Acute altitude exposure and altered acid-base states. II. Effects on exercise performance and muscle and blood lactate

This study examined the influence of the respiratory alkalosis of acute altitude (AL) exposure alone or in combination with metabolic acid-base manipulations on exercise performance and muscle and blood lactate accumulation. Four subjects exercised for 10 min at 50% and 75% and to exhaustion at 90% of ground level (GL) VO2max, and at the same relative exercise intensities during three exposures to a simulated altitude of 4200 m; (i) normal (NAL), (ii) following 0.2 g.kg-1 ingestion of sodium bicarbonate (BAL), and (iii) following 0.5 g.day-1 ingestion of acetazolamide for 2 days prior to exposure (AAL). Muscle and blood lactate values were similar throughout exercise for GL and NAL. Although muscle lactates were similar among AL conditions blood lactate was reduced for AAL and increased following exhaustive exercise for BAL compared with NAL. Time to exhaustion at 90% VO2max was increased for NAL (10.4 +/- 1.6 min) compared with GL (7.1 +/- 0.2 min). Performance time was decreased for AAL (6.3 +/- 2.8 min) compared with NAL and BAL (12.4 +/- 4.2 min). These data suggest that the induced respiratory alkalosis of acute AL exposure may enhance exercise performance at high relative intensities. In contrast, the ingestion of acetazolamide before AL exposure would have detrimental effects on performance. The mechanism responsible for these changes may relate to the possible influence of altered extracellular acid-base states on intracellular hydrogen ion accumulation and lactate release.     

Effects of the menstrual cycle phase on the blood lactate responses to exercise

The effects of menstrual cycle phase on the blood lactate response to exercise were examined in eumenorrheic women (n=9). Exercise tests were performed at the mid-follicular and mid-luteal points in the menstrual cycle (confirmed by basal body temperature records and hormone levels). Blood lactates were measured at rest and during the recovery from exercise. Resting lactates were not different between the exercise tests; however, recovery lactates were significantly (p < 0.05) lower in the luteal compared to the follicular phase. The mechanism for these differences is unclear, but may be related to an estrogen mediated increased lipid metabolism inducing a concurrent reduction in carbohydrate metabolism. The present findings question the use of blood lactate monitoring as a suitable technique to measure exercise intensity in eumenorrheic women.     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

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)     

Muscle and blood ammonia and lactate responses to prolonged exercise with hyperoxia

Investigations using nonsteady-state and fatiguing exercise protocols have demonstrated a strong relationship between ammonia and lactate metabolism and have suggested a cause and effect relationship between these two variables. We investigated the lactate-ammonia response using prolonged exercise and inspiration of hyperoxic gas (60% O2-40% N2). The exercise consisted of either 70-75% maximal O2 uptake (VO2 max) for 40 min (series 1, n = 6) or 75-80% VO2max for 30 min (series 2, n = 6) with the subjects inspiring room air on one occasion and hyperoxia in the other test. In both series blood ammonia rose continuously throughout the exercise regardless of the inspired gas treatment; in contrast blood lactate did not increase after 10 min with room air, and with hyperoxia blood lactate was reduced. Muscle lactate and ammonia (series 2; vastus lateralis) had responses similar to the blood data. The data demonstrated no apparent lactate-ammonia relationship with prolonged exercise or in response to hyperoxia, suggesting that ammonia production can be independent of lactate metabolism. The data also suggest that type I fibers can be a major source of ammonia in humans.     

Influence of moderate altitude on blood lactate and heart rate in a standardized exercise test in healthy volunteers

Nineteen healthy volunteers were exposed to a standardized exercise test at sea level (SLa), at an altitude of 1700 m before (1700a) and after a moderate 10-day mountain training (1700b), with a final control four weeks later at sea level (SLb). Vital signs, blood lactate and arterial oxygen saturation were determined prior, during or after the exercise test. Whereas systolic blood pressure and heart rate at rest did not change substantially, diastolic blood pressure decreased at the final control (SLb, p<0.05) and oxygen saturation was significantly lower at 1700 m (1700a, 1700b, p<0.01). Lactate at rest increased from 1.16 (SLa) to 1.97 (1700a) mmol/l after acute exposure followed by a slight reduction after adaptation (p<0.05). The mean maximum lactate levels were as follows: 6.03, 10.56, 6.22 and 8.75 (p<0.01). The mean maximum performance increased during the study (225.6, 223.3, 231.6, 248.1 Watt, p<0.01). Lactate versus workload curves did not show a marked shift to the right. No significant changes of maximum heart rates during the exercise test were found. In conclusion, a sojourn at 1700 m provokes an increase of lactate levels with subsequent reduction after acclimatization and has a significant positive impact on the mean maximum performance after moderate mountain training.     

