanding the organisation of postural and respiratory activities and suggest that stability of the body may be compromised in situations in which respiratory demand increases and requires voluntary control.

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [Formula: see text] (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [Formula: see text] separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T (es)), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ([Formula: see text]) during exercise. The training lowered the T (es) threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T (es) and the peak FVC during exercise. It also lowered minute ventilation ([Formula: see text]) during exercise, but this effect disappeared after removing the influence of [Formula: see text] on [Formula: see text]. The training did not change the slope relating ventilatory variables to T (es). We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.

We have reported that minute ventilation [[Formula: see text]] and end-tidal CO(2) tension [[Formula: see text]] are determined by the interaction between central controller and peripheral plant properties. During exercise, the controller curve shifts upward with unchanged central chemoreflex threshold to compensate for the plant curve shift accompanying increased metabolism. This effectively stabilizes [Formula: see text] within the normal range at the expense of exercise hyperpnea. In the present study, we investigated how endurance-trained athletes reduce this exercise hyperpnea. Nine exercise-trained and seven untrained healthy males were studied. To characterize the controller, we induced hypercapnia by changing the inspiratory CO(2) fraction with a background of hyperoxia and measured the linear [Formula: see text] relation [[Formula: see text]]. To characterize the plant, we instructed the subjects to alter [Formula: see text] voluntarily and measured the hyperbolic [Formula: see text] relation ([Formula: see text]). We characterized these relations both at rest and during light exercise. Regular exercise training did not affect the characteristics of either controller or plant at rest. Exercise stimulus increased the controller gain (S) both in untrained and trained subjects. On the other hand, the [Formula: see text]-intercept (B) during exercise was greater in trained than in untrained subjects, indicating that exercise-induced upward shift of the controller property was less in trained than in untrained subjects. The results suggest that the additive exercise drive to breathe was less in trained subjects, without necessarily a change in central chemoreflex threshold. The hyperbolic plant property shifted rightward and upward during exercise as predicted by increased metabolism, with little difference between two groups. The [Formula: see text] during exercise in trained subjects was 21% lower than that in untrained subjects (P < 0.01). These results indicate that an adaptation of the controller, but not that of plant, contributes to the attenuation of exercise hyperpnea at an iso-metabolic rate in trained subjects. However, whether training induces changes in neural drive originating from the central nervous system, afferents from the working limbs, or afferents from the heart, which is additive to the chemoreflex drive to breathe, cannot be determined from these results.

Since playing wind instrument impedes normal respiratory functions, its effect on expiratory and blood gases as well as on cardiac function was investigated. In 15 skilled clarinettists expiratory PO(2) and PCO(2) were measured in gas drawn from a modified clarinet barrel when playing a composition (Robert Schumann's "Phantasiestücke" Op. 73 for clarinet and piano) with increasing difficulty from movement 1 to movement 3. Blood gases were measured in arterialized ear lobe blood at the end of each movement and the electrocardiogram was recorded continuously. From the expiratory gas pressures one may conclude that the most advanced players adapt their ventilation to the requirements of the composition and sustain expiration during difficult parts of the composition until hypoxic alveolar PO(2) values are reached (minimum 77 mmHg). Less trained clarinettists tend to hyperventilation or shallow breathing. Oxygen saturation in arterialized blood showed a slight step-wise decrease from movement to movement [control 96.6 ± 0.5 (SD)%, end of concert 95.6 ± 1.0%]. SO(2) was significantly higher because of possibly more effective ventilation in instrumentalists with practise time exceeding 2 h daily. Mean heart rate increased to values like during moderate to heavy physical exercise depending on artistic fitness and the difficulty of the movement (maximal individual value 173 beats/min). Additionally, a large variation might be caused through intrathoracic pressure changes, changing exertion, respiratory influences and emotion. The electrocardiogram showed no pathological events. In general, clarinet playing at a professional level imposes strain on ventilation and circulation but usually not on a pathophysiological level.

The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O(2) uptake (VO(2p)) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P(ET)CO(2) approximately 40 mmHg) and (2) controlled hyperventilation (HYPO, P(ET)CO(2) approximately 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Delta50%); each transition lasted 6 min and was preceded by 20 W cycling. VO(2p) was measured breath-by-breath and concentration changes in oxy- and deoxy-hemoglobin/myoglobin (Delta[HHb]) of the vastus lateralis muscle were measured by near-infrared spectroscopy. Adjustment of VO(2p) and Delta[HHb] were modeled using a mono-exponential equation by non-linear regression. During MOD1, the phase 2 time constant (tau) for VO(2p)(tauVO(2p)) was greater (P < 0.05) in HYPO (45 +/- 24 s) than CON (28 +/- 17 s). During MOD2, tauVO(2p) was reduced (P < 0.05) in both conditions (HYPO: 24 +/- 7 s, CON: 20 +/- 8 s). The Delta[Hb(TOT)] and Delta[O(2)Hb] were greater (P < 0.05) prior to and throughout MOD2. The Delta[HHb] mean response time was similar in MOD1 and MOD2, and between conditions, however, the MOD1 Delta[HHb] amplitude was greater (P < 0.05) in HYPO compared to CON, with no differences between conditions in MOD2. These findings suggest that the speeding of VO(2p) kinetics after prior HVY in HYPO was related, in part, to an increase in microvascular perfusion.

