Lactate during exercise at high altitude

In acclimatized humans at high altitude the reduction, compared to acute hypoxia, of the blood lactate concentration (1a) at any absolute oxygen uptake ( ), as well as the reduction of maximum la (la_max) after exhaustive exercise, compared to both acute hypoxia or normoxia, have been considered paradoxical, and these phenomena have therefore become known as the lactate paradox. Since, at any given power output and , mass oxygen transport to the contracting locomotor muscles is not altered by the process of acclimatization to high altitude, the gradual reduction in [la^–]_max in lowlanders exposed to chronic hypoxia seems not to be due to changes in oxygen availability at the tissue level. At present, it appears that the acclimatization-induced changes in [la^–] during exercise are the result of at least two mechanisms: (1) a decrease in maximum substrate flux through aerobic glycolysis due to the reduced in hypoxia; and (2) alterations in the metabolic control of glycogenolysis and glycolysis at the cellular level, largely because of the changes in adrenergic drive of glycogenolysis that ensue during acclimatization, although effects of changes in peripheral oxygen transfer and the cellular redox state cannot be ruled out. With regard to the differences in lactate accumulation during exercise that have been reported to occur between lowlanders and highlanders, both groups either being acclimatized or not, these do not seem to be based upon fundamentally different metabolic features. Instead, they seem merely to reflect points along the same continuum of phenotypic adaptation of which the location depends on the time spent at high altitude.     

Alpha-motoneuron excitability at high altitude

Summary It has been hypothesized that chronic hypobaric hypoxia could lead to inhibition of the-motoneuron pool, thus limiting the maximal activation of working skeletal muscles. To test this hypothesis six subjects [32 (SEM 2) years] were evaluated in resting conditions, at sea level and after acclimatization at 5,050 m. The recruitment curves of the Hofmann-reflex (H-) and the direct muscle-response (M-) of the right soleus muscle were obtained by stimulating the posterior tibeal nerve with different intensities while recording the electromyogram of the soleus muscle. From the recorded data the net-motoneuron excitability (ratio of maximal H-reflex to M-response H_max : M_max ratio), the threshold and gain for both responses, obtained from linear regressions through the rising phase of the recruitment curves of both responses, as well as the latency times of both responses were determined. The latency times and the H_max :M_max ratio were unchanged at altitude. The thresholds of both responses and the gain of the M-response were unaltered. The gain of the H-response was significantly higher at altitude when compared to sea level. It is concluded that in the acclimatized subjects at rest the signal conduction velocity through the different parts of both pathways was unaltered and therefore nerve and muscle conduction velocity as well as synaptic and muscle end-plate transmission were unchanged, that the recruitment of the H-reflex was slightly facilitated after acclimatization to high altitude suggesting increased excitability of the-motoneurons, through either postsynaptic facilitatory changes in the soma or a different descending drive, and that the unchanged H_max:M_max ratio indicated no change in the net excitatory and inhibitory influences on the-motoneuron pool. The above hypothesis is thus not strengthened by the results that were, however, obtained in resting conditions.     

Effects of Β blockade and atropinisation on plasma catecholamine concentration during exercise

The changes in plasma catecholamine concentration (C) following -blockade (practolol, 15 mg) and atropinisation (Atropine, 1.8 mg) have been studied on 5 healthy male subjects during exercise on a motor driven treadmill.The results showed that for a given VO₂ and % VO_{2 max}, blockade was without effect on C (except in one athletic subject), but atropine produced a rise in C. In relation to Q, both drugs produced an increase in C, but for a given cardiac frequency (f _H ) C was higher with blockade, and lower with atropinisation than found in control experiments. The intra- and inter-subject variability of C in relation to f _H was resolved by considering the change in cardiac frequency calculated from baseline value obtained during walking at 6.44 km/h on the level, and expressed as a percentage of the maximal f _H attainable for given individuals under the different drug and control conditions (% f _H ).It was concluded that during short term exercise, the rise of C in relation to % f _H reflects both the myocardial sensitivity to vagal and blockade, and the circulatory vasoconstrictor control of blood vessels which is required to sustain increases in systemic and muscle blood flow.     

