Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Restoration of blood pH between repeated bouts of high-intensity exercise: effects of various active-recovery protocols

To determine which active-recovery protocol would reduce faster the high blood H⁺ and lactate concentrations produced by repeated bouts of high-intensity exercise (HIE). On three occasions, 11 moderately trained males performed 4 bouts (1.5 min) at 163% of their respiratory compensation threshold (RCT) interspersed with active-recovery: (1) 4.5 min pedalling at 24% RCT (S_HORT); (2) 6 min at 18% RCT (M_EDIUM); (3) 9 min at 12% RCT (L_ONG). The total work completed during recovery was the same in all three trials. Respiratory gases and arterialized-blood samples were obtained during exercise. At the end of exercise, L_ONG in comparison to S_HORT and M_EDIUM increased plasma pH (7.32 ± 0.02 vs. ~7.22 ± 0.03; P < 0.05), while reduced lactate concentration (8.5 ± 0.9 vs. ~10.9 ± 0.8 mM; P < 0.05). Ventilatory equivalent for CO₂ was higher in L_ONG than S_HORT and M_EDIUM (31.4 ± 0.5 vs. ~29.6 ± 0.5; P < 0.05). Low-intensity prolonged recovery between repeated bouts of HIE maximized H⁺ and lactate removal likely by enhancing CO₂ unloading.     

Plasma K+ changes during intense exercise in endurance-trained and sprint-trained subjects

Active muscle releases K⁺, and the plasma K⁺ concentration is consequently raised during exercise. K⁺ is removed by the NaK pump, and training may influence the number of pumps. The plasma K⁺ concentration was therefore studied in five endurance-trained (ET) and six sprint-trained (ST) subjects during and after 1 min of exhausting treadmill running. Non-exhausting bouts of exercise at either lower speed or of shorter duration were also carried out. Blood samples were taken from a catheter in the femoral vein before and at frequent intervals after exercise. The pre-exercise venous plasma [K⁺] was (mean ± SEM) 3.68±0.10mmol l^-1 (ET) and 3.88 ± 0.06 mmol l^-1 (ST). One minute of exhausting exercise was sustained at 5.27 ±0.08 m s^-1 (ET) and 5.59 ± 0.06 m s^-1 (ST) and caused the plasma K⁺ concentration to rise by 4.4 ± 0.3 (ET) and 4.7 ± 0.3 mmol l^-1 (ST; ns) respectively. Three minutes after exercise the K⁺ concentration was 0.48 + 0.08 mmol l^-1 (ST) and 0.50 ± 0.07 mmol l^-1 (ST) below the pre-exercise value. During the following 6 min of recovery, the value was unchanged for the ET subjects, while a 0.32 ± 0.06 mmol l^-1 rise was seen for the ST subjects. Exercise at reduced intensity or of reduced duration resulted in smaller changes in the K⁺ concentration both during exercise and in the post-exercise recovery, and for each subject the lowest post-exercise K⁺ concentration was therefore inversely related to the peak K⁺ concentration during exercise. For a given peak K⁺ concentration, the ST subjects had higher plasma K⁺ concentrations than the ET subjects in the recovery period, suggesting that the two groups of subjects may regulate the K⁺ concentration differently after exercise.     

Effects of acute carbohydrate supplementation during sessions of high-intensity intermittent exercise

Abs tract The present study evaluated the acute effects of carbohydrate supplementation on heart rate (HR), rate of perceived exertion (RPE), metabolic and hormonal responses during and after sessions of high-intensity intermittent running exercise. Fifteen endurance runners (26 ± 5 years, 64.5 ± 4.9 kg) performed two sessions of intermittent exercise under carbohydrate (CHO) and placebo (PLA) ingestion. The sessions consisted of 12 × 800 m separated by intervals of 1 min 30 s at a mean velocity corresponding to the previously performed 3-km time trial. Both the CHO and PLA sessions were concluded within ∼28 min. Blood glucose was significantly elevated in both sessions (123.9 ± 13.2 mg dl⁻¹ on CHO and 147.2 ± 16.3 mg dl⁻¹ on PLA) and mean blood lactate was significantly higher in the CHO (11.4 ± 4.9 mmol l⁻¹) than in the PLA condition (8.4 ± 5.1 mmol l⁻¹) (P < 0.05). The metabolic stress induced by the exercise model used was confirmed by the elevated HR (∼182 bpm) and RPE (∼18 on the 15-point Borg scale) for both conditions. No significant differences in plasma insulin, cortisol or free fatty acids were observed during exercise between the two trials. During the recovery period, free fatty acid and insulin concentrations were significantly lower in the CHO trial. Supplementation with CHO resulted in higher lactate associated with lipolytic suppression, but did not attenuate the cortisol, RPE or HR responses.     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

