Explaining pH change in exercising muscle: lactic acid, proton consumption, and buffering vs. strong ion difference.
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Biomedical subjects
Publications and source records attributed to Ralph Beneke.
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The pathophysiology of exercise related haemolysis is not thoroughly understood. We investigated whether exercise related haemolysis (1) is associated with alterations of red blood cell (RBC) membrane proteins similar to those found in inherited anaemic diseases, (2) can be induced with a non-running exercise mode, (3) is related to exercise intensity, and (4) coincides with indicators of oxidative stress. In ten triathletes [median (P25/P75-percentiles) age: 28.0 (26.3/28.5) years, height: 1.84 (1.78/1.87) m, body mass: 78.5 (74.8/80.8) kg, maximal oxygen uptake: 60.0 (57.3/64.8) ml kg(-1) min(-1)], haptoglobin, alpha- and beta-spectrin bands, malondialdehyde (MDA) and H2O2-induced chemiluminescence (H2O2-Chem) were determined immediately pre- and post-both, a 35 min low intensity and a high intensity cycling exercise [240 (218/253) vs 290 (270/300) W, P<0.05) requiring similar amounts of metabolic energy [28.3 (25.9/29.9) vs 24.9 (18.4/30.5) kJ kg(-1), P>0.05]. At high exercise intensity haptoglobin [1.10 (0.81/2.53) vs 1.01 (0.75/2.00) g l(-1)] decreased (P<0.05) whilst MDA [2.80 (2.65/3.20) vs 3.13 (2.78/3.31) nmol ml(-1)] and H2O2-Chem [29.70 (22.55/37.10) vs 37.25 (35.20/52.63) rel. U min] increased (P<0.05), coinciding with the disappearance of the spectrin bands in six out of ten gels. No corresponding changes were found at low intensity exercise. Ten to 35 min of non-running exercise in a regularly used intensity domain causes intra-vascular haemolysis associated with alterations in the RBC membrane proteins similar to those found after in vitro oxidative stress and in inherited anaemic diseases like Sphaerocytosis and Fanconi's anaemia.
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Whether age-related differences in blood lactate concentrations (BLC) reflect specific BLC kinetics was analyzed in 15 prepubescent boys (age 12.0 +/- 0.6 yr, height 1.54 +/- 0.06 m, body mass 40.0 +/- 5.2 kg), 12 adolescents (16.3 +/- 0.7 yr, 1.83 +/- 0.07 m, 68.2 +/- 7.5 kg), and 12 adults (27.2 +/- 4.5 yr, 1.83 +/- 0.06 m, 81.6 +/- 6.9 kg) by use of a biexponential four-parameter kinetics model under Wingate Anaerobic Test conditions. The model predicts the lactate generated in the extravasal compartment (A), invasion (k(1)), and evasion (k(2)) of lactate into and out of the blood compartment, the BLC maximum (BLC(max)), and corresponding time (TBLC(max)). BLC(max) and TBLC(max) were lower (P < 0.05) in boys (BLC(max) 10.2 +/- 1.3 mmol/l, TBLC(max) 4.1 +/- 0.4 min) than in adolescents (12.7 +/- 1.0 mmol/l, 5.5 +/- 0.7 min) and adults (13.7 +/- 1.4 mmol/l, 5.7 +/- 1.1 min). No differences were found in A related to the muscle mass (A(MM)) and k(1) between boys (A(MM): 22.8 +/- 2.7 mmol/l, k(1): 0.865 +/- 0.115 min(-1)), adolescents (22.7 +/- 1.3 mmol/l, 0.692 +/- 0.221 min(-1)), and adults (24.7 +/- 2.8 mmol/l, 0.687 +/- 0.287 min(-1)). The k(2) was higher (P < 0.01) in boys (2.87 10(-2) +/- 0.75 10(-2) min(-1)) than in adolescents (2.03 x 10(-2) +/- 0.89 x 10(-2) min(-1)) and adults (1.99 x 10(-2) +/- 0.93 x 10(-2) min(-1)). Age-related differences in the BLC kinetics are unlikely to reflect differences in muscular lactate or lactate invasion but partly faster elimination out of the blood compartment.
