Comparison of heart rate as a non-invasive determinant of anaerobic threshold with the lactate threshold when cycling

In 9 trained athletes and 4 sedentary subjects the anaerobic threshold was assessed on a cycle ergometer, using the deflection point of heart rate in a protocol in which the workload increased by 10 W every 45 s. The workload at which plasma lactate concentration equalled 4 mmol.l-1 was assessed under steady state conditions on separate occasions. In addition, in 3 subjects the non-invasive anaerobic threshold and the 4 mmol.l-1 lactate level under steady state conditions were assessed on a treadmill. On the cycle ergometer 6 subjects demonstrated a deflection point in the heart rate record, whereas the others failed to do so. The workload at which heart rate departed from linearity in the progressive protocol did not coincide with the steady state 4 mmol.l-1 workload but occurred at a higher workload. On the treadmill no deflection in heart rate was observed. It is concluded that in cyclists a deflection in heart rate does not always occur, and when it does, it does not coincide with the anaerobic threshold determined under steady state conditions.     

Heart rate deflection compared to 4 mmol?·?l?1 lactate threshold during incremental exercise and to lactate during steady-state exercise on an arm-cranking ergometer in paraplegic athletes

The deflection point (DP) of the heart rate in relation to the work rate (WR) of 8 male endurance-trained paraplegics and 11 male physically active sports students was investigated during nonsteady-state incremental arm cranking ergometry (IT) and compared to the 4 mmol · l⁻¹ blood lactate concentration threshold and to blood lactate concentration in steady-state exercise (SST). Heart rate, and lactate concentration from capillary blood, were determined at rest, during IT and SST. The DP was calculated by linear regression analysis of the heart rate during IT. The SST consisted of three consecutive exercise intensities over a period of 8 min at exercise intensities of 10 W below, and at 10 W above the work rate at deflection point (WR_DP). No difference was found between the paraplegics and non-handicapped subjects regarding heart rate and blood lactate concentration at rest and during exercise. A DP was established in all the paraplegics and in 72.7% of the non-handicapped subjects, but lactate accumulation was observed in 75% of the paraplegics and in 62.5% of the non-handicapped subjects at the lowest intensity of SST. In summary, endurance-trained paraplegics with an injury level below T₅ showed heart rate and blood lactate concentration values comparable to non-handicapped subjects during IT. A linear increase at moderate exercise intensities and a levelling-off at higher to maximal intensities could be identified in all the paraplegics and in 72.7% of non-handicapped subjects. The determination of the anaerobic threshold by DP should be applied with caution, since no causal relationship of DP and the anaerobic threshold was found and the WR_DP tended to overestimate threshold values. Accepted: 9 February 1998     

Mathematical analysis of the heart rate performance curve during incremental exercise testing

In this study we performed laboratory treadmill protocols of increasing load. Heart rate was continuously recorded and blood lactate concentration was measured for determination of lactate threshold by means of LTD-max and LT4.0 methods.Our results indicate that the shape of heart rate performance curve (HRPC) during incremental testing depends on the applied exercise protocol (change of initial speed and the step of running speed increase, with the constant stage duration). Depending on the applied protocol, the HRPC can be described by linear, polynomial (S-shaped), and exponential mathematical expression.We presented mathematical procedure for estimation of heart rate threshold points at the level of LTD-max and LT4.0, by means of exponential curve and its relative deflection from the initial trend line (tangent line to exponential curve at the point of starting heart rate). The relative deflection of exponential curve from the initial trend line at the level of LTD-max and/or LT4.0 can be defined, based on the slope of the initial trend line. Using originally developed software that allows mathematical analysis of heart rate-load relation, LTD-max and/or LT4.0 can be estimated without direct measurement of blood lactate concentration.     