Abnormal blood flow in the sublingual microcirculation at high altitude

We report the first direct observations of deranged microcirculatory blood flow at high altitude, using sidestream dark-field imaging. Images of the sublingual microcirculation were obtained from a group of 12 volunteers during a climbing expedition to Cho Oyu (8,201 m) in the Himalayas. Microcirculatory flow index (MFI) was calculated from the moving images of microcirculatory red blood cell flow, and comparison was made between the baseline and high altitude measurements. Peripheral oxygen saturation (SpO₂) and Lake Louise scores (LLS) were recorded along with MFI. Our data demonstrate that there was a significant reduction in MFI from baseline to 4,900 m in small (less than 25 μm) and medium (26–50 μm) sized blood vessels (P = 0.025 and P = 0.046, respectively). There was no significant correlation between MFI and SpO₂ or MFI and LLS. Disruption of blood flow within microcirculatory may explain persistent abnormal oxygen flux to tissues following the normalisation of systemic oxygen delivery that accompanies acclimatisation to high altitude.     

Changes in plasma lipids and lipoprotein cholesterol during a high altitude mountaineering expedition (4800 m)

Summary Effects of high altitude exposure on plasma lipids and lipoprotein cholesterol were studied in 8 mountaineers who spent 3 weeks at the Annapurna IV base camp (4800 m) after a 12 day trek. In spite of the moderate physical exertion at the camp, the loss of body weight was more pronounced during the stay at high altitude than during the trekking period. Compared with baseline values observed at sea level, marked reductions in plasma cholesterol (–27%) and phospholipids (–19%) were found 3 days after arrival at the camp and persisted during the next 17 days. A less marked fall in plasma triglycerides occurred, weakly significant at the end of the stay. Because there were no relevant changes in very low density lipoproteins or in high density lipoprotein (HDL)-cholesterol, the low plasma cholesterol levels at the high altitude resulted mainly from the reduction in low density lipoprotein (LDL)-cholesterol: the mean HDL/LDL cholesterol ratio changed from 0.39 at sea level to 0.63 at the end of the stay at 4800 m. Fluctuations in LDL-cholesterol were not concomitant with those in body weight and were independent of the exercise training during the expedition. This study shows moreover that the early drop in LDL-cholesterol was associated with an opposite change in plasma levels of catecholamines and thyroid hormones. Taking into account that such hormonal responses are classically observed at high altitude, the concomitant decrease in LDL-cholesterol might be interpreted as being a relevant adaptative response to hypoxic conditions at high altitude.Abbreviations VLDL very low density lipoproteins - LDL low density lipoproteins - HDL high density lipoproteins     

Branched-chain amino acid supplementation during trekking at high altitude

Summary To investigate the influence of a branched-chain amino acid (BCAA) supplementation on chronic hypoxia-related loss of body mass and muscle loss, 16 subjects [age 35.8 (SD 5.6) years] participating in a 21-day trek at a mean altitude of 3,255 (SD 458) m, were divided in two age-, sex- and fitness-matched groups and took either a dietary supplementation of BCAA (5.76, 2.88 and 2.88 g per day of leucine, isoleucine and valine, respectively) or a placebo (PLAC) in a controlled double-blind manner. Daily energy intake at altitude decreased by 4% in both groups compared with sea level. After altitude exposure both groups showed a significant loss of body mass, 1.7% and 2.8% for BCAA and PLAC, respectively. Fat mass had decreased significantly by 11.7% for BCAA and 10.3% for PLAC, whereas BCAA showed a significantly increased lean mass of 1.5%, as opposed to no change in PLAC. Arm muscle cross-sectional area tended to increase in BCAA, whereas there was a significant decrease of 6.8% in PLAC (P<0.05 between groups). The same tendency, although not significant, was observed for the thigh muscle cross-sectional area. On the whole it seemed that PLAC had been catabolizing whereas BCAA had been synthesizing muscle tissue. Single jump height from a squatted position showed a similar tendency to increase in both groups. Lower limb maximal power decreased less in BCAA than in PLAC (2.4% vs 7.8%, P<0.05). We concluded that BCAA supplementation may prevent muscle loss during chronic hypobaric hypoxia.     

