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The effect of environmental heat on lactate threshold testing
Abstract
Eight physical education students, healthy, moderately trained (VO2max: 57 ± 4 ml·kg-1·min-1) and non acclimated to the heat, performed two lactate threshold cycloergometer trials. The subjects pedaled for 5 incremental workloads up to 225 watts in the HEAT (38±1°C; 28±3% relative humidity) and performed the same protocol in a NEUTRAL environment (21 ± 2° C; 43 ± 4% relative humidity). The trial order was randomly selected (HEAT or NEUTRAL) and trials were separated for at least 45 min in a thermoneutral environment (21° C). At the end of the trials body weight loss through sweat was 0,41 ± 0,02 kg and tympanic temperature was similar in the HEAT and NEUTRAL environments (37.6 ± 0.3 vs. 37.5 ± 0.3 °C). However, at the end of the test (225 watts) in the HEAT heart rate was 8 beats/min, ventilation rate was 6 L/min and the rate of perceived exertion (Borg scale) was 13% higher than in the NEUTRAL trial (all p<0.05). Similarly at the highest workload blood lactate level was 30% higher during HEAT than in the NEUTRAL environment (4.6 ± 1.0 vs 3.5 ± 0.6 mmol/ L; respectively, p<0.05). In the HEAT the rate of blood lactate accumulation increased and lactate threshold took place at 175 watts while it took place at 200 watt in the NEUTRAL trial. Due to the increase in heart rate in the HEAT, heart rate at lactate threshold was similar in the HEAT and NEUTRAL environments (150 ± 1 beats/min). In summary, environmental HEAT in non heat-acclimated athletes reduced lactate threshold and may underestimate training adaptations of the metabolic and cardiovascular systems.
Since 1920 until ours days, it has been acepted in a common and generalizable way, the belief of considering the lactic acidosis as reason of metabolic acidosis. However, a lot of studies confirm that such affirmation has not any bio-chemical support. In this study we try to check all the works that support this idea, clarify why this controversy exists and show a future scenario. A lot of publications since 1966 propose others explanations to the metabolic acidosis and the role that lactate plays in it, like: a) Metabolic acidosis is caused by an increase in ATP's non-mitocondrial production; b) The lactate production is fundamental to continue the regeneration of the glucolitic ATP; c) The lactate production consumes two protons and delays the acidosis; d) Lactate facilitates the elimination of the proton of the muscle across the MCTs (monocarboxylates transporters); e) Exists a lactate shuttle intracellular; f) Lactate competes with the glucose as source of carbohydrates; g) Lactate is a protector of the muscular fatigue, between others. All these roles that lactate plays grant a special protagonism to it in the intermediary metabolism of the different tissues, between cells and intracellular. The correct knowledge of the lactate metabolism must help to eliminate the mistakes of valuation and the inadequate training prescription that have been produced till now. The new era of the lactic acid and its biochemistry, will must take us, unavoidablement, to change the evaluate tests and the parameters measured, to eradicate the inadequate terminology (anaerobic, anaerobic threshold, anaerobic capacity), eliminate the threshold lactic acid values established beforehand and prescribe the trainings with the maximum specifity.
To investigate the influence of heat stress on the regulation of skeletal muscle carbohydrate metabolism, six active, but not specifically trained, men performed 5 min of cycling at a power output eliciting 70% maximal O2 uptake in either 20 degrees C (Con) or 40 degrees C (Heat) after 20 min of passive exposure to either environmental condition. Although muscle temperature (T(mu)) was similar at rest when comparing trials, 20 min of passive exposure and 5 min of exercise increased (P < 0.05) T(mu) in Heat compared with Con (37.5 +/- 0.1 vs. 36.9 +/- 0.1 degrees C at 5 min for Heat and Con, respectively). Rectal temperature and plasma epinephrine were not different at rest, preexercise, or 5 min of exercise between trials. Although intramuscular glycogen phosphorylase and pyruvate dehydrogenase activity increased (P < 0.05) at the onset of exercise, there were no differences in the activities of these regulatory enzymes when comparing Heat with Con. Accordingly, glycogen use in the first 5 min of exercise was not different when comparing Heat with Con. Similarly, no differences in intramuscular concentrations of glucose 6-phosphate, lactate, pyruvate, acetyl-CoA, creatine, phosphocreatine, or ATP were observed at any time point when comparing Heat with Con. These results demonstrate that, whereas mild heat stress results in a small difference in contracting T(mu), it does not alter the activities of the key regulatory enzymes for carbohydrate metabolism or glycogen use at the onset of exercise, when plasma epinephrine levels are unaltered.
Eight physically fit men performed two incremental bicycle ergometer tests, one in an ambient temperature of 25 degrees C and the other at 40 degrees C. Oesophageal temperature (Tes) increased continuously throughout the tests up to 38.0 and 38.3 degrees C, respectively. In both environments, forearm blood flow (plethysmography) was linearly related to Tes above the Tes threshold for vasodilation, but at the heaviest work loads this relationship was clearly attenuated and therefore indicated skin vasoconstriction, which tended to be more pronounced at 25 degrees C. During recovery at 25 degrees C, in some subjects the forearm blood flow increased above the levels observed at the end of the graded exercise in spite of a decreasing Tes. Skin blood flow, measured by laser Doppler flow meter at the shoulder, was quantitatively different but, on average, seemed to reveal the same response pattern as the forearm blood flow. In spite of the higher level of skin blood flow in the heat, blood lactate accumulation did not differ between the two environments. The present results suggest that there is competition between skin vasoconstriction and vasodilation at heavy work rates, the former having precedence in a thermoneutral environment to increase muscle perfusion. During short-term graded exercise in a hot environment, skin vasoconstriction with other circulatory adjustments seems to be able to maintain adequate muscle perfusion at heavy work levels, but probably not during maximum exercise.
In an investigation of the effect of acute heat exposure on aerobic and anaerobic metabolism, eight unacclimated men performed two incremental bicycle ergometer tests in random order, once under thermoneutral conditions (25 degrees C) and once in a hot dry (40 degrees C) environment. Oxygen consumption (VO2) and pulmonary ventilation were measured every minute. Fingertip blood samples were taken at each work level for blood lactate (LA) determination. Compared to the results at 25 degrees C, the mean VO2 was significantly (P less than 0.01) lower during exercise at 40 degrees C. In the hot dry environment the blood lactate threshold was slightly reduced in four subjects, but neither the average peak nor the post-exercise blood LA values differed from the findings at 25 degrees C. During the exercise-heat stress, the ventilatory threshold did not change significantly. The results indicated that, during relatively short-term incremental exercise in a hot environment, almost adequate muscle metabolism can be maintained.