Relation between the change of slope of heart rate and second lactic and ventilatory thresholds in muscular exercise with large load]

The time-course of heart rate, blood lactate, and ventilatory gas exchange was studied during an incremental exercise test on cycloergometer in order to ascertain whether heart rate deflection occurred at the same load as the second lactate S[La]2) and ventilatory (SV2) thresholds. Twelve moderately trained subjects, 22 to 30 years old, participated in the study. The initial power setting was 30 W for 3 min with successive increases of 30 W every min except at the end of the test where the increase was reduced to 20 and 10 W.min-1. Ventilatory flow (VE), oxygen uptake (VO2), carbon dioxide production (VCO2, ventilatory equivalents of O2 (EO2 = VE/VO2) and CO2 (ECO2 = VE/VCO2), and heart rate (HR) were determined during the last 20 s of every min. Venous blood samples were drawn at the end of each stage of effort and analyzed enzymatically for lactate concentration ([La]). The HR deflection, S[La]2, and SV2 were represented graphically by two investigators using a double blind procedure. Following the method proposed by Conconi et al. 1982, the deflection in HR was considered to begin at the point beyond which the increase in work intensity exceeded the increase in HR and the linearity of the work rate/HR relationship was lost. S[La]2 corresponded to the second breaking point of the lactate time-course curve (onset of blood lactate accumulation) and SV2 was identified at the second breaking point in the increase in VE and ventilatory equivalent for O2 uptake accompanied by a concomitant increase in ventilatory equivalent for CO2 output. We observed that the deflection point in HR was present only in 7 subjects. The work load, VO2, HR, and [La] levels at which heart rate departed from linearity did not differ significantly from those determined with S[La]2 ans SV2. The VO2 and HR values at HR deflection point were significantly correlated with those measured at S[La]2 and SV2. It is concluded that deflection in heart rate does not always occur, and when it does, it coincides with the second lactate and ventilatory gas exchange thresholds. It can thus be used for the determination of optimal intensity for individualized aerobic training.     

Effects of acute hypoxia on the estimation of lactate threshold from ventilatory gas exchange indices during an incremental exercise test

The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.4+/-1.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.91+/-0.10 l/min (for the VE/VO2) vs. 1.89+/-0.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.67+/-0.1 l/min (for the lactate) vs. 1.37+/-0.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.     

Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys

To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4-12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO2max), ventilation and the "ventilatory anaerobic threshold" were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% of VO2max and increasing it during the next run by 0.5 or 1.0 km.h-1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. "Anaerobic threshold" was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol.l-1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional "anaerobic threshold" was only 2.6 mmol.l-1, which corresponded to 78% of the VO2max. The correlations between the parameters of "anaerobic threshold", "ventilatory anaerobic threshold" and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.     

Effect of breathing of a helium-oxygen mixture on adaptation to effort in humans during high-altitude hypoxia

The study was carried out on 17 healthy males aged 20-27 years subjected for 15 minutes to submaximal effort on a cycle ergometer (Elema-Schonander) under conditions of breathing ambient atmospheric air or a helium-oxygen mixture (20% O2 + 80% He) and under hypobaric pressure simulating an altitude of 3500 m above sea level. During the experiment the heart rate was recorded with ECG, and determinations were performed of the minute volume, respiratory rate, tidal volume and systolic arterial blood pressure. In the serum of venous blood obtained before and 3 minutes after the exercise the concentrations were measured of lactate (LA), pyruvate (PA) and glucose. High-altitude hypoxia caused unifavourable changes in the adaptation to effort manifesting themselves as an increase of the values of the determined physiological and biochemical indices. On the other hand, favourable changes were observed of the reaction to exercise while the subjects were breathing the helium-oxygen mixture during high-altitude hypoxia. The minute volume increased owing to increased tidal volume, and the exercise-induced rise of lactate (LA), pyruvate (PA) and the LA/PA ratio was lower. This may suggest reduced energy cost of respiration and reduced anaerobic metabolism under these conditions.     