Postural ataxia at high altitude is not related to mild to moderate acute mountain sickness

To evaluate the role of acute mountain sickness (AMS) in the pathogenesis of stance abnormalities occurring at high altitude, static posturography was applied to 22 healthy subjects at an altitude of 450 m and during a 3-day sojourn at 4559 m. Subjects stood on a platform and sway velocity (S), and sway velocity in the antero-posterior (S_AP) and medio-lateral (S_ML) directions was recorded for 20 s with eyes open (EO) and 20 s with eyes closed (EC). Arterialized blood from an ear lobe was analyzed to determine the arterial partial pressures of oxygen (P _aO₂) and carbon dioxide, and oxygen saturation (S _aO₂). AMS was assessed by the environmental symptom questionnaire (ESQ) of Sampson (cerebral AMS, AMS-C score >0.7). AMS affected four subjects on day 1, ten subjects on day 2, and five subjects on day 3. Posturographic findings showed no difference between subjects with AMS and healthy subjects, and no correlation with the ESQ score. P _aO₂ and S _aO₂ showed non-significant trends toward lower values in subjects with AMS than in those without AMS. Posturographic parameters significantly worsened on the 1st (EO-S, P<0.001; EC-S, P<0.01; EO-S_ML, P<0.05), 2nd (EO-S, EC-S and EO-S_ML, P<0.01) and 3rd days (EC-S, P<0.05) at high compared to low altitude. Differences in AMS-C score, S _aO₂ and P _aO₂ were significant between low and high altitude (P<0.0001). Our data suggest that AMS is not important in the pathogenesis of postural ataxia occurring at high altitude. Electronic Publication     

Physiological changes induced by pre-adaptation to high altitude

To study the physiological effects of pre-adaptation to high altitude, seven subjects were submitted to acclimatization at 4350 m followed by intermittent acclimation in a low barometric pressure chamber (5000 m to 8500 m). The subjects then spent 25 days in the Himalayas. Ventilatory and cardiac responses were studied during a hypobaric poikilocapnic hypoxic test performed both at rest and during exercise (100 W) in normoxia and in hypoxia (barometric pressure: 589 hPa, altitude: 4500 m). Haemoglobin, erythrocytes, reticulocytes, packed cell volume, 2,3-diphosphoglycerate (2,3-DPG) and erythropoietin (EPO) were measured. All variables were studied before pre-adaptation to high altitude (A), after the acclimatization period (B), after the acclimation period (C) and after the expedition (D). The ventilatory and cardiac responses were characterized by an increased tidal volume in hypoxia (+ 33% during exercise in B,P < 0.05; + 100% at rest and + 33% during exercise in C,P < 0.05) without any change in respiratory frequency, whereas an increased systolic blood pressure was only observed in C during exercise in hypoxia [+23 mmHg (3.07 kPa),P<0.01]. Arterial O2 saturation was higher in hypoxia in C and D, both at rest (+8.2% and +4.7%,P<0.01, respectively), and during exercise (+6.3% and +6.3%,P<0.01, respectively). Erythrocytes, haemoglobin and packed cell volume did not vary significantly. The number of reticulocytes was higher in B (+172%,P<0.05) and in C (+249%,P<0.05). EPO and 2,3-DPG increased only in C (+ 770%,P<0.01 and +23%,P<0.05, respectively). These results showed that a combination of continuous pre-acclimatization on Mont Blanc and intermittent acclimation in the hypobaric chamber triggered efficient pre-adaptation mechanisms allowing climbers to save 1 to 2 weeks of acclimatization on the mountain without clinical inconvenience.     

