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.     

Extracellular pH defense against lactic acid in untrained and trained altitude residents

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Δ) in lactic acid ([La]), [HCO₃ ⁻], pH and PCO₂ in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (β _nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃ ⁻] · ΔpH⁻¹) amounted to 40 ± 2 (SEM) and 28 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.01). During recovery β _nbi decreased to 20 (UT) and 16 (TR) mmol l⁻¹ (P < 0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Δ[La]. β _bi amounted to 37–41 mmol l⁻¹ being lower than at sea level. The large exercise β _nbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower β _nbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders β _nbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO₃ ⁻]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.     

In vivo 4-androstene-3,17-dione and 4-androstene-3β,17β-diol supplementation in young men

To determine if known androgenic hormone precursors for testosterone in the androgen pathway would be readily transformed to testosterone, eight male subjects [mean age 23.8 (SEM 3) years, bodymass 83.1 (SEM 8.7) kg, height 175.6 (SEM 8.5) cm] underwent a randomized, double-blind, cross-over, placebo-controlled oral treatment with 200 mg of 4-androstene-3,17-dione (Δ4), 4-androstene-3β,17β-diol (Δ4Diol), and placebo (PL). The periods of study were separated by 7 days of washout. Blood was drawn at baseline and subsequently every 30 min for 90 min after treatment. Analysis revealed mean area-under-the-curve (AUC) serum Δ4 concentrations to be higher during Δ4 treatment [2177 (SEM 100) nmol · l⁻¹] than Δ4Diol [900 (SEM 96) nmol · l⁻¹] or PL [484 (SEM 82) nmol · l⁻¹; P < 0.0001]. The Δ4 treatment also revealed a significant effect on total testosterone with a mean AUC [1632.5 (SEM 121) nmol · l⁻¹] that was greater than PL [1418.5 (SEM 131) nmol · l⁻¹; P < 0.05] but not significantly different from those observed after Δ4Diol treatment [1602.9 (SEM 119) nmol · l⁻¹; P = 0.77]. Free testosterone concentrations followed a similar pattern where mean AUC for the Δ4 treatment [6114.0 (SEM 600) pmol · l⁻¹] was greater than after PL [4974.6 (SEM 565) pmol · l⁻¹; P < 0.06] but not significantly different from those observed after Δ4Diol [5632.0 (SEM 389) pmol · l⁻¹; P = 0.48]. The appearance and apparent conversion to total and free testosterone over 90 min was stronger for the Δ4 treatment (r = 0.91, P < 0.045) than for Δ4Diol treatment (r = 0.69, NS) and negatively correlated for PL (r = −0.90, P < 0.02). These results would suggest that Δ4, and perhaps Δ4Diol, taken by month are capable of producing in vivo increases in testosterone concentrations in apparently healthy young men as has already been observed in women after treatment with Δ4. Accepted: 26 August 1999     

The effects of 3000-m swimming on subsequent 3-h cycling performance: implications for ultraendurance triathletes

The purpose of this study was to examine the physiological effects of 3000-m swimming on subsequent 3-h cycling time trial performance in ultraendurance triathletes. Eight highly trained ultraendurance triathletes [mean (SEM) age 34 (2) years, body fat 12.5 (0.8)%, maximum oxygen consumption 63.2 (2.1) ml · kg⁻¹ · min⁻¹] completed two randomly assigned trials 1 week apart. The swim/bike trial (SB) involved 3000 m of swimming [min:s 52:28 (1:48)] immediately followed by a 3-h cycling performance at a self-selected time-trial pace. The control trial (CON) consisted of an identical 3-h cycling time trial but without prior swimming. Subjects consumed an 8% carbohydrate (CHO)/electrolyte beverage during both trials at the rate of 60 g CHO · h⁻¹ and 1 l · h⁻¹. No significant differences were evident between CON and SB on the dependent measures (CON vs SB): power output [W˙, 222 (14) W vs 212 (13) W], heart rate [f _c, 147 (5) beats · min⁻¹ vs 143 (4) beats · min⁻¹; %f _cmax 80.0 (1.6)% vs 78.4 (1.5)%], oxygen uptake [3.10 (0.12) l · min⁻¹ vs 2.97 (0.15) l · min⁻¹], minute ventilation [82.5 (4.4) l · min⁻¹ vs 77.3 (3.7) l · min⁻¹], rating of perceived exertion [14.6 (0.4) vs 14.0 (0.1)], blood lactate [6.1 (0.5) mmol · l⁻¹ vs 4.8 (0.5) mmol · l⁻¹], and blood glucose [5.0 (0.2) mmol · l⁻¹ vs 5.3 (0.1) mmol · l⁻¹; all non-significant at the P > 0.05 level]. However, the CON respiratory exchange ratio was significantly greater than for SB [0.91 (0.01) vs 0.89 (0.01); P < 0.05], suggesting that the SB trial required a greater reliance on lipid as a fuel substrate. Hence, the main finding in the present study was that 3000 m of swimming had no significant performance effect (in terms of W˙) on subsequent 3-h cycling performance in ultraendurance triathletes. Accepted: 2 March 2000     