A reduction in the hyperventilation threshold by intravenous infusion of adrenaline in the treadmill exercise

Seven healthy male subjects underwent a treadmill incremental work test in control conditions and during an intravenous epinephrine infusion (10 micrograms/min). At all exercise intensities, epinephrine increased heart rate, ventilation, respiratory quotient and plasma lactate levels without significant changes in oxygen consumption. Under epinephrine infusion, the "anaerobic threshold", considered as the critical intensity at which ventilation began to increase non linearly with oxygen consumption, appeared at a lower intensity and for a higher plasma lactate level than in control conditions. We conclude that the hyperventilation threshold does not necessarily reflect a muscular hypoxia. It could be due to an effect of catecholamines on peripheral chemoreceptors, maybe by alpha-adrenergic vasoconstriction in the carotid bodies.     

The relationship between anaerobic threshold and heart rate linearity during cycle ergometry

Recent studies have demonstrated there is a definitive deflection in the heart rate response to incremental velocity work that coincides with the anaerobic threshold. These studies were conducted with elite athletes who performed the specific activities in which they were trained. The purpose of this study was to determine if the same relationship in heart rate and ventilatory response to increasing velocity was evident in nine untrained healthy subjects aged 22 to 36 years performing leg ergometry under controlled laboratory conditions. All subjects began pedaling at 50 rpm with an initial power output of 100 W. Pedaling rates were increased by 5 rpm every 30 s. This increment was equivalent to a power increase of 11.1 W. The subjects cycled to the point of exhaustion or until they could no longer maintain the pedaling speed at the higher velocities. Heart rate and expiration gases were collected at 30-s intervals. The results indicated that the heart rate and ventilatory response to increasing velocity as previously reported under field conditions does not exist under laboratory conditions. While there was a definitive and statistically significant inflection in the ventilatory response to increasing velocity, heart rate remained linear. Therefore, caution should be used when determining the anaerobic threshold from the single measure of heart rate response.     

Effect of training on treadmill performance,aerobic capacity,and body responses to acute cold exposure

An attempt was made to test the hypothesis that regular physical activity at the anaerobic threshold can stimulate an increase in the amount of brown or beige body fat, which can manifest itself in increased lactate utilization during exercise and increased reactivity in response to acute regional cooling. The methods used in the study included the ramp test; regional acute cold exposure; measurement of gas exchange; lactate and glucose in the blood; heart rate; heart rate, blood pressure, and respiration variability at rest and during standard functional tests; infrared thermal imaging; and statistical methods of analysis of results. Training of ten physically active volunteers (7 males and 3 females) on a treadmill at a speed corresponding to 75–80% of personal maximum oxygen consumption \(\left( {V_{O_{2\max } } } \right)\) for 30 min 3 times per week at a fixed ambient temperature of 21–22°C for 6 weeks resulted in a significant (from 19 to 39%) increase in exercise duration in the ramp test, whereas \(V_{O_{2\max } }\) changed, on average, only slightly. The increase in the anaerobic threshold power was associated with a sharp slowdown in the accumulation of lactate during the ramp test. The lactate utilization rate during the recovery period, on the contrary, increased. In general, work efficiency during test load significantly increased. Noticeable changes in the condition and responses to the standard functional tests of the autonomic system were not found, as judged by the heart rate variability, blood pressure, and respiration variability at rest and during orthostatic tests and imposed breathing rhythm. The functional response of the body to acute cold exposure (1-min cooling of the feet in ice water) did not change after a cycle of training, both in terms of metabolism (oxygen consumption, etc.) and the skin temperature dynamics in the areas of most probable location of brown adipose tissue (BAT). These data do not confirm our previous hypothesis (2010) about the function of BAT as a universal homeostatic instrument in the body. Probably, if the formation of the beige adipose tissue is stimulated by physical activity and hormone irisin, produced by muscles, this tissue is involved in lactate utilization but is not involved in the thermoregulatory responses.     