Effect of plasma volume loss during graded exercise testing on blood lactate concentration

Previous studies have shown that plasma volume (PV) loss can be a confounding variable in the interpretation of changes in blood constituents. We examined the effect of PV loss on three features of the blood lactate versus work-rate relationship, namely, slight blood lactate increase during the early stages of graded exercise testing (GXT); work rate at the onset of a systematic increase in blood lactate, i.e., lactate threshold (LT); and work rate at a blood lactate concentration of 4 mM, i.e., onset of blood lactate accumulation (OBLA). Fourteen subjects underwent cycle ergometer GXT. Blood samples were obtained at rest and at the end of each 3-min work-rate increment and analyzed for hematocrit and lactate concentration. For exercise levels up to and including LT, PV loss was relatively stable at approximately 2.8%. Beyond LT, PV loss accelerated. From the first work rate to LT, blood lactate concentration uncorrected for PV loss increased 0.24 +/- 0.07 mM (P < 0.05). After correction for PV loss, the increase was 0.21 +/- 0.08 mM (P < 0.05). These mean increases were not significantly different from each other. For the four exercise levels above LT common to most subjects, PV-corrected lactate values were significantly lower than uncorrected values. Correction of lactate values for PV loss did not alter LT for any subject, but it did result in a significant increase in OBLA. Thus, PV loss has the potential to be a confounding variable for the interpretation of blood lactate parameters that are determined at exercise levels above LT.     

Cardiovascular adjustments for life at high altitude

The effects of hypobaric hypoxia in visitors depend not only on the actual elevation but also on the rate of ascent. There are increases in sympathetic activity resulting in increases in systemic vascular resistance, blood pressure and heart rate. Pulmonary vasoconstriction leads to pulmonary hypertension, particularly during exercise. The sympathetic excitation results from hypoxia, partly through chemoreceptor reflexes and partly through altered baroreceptor function. Systemic vasoconstriction may also occur as a reflex response to the high pulmonary arterial pressures. Many communities live permanently at high altitude and most dwellers show excellent adaptation although there are differences between populations in the extent of the ventilatory drive and the erythropoiesis. Despite living all their lives at altitude, some dwellers, particularly Andeans, may develop a maladaptation syndrome known as chronic mountain sickness. The most prominent characteristic of this is excessive polycythaemia, the cause of which has been attributed to peripheral chemoreceptor dysfunction. The hyperviscous blood leads to pulmonary hypertension, symptoms of cerebral hypoperfusion, and eventually right heart failure and death.     

Metabolic consequences of reduced frequency breathing during submaximal exercise at moderate altitude

Summary The intention of this study was to determine the metabolic consequences of reduced frequency breathing (RFB) at total lung capacity (TLC) in competitive cyclists during submaximal exercise at moderate altitude (1520 m; barometric pressure, P _B=84.6 kPa; 635 mm Hg). Nine trained males performed an RFB exercise test (10 breaths · min ^–1) and a normal breathing exercise test at 75–85% of the ventilatory threshold intensity for 6 min on separate days. RFB exercise induced significant (P<0.05) decreases in ventilation (V _E), carbon dioxide production (VCO₂), respiratory exchange ratio. (RER), ventilatory equivalent for O₂ consumption (V _E/VO₂), arterial O₂ saturation and increases in heart rate and venous lactate concentration, while maintaining a similar OZ consumption (VO₂). During recovery from RFB exercise (spontaneous breathing) a significant (P< 0.05) decrease in blood pH was detected along with increases in V _E, VO₂, VCO₂, RER, and venous partial pressure of carbon dioxide. The results indicate that voluntary hypoventilation at TLC, during submaximal cycling exercise at moderate altitude, elicits systemic hypercapnia, arterial hypoxemia, tissue hypoxia and acidosis. These data suggest that RFB exercise at moderate altitude causes an increase in energy production from glycolytic pathways above that which occurs with normal breathing.     