PURPOSE: To analyze the effect of an 8-wk training program on the energy cost of running (C) and the performance of 16 recreational males. METHODS: A training group (TG, N = 8, 25.3 +/- 2.9 yr, 183.6 +/- 7.3 cm, 80.9 +/- 9.6 kg) and a control group (CG, N = 8, 24.3 +/- 3.7 yr, 179.3 +/- 6.1 cm, 75.5 +/- 8.0 kg) performed three two-stage tests (TST) at weeks 0, 4, and 8 (W0, W4, W8). Speeds of the first (v-slow) and second stage (v-fast) were 2.4 +/- 0.3 vs 2.5 +/- 0.4 m x s(-1) and 3.7 +/- 0.3 vs 3.9 +/- 0.4 m.s (TG vs CG), respectively. Maximum running time at v-fast (T) served as the measure of performance. C was calculated from oxygen uptake above rest, blood lactate concentration, and speed. The TG trained 3-5x wk(-1) at an HR of +/-10 beats of the HR measured at v-slow at W0 (161 +/- 12 bpm). The CG did not train. RESULTS: At W0, there were no significant differences between the groups in T (377 +/- 47 vs 335 +/- 34 s) and C (v-slow: 4.1 +/- 0.3 vs 4.3 +/- 0.4 J x kg(-1) x m(-1); v-fast: 4.2 +/- 0.4 vs 4.0 +/- 0.4 J x kg(-1) x m(-1)). In the CG, T and C remained almost unchanged at W4 (363 +/- 38 s, 4.0 +/- 0.4 J x kg(-1) x m(-1)) and at W8 (342 +/- 49 s, 4.0 +/- 0.3 J x kg(-1) x m(-1)). In the TG, T increased (P < 0.05) at W4 (469 +/- 45 s) and at W8 (591 +/- 109 s). At v-fast, also C increased (P < 0.05) at W8 (4.6 +/- 0.4 J x kg(-1) x m(-1)), whereas at v-slow, C decreased (P < 0.05) at W4 (3.7 +/- 0.4 J x kg(-1) x m(-1)) with no further change at W8 (3.7 +/- 0.4 J x kg(-1) x m(-1)). CONCLUSION: The training successfully increased running performance in terms of T. During the initial training period, C could be reduced at the speed predominantly used in training. However, at high running speeds, C may even increase if the corresponding running time is largely increased.
It is speculated that anaerobic metabolism is the predominant source of energy in karate kumite. However, no experimental proof is currently available. The metabolic cost and fractions of aerobic and anaerobic energy of karate kumite fighting were investigated. Ten male nationally or internationally ranked karateka [means (SD) age 26.9 (3.8) years, height 1.80 (0.08) m, mass 77.2 (12.8) kg] performed two to four fights scheduled and judged like a championship. Oxygen uptake was measured continuously with a portable spirometric device. Blood lactate was determined immediately before, and minute by minute after, each fight. Aerobic, anaerobic alactic and anaerobic lactic energy were calculated from oxygen uptake during the fight ( VO(2)), the fast component of the post-fight oxygen uptake ( VO(2PCr)) above resting values and changes in blood lactate concentration (Net-BLC), respectively. Altogether, 36 fights lasting 267 (61) s were analysed. The referee's decisions caused an activity-to-break ratio of approximately 2:1. VO(2), VO(2PCr), and Net-BLC per fight were 165.3 (52.4) ml(.)kg(-1), 32.2 (7.2) ml(.)kg(-1)and 4.2 (1.9) mmol(.)l(-1); the overall energy cost above rest was 334.3 (86.3) kJ per fight. Fractions of aerobic, anaerobic alactic, and lactic energy sources were 77.8 (5.8)%, 16.0 (4.6)%, and 6.2 (2.4)%, respectively. The results indicate a high metabolic rate in karate kumite. However, the acyclic activity profile implies that aerobic metabolism is the predominant source of energy and there is anaerobic supplementation, mainly by high-energy phosphates.
