Effect of respiratory alkalosis during exercise on blood lactate

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.     

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)     

Effect of respiratory acidosis on metabolism in exercise

Five healthy males took part in two separate studies. In one study subjects breathed air (control, C) and in the other 5% CO2 in 21% O2 (respiratory acidosis, RA). Measurements were made at rest, during exercise at 30 and 60% maximal O2 uptake (VO2 max), (20 min each) and in recovery. RA was associated with higher arterial CO2 partial pressure (PCO2) and bicarbonate and lower pH than C. The increase with exercise in plasma lactate (mmol . l-1) was less in RA than C from 1.0 +/- 0.15 (SE) (C = 1.1 +/- 0.17) at rest to 5.3 +/- 1.25 (C = 6.8 +/- 0.98) at 60% VO2 max (P less than 0.10). Plasma pyruvate, alanine, and glycerol concentrations increased with exercise; free fatty acids did not change. There were no significant differences between RA and C in any of these metabolites. Norepinephrine concentrations were similar at rest but increased to a greater extent during exercise in RA than C (P less than 0.02). Epinephrine levels were also higher in RA than C at 60% VO2 max (NS); the two subjects in whom lactate was not lower with RA showed the greatest increase in epinephrine. Exercise in RA was associated with higher heart rates (P less than 0.05), blood pressures (NS), and ventilation (P less than 0.01). In hypercapnia the metabolic effects of acidosis are modified by increased levels of circulating catecholamines.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40 min of bench stepping (knee high step; 15 steps · min⁻¹). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150 W, with increments of 50 W every 2 min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P < 0.05). Endurance time and peak V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P < 0.05) during cycling after eccentric exercise compared with the control condition. Peak blood lactate concentration, observed at 2 min post-exercise was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The higher blood lactate concentration during cycling exercise after prior eccentric exercise may be attributable to an increased rate of glycogenolysis possibly arising from an increased recruitment of Type II muscle fibres. It follows that determination of lactate thresholds for the purpose of fitness assessment in subjects experiencing DOMS is not appropriate. Accepted: 27 September 1997     

Failure to obtain a unique threshold on the blood lactate concentration curve during exercise

The purpose of this study was to compare various methods and criteria used to identify the anaerobic threshold (AT), and to correlate the AT obtained with each other and with running performance. Furthermore, a number of additional points throughout the entire range of lactate concentrations [La⁻] were obtained and correlated with performance. A group of 19 runners [mean age 33.7 (SD 9.6) years, height 173 (SD 6.3) cm, body mass 68.3 (SD 5.4) kg, maximal O₂ uptake (V˙O_{2 max} ) 55.2 (SD 5.9) ml · kg⁻¹ · min⁻¹] performed a maximal multistage treadmill test (1 km · h⁻¹ every 3.5 min) with blood sampling at the end of each stage while running. All AT points selected (visual [La⁻], 4 mmol · l⁻¹ [La⁻], 1 mmol · l⁻¹ above baseline, log-log breakpoint, and 45° tangent to the exponential regression) were highly correlated one with another and with performance (r > 0.90) even when there were many differences among the AT (P < 0.05). The additional points (ranging from 3 to 8 mmol · l⁻¹ [La⁻], 1 to 6 mmol · l⁻¹ [La⁻] above the baseline, and 30 to 70° tangent to the exponential curve of [La⁻]) were also highly correlated with performance (r > 0.90). These results failed to demonstrate a distinct AT because many points of the curve provided similar information. Intercorrelations and correlations between AT and performance were, however, reduced when AT were expressed as the percentage of maximal treadmill speed obtained at AT or percentage of V˙O_{2 max} . This would indicate that different attributes of aerobic performance (i.e. maximal aerobic power, running economy and endurance) are measured when manipulating units. Thus, coaches should be aware of these results when they prescribe an intensity for training and concentrate more on the physiological consequences of a chosen [La⁻] rather than on a “threshold”. Accepted: 22 October 1997     

Modelling the lactate response to short-term all out exercise

Background

The maximum post exercise blood lactate concentration (BLC_max) has been positively correlated with maximal short-term exercise (MSE) performance. However, the moment when BLC_max occurs (TBLC_max) is rather unpredictable and interpretation of BLC response to MSE is therefore difficult.

Methods

We compared a 3- and a 4-parameter model for the analysis of the dynamics of BLC response to MSEs lasting 10 (MSE10) and 30 s (MSE30) in eleven males (24.6 ± 2.3 yrs; 182.4 ± 6.8 cm; 75.1 ± 9.4 kg). The 3-parameter model uses BLC at MSE-start, extra-vascular increase (A) and rate constants of BLC appearance (k₁) and disappearance (k₂). The 4-parameter model includes BLC at MSE termination and amplitudes and rate constants of increase (A₁, y₁) and decrease (A₂, y₂) of post MSE-BLC.

Results

Both models consistently explained 93.69 % or more of the variance of individual BLC responses. Reduction of the number of parameters decreased (p < 0.05) the goodness of the fit in every MSE10 and in 3 MSE30. A (9.1 ± 2.1 vs. 15.3 ± 2.1 mmol l^-1) and A₁ (7.1 ± 1.6 vs. 10.9 ± 2.0 mmol l^-1) were lower (p < 0.05) in MSE10 than in MSE30. k₁ (0.610 ± 0.119 vs. 0.505 ± 0.107 min^-1), k₂ (4.21 10^-2 ± 1.06 10^-2 vs. 2.45 10^-2 ± 1.04 10^-2 min^-1), and A₂ (-563.8 ± 370.8 vs. -1412.6 ± 868.8 mmol l^-1), and y₁ (0.579 ± 0.137 vs. 0.489 ± 0.076 min^-1) were higher (p < 0.05) in MSE10 than in MSE30. No corresponding difference in y₂ (0.41 10^-2 ± 0.82 10^-2 vs. 0.15 10^-2 ± 0.42 10^-2 min^-1) was found.