Respiratory and leg muscles perceived exertion during exercise at altitude

We compared the rate of perceived exertion for respiratory (RPE,resp) and leg (RPE,legs) muscles, using a 10-point Borg scale, to their specific power outputs in 10 healthy male subjects during incremental cycle exercise at sea level (SL) and high altitude (HA, 4559 m). Respiratory power output was calculated from breath-by-breath esophageal pressure and chest wall volume changes. At HA ventilation was increased at any leg power output by ～ 54%. However, for any given ventilation, breathing pattern was unchanged in terms of tidal volume, respiratory rate and operational volumes of the different chest wall compartments. RPE,resp scaled uniquely with total respiratory power output, irrespectively of SL or HA, while RPE,legs for any leg power output was exacerbated at HA. With increasing respective power outputs, the rate of change of RPE,resp exponentially decreased, while that of RPE,legs increased. We conclude that RPE,resp uniquely relates to respiratory power output, while RPE,legs varies depending on muscle metabolic conditions.     

Effect of alkalosis on plasma epinephrine responses to high intensity cycle exercise in humans

The purpose of this study was to determine the effects of alkalosis on epinephrine concentrations in response to a 90 s maximal exercise test. A group of ten healthy men ingested either a bicarbonate (BS) supplement (0.3 g·kg^–1 of body mass of sodium bicarbonate) or placebo mixture (P) prior to performing a 90 s maximal cycle ergometer test. An indwelling Teflon cannula was placed in the antecubital vein and blood samples were drawn at three times at rest separated by 10 min, immediately following the protocol, and at 2.5, 5, and 10 min post exercise to determine plasma epinephrine concentrations. Sodium bicarbonate ingestion significantly (P<0.05) induced alkalosis both at rest [mean (SD) pH=7.42 (0.02) BS, 7.38 (0.02) P] and after the exercise protocol [pH=7.16 (0.02) BS, 7.12 (0.02) P]. Plasma epinephrine concentrations were not significantly different immediately post exercise between the two conditions [4.2 (0.6) compared to 4.2 (0.7) pmol·ml^–1 in BS and P, respectively]. Work performed and power output attained were not significantly different between the two treatment conditions [mean power=258.7 (35.1) W BS, 260.3 (35.4) W P; peak power=534.7 (61.6) W BS, 535.7 (54.4) W P]. The primary finding of this investigation was that orally-induced alkalosis does not significantly affect plasma epinephrine concentrations or performance following 90 s of maximal cycle exercise in untrained men. Electronic Publication     

Capillary-venous differences of free plasma catecholamines at rest and during graded exercise

Summary Levels of free plasma catecholamines were simultaneously determined in 10 cyclists using capillary blood from one ear lobe and venous blood from one cubital vein. Catecholamine concentrations were higher in the ear lobe blood than in the venous blood at rest and during graded exercise. Average differences amounted to 1.7 nmol · l^–1 (dopamine), 2.1 nmol · l^–1 (noradrenaline) and 1.9 nmol · l^–1 (adrenaline) at rest and increased only to 8.8 nmol · l^–1 for noradrenaline during exercise. We assume that higher concentrations of dopamine and adrenaline in the capillary blood point to a significant neuronal release of these catecholamines, similar to noradrenaline. Catecholamine concentrations in capillary blood may better reflect sympathetic drive and delivery of catecholamines to the circulation than the concentrations in venous blood.Supported by Bundesinstitut für Sportwissenschaften, Köln-Lövenich, FRG     

Rapidity of responding to a hypoxic challenge during exercise

The ability to modify power output (PO) in response to a changing stimulus during exercise is crucial for optimizing performance involving an integration system involving a performance template and feedback from peripheral receptors. The rapidity with which PO is modified has not been established, but would be of interest relative to understanding how PO is regulated. The objective is to determine the rapidity of changes in PO in response to a hypoxic challenge, and if change in PO is linked to changes in arterial O₂ saturation (S _aO₂). Well-trained cyclists performed randomly ordered 5-km time trials. Subjects began the trials breathing room air and switched to hypoxic (HYPOXIC, F_IO₂ = 0.15) or room (CONTROL, F_IO₂ = 0.21) air at 2 km, then to room air at 4 km. The time delay to begin decreasing S _aO₂ and PO and to recover S _aO₂ and PO on to room air was compared, along with the half time (t _1/2) during the HYPOXIC trial. Mean S _aO₂ and PO between 2 and 4 km were significantly different between CONTROL and HYPOXIC (94 ± 2 vs. 83 ± 2% and 285 ± 16 vs. 245 ± 19 W, respectively). There was no difference between the time delay for S _aO₂ (31.5 ± 12.8 s) and in PO (25.8 ± 14.4 s) or the recovery of S _aO₂ (29.0 ± 7.7 s) and PO (21.5 ± 12.4 s). The half time for decreases in S _aO₂ (56.6 ± 14.4 s) and in PO (62.7 ± 20.8 s) was not significantly different. Modifications of PO due to the abrupt administration of hypoxic air are related to the development of arterial hypoxemia, and begin within ~30 s.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary 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°C or at 10°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. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, 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°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°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