Causes of differences in exercise-induced changes of base excess and blood lactate

It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H⁺ than La⁻ leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid–base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (−ΔABE) was 2.2 ± 0.5 (SEM) mmol l⁻¹ larger than the increase of [La]_blood at exhaustion, and the difference rose to 4.8 ± 0.5 mmol l⁻¹ during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (Δ[La]_if+blood) during exercise and only slightly larger during recovery. The discrepancy between −ΔABE and Δ[La]_blood mainly results from the Donnan effect hindering the rise of [La]_erythrocyte to equal values like [La]_plasma. The changing Donnan effect during acidosis causes that Cl⁻ from the interstitial fluid enter plasma and erythrocytes in exchange for HCO₃⁻. A corresponding amount of La⁻ remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to Δ[La]_blood instead to Δ[La]_if+blood. When performing correct comparisons and considering Cl⁻/HCO₃⁻ exchange between erythrocytes and extracellular fluid, neither the use of ΔABE nor of ΔSBE provides evidence for differences in H⁺ and La⁻ transport across the tissue cell membranes.     

Physiological and metabolic responses of female games and endurance athletes to prolonged, intermittent, high-intensity running at 30° and 16°C ambient temperatures

Eight female games players (GP) and eight female endurance athletes (EA) ran intermittently at high-intensity and for prolonged periods in hot (30°C) and moderate (16°C) ambient temperatures. The subjects performed a two-part (A, B) test based on repeated 20-m shuttle runs. Part A comprised 60 m of walking, a maximal 15-m sprint, 60 m of cruising (90% maximal oxygen uptake, V˙O_2max) and 60 m of jogging (45% V˙O_2max) repeated for 75 min with a 3-min rest every 15 min. Part B involved an exercise and rest pattern of 60-s running at 100% V˙O_2max and 60-s rest which was continued until fatigue. Although the GP and EA did not respond differently in terms of distances completed, performance was 25 (SEM 4)% less (main effect trial, P < 0.01) in the hot (HT) compared with the moderate trial (MT). Sprints of 15 m took longer to complete in the heat (main effect, trial, P < 0.01), and sprint performance declined during HT but not MT (interaction, trial × time, P < 0.01). A very high correlation was found between the rate of rise in rectal temperature in HT and the distance completed [GP, r =−0.94, P < 0.01; EA (n = 7), r = −0.93, P < 0.01]. Blood lactate [La⁻ ]_b and plasma ammonia [NH₃]_p1 concentrations were higher for GP than EA, but were similar in HT and MT [La⁻ ]_b, HT: GP vs EA, 8.0 (SEM 0.9) vs 4.9 (SEM 1.1) mmol · l⁻¹; MT: GP vs EA, 8.0 (SEM 1.3) vs 4.4 (SEM 1.2) mmol · l⁻¹; interaction, group × time, P < 0.01; [NH₃]_p1, HT: GP vs EA, 70.1 (SEM 12.7) vs 43.2 (SEM 6.1) mmol · l⁻¹; MT: GP vs EA, 76.8 (SEM 8.8) vs 32.5 (SEM 3.8) μmol · l⁻¹; interaction, group × time, P < 0.01. Ad libitum water consumption was higher in HT [HT: GP vs EA, 18.9 (SEM 2.9) vs 13.5 (SEM 1.7) ml · kg⁻¹ · h⁻¹; MT: GP vs EA, 12.7 (SEM 3.7) vs 8.5 (SEM 1.5) ml · kg⁻¹ · h⁻¹; main effect, group, n.s.; main effect, trial, P < 0.01]. These results would suggest that elevated body temperature is probably the key factor limiting performance of prolonged, intermittent, high-intensity running when the ambient temperature is high, but not because of its effect on the metabolic responses to exercise. Accepted: 19 July 1999     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