To test the hypothesis that the hyperthermia-induced ventilatory response relates to aerobic power and/or the cutaneous vasodilatory response during exercise, we asked 18 subjects to perform 3 kinds of exercise: an incremental exercise to determine peak oxygen consumption (V(O)(2peak)), a steady state exercise at 50% of V(O)(2peak) to determine the ventilatory response to increasing body temperature, and a steady state exercise at 60% of V(O)(2peak) to determine the cutaneous vasodilatory response to increasing body temperature. The ventilatory and cutaneous vasodilatory responses were evaluated by plotting the increase in minute ventilation or in forearm vascular conductance against the increase in oesophageal temperature. Regression analysis revealed that: (1) there was a negative relationship between the hyperthermic ventilatory response and cutaneous vasodilatory response, (2) there was a negative relationship between the hyperthermic ventilatory response and V(O)(2peak), and (3) there was a positive relationship between the cutaneous vasodilatory response and V(O)(2peak). These results support our hypothesis and suggest that exercise training suppresses the hyperthermic ventilatory response and improves the thermoregulatory response.

Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction. To investigate this, we tested the hypothesis that IMT would attenuate the increase in [lac(-)](B) caused by mimicking, at rest, the breathing pattern observed during high-intensity exercise. Twenty-two physically active males were matched for 85% maximal exercise minute ventilation (.V(E) max) and divided equally into an IMT or a control group. Prior to and following a 6 week intervention, participants performed 10 min of volitional hyperpnoea at the breathing pattern commensurate with 85% .V(E) max. The IMT group performed 6 weeks of pressure-threshold IMT; the control group performed no IMT. Maximal inspiratory mouth pressure increased (mean +/- SD) 31 +/- 22% following IMT and was unchanged in the control group. Prior to the intervention in the control group, [lac(-)](B) increased from 0.76 +/- 0.24 mmol L(-1) at rest to 1.50 +/- 0.60 mmol L(-1) (P < 0.05) following 10 min volitional hyperpnoea. In the IMT group, [lac(-)](B) increased from 0.85 +/- 0.40 mmol L(-1) at rest to 2.02 +/- 0.85 mmol L(-1) following 10 min volitional hyperpnoea (P < 0.05). After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05). In conclusion, increases in [lac(-)](B) during volitional hyperpnoea at 85% .V(E) max were attenuated following IMT. These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.

High arterial CO(2) pressure (P(a)CO(2)) measured in athletes during exercise suggests inadequate hyperventilation. End-tidal CO(2) pressure (P (ET)CO(2)) is used to estimate P(a)CO(2.) However, P(ET)CO(2) also depends on exercise intensity (CO(2) production, .VCO2) and ventilation efficiency (being P(ET)CO(2) function of respiratory rate). We evaluated P(ET)CO(2) as a marker, which combines efficiency of ventilation and performance. A total of 45 well-trained volunteers underwent cardiopulmonary tests and were grouped according to P(ET)CO(2) at respiratory compensation (RC): Group 1 (P(ET)CO(2) 35.1-41.5 mmHg), Group 2 (41.6-45.7) and Group 3 (45.8-62.6). At anaerobic threshold, RC and peak exercise, ventilation (.VE) was similar, but in Group 3, a greater tidal volume (Vt) and lower respiratory rate (RR) were observed. Peak exercise workload and .VO2 were lowest in Group 1 and similar between Group 2 and 3. Group 3 subjects also showed high peak .VCO2 suggesting a greater glycolytic metabolism. In conclusion, a high P(ET)CO(2) during exercise is useful in identifying a specific respiratory pattern characterized by high tidal volume and low respiratory rate. This respiratory pattern may belong to subjects with potential high performance.

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Delta) in lactic acid ([La]), [HCO3-], pH and PCO2 in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (betanbi=-Delta[La]. DeltapH(-1)-Delta[HCO3-]. DeltapH(-1)) amounted to 40+/-2 (SEM) and 28+/-2 mmol l(-1) in UT and TR, respectively (P<0.01). During recovery beta (nbi) decreased to 20 (UT) and 16 (TR) mmol l(-1) (P<0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Delta[La]. betabi amounted to 37-41 mmol l(-1) being lower than at sea level. The large exercise betanbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower betanbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders betanbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO3-]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.