Summary 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° C (MT) or at –2° C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption ( ) 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 1^st, 4^th, 7^th, and the 10^th min following exercise for the determination of blood lactate (LA) concentration. The , 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 , 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 of FFA was found only during CT. The difference in FFA level suggests that alterations in fat metabolism, possibly initiated by an enhanced secretion of NE, may have contributed to a decrease in lactate production.     

Interleukin-6 response to exercise during acute and chronic hypoxia

Prolonged exercise is associated with increased plasma levels of the cytokine interleukin-6 (IL-6). Both circulating catecholamine levels and exercise intensity have been related to the exercise-derived IL-6. During hypoxia and acclimatization, changes in sympathetic activity is seen, and also a given workload becomes more intense in hypoxia. Therefore, hypoxia offers a unique opportunity to study the effect of catecholamines and intensity on exercise-derived IL-6. In the present study, eight Danish sea-level residents performed 60 min of cycle ergometer exercise at sea level (SL) (154 W, 45% maximal O₂ consumption, O₂max), in acute (AH) and chronic hypoxia (CH), at the same absolute (_abs) (AH_abs=154 W, 54% O₂max; CH_abs=154 W, 59% O₂max) and same relative (_rel) (AH_rel=130 W, 46% O₂max; CH_rel=120 W, 44% O₂max) workload. We hypothesized that the IL-6 response to exercise at the same absolute workload would be augmented during hypoxia compared with sea level, and that these changes would not correlate with changes in catecholamines. In AH_abs (2.35 pg·ml^–1) and CH_abs (3.34 pg·ml^–1) the IL-6 response to exercise was augmented (p<0.05) compared with that at sea level (0.78·ml^–1). In addition, after 60 min of bicycling at sea level, AH_rel (1.02 pg·ml^–1) and CH_rel (1.31 pg·ml^–1) resulted in similar IL-6 responses. The augmented IL-6 response during AH_abs and CH_abs did not match changes in circulating catecholamine levels when comparing all trials. We conclude that the plasma IL-6 concentration during exercise in hypoxia is intensity dependent, and that factors other than catecholamine levels are more important for its regulation.     

The effect of moderate altitude on post-exercise blood lactate

Summary Post-exercise blood lactate levels were studied after a short exhaustive bicycle ride in 3 males at sea level control, at altitude (2300 m) and on return to sea level. The short exhaustive bicycle ride was performed at a work rate of 2730 kpm · min^–1 and ride times ranged from 55 to 105 sec. Compared to sea level controls, performance time of the tests at altitude were of similar intensity and duration. Although the changes were small, the oxygen uptakes during the ride and oxygen debts following the rides increased with each test. However, in comparison with sea level controls the blood lactate concentrations were reduced. The reduction on the average reached 44% after 4 days at altitude, and 51% after 22 days at altitude. This reduction in blood lactate concentration of the same subject at altitude as compared with his sea level values may indicate a decrease in the activity of the glycolytic pathway relative to the activity of the aerobic pathway. This appears to be a contradiction to what would be expected in the mild hypoxic conditions present at altitude.Work done while at the University of Michigan, Ann Arbor, Michigan.This study was supported in part by a grant from the Fitness and Amateur Sport Directorate, Ottawa, Canada.