An improved estimation of mean body temperature using combined direct calorimetry and thermometry

The conventional method used to estimate the change in mean body temperature (dMBT) is by taking X% of a body core temperature and (1−X)% of weighted mean skin temperature, the value of X being dependent upon ambient temperature. This technique is used widely, despite opposition from calorimetrists. In the present paper we attempt to provide a better method. Minute-by-minute changes in dMBT, as assessed using calorimetry, and 21 (20 if esophageal temperature was unavailable) various regional temperatures (dRBTs), as assessed using thermometry, including 6 subcutaneous measures, were collected from 7 young male adults at 6 calorimeter temperatures. Since a calorimeter measures only changes in heat storage, which can be converted to dMBT, all body temperatures are expressed as changes from the reasonably constant pre-exposure temperatures. The following three aspects were investigated. (1) The prediction of dMBT from the 21 (or 20) dRBTs with multi-linear regression analysis (MLR). This yields two results, model A with rectal temperature (dT _re) alone, and model B with dT _re and esophageal temperature (dT _es). (2) The prediction of dMBT from dT _re with or without dT _es and 13 skin surface temperatures combined to one weighted mean skin temperature (dTˉ _sk), using MLR. This results in models C and D. Six more models (E–J) were added, representing the above two sets in various combinations with four factors. (3) The conventional method calculated with four values for X. Model A predicted better than 0.3 °C in 70% of the cases. Model I was the best amongst the models with 13 weighted skin temperatures (better than 0.3 °C in 60% of the cases). The conventional method was erratic. Accepted: 14 January 2000     

Muscle glycogen resynthesis rate in humans after supplementation of drinks containing carbohydrates with low and high molecular masses

The rate of muscle glycogen synthesis during 2 and 4 h of recovery after depletion by exercise was studied using two energy equivalent carbohydrate drinks, one containing a polyglucoside with a mean molecular mass of 500 000–700 000 (C drink), and one containing monomers and oligomers of glucose with a mean molecular mass of approximately 500 (G drink). The osmolality was 84 and 350 mosmol · l⁻¹, respectively. A group of 13 healthy well-trained men ingested the drinks after glycogen depleting exercise, one drink at each test occasion. The total amount of carbohydrates consumed was 300 g (4.2 g · kg⁻¹) body mass given as 75 g in 500 ml water immediately after exercise and again 30, 60 ad 90-min post exercise. Blood glucose and insulin concentrations were recorded at rest and every 30 min throughout the 4-h recovery period. Muscle biopsies were obtained at the end of exercise and after 2 and 4 h of recovery. Mean muscle glycogen contents after exercise were 52.9 (SD 27.4) mmol glycosyl units · kg⁻¹ (dry mass) in the C group and 58.3 (SD 35.4) mmol glycosyl units · kg⁻¹ (dry mass) in the G group. Mean glycogen synthesis rate was significantly higher during the initial 2 h for the C drink compared to the G drink: 50.2 (SD 13.7) mmol · kg⁻¹ (dry mass) · h⁻¹ in the C group and 29.9 (SD 12.5) mmol · kg⁻¹ (dry mass) · h⁻¹ in the G group. During the last 2 h the mean synthesis rate was 18.8 (SD 33.3) and 23.3 (SD 22.4) mmol · kg⁻¹ (dry mass) · h⁻¹ in the C and G group, respectively (n.s.). Mean blood glucose and insulin concentrations did not differ between the two drinks. Our data indicted that the osmolality of the carbohydrate drink may influence the rate of resynthesis of glycogen in muscle after its depletion by exercise. Accepted: 9 September 1999     