The purpose of this study was to determine if increased environmental heat leads to hyperthermic-induced hypocapnia and associated alkalosis during prolonged self-paced cycling. Nine male cyclists completed three 100 km stochastic time trials in hot (34 degrees C), neutral (22 degrees C) and cold (10 degrees C) environments. Intermittent measurements of rectal and skin temperature, expired gases, blood pH, PaCO(2), PaO(2), and bicarbonate were made throughout. Rectal temperature increased significantly throughout all trials (P < 0.001) and was significantly correlated with increases in the ventilatory equivalent for carbon dioxide (Ve/ VCo2; r = 0.77; P < 0.001) and blood pH (r = 0.69; P < 0.05). Rectal temperature was also negatively correlated with a reduction in PaCO(2) (r = -0.80; P < 0.001). PaO(2) and bicarbonate concentration remained constant throughout all trials. This study has shown that prolonged self-paced cycling is associated with a hyperthermic-induced hyperventilation, causing a decrease in arterialized carbon dioxide tension and consequential respiratory alkalosis.

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac-]B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207+/-8 W, mean +/- SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20-28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3+/-2.4 and 168.3+/-7.0 l min(-1) (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9+/-6.8 l min(-1)), 3.46+/-0.20 and 3.83 +/- 0.20 l min(-1) (P<0.01), and 158.5+/-2.7 and 166.8+/-2.7 beats min(-1) (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac-]B increased from 3.7+/-0.2 to 4.7+/-0.3 mmol l(-1) (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac-]B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac-]B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.

Weight-training is recommended as a complement to conventional aerobic-training for most low to moderate risk patients suffering from coronary artery disease (CAD). The purpose of this study was to evaluate the effect of a 1 year exercise programme combining weight- and aerobic-training on peak oxygen uptake (V*O2,peak) and ventilatory threshold (VT). We studied 40 men suffering CAD who were divided into three groups: 14 subjects to weight-training plus aerobic-training [mean (SD] [combined exercise group, age 55 (10) years], 14 to aerobic-training only [aerobic-training group, age 57 (11) years], and 12 to a control group [standard care, age 57 (11) years]. A symptom-limited graded exercise test using the standard Bruce protocol was performed using a 12-lead electrocardiogram, and gas analysis techniques. Muscle strength was determined only in the combined exercise group using the one-repetition maximum method on each of eight weight exercises. Arm and leg strength increased by 21.9% and 27.8% respectively ( P<0.0001) from pre to post-tests. The V*O2,peak did not differ between the combined and aerobic-training groups but their adjusted means were greater than those of the control group [39 (1.8) and 35.3 (1.8) compared to 26.2 (2.7) ml.kg(-1).min(-1) ( P<0.001)]. The oxygen uptake at VT was higher in the combined group [24.7 (1.4) ml.kg(-1).min(-1)] compared to aerobic [18.7 (1.4) ml.kg(-1).min(-1)] and control [13.6 (1.7) ml.kg(-1)min(-1)] groups ( P<0.001). Similar results were found for exercise tolerance (treadmill time to peak and at VT). Combined exercise training increased the VT more than aerobic-training alone. Combined exercise training did not improve the V*O2,peak or the functional capacity more than aerobic-training alone.

The slope of the expired alveolar partial pressure of carbon dioxide profile increases during exercise. Its relationship to metabolic rate, however, remains to be determined at high exercise intensities. We therefore determined the slope of alveolar partial pressures of carbon dioxide and oxygen (PACO2, PAO2, respectively) during incremental cycle ergometer exercise (an increment of 40 W each minute) to exhaustion in 11 normal subjects. The PACO2 and PAO2 increased as linear functions of carbon dioxide production and oxygen uptake (VO2), respectively, up to the estimated lactate threshold (thetaLa-). At higher intensities PACO2 increased disproportionately but PAO2 continued to increase at the same rate in 7 subjects but increased more rapidly in the remainder. The rate of change in PACO2 per unit rate of change in VO2 averaged 3.15 (SD 1.05) (mmHg.s(-1)). (l.min(-1))-1 while the rate of change in PAO2 per unit rate of change in VO2 averaged -3.53 (SD 0.79) (mmHg.s(-1)) (l.min(-1))-1 over this range. The more rapid increase in PACO2 above thetaLa- was consistent with an accelerated CO2 exchange, whereas the more rapid rate of change in PAO2 in 3 of the subjects may have reflected the development of an increased distribution of the ventilation perfusion ratio in addition to the effects of hyperventilation.