Effects of high altitude exposure on components of blood and urine in mountaineers

Physiological correlations with impaired or umimpaired performance at high altitude were sought among 24 blood and urine parameters measured in 50 mountaineers and 21 observers before (preclimb) and after (postclimb) expeditions on Mt. McKinley. Values and per cent changes were compared for five degrees of impairment at high altitude. Average preclimb values were all near established normal levels and no correlations with subsequent involvement at high altitude were found. Postclimb samples contained more Hb, PCV, urea, LDH, and HBD and less bilirubin (P < 0.05). But no association was found between degrees of altitude impairment and preclimb/postclimb changes in any of the 24 blood and urine parameters. Additional results from samples collected at 4300 m showed "weaker" mountaineers excreted 1/4 as much Na in urine and had 50% more serum FFA concentration than stronger mountaineers.

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Zusammenfassung Bei 50 Bergsteigern und 21 Beobachtern wurden vor und nach einer Expedition zum Mt. McKinley (Alaska) für 24 Parameter im Blut und Harn die Beziehungen zur Abschwächung der Leistung in grosser Höhe untersucht. Zum Vergleich wurden 5 Grade von unbeeinflusster bis schwerer Schädigung in der Höhe verwendet. Die mittleren Werte vor dem Aufstieg lagen alle im Bereich der Normbreite. Beziehungen zu nachfolgenden Komplikationen in der Höhe bestanden nicht. Nach dem Aufstieg waren Hgb, Hämatokrit, Harnstoff, LDH, Hydroxybutyric Dehydrogenase erhöht und Bilirubin erniedrigt (P < 0, 05). Es liess sich jedoch für keinen Parameter eine Beziehung zwischen dem Ausmass der Höhenschädigung und den Veränderungen vor und nach dem Aufstieg nachweisen. Zusätzliche Ergebnisse von Proben, die in 4300 m Höhe gesammelt wurden, ergaben, dass schwache Bergsteiger ein Viertel soviel Na im Harn ausschieden und 50% mehr freie Fettsäuren im Blut aufwiesen als starke Bergsteiger.

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Resume On a mesuré 24 paramètre du sang et de l'urine de 50 alpinistes et 21 observateurs avant et après l'ascension du Mont McKinley (Canada). On a établi ensuite la corrélation physiologique existant entre ces paramètres et une diminution éventuelle des performances. Les valeurs absolues et le taux de modification ont été comparés à 5 degrés de diminution des capacités physiques à haute altitude. Les valeurs moyennes des analyses faites avant l'ascension ont toutes été voisines du niveau normal et on n'a pas constaté de corrélation avec les performances individuelles subséquentes. Les échantillons recueillis après l'ascension contenaient davantage de Hb, PCV, urée, LDH, et HBD, mais moins de bilirubine (P < 0, 05). On n'a cependant trouvé aucune relation entre le degré de diminution des performances et les modifications d'aucun des 24 paramètres retenus du sang ou de l'urine avant et après l'ascension. Des échantillons prélevés à 4300 m d'altitude ont montré que les alpinistes peu aguerris ne sécrétaient que le 1/4 du Na par l'urine, mais avaient 50% d'acides gras libres de plus dans le sang que les montagnards les plus résistants.

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Work supported by Themis Contract No DADA 17-68-C-8018     

Physiological responses during prolonged exercise at the power output corresponding to the blood lactate threshold

Heart rate (HR) and oxygen uptake (VO2) at the mechanical power (W) corresponding to the capillary blood lactate ([la]cap) of 4 mmol.l-1 (Wlt) were measured in 34 healthy male subjects during incremental exercise (Winc). On the basis of these measurements, the subjects were asked to cycle at Wlt for 60 min (steady-state exercise, Wss). Twenty subjects could not reach the target time (mean exhaustion time, te, 38.2 min, SD 5.3), while 6 of the 14 remaining subjects declared themselves exhausted at the end of exercise. The final [la]cap if the two groups of exhausted subjects were 5.3 mmol.l-1, SD 2.3 and 4.3 mmol.l-1, SD 1.1, respectively. At the end of Wss, [la]cap and HR were significantly lower in the 8 unexhausted subjects than in the other subjects. This group also had a lower HR at Wlt during Winc. The HR and VO2 appeared to be higher during Wss than during Winc. When all subjects were ranked according to their te during Wss, Wlt (expressed per kilogram of body mass) was found to be negatively related to te. In conclusion, during Winc, measurements of physiological variables at fixed [la]cap give a poor prediction of their trends during Wss and of the relative te; at the same work load [la]cap can be quite different in the two experimental conditions. Furthermore, resistance to exercise fatigue at Wlt seems lower in the fitter subjects.     

Effects of exercise training on thermoregulatory responses and blood volume in older men.