Cystic fibrosis (CF) is a life-limiting inherited disorder characterised by pulmonary disease, pancreatic dysfunction and symptoms of malnutrition that are all interrelated with low exercise capacity and poor survival rate. Therapy with growth hormone (GH) may improve the reduced dimensional and functional capacity associated with poor nutritional status and catabolism and therefore improve exercise tolerance, quality of life and survival rate in patients with CF. The literature about GH treatment and its effect on exercise tolerance are rather limited, not always consistent and methodological concerns restrict further analysis. GH treatment may have beneficial effects on both growth and exercise tolerance without serious complications in prepubertal children with CF. The observed dimensional changes of the muscular, cardiovascular and pulmonary system seem to improve aerobic exercise capacity and respiratory and peripheral muscle strength. The physiological background of the observed changes is not yet fully understood, therefore, larger-scale studies with an optimised design are required.
The maximal lactate steady state (MLSS) is the highest blood lactate concentration (BLC) that can be identified as maintaining a steady-state during a prolonged submaximal constant workload. Comparative interpretation of published data about MLSS is complicated by the fact that different methods of testing have been utilized. Thus, three methods, corresponding to the time course of changes in BLC incurred during either 30 min (MLSS I) or 20 min (MLSS II and III) of constant submaximal workload exercise, were compared in 26 male subjects [mean (SD) age 24.6 (5.6) years, height 181.6 (4.9) cm, body mass 74.4 (5.2) kg]. MLSS I [5.1 (1.3) mmol x l(-1)], II [4.9 (1.3) mmol x l(-1)], and III [4.3 (1.3) mmol x l(-1)] were different (P<0.01). The workload corresponding to MLSS III [244.8 (44.0) W] was lower (P<0.01) than that at MLSS I [254.0 (40.8) W] and II [251.9 (40.4) W]. No difference could be confirmed between the workloads established for MLSS I and MLSS II. The differences between MLSS I, MLSS II, and MLSS III and corresponding workloads reflect insufficient contribution to lactate kinetics by testing procedures that depend strongly upon the time course of changes in BLC during the initial 20-25 min of constant-workload exercise. Based on the present findings, constant-load tests lasting at least 30 min and a BLC increase of no more than 1.0 mmol x l(-1) after the 10th testing minute appear to be the most reasonable with respect to valid testing results.
OBJECTIVE: To determine whether repetitive test interruptions (TI) during constant load testing influence blood lactate concentration (BLC), maximal lactate steady state (MLSS), MLSS workload (P-MLSS), and relative MLSS intensity (Int-MLSS). METHODS: Nineteen males participated in this study. In experiment A, 10 subjects (27.5 +/- 2.9 yr; 183.7 +/- 5.2 cm; 77.4 +/- 3.7 kg) performed 30-min constant load tests: one without TI, one with TI of 30 s, and one with TI of 90 s after every 5 min of cycling at a given workload. In experiment B, nine subjects (28.0 +/- 2.7 yr; 182.9 +/- 6.8 cm; 76.2 +/- 4.5 kg) performed 30-min constant load tests at different workloads until MLSS had been determined for all three TI protocols. RESULTS: In experiment A, the BLC after 30 min net working time (BLC30) was higher (P < 0.001) without TI (6.0 +/- 1.3 mmol.l(-1)) than with TI of 30 s (4.9 +/- 1.4 mmol.l(-1)) or 90 s (4.5 +/- 1.1 mmol.l(-1)). The change in BLC during the final 20 min (DeltaBLC10-30) was greater (P < 0.01) without TI (1.2 +/- 1.0 mmol.l(-1)) than with TI of 30 s (0.2 +/- 0.7 mmol.l(-1)) or 90 s (-0.3 +/- 0.7 mmol.l(-1)). In experiment B, the MLSS was not affected, but P-MLSS and Int-MLSS were lower (P < 0.01) without TI (277.8 +/- 24.4W and 73.7 +/- 7.6%) than with TI of 30 s (300.4 +/- 30.4W and 79.2 +/- 8.0%) or 90 s (310.0 +/- 31.2W and 81.5 +/- 7.1%). Approximately 35% of the variance of BLC30 and DeltaBLC10-30, and 70% of the variance of P-MLSS and Int-MLSS were explained by TI duration (P < 0.001). CONCLUSIONS: TI decreased BLC30 and DeltaBLC10-30 but has no effect on MLSS. Consequently, with TI, the MLSS is achieved at higher P-MLSS and Int-MLSS.