Conclusion

The 3-parameter model estimates of lactate appearance and disappearance were sensitive to differences in test duration and support an interrelation between BLC level and halftime of lactate elimination previously found. The 4-parameter model results support the 3-parameter model findings about lactate appearance; however, parameter estimates for lactate disappearance were unrealistic in the 4-parameter model. The 3-parameter model provides useful information about the dynamics of the lactate response to MSE.

     

Acute renal response to rapid onset respiratory acidosis

Renal strong ion compensation to chronic respiratory acidosis has been established, but the nature of the response to acute respiratory acidosis is not well defined. We hypothesized that the response to acute respiratory acidosis in sheep is a rapid increase in the difference in renal fractional excretions of chloride and sodium (Fe(Cl) - Fe(Na)). Inspired CO(2) concentrations were increased for 1 h to significantly alter P(a)CO(2) and pH(a) from 32 ± 1 mm Hg and 7.52 ± 0.02 to 74 ± 2 mm Hg and 7.22 ± 0.02, respectively. Fe(Cl) - Fe(Na) increased significantly from 0.372 ± 0.206 to 1.240 ± 0.217% and returned to baseline at 2 h when P(a)CO(2) and pH(a) were 37 ± 0.6 mm Hg and 7.49 ± 0.01, respectively. Arterial pH and Fe(Cl) - Fe(Na) were significantly correlated. We conclude that the kidney responds rapidly to acute respiratory acidosis, within 30 min of onset, by differential reabsorption of sodium and chloride.     

The influence of straining maneuvers on the pressor response during isometric exercise

Experiments were performed to determine to what extent increments in esophageal and abdominal pressure would have on arterial blood pressure during fatiguing isometric exercise. Arterial blood pressure was measured during handgrip and leg isometric exercise performed with both a free and occluded circulation to active muscles. Handgrip contractions were exerted at 33 and 70% MVC (maximum voluntary contraction) by 4 volunteers in a sitting position and calf muscle contractions at 50 and 70% MVC with the subjects in a kneeling position. Esophageal pressure measured at the peak of inspirations did not change during either handgrip or leg contractions but peak expiratory pressures increased progressively during both handgrip and leg contractions as fatigue occurred. These increments were independent of the tensions of the isometric contractions exerted. Intra-abdominal pressures measured at the peak of either inspiration or expiration did not change during inspiration with handgrip contractions but increased during expiration. During leg exercise, intraabdominal pressures increased during both inspiration and expiration, reaching peak levels at fatigue. The arterial blood pressure also reached peak levels at fatigue, independent of circulatory occlusion and tension exerted, averaging 18.5-20 kPa (140-150 mm Hg) for both handgrip and leg contractions. While blood pressure returned to resting levels following exercise with a free circulation, it declined by only 2.7-3.8 kPa after leg and handgrip exercise, respectively, during circulatory occlusion. These results indicate that straining maneuvers contribute 3.5 to 7.8 kPa to the change in blood pressure depending on body position.     

Continuous blood gas and lactate monitoring during exercise

An improved computer method for continuous monitoring of arterial blood gases synchronized with an analysis of ventilatory variables was developed. Lactate was determined every 30 s. Sixteen healthy male volunteers who exercised regularly were included in this study. To evaluate the different transients of ventilation and metabolism, a gradual increase in the work load was used, starting with 40 W and increasing the load by 20 W every 2 min. This method generates large amounts of data and requires the development of computer programs for automatic determination of break points and general data reduction.     

Anemia causes a relative decrease in blood lactate concentration during exercise

The purpose of the present study was to examine to what degree a reduction in systemic oxygen transport capacity influences the absolute and relative levels (% of maximal oxygen uptake) of submaximal blood lactate accumulation. Anemia was induced by repeated venesections in eight healthy males. After 9-10 weeks of anemia, hemoglobin concentration [Hb] was restored by retransfusion of packed erythrocytes. The [Hb] values obtained were, before venesections, in control (C) = 145 +/- 10, in the anemic state (A) = 110 +/- 8, and after retransfusion (R) = 143 +/- 8 g X l-1 respectively. In all states, muscle biopsies were taken and measurements made of VO2max and VO2 at a running velocity corresponding to a blood lactate concentration of 4 mM (upsilon Hla 4.0). In the A condition Vo2max decreased by 19% as compared to C (P less than 0.01). upsilon Hla 4.0 was 14% lower in A as compared to C and R (p less than 0.01). VO2 at upsilon Hla 4.0 was 13% lower in A as compared to C (P less than 0.01). However, VO2 at upsilon Hla 4.0 expressed as a percentage of VO2max was increased (P less than 0.01) in the anemic state, the values obtained being C = 83.3%, A = 89.8% and R = 84.8%. Ventilation at upsilon Hla 4.0 was higher in A as compared to C and R (P less than 0.05). R and C values were not significantly different for any of the values presented above. The maximal activity of citrate synthase in muscle did not differ between the three different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.