We assessed the effects of aerobic and/or resistance training on thermoregulatory responses in older men and analyzed the results in relation to the changes in peak oxygen consumption rate (VO(2 peak)) and blood volume (BV). Twenty-three older men [age, 64 +/- 1 (SE) yr; VO(2 peak), 32.7 +/- 1.1 ml. kg(-1). min(-1)] were divided into three training regimens for 18 wk: control (C; n = 7), aerobic training (AT; n = 8), and resistance training (RT; n = 8). Subjects in C were allowed to perform walking of ~10,000 steps/day, 6-7 days/wk. Subjects in AT exercised on a cycle ergometer at 50-80% VO(2 peak) for 60 min/day, 3 days/wk, in addition to the walking. Subjects in RT performed a resistance exercise, including knee extension and flexion at 60-80% of one repetition maximum, two to three sets of eight repetitions per day, 3 days/wk, in addition to the walking. After 18 wk of training, VO(2 peak) increased by 5.2 +/- 3.4% in C (P > 0.07), 20.0 +/- 2.5% in AT (P < 0.0001), and 9.7 +/- 5.1% in RT (P < 0.003), but BV remained unchanged in all trials. In addition, the esophageal temperature (T(es)) thresholds for forearm skin vasodilation and sweating, determined during 30-min exercise of 60% VO(2 peak) at 30 degrees C, decreased in AT (P < 0.02) and RT (P < 0.02) but not in C (P > 0.2). In contrast, the slopes of forearm skin vascular conductance/T(es) and sweat rate/T(es) remained unchanged in all trials, but both increased in subjects with increased BV irrespective of trials with significant correlations between the changes in the slopes and BV (P < 0.005 and P < 0.0005, respectively). Thus aerobic and/or resistance training in older men increased VO(2 peak) and lowered T(es) thresholds for forearm skin vasodilation and sweating but did not increase BV. Furthermore, the sensitivity of the increase in skin vasodilation and sweating at a given increase in T(es) was more associated with BV than with VO(2 peak).     

Supramaximal exercise after training-induced hypervolemia. I. Gas exchange and acid-base balance

The effect of an exercise-induced reduction in blood O2-carrying capacity on ventilatory gas exchange and acid-base balance during supramaximal exercise was studied in six males [peak O2 consumption (VO2peak), 3.98 +/- 0.49 l/min]. Three consecutive days of supramaximal exercise resulted in a preexercise reduction of hemoglobin concentration from 15.8 to 14.0 g/dl (P less than 0.05). During exercise (120% VO2peak) performed intermittently (1 min work to 4 min rest); a small but significant (P less than 0.05) increase was found for both O2 consumption (VO2) (l X min) and heart rate (beats/min) on day 2 of the training. On day 3, VO2 (l/min) was reduced 3.2% (P less than 0.05) over day 1 values. No changes were found in CO2 output and minute ventilation during exercise between training days. Similarly, short-term training failed to significantly alter the changes in arterialized blood PCO2, pH, and [HCO-3] observed during exercise. It is concluded that hypervolemia-induced reductions in O2-carrying capacity in the order of 10-11% cause minimal impairment to gas exchange and acid-base balance during supramaximal non-steady-state exercise.     

Effect of acute exposure to 3660 m altitude on orthostatic responses and tolerance.

Orthostatic reflexes were examined at 375 m and after 60 min of exposure in a hypobaric chamber at 3660 m using a 20-min 70 degrees head-up tilt (HUT) test. Mean arterial blood pressure, R wave-R wave interval (RRI), and mean cerebral blood flow velocity (MFV) were examined with coarse-graining spectral analysis. Of 14 subjects, 7 at 375 m and 12 at 3660 m were presyncopal. Immediately on arrival to high altitude, breathing frequency and MFV increased, and endtidal PCO2, RRI, RRI complexity, and the parasympathetic nervous system indicator decreased. MFV was similar in HUT at both altitudes. The sympathetic nervous system indicator increased with tilt at 3660 m, whereas parasympathetic nervous system indicator decreased with tilt at both altitudes. Multiple regression analysis of supine variables from either 375 or 3660 m and the time to presyncope at 3660 m indicated that, after 1 h of exposure, increased presyncope at altitude was the result of 1). ineffective peripheral vasoconstriction, despite increased cardiac sympathetic nervous system activity with HUT, and 2). insufficient cerebral perfusion owing to cerebral vasoconstriction as the result of hypoxic hyperventilation-induced hypocapnia.     

Effects of altered CSF [H+] on ventilatory responses to exercise in the awake goat

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.     

Effects of carbon dioxide inhalation prior to maximal exercise on blood lactate and physical performance

In order to examine the effect of acute respiratory acidosis induced by CO2 inhalation prior to maximal exercise on blood lactate and physical performance, double determinations were carried out for each subject on separate days; one day, after CO2 inhalation and other day, after inhalation of room air. It was observed that in the untrained subjects the CO2 inhalation prior to maximal treadmill exercise does not affect endurance time and maximum aerobic power, whereas blood lactate during recovery was lower in CO2 breathing than that in room air. In addition, no significant difference of 200m sprint time in the athletes was noticed between CO2 and room air while blood lactate after 200m sprint running was significantly lower in the CO2 than that in room air. From these results, it was suggested that the effect of CO2 inhalation prior to maximal exercise as applied here appeared to be mediate through metabolic rather than oxygen transport mechanism, but not related to physical performance.