Blood lactate response to overtraining in male endurance athletes

Many physiological markers vary similarly during training and overtraining. This is the case for the blood lactate concentration ([La⁻]_b), since a right shift of the lactate curve is to be expected in both conditions. We examined the possibility of separating the changes in training from those of overtraining by dividing [La⁻]_b by the rating of perceived exertion ([La⁻]_b/RPE) or by converting [La⁻]_b into a percentage of the peak blood lactate concentration ([La⁻]_b,peak). Ten experienced endurance athletes increased their usual amount of training by 100% within 4 weeks. An incremental test and a time trial were performed before (baseline) and after this period of overtraining, and after 2 weeks of recovery (REC). The [La⁻]_b and RPE were measured during the recovery of each stage of the incremental test. We diagnosed overtraining in seven athletes, using both physiological and psychological criteria. We found a decrease in mean [La⁻]_b,peak from baseline to REC [9.64 (SD 1.17), 8.16 (SD 1.31) and 7.69 (SD 1.84) mmol · l⁻¹, for the three tests, respectively; P < 0.05] and a right shift of the lactate curve. Above 90% of maximal aerobic speed (MAS) there was a decrease of mean [La⁻]_b/RPE from baseline to REC [at 100% of MAS of 105.41 (SD 17.48), 84.61 (SD 12.56) and 81.03 (SD 22.64) arbitrary units, in the three tests, respectively; P < 0.05), but no difference in RPE, its variability accounting for less than 25% of the variability of [La⁻]_b/RPE (r=0.49). Consequently, [La⁻]_b/RPE provides little additional information compared to [La⁻]_b alone. Expressing [La⁻]_b as a %[La⁻]_b,peak resulted in a suppression of the right shift of the lactate curve, suggesting it was primarily the consequence of a decreased production of lactate by the muscle. Since the right shift of the curve induced by optimal training is a result of improved lactate utilization, the main difference between the two conditions is the decrease of [La⁻]_b,peak during overtraining. We propose retaining it as a marker of overtraining for long duration events, and repeating its measurement after a sufficient period of rest to make the distinction with overreaching. Accepted: 26 September 2000     

Gender differences in sweat lactate

Sweat rate may affect sweat lactate concentration. The current study examined potential gender differences in sweat lactate concentrations because of varying sweat rates. Males (n=6) and females (n=6) of similar age, percentage body fat, and maximal oxygen consumption (VO_2max) completed constant load (CON) cycling (30 min – approximately 40% VO_2max) and interval cycling (INT) (15 1-min intervals each separated by 1 min of rest) trials at 32 (1) °C wet bulb globe temperature (WBGT). Trials were preceded by 15 min of warm-up (0.5 kp, 60 rpms) and followed by 15 min of rest. Blood and sweat samples were collected at 15, 25, 35, 45, and 60 min during each trial. Total body water loss was used to calculate sweat rate. Blood lactate concentrations (CON ≅ 2 mmol · l⁻¹, INT ≅ 6 mmol · l⁻¹) and sweat lactate concentrations (CON and INT ≅ 12 mmol · l⁻¹) were not significantly different (P > 0.05) at any time between genders for CON or INT. Overall sweat rates (ml · h⁻¹) were not significantly different (P > 0.05) between trials but were significantly greater (P ≤ 0.05) for males than for females for CON [779.7 (292.6) versus 450.3 (84.6) ml · h⁻¹] and INT [798.0 (268.3) versus 503.0 (41.4) ml · h⁻¹]. However, correcting for surface area diminished the difference [CON: 390.7 (134.4) versus 277.7 (44.4) ml · h⁻¹, INT: 401.5 (124.1) versus 310.6 (23.4) ml · h⁻¹ (P ≤ 0.07)]. Estimated total lactate secretion was significantly greater (P ≤ 0.05) in males for CON and INT. Results suggest that sweat rate differences do not affect sweat lactate concentrations between genders. Accepted: 7 February 2000     

Measurement and prediction of peak shivering intensity in humans

Prediction equations of shivering metabolism are critical to the development of models of thermoregulation during cold exposure. Although the intensity of maximal shivering has not yet been predicted, a peak shivering metabolic rate (Shiv_peak) of five times the resting metabolic rate has been reported. A group of 15 subjects (including 4 women) [mean age 24.7 (SD 6) years, mean body mass 72.1 (SD 12) kg, mean height 1.76 (SD 0.1) m, mean body fat 22.3 (SD 7)% and mean maximal oxygen uptake (V˙O_2max) 53.2 (SD 9) ml O₂ · kg⁻¹ · min⁻¹] participated in the present study to measure and predict Shiv_peak. The subjects were initially immersed in water at 8°C for up to 70 min. Water temperature was then gradually increased at 0.8 °C · min⁻¹ to a value of 20 °C, which it was expected would increase shivering heat production based on the knowledge that peripheral cold receptors fire maximally at approximately this temperature. This, in combination with the relatively low core temperature at the time this water temperature was reached, was hypothesized would stimulate Shiv_peak. Prior to warming the water from 8 to 20 °C, the oxygen consumption was 15.1 (SD 5.5) ml · kg⁻¹ · min⁻¹ at core temperatures of approximately 35 °C. After the water temperature had risen to 20 °C, the observed Shiv_peak was 22.1 (SD 4.2) ml O₂ · kg⁻¹ · min⁻¹ at core and mean skin temperatures of 35.2 (SD 0.9) and 22.1 (SD 2.2) °C, respectively. The Shiv_peak corresponded to 4.9 (SD 0.8) times the resting metabolism and 41.7 (SD 5.1)% of V˙O_2max. The best fit equation predicting Shiv_peak was Shiv_peak (ml O₂ · kg⁻¹ · min⁻¹)=30.5 + 0.348 ×V˙O_2max (ml O₂ · kg⁻¹ · min⁻¹) − 0.909 × body mass index (kg · m⁻²) − 0.233 × age (years); (P=0.0001; r ²=0.872). Accepted: 7 September 2000     