Blood lactate and metabolic responses to controlled frequency breathing during graded swimming

Controlled frequency breathing (CFB) is a training technique used by swimmers in an effort to simulate high-intensity workloads by limiting oxygen availability to the body and stimulating anaerobic metabolism. During CFB, a swimmer voluntarily restricts breathing, which, theoretically, limits oxygen availability and stimulates anaerobic metabolism. The purpose of this study was to determine the influence of CFB on blood lactate and metabolic responses during graded increases in swimming intensity. A free swimming (FS) protocol was used to determine blood lactate and heart rate (HR) responses to CFB, while a tethered swimming (TS) protocol was used to determine blood lactate, HR, and ventilatory responses to CFB. The subjects swam four 3-minute trials at workloads of 55, 65, 75, and 85% of peak intensity during both protocols. A total of 46 competitive collegiate swimmers participated in the study. Thirty-four subjects (14 men and 20 women) completed the FS protocol, and 12 subjects (7 men and 5 women) completed the TS protocol. CFB reduced ventilation and Vo(2) (p < 0.05) during the TS protocol and reduced HR (p < 0.05) during the FS protocol when compared to normal breathing. However, CFB did not alter blood lactate concentrations for either protocol (p > 0.05). Our findings demonstrate that although CFB does not alter the blood lactate response to graded increases in swimming intensity, it appears to reduce the ventilatory and HR responses to exercise. Thus, swim coaches can use CFB at moderate intensities to simulate high-intensity training but should consider adjusting HR training zones to reflect the reduction in HR associated with reduced ventilation.     

Anaerobic energy provision does not limit Wingate exercise performance in endurance-trained cyclists.

The aim of this study was to evaluate the effects of severe acute hypoxia on exercise performance and metabolism during 30-s Wingate tests. Five endurance- (E) and five sprint- (S) trained track cyclists from the Spanish National Team performed 30-s Wingate tests in normoxia and hypoxia (inspired O(2) fraction = 0.10). Oxygen deficit was estimated from submaximal cycling economy tests by use of a nonlinear model. E cyclists showed higher maximal O(2) uptake than S (72 +/- 1 and 62 +/- 2 ml x kg(-1) x min(-1), P < 0.05). S cyclists achieved higher peak and mean power output, and 33% larger oxygen deficit than E (P < 0.05). During the Wingate test in normoxia, S relied more on anaerobic energy sources than E (P < 0.05); however, S showed a larger fatigue index in both conditions (P < 0.05). Compared with normoxia, hypoxia lowered O(2) uptake by 16% in E and S (P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not altered by hypoxia in any group. Endurance cyclists, unlike S, maintained their mean power output in hypoxia by increasing their anaerobic energy production, as shown by 7% greater oxygen deficit and 11% higher postexercise lactate concentration. In conclusion, performance during 30-s Wingate tests in severe acute hypoxia is maintained or barely reduced owing to the enhancement of the anaerobic energy release. The effect of severe acute hypoxia on supramaximal exercise performance depends on training background.     

Validity of the heart rate deflection point as a predictor of lactate threshold during running.

During an incremental run test, some researchers consistently observe a heart rate (HR) deflection at higher speeds, but others do not. The present study was designed to investigate whether differences in test protocols could explain the discrepancy. Additionally, we sought to determine whether the HR deflection point accurately predicts lactate threshold (LT). Eight trained runners performed four tests each: 1) a treadmill test for maximal O(2) uptake, 2) a Conconi test on a 400-m track with speeds increasing approximately 0.5 km/h every 200 m, 3) a continuous treadmill run with speeds increasing 0.5 km/h every minute, and 4) a continuous LT treadmill test in which 3-min stages were used. All subjects demonstrated an HR deflection on the track, but only one-half of the subjects showed an HR deflection on the treadmill. On the track the shortening of stages with increasing speeds contributed to a loss of linearity in the speed-HR relationship. Additionally, the HR deflection point overestimated the LT when a continuous treadmill LT protocol was used. In conclusion, the HR deflection point was not an accurate predictor of LT in the present study.     