Summary The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (T _db=33.4°C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% , with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml·kg BW⁻¹ of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol·l⁻¹ Na⁺, 3.2 mmol·l⁻¹ K⁺). Beverages were administered in double blind, counterbalanced order. Mean (±SE) times for the 1200 cycling task differed significantly: WP=13.62±0.33 min, *6%=13.03±0.24 min, 8%=13.30±0.25 min, 10%=13.57±0.22 min (*=different from WP and 10%,P<0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P<0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance. Compared to ingestion of a water placebo, consumption of beverages containing 6% to 10% sucrose resulted in similar physiologic and sensory response, while ingestion of the 6% sucrose beverage resulted in significantly improved end-exercise performance following only 60 min of intermittent cycling exercise.     

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CV_drift) during cycling. Twelve healthy males (23.4 ± 0.5 years, mean ± SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CV_drift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (ΔSV = −16.2 ± 2.0 and −17.1 ± 1.0 ml beat⁻¹; ΔHR = 18.3 ± 2.0 and 17.5 ± 3.0 beats min⁻¹ for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO₂ rebreathing) was 14.7 ± 0.3 l min⁻¹ and 15.0 ± 0.3 l min⁻¹, and mean arterial pressure was 100.0 ± 1.0 mmHg and 96.7 ± 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 ± 1.2% and 11.0 ± 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 ± 0.8 (AU) for 40 rpm and 53.0 ± 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CV_drift during cycling, at least under the present experimental conditions.     

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

To evaluate the relationship between lactate release and [lac]_art and to investigate the influence of the catecholamines on the lactate release, 14 healthy men [age 25±3 (SE) year] were studied by superimposing cycle on forearm exercise, both at 65% of their maximal power reached in respective incremental tests. Handgrip exercise was performed for 30 min at 65% of peak power. In addition, between the tenth and the 22nd minute, cycling with the same intensity was superimposed. The increase in venous lactate concentration ([lac]_ven) (rest: 1.3±0.4 mmol·l⁻¹; 3rd min: 3.9±0.8 mmol·l⁻¹) begins with the forearm exercise, whereas arterial lactate concentration ([lac]_art) remains almost unchanged. Once cycling has been added to forearm exercise (COMB), [lac]_art increases with a concomitant increase in [lac]_ven (12th min: [lac]_art, 3.2±1.3 mmol·l⁻¹; [lac]_ven, 5.7±2.2 mmol·l⁻¹). A correlation between oxygen tension (P_vO₂) and [lac]_ven cannot be detected. There is a significant correlation between [lac]_art and norepinephrine ([NE]) (y=0.25x+1.2; r=0.815; p<0.01) but no correlation between lactate release and epinephrine ([EPI]) at moderate intensity. Our main conclusion is that lactate release from exercising muscles at moderate intensities is neither dependent on P_vO₂ nor on [EPI] in the blood.     

The effect of prolonged submaximal exercise on gas exchange kinetics and ventilation during heavy exercise in humans

This study compared ventilation, gas exchange (oxygen uptake, V̇O₂) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% V̇O_2peak. The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [V̇O_2peak=60.2 (1.7) ml·kg⁻¹·min⁻¹] completed two identical 6-min bouts of cycling performed at high intensity [~90% V̇O_2peak; 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). V̇O₂ at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml·min⁻¹, respectively, P<0.05) than in Pre-Ex but there was a ~25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml·min⁻¹, respectively, P<0.05]. The greater whole-body V̇O₂ after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (~12–16 l·min⁻¹ and ~10 beats·min⁻¹, respectively, P<0.05) as were the ratios V̇ _E/O₂ and V̇ _E/V̇CO₂ in the Post-Ex tests. It was concluded that the V̇O₂ and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.     

Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Δ) in lactic acid ([La]), [HCO₃⁻], pH and PCO₂ in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (β_nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃⁻] · ΔpH⁻¹) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 ± 2(SEM) and 20 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.02). During recovery β_nbi decreased to 14 (UT) and 12 (TR) mmol l⁻¹ (both P < 0.001) corresponding to values previously found at rest by in vivo CO₂ titration. Bicarbonate buffering (β_bi) amounted to 44–48 mmol l⁻¹ during and after exercise. The large exercise β_nbi seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO₃⁻ or H⁺ with cells and delayed HCO₃⁻ equilibration between plasma and interstitial fluid. Increase of [HCO₃⁻] during titration by these mechanisms augments total β and thus the calculated β_nbi more than β_bi because it reduces ΔpH and Δ[HCO₃⁻] at constant Δ[La]. The smaller rise in exercise β_nbi in TR than UT may be caused by an increased extracellular volume and an improved exchange of La⁻, HCO₃⁻ and H⁺ between trained muscles and blood.     

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists

We tested the hypothesis that intense short duration hypoxic exercise would result in an increase in extravascular lung water (EVLW), as evidenced by an increase in lung density. Using computed tomography (CT), baseline lung density was obtained in eight highly trained male cyclists (mean ± SD: age = 28 ± 8 years; height = 180 ± 9 cm; mass = 71.6 ± 8.2 kg; = 65.0 ± 5.2 ml kg min⁻¹). Subjects then completed an intense hypoxic exercise challenge on a cycle ergometer and metabolic data, HR and %S_pO₂ were recorded throughout. While breathing 15% O₂, subjects performed five 3 km cycling intervals (mean power, 286 ± 20 W; HR = 91 ± 4% HR_max) separated by 5 min of recovery. From a resting hypoxic S_pO₂ of 92 ± 4%, subjects further desaturated during exercise to 76 ± 3%. CT scans were repeated 76 ± 10 min (range 63–88 min) following the completion of exercise. There was no change in lung density from pre (0.18 ± 0.02 g ml⁻¹) to post-exercise (0.18 ± 0.04 g ml⁻¹). The substantial reduction in S_pO₂ may be explained by a number of potential mechanisms, including decreased pulmonary diffusion capacity, alveolar hypoventilation, reduced red cell transit time, ventilation/perfusion inequality or a temperature and pH induced rightward-shift in the oxyhaemoglobin dissociation curve. Alternatively, the integrity of the blood gas barrier may have been disrupted without any measurable increase in lung density.     

Arterio‐venous differences of blood acid–base status and plasma sodium caused by intense bicycling

After intense exercise muscle may give off hydrogen ions independently of lactate, perhaps by a mechanism involving sodium ions. To examine this possibility further five healthy young men cycled for 2 min to exhaustion. Blood was drawn from catheters in the femoral artery and vein during exercise and at 1‐h intervals after exercise. The blood samples were analysed for pH, blood gases, lactate, haemoglobin, and plasma proteins and electrolytes. Base deficit was calculated directly without using common approximations. The leg blood flow was also measured, thus allowing calculations of the leg’s exchange of metabolites. The arterial blood lactate concentration rose to 14.2 ± 1.0 mmol L^–1, the plasma pH fell to 7.18 ± 0.02, and the base deficit rose 22% more than the blood lactate concentration did. The femoral‐venous minus arterial differences peaked at 1.8 ± 0.2 mmol L^–1 (lactate), –0.24 ± 0.01 (pH), and 4.5 ± 0.4 mmol L^–1 (base deficit), and –2.5 ± 0.7 mmol L^–1 (plasma sodium concentration corrected for volume changes). Thus, near the end of the exercise and for the first 10 min of the recovery period the leg gave off more hydrogen ions than lactate ions to the blood, and sodium left plasma in proportion to the extra hydrogen ions appearing. The leg’s integrated excess release of hydrogen ions of 0.88 ± 0.45 mmol kg^–1 body mass was 67% of the integrated lactate release. Base deficit calculated by the traditional approximate equations underestimated the true value, but the error was less than 10%. We conclude that intense exercise and lactic acidosis may lead to a muscle release of hydrogen ions independent of lactate release, possibly by a Na⁺,H⁺ exchange. Hydrogen ions were largely buffered in the red blood cells.     