Effects of heavy resistance training on maximal and explosive force production, endurance and serum hormones in adolescent handball players

To determine the effects of 6-weeks of heavy-resistance training on physical fitness and serum hormone status in adolescents (range 14–16 years old) 19 male handball players were divided into two different groups: a handball training group (NST, n = 10), and a handball and heavy-resistance strength training group (ST, n = 9). A third group of 4 handball goalkeepers of similar age served as a control group (C, n = 4). After the 6-week training period, the ST group showed an improvement in maximal dynamic strength of the leg extensors (12.2%; P < 0.01) and the upper extremity muscles (23%; P < 0.01), while no changes were observed in the NST and C groups. Similar differences were observed in the maximal isometric unilateral leg extension forces. The height of the vertical jump increased in the NST group from 29.5 (SD 4) cm to 31.4 (SD 5) cm (P < 0.05) while no changes were observed in the ST and C groups. A significant increase was observed in the ST group in the velocity of the throwing test [from 71.7 (SD 7) km · h⁻¹ to 74.0 (SD 7) km · h⁻¹; P < 0.001] during the 6-week period while no changes were observed in the NST and C groups. During a submaximal endurance test running at 11 km · h⁻¹, a significant decrease in blood lactate concentration occurred in the NST group [from 3.3 (SD 0.9) mmol · l⁻¹ to 2.4 (SD 0.8) mmol · l⁻¹; P < 0.01] during the experiment, while no change was observed in the ST or C groups. Finally, a significant increase (P < 0.01) was noted in the testosterone:cortisol ratio in the C group, while the increase in the NST group approached statistical significance (P < 0.08) and no changes in this ratio occurred in the ST group. The present findings suggested that the addition of 6-weeks of heavy resistance training to the handball training resulted in gains in maximal strength and throwing velocity but it compromised gains in leg explosive force production and endurance running. The tendency for a compromised testosterone:cortisol ratio observed in the ST group could have been associated with a state of overreaching or overtraining. Accepted: 22 April 1999     

Cultured ruminal epithelial cells express a large-conductance channel permeable to chloride, bicarbonate, and acetate

The absorption of short-chain fatty acids (SCFA) from the rumen requires efficient mechanisms for both apical uptake and basolateral extrusion. Previous studies suggest that the rumen expresses a basolateral chloride conductance that might be permeable to SCFA. In order to characterize this conductance in more detail, isolated cultured ruminal epithelial cells were studied with the patch-clamp technique, revealing a whole-cell conductance with p(Cl⁻) ≈ p(NO₃ ⁻) > p(HCO₃ ⁻) > p(acetate⁻) > p(gluconate⁻). Currents could be blocked by diisothiocyanato-stilbene-2,2′-disulfonic acid (1 mmol l⁻¹ > 100 μmol l⁻¹), 5-nitro-2-(3-phenylpropyl-amino)benzoic acid (50 μmol l⁻¹), niflumic acid (100 μmol l⁻¹), and p-chloromercuribenzoate (1 mmol l⁻¹). Single-channel conductance was 350 ± 7 pS for chloride and 142 ± 7 pS for acetate. Open probability could be fitted with a three-state gating model. We propose a role for this channel in mediating the permeation of chloride, bicarbonate, and acetate across the basolateral membrane of the ruminal epithelium.     