It is assumed that the maximal lactate steady state (MLSS) can be used to establish the highest workload that can be maintained over time without continual blood lactate accumulation. In untrained subjects, and in both elite and junior athletes, MLSS occurs at different blood lactate concentrations (BLC) for different exercise modes. This suggests that MLSS depends on the motor pattern of exercise and may be a function of the relationship between power output per unit muscle mass and the mass of the muscle primarily engaged in the activity. A computer model has been developed that takes account of current theories relating to the effect of exercise on BLC and to the factors that limit oxygen transport to the muscle cell. Simulations using this model support the suggestion that load per unit of engaged muscle mass accounts for task-specific levels of MLSS. Simulated differences in MLSS appear because the MLSS does not necessarily reflect the real maximal equilibrium between lactate formation and utilization, the LLSS. The higher difference between MLSS and LLSS measured in rowing ergometry compared to cycle ergometry seems to indicate a greater task sensitivity of the BLC response to given changes of exercise intensity during rowing. Whether such a difference may be relevant for a deeper understanding of task-specific training strategies remains a matter for further investigation.
PURPOSE: The effect of growth hormone (GH) treatment on exercise tolerance in children with cystic fibrosis was investigated. METHODS: 10 prepubertal children (mean +/- SD; age: 12.1 +/- 1.7 yr; height: 137.4 +/- 9.2 cm; body mass: 27.8 +/- 4.2 kg; forced expiratory volume in 1 s (FEV1): 68 +/- 22% predicted) were randomly assigned to either control period (CON, standard therapy) or recombinant human growth hormone (GH) period (additional GH treatment, 0.11-0.14 IU.kg-1, daily, s.c.) for the first 6 months, and then assigned to the other period for the next 6 months. At study entry and after each period, anthropometric data, pulmonary function, and exercise capacity (peak exercise capacity, .VO(2peak), and isokinetic muscle strength) were measured. RESULTS: Changes in height (+4.3 +/- 1.0 cm), total body mass (+2.2 +/- 0.8 kg), and lean body mass (LBM, +2.9 +/- 0.7 kg) were significantly higher (P < 0.01) after GH treatment compared with CON. Pulmonary function did not significantly change in either of the periods. In contrast to CON, GH treatment improved absolute .VO(2peak) (+19%, P < 0.01), peak ventilation (+14%, P < 0.01), and peak oxygen pulse (+18%, P < 0.01). Analysis of variance revealed that most of the changes (71%) in .VO(2peak) could be explained by those in LBM and FEV1 (P = 0.001). CONCLUSION: GH treatment clearly improved exercise tolerance, presumably resulting from the combined effects of GH on the muscular, cardiovascular, and pulmonary capacity.
Numerous studies have confirmed that performance can be impaired when athletes are dehydrated. Endurance athletes should drink beverages containing carbohydrate and electrolyte during and after training or competition. Carbohydrates (sugars) favor consumption and Na(+) favors retention of water. Drinking during competition is desirable compared with fluid ingestion after or before training or competition only. Athletes seldom replace fluids fully due to sweat loss. Proper hydration during training or competition will enhance performance, avoid ensuing thermal stress, maintain plasma volume, delay fatigue, and prevent injuries associated with dehydration and sweat loss. In contrast, hyperhydration or overdrinking before, during, and after endurance events may cause Na(+) depletion and may lead to hyponatremia. It is imperative that endurance athletes replace sweat loss via fluid intake containing about 4% to 8% of carbohydrate solution and electrolytes during training or competition. It is recommended that athletes drink about 500 mL of fluid solution 1 to 2 h before an event and continue to consume cool or cold drinks in regular intervals to replace fluid loss due to sweat. For intense prolonged exercise lasting longer than 1 h, athletes should consume between 30 and 60 g/h and drink between 600 and 1200 mL/h of a solution containing carbohydrate and Na(+) (0.5 to 0.7 g/L of fluid). Maintaining proper hydration before, during, and after training and competition will help reduce fluid loss, maintain performance, lower submaximal exercise heart rate, maintain plasma volume, and reduce heat stress, heat exhaustion, and possibly heat stroke.