Increased blood ammonia in hypoxia during exercise in humans

The effect of acute hypoxia on blood concentration of ammonia ([NH3]b) and lactate (la-]b) was studied during incremental exercise(IE), and two-step constant workload exercises (CE). Fourteen endurance-trained subjects performed incremental exercise on a cycle ergometer under normoxic (21% O2) and hypoxic (10.4% O2) conditions. Eight endurance-trained subjects performed two-step constant workload exercise at sea level and at a simulated altitude of 5000 m (hypobaric chamber, P(B)=405 Torr; P(O2)=85 Torr) in random order. In normoxia, the first step lasted 25 minutes at an intensity of 85 % of the individual ventilatory anaerobic threshold (AT(vent), ind) at sea level. This reduced workload was followed by a second step of 5 minutes at 115% of their AT(vent), ind. This test was repeated into a hypobaric chamber, at a simulated altitude of 5,000 m. The first step in hypoxia was at an intensity of 65 % of AT(vent), ind., whereas workload for the second step at simulated altitude was the same as that of the first workload in normoxia (85 % of AT(vent), ind). During IE, [NH3]b and [la-]b were significantly higher in hypoxia than in normoxia. Increases in these metabolites were highly correlated in each condition. The onset of [NH3]b and [la-]b accumulation occurred at different exercise intensity in normoxia (181W for lactate and 222W for ammonia) and hypoxia (100W for lactate and 140W for ammonia). In both conditions, during CE, [NH3]b showed a significant increase during each of the two steps, whereas [la-]b increased to a steady-state in the initial step, followed by a sharp increase above 4 mM x L(-1) during the second. Although exercise intensity was much lower in hypoxia than in normoxia, [NH3]b was always higher at simulated altitude. Thus, for the same workload, [NH3]b in hypoxia was significantly higher (p<0.05) than in normoxia. Our data suggest that there is a close relationship between [NH3]b and [la-]b in normoxia and hypoxia during graded intensity exercises. The accumulation of ammonia in blood is independent of that of lactate during constant intense exercise. Hypoxia increases the concentration of ammonia in blood during exercise.     

Effects of L-carnitine administration on VO2max and the aerobic-anaerobic threshold in normoxia and acute hypoxia

Seven healthy young male adults were subjected to a total of 56 tests to ascertain the effects of L-carnitine (L-C) and a placebo (P) on ventilation, O2 intake (VO2), CO2 output, heart rate, blood pressure and serum lactic acid, non-esterified fatty acid, glycerol and glucose during strenuous and aerobic/anaerobic threshold-level treadmill exercise. The tests were made in conditions of normoxia (O2 = 20.9%) and hypoxia (O2 = 13.0%, equivalent to 3,500 m above sea level). The only clear difference was in the respiratory quotient (RQ = 0.883, SD 0.025 vs 0.904, SD 0.035) after L-C and P administration respectively (P less than 0.01), under normal oxygenation and 0.861, SD 0.052 following L-C vs 0.926, SD 0.040 after P (P less than 0.01) in acute hypoxia at VO2 levels around the anaerobic threshold. The lower RQ values of the L-C-treated subjects during hypoxia indicate a lower rate of carbohydrate transformation.     

On the kinetics of anaerobic power

ABSTRACT: BACKGROUND: This study investigated two different mathematical models for the kinetics of anaerobic power. Model 1 assumes that the work power is linear with the work rate, while model 2 assumes a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power. In order to test these models, a cross country skier ran with poles on a treadmill at different exercise intensities. The aerobic power, based on the measured oxygen uptake, was used as input to the models, whereas the simulated blood lactate concentration was compared with experimental results. Thereafter, the metabolic rate from phosphocreatine break down was calculated theoretically. Finally, the models were used to compare phosphocreatine break down during continuous and interval exercises. RESULTS: Good similarity was found between experimental and simulated blood lactate concentration during steady state exercise intensities. The measured blood lactate concentrations were lower than simulated for intensities above the lactate threshold, but higher than simulated during recovery after high intensity exercise when the simulated lactate concentration was averaged over the whole lactate space. This fit was improved when the simulated lactate concentration was separated into two compartments; muscles + internal organs and blood. Model 2 gave a better behavior of alactic energy than Model 1 when compared against invasive measurements presented in the literature. During continuous exercise, model 2 showed that the alactic energy storage decreased with time, whereas model 1 showed a minimum value when steady state aerobic conditions were achieved. During interval exercise the two models showed similar patterns of alactic energy. CONCLUSIONS: The current study provides useful insight on the kinetics of anaerobic power. Overall, our data indicates that blood lactate levels can be accurately modeled during steady state, and suggests a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power.     