Effects of gradient and load carried on human haemodynamic responses during treadmill walking

This study examined the effects of different loads carried and gradients, on haemodynamic and cardiovascular responses during 45 min of treadmill walking. A group of 20 male endurance-trained athletes [mean maximal oxygen uptake 61.4 (SD 4) ml · kg⁻¹ · min⁻¹] volunteered for this study. The subjects took part in three separate trials. The first involved a backpack weighing 25 kg , the second a 35 kg backpack, and the third trial, unladen, while walking on a treadmill at a speed of 5 km · h⁻¹. The subjects began walking on the treadmill with the randomized load at 0% gradient. After 15 min, the gradient was increased by 5% every 15 min for a total of 45 min. The order of the loads carried was randomized among subjects. No significant differences were noted for all the variables measured attributable to loads between 25 kg and 35 kg. However, significant (P < 0.05) differences were seen for all variables each time the gradient was increased. Cardiac output increased from 11.4 (SD 0.6) l · min⁻¹ at 0% to 13.6 (SD 0.8) l · min⁻¹ at 5% and to 17.6 (SD 1.3) l · min⁻¹ at 10% carrying the 35 kg load. Similarly, lactic acid concentrations in the blood increased from 2.8 (SD 0.2) to 3.1 (SD 0.6) and to 5.3 (SD 1.3) mmol · l⁻¹, respectively. Similar changes were observed for all variables while carrying the 25 kg load. In addition, steady states in oxygen uptake and other physiological variables were obtained throughout the course of the tests. These data suggest that during isodynamic exercise, one of the main factors determining metabolic and haemodynamic responses will be the change in gradient and to a lesser extent, the mass of the load carried. Accepted: 12 May 2000     

Effect of creatine supplementation on metabolism and performance in humans during intermittent sprint cycling

This double blind study investigated the effect of oral creatine supplementation (CrS) on 4 × 20 s of maximal sprinting on an air-braked cycle ergometer. Each sprint was separated by 20 s of recovery. A group of 16 triathletes [mean age 26.6 (SD 5.1) years. mean body mass 77.0 (SD 5.8) kg, mean body fat 12.9 (SD 4.6)%, maximal oxygen uptake 4.86 (SD 0.7) l · min⁻¹] performed an initial 4 × 20 s trial after a muscle biopsy sample had been taken at rest. The subjects were then matched on their total intramuscular creatine content (TCr) before being randomly assigned to groups to take by mouth either a creatine supplement (CRE) or a placebo (CON) before a second 4 × 20 s trial. A muscle biopsy sample was also taken immediately before this second trial. The CrS of 100 g comprised 4 × 5 g for 5 days. The initial mean TCr were 112.5 (SD 8.7) and 112.5 (SD 10.7) mmol · kg⁻¹ dry mass for CRE and CON, respectively. After creatine loading and placebo ingestion respectively, CRE [128.7 (SD 11.8) mmol · kg⁻¹ dry mass] had a greater (P=0.01) TCr than CON [112.0 (SD 10.0) mmol · kg⁻¹ dry mass]. While the increase in free creatine for CRE was statistically significant (P=0.034), this was not so for the changes in phosphocreatine content [trial 1: 75.7 (SD 6.9), trial 2: 84.7 (SD 11.0) mmol · kg⁻¹ dry mass, P=0.091]. There were no significant differences between CRE and CON for citrate synthase activity (P=0.163). There was a tendency towards improved performance in terms of 1 s peak power (in watts P=0.07; in watts per kilogram P=0.05), 5 s peak power (in watts P=0.08) and fatigue index (P=0.08) after CrS for sprint 1 of the second trial. However, there was no improvement for mean power (in watts P=0.15; in watts per kilogram P=0.1) in sprint 1 or for any performance values in subsequent sprints. Our results suggest that, while CrS elevates the intramuscular stores of free creatine, this does not have an ergogenic effect on 4 × 20 s all-out cycle sprints with intervening 20-s rest periods. Accepted: 2 October 2000     

Involvement of muscarinic cholinergic and α2-adrenergic mechanisms in growth hormone secretion during exercise in humans

The purpose of this study was to examine the role of muscarinic cholinergic and α₂-adrenergic mechanisms in growth hormone (GH) secretion during exercise in humans. The GH responses induced during moderate-intensity exercise (using a cycle ergometer at 60% maximal oxygen uptake, V˙O_2max, for 30 min) without treatment (control) and after the administration of a muscarinic cholinergic antagonist (atropine 1 mg) or after an α₂-adrenergic antagonist (yohimbine 15 mg) were compared in seven healthy men. Although, serum GH concentration had increased significantly after exercise in the control experiment [mean peak GH concentration 52.64