Effect of intravenous infusion of hypertonic glucose solutions on pancreatic HCO3 secretion

To examine why intravenous infusion of hypertonic non-electrolyte solutions inhibit pancreatic HCO₃^- secretion, the relationship between pancreatic HCO₃^- secretion and plasma pH was examined before and following intravenous infusion of hypertonic glucose to 5 anesthetized, secretin infused (2.7 C.U./kg b. wt. h^-1) pigs. Hyperglycemia (plasma glucose 103±6 mmol/l) did not significantly change plasma pH, NaM⁺, K⁺, Cl^- and HCO₃^- concentrations. Hyperglycemia reduced pancreatic water flux by 48±5% and raised pancreatic juice HCO₃^- concentration by 43±4 mmol/l. Concurrently, HCO₃^- secretion fell by 34±5%. Acidosis, produced through intravenous HC1 infusion and CO₂ addition to inspired air, reduced HCO₃^- secretion by 40±6 ±mol/min and 30±5 ±mol/min per 0.1 pH unit reduction in plasma pH before and during hyperglycemia, respectively, and abolished HCO₃ secretion at an estimated plasma pH of 6.51 ±0.06 before and a pH of 6.63±0.05 during hyperglycemia. We conclude that hypertonic glucose infusions inhibit pancreatic water flux and cause an increase in pancreatic juice HCO₃^- concentration which may inhibit HCO₃^- secretion through an effect on acid-base balance in secretory cells.     

The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise

Summary The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate (C) or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg⁻¹ body weight. Pre-exercise blood pH was 7.44±0.06, 7.42±0.05, 7.41±0.05 and 7.38±0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p<0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO₃ ⁻], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.     

The effect of induced alkalosis and acidosis on plasma lactate and work output in elite oarsmen

Summary In order to test the effect of artificially induced alkalosis and acidosis on the appearance of plasma lactate and work production, six well-trained oarsmen (age=23.8±2.5 years; mass=82.0±7.5 kg) were tested on three separate occasions after ingestion of 0.3 g·kg⁻¹. NH₄Cl (acidotic), NaHCO₃ (alkalotic) or a placebo (control). Blood was taken from a forearm vein immediately prior to exercise for determination of pH and bicarbonate. One hour following the ingestion period, subjects rowed on a stationary ergometer at a pre-determined sub-maximal rate for 4 min, then underwent an immediate transition to a maximal effort for 2 min. Blood samples from an indwelling catheter placed in the cephalic vein were taken at rest and every 30 s during the 6 min exercise period as well as at 1, 3, 6, 9, 12, 15, 18, 21, 25 and 30 min during the passive recovery period. Pre-exercise blood values demonstrated significant differences (p<0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p>0.05), although a trend toward decreased production was evident in the acidotic condition. Analysis of exercise blood samples using ANOVA with repeated measures revealed that the linear increase in plasma lactate concentration during control was significantly greater than acidosis (p<0.01). Although plasma lactate values during alkalosis were consistantly elevated above control there was no significant difference in the linear trend (p>0.05). During recovery, there was no significant difference in the rate of lactate disappearance amongst the three conditions. It is concluded that under this protocol artificial manipulation of the acid-base status of the blood does not significantly influence work production despite significantly reduced plasma lactate concentrations during acidosis. The inability of these pH changes to alter exercise performance emphasizes the relative importance of the intracellular and the extracellular buffer systems in well trained athletes.     

Changes in ventilation related to changes in electromyograph activity during repetitive bouts of isometric exercise in simulated sailing

This study examined the control of ventilation during repetitive bouts of isometric exercise in simulated sailing. Eight male sailors completed four successive 3-min bouts of similar isometric effort on a dinghy simulator, bouts were separated by 15-s rest intervals. Quadriceps muscle integrated electromyograph activity (iEMG) was recorded during each bout and expressed as a percentage of activity during maximal voluntary contraction (%iEMG_max). From the first to the fourth bout, the 3-min mean averages for ventilation and for %iEMG_max increased from 19.8 (SEM 1.1) to 37.5 (SEM 3.0) l · min^–1 and from 31 (SEM 4) to 39 (SEM 4)% respectively; also, ventilation and %iEMG_max over each minute throughout the four bouts were significantly correlated (r = 0.85;P < 0.05). Progressive hyperventilation reduced the mean end-tidal partial pressure of carbon dioxide from 5.0 (SEM 0.3) kPa during bout 1 to 4.3 (SEM 0.4) kPa during bout 4 [37.7 (SEM 2.0) to 32.4 (SEM (3.0) mmHg]. From the first to the fourth bout the end-of-bout blood lactate concentration did not increase significantly although the concentration from the third bout onwards was significantly greater than at rest. The results suggested that the development of muscle fatigue, which was enhanced by the insufficiency of recovery during the 15-s intervals and mirrored in the progressive increase in iEMG, was linked with stimuli causing progressive hyperventilation. Though these changes in ventilation and iEMG could not be associated with changes in blood lactate concentration, they could both have been related to accumulating metabolites within the muscles themselves.     