Carbohydrate management, anaerobic metabolism, and adenosine levels in the armoured catfish, Liposarcus pardalis (castelnau), during hypoxia

The armoured catfish, Liposarcus pardalis, tolerates severe hypoxia at high temperatures. Although this species can breathe air, it also has a strong anaerobic metabolism. We assessed tissue to plasma glucose ratios and glycogen and lactate in a number of tissues under "natural" pond hypoxia, and severe aquarium hypoxia without aerial respiration. Armour lactate content and adenosine in brain and heart were also investigated. During normoxia, tissue to plasma glucose ratios in gill, brain, and heart were close to one. Hypoxia increased plasma glucose and decreased tissue to plasma ratios to less than one, suggesting glucose phosphorylation is activated more than uptake. High normoxic white muscle glucose relative to plasma suggests gluconeogenesis or active glucose uptake. Excess muscle glucose may serve as a metabolic reserve since hypoxia decreased muscle to plasma glucose ratios. Mild pond hypoxia changed glucose management in the absence of lactate accumulation. Lactate was elevated in all tissues except armour following aquarium hypoxia; however, confinement in aquaria increased armour lactate, even under normoxia. A stress-associated acidosis may contribute to armour lactate sequestration. High plasma lactate levels were associated with brain adenosine accumulation. An increase in heart adenosine was triggered by confinement in aquaria, although not by hypoxia alone.     

Decreased exercise muscle lactate release after high altitude acclimatization

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.     

Metabolic effects of exposure to hypoxia plus cold at rest and during exercise in humans

To determine effects on metabolic responses, subjects were exposed to four environmental conditions for 90 min at rest followed by 30 min of exercise: breathing room air with an ambient temperature of 25 degrees C (NN); breathing room air with an ambient temperature of 8 degrees C (NC); hypoxia (induced by breathing 12% O2 in N2) with a neutral temperature (HN); and hypoxia in the cold (HC). Hypoxia increased heart rate (HR), systolic blood pressure (SBP), pulmonary ventilation (VE), respiratory exchange ratio (R), blood lactate, and perceived exertion during exercise while depressing rectal temperature (Tre) and O2 uptake (VO2). Cold exposure elevated SBP, diastolic blood pressure (DBP), VE, VO2, blood glucose, and blood glycerol but decreased HR, Tre, and R. Shivering and DBP were higher and Tre was lower in HC compared with NC. HR, SBP, VE, R, and lactate tended to be higher in HC compared with NC, whereas VO2 and blood glycerol tended to be depressed. These results suggest that cold exposure during hypoxia results in an increased reliance on shivering for thermogenesis at rest whereas, during exercise, heat loss is accelerated.     

Lactate accumulation during incremental exercise with varied inspired oxygen fractions

Six subjects pedaled a stationary cycle ergometer to exhaustion on three separate occasions while breathing gas mixtures of 17, 21, or 60% O2 in N2. Each subject rode for 3 min at work rates of 60, 90, 105 W, followed by 15-W increases every 3 min until exhaustion. Inspired and expired gas fractions, ventilation (V), heart rate, and blood lactate were measured. O2 uptake (VO2) and CO2 output (VCO2) were calculated for the last minute of each work rate; blood samples were drawn during the last 5 s. "Break points" for lactate, V, VCO2, V/VO2, and expired oxygen fraction (FEO2) were mathematically determined. VO2 was not significantly different at any work rate among the three different conditions. Nor did maximal VO2 differ significantly among the three treatments (P greater than 0.05). Lactate concentrations were significantly lower during hyperoxia and significantly higher during hypoxia compared with normoxia. Lactate values at exhaustion were not significantly different among the three treatments. Four subjects were able to work for a longer period of time during hyperoxic breathing. The variations in lactate accumulation as reported in this study cannot be explained on the basis of differences in VO2. The results of this research lend support to the hypothesis that differences in the performance of subjects breathing altered fractions of inspired oxygen may be caused by differences in lactate (or H+) accumulation.