Effects of compression stockings during exercise and recovery on blood lactate kinetics

This study aimed to investigate if wearing compression stockings (CS) during exercise and recovery could affect lactate profile in sportsmen. Eight young healthy trained male subjects performed two maximal exercise tests on a cycle ergometer on two different occasions performed randomly: CS during both exercise and recovery, and no CS. Blood lactate concentration was taken during exercise and at 0, 3, 5, 10, 15, 30 and 60 min post-exercise. The individual blood lactate recovery curves were fitted to a biexponential time function: \textLa_(t) = \textLa₍₀₎ + A ₁ ( 1- \texte ^{- g₁ t} ) + A ₂ ( 1- \texte ^{- g₂ t} ) {\text{La}}_{(t)} = {\text{La}}_{(0)} + A_{ 1} ( 1- {\text{e}}^{{ - \gamma_{1} t}} ) + A_{ 2} ( 1- {\text{e}}^{{ - \gamma_{2} t}} ) , where γ ₁ and γ ₂ denote the abilities to exchange lactate between the previously active muscles and the blood and to remove lactate from the organism, respectively. A significantly higher blood lactate value at the end of the maximal exercise was found (12.1 ± 0.5 vs. 10.8 ± 0.5 mmol l⁻¹) wearing CS as compared to no CS (P < 0.05). Lower γ ₁ and higher γ ₂ values were observed with CS during recovery, as compared to no CS. It was concluded that CS during graded exercise leads to a significant higher blood lactate value at exhaustion. Since lactate exchanges were expected to be decreased during exercise due to CS, this result was likely attributable to a higher lactate accumulation related to a greater overall contribution of anaerobic glycolysis. Although the lactate removal ability was significantly improved when wearing CS during recovery, its efficacy in promoting blood lactate clearance after high-intensity exercise is limited.     

Effects of pre-cooling procedures on intermittent-sprint exercise performance in warm conditions

The aim of this study was to determine whether pre-cooling procedures improve both maximal sprint and sub-maximal work during intermittent-sprint exercise. Nine male rugby players performed a familiarisation session and three testing sessions of a 2 × 30-min intermittent sprint protocol, which consisted of a 15-m sprint every min separated by free-paced hard-running, jogging and walking in 32°C and 30% humidity. The three sessions included a control condition, Ice-vest condition and Ice-bath/Ice-vest condition, with respective cooling interventions imposed for 15-min pre-exercise and 10-min at half-time. Performance measures of sprint time and % decline and distance covered during sub-maximal exercise were recorded, while physiological measures of core temperature (T _core), mean skin temperature (T _skin), heart rate, heat storage, nude mass, rate of perceived exertion, rate of thermal comfort and capillary blood measures of lactate [La⁻], pH, Sodium (Na⁺) and Potassium (K⁺) were recorded. Results for exercise performance indicated no significant differences between conditions for the time or % decline in 15-m sprint efforts or the distance covered during sub-maximal work bouts; however, large effect size data indicated a greater distance covered during hard running following Ice-bath cooling. Further, lowered T _core, T _skin, heart rate, sweat loss and thermal comfort following Ice-bath cooling than Ice-vest or Control conditions were present, with no differences present in capillary blood measures of [La⁻], pH, K⁺ or Na⁺. As such, the ergogenic benefits of effective pre-cooling procedures in warm conditions for team-sports may be predominantly evident during sub-maximal bouts of exercise.     

The effect of beta-blockade on plasma potassium concentrations and muscle excitability following static exercise

 The effects of β-blockade on plasma [K⁺], muscle excitability and force during fatiguing exercise were examined. Nine healthy males (mean age 22.3±1.7 yr) performed a 3-min fatigue protocol that consisted of a sustained submaximal contraction (30% of the maximal voluntary contraction, MVC) of the right quadriceps muscle. Subjects performed the exercise after treatment with either placebo, β₁-selective (metoprolol, 100 mg) or an equipotent dose of non-selective β_1,2-blockade (propranolol, 80 mg, n=6; 100 mg, n=2; 120 mg, n=1) twice daily for 3 days before testing according to a randomized double–blind design. Brachial arterial and femoral venous blood samples were drawn before, during, and for 15 min following the contraction, together with maximal stimulation of the right femoral nerve to evoke a twitch and a compound muscle action potential (M-wave); the M-wave amplitude being used as an index of sarcolemmal excitability. The exercise-induced rise in plasma [K⁺] did not differ between treatments, but K⁺ re-uptake during recovery was slower following propranolol. The recovery of the twitch was significantly related to the recovery of plasma [K⁺] in all trials, but the evoked M-waves were unaffected by either the contraction or the drug treatment. Propranolol resulted in a significantly (P<0.05) greater reduction (51.9±7.3%) in MVC following the 3-min contraction compared with metoprolol (40.7±3.6%) or placebo (38.9±3.6%). These results suggest that while β_1,2-blockade may significantly affect the recovery of muscle force and K⁺ homeostasis after fatiguing exercise (presumably through an inhibition of the Na⁺,K⁺-ATPase), it does not appear to affect surface membrane excitability. Received: 22 July 1997/Received after revision: 20 January 1998/Accepted: 23 January 1998     

The relationship between plasma potassium,muscle membrane excitability and force following quadriceps fatigue

To examine the simultaneous changes in plasma [K⁺], muscle excitability and force during fatigue, ten male adults (mean age = 22 ± 0.5 years) held an isometric contraction of their right quadriceps muscle at an intensity of 30% maximum voluntary contraction (MVC) for 3 min. Femoral venous and brachial arterial [K⁺] were determined from serial samples drawn before, during, and for 15 min following the 3-min contraction. Each blood sample was synchronized with a maximal stimulation of the right femoral nerve to evoke a twitch and compound muscle action potential (M-wave). Immediately post-exercise, twitch torque was only 42% of baseline and femoral venous plasma [K⁺] had increased significantly from 4.02 ± 0.08 mmol/l to 5.9 ± 0.22 mmol/l. Femoral venous plasma lactate rose to a peak level of 10.0 ± 0.8 mmol/l at 1 min post exercise. The recovery of the twitch torque was exponentially related to the recovery of femoral venous plasma [K⁺] (r ² = 0.93, P < 0.01). There was no evidence for any loss of muscle membrane excitability during the period of increased extracellular [K⁺], in fact, the M-waves tended to be potentiated in the early phases of the recovery period. These results suggest that muscle membrane excitability is maintained in spite of increased extracellular [K⁺] following fatigue induced by a sustained submaximal quadriceps contraction. However, the strong relationship between twitch torque and femoral venous plasma [K⁺] suggests that K⁺ may be exerting its effect distal to surface membrane action potential propagation, most likely in the T-tubular region. Received: 20 April 1995/Received after revision and accepted: 8 January 1996     

Effect of ageing on the ventilatory response and lactate kinetics during incremental exercise in man

We investigated the effects of age on breathing pattern, mouth occlusion pressure, the ratio of mouth occlusion pressure to mean inspiratory flow, and venous blood lactate kinetics during incremental exercise. Mouth occlusion pressure was used as an index of inspiratory neuromuscular activity, and its ratio to mean inspiratory flow was used as an index of the “effective impedance” of the respiratory system. Nine elderly male subjects [mean (SD) age: 68.1 (4.8) years] and nine young male subjects [mean (SD) age: 23.4 (1.3) years] performed an incremental exercise test on a bicycle ergometer. After a warm-up at 30 W, the power was increased by 30 W every 1.5 min until exhaustion. Our results showed that at maximal exercise, power output, breathing pattern, and respiratory exchange values, with the exception of tidal volume and the “effective impedance” of the respiratory system, were significantly higher in the young subjects. The power output and oxygen consumption values at the anaerobic threshold were also significantly higher in the young men. At the same power output, the elderly subjects showed significantly higher values for minute ventilation, respiratory equivalents for oxygen uptake and carbon dioxide output (CO₂), mean inspiratory flow, occlusion pressure and lactate concentration than the young subjects. At the same CO₂ below the anaerobic threshold (0.5, 0.75, 1.00 and 1.25 l · min⁻¹), minute ventilation and lactate concentration were also significantly higher in the elderly subjects. We observed a significantly higher minute ventilation at CO₂ values of 0.5, 0.75, 1.00 (P < 0.001) and 1.25 l · min⁻¹ (P < 0.05) in the elderly men, and a significantly higher lactate concentration at CO₂ values of 1.00 (P < 0.05) and 1.25 l · min⁻¹ (P < 0.01). In conclusion, the ventilatory response in elderly subjects is elevated in comparison with that in young subjects, both below and above the anaerobic threshold. This study demonstrates for the first time that this ventilatory increase, both below and above the threshold, is partly due to an increased lactate concentration. Received: 30 March 1999 / Accepted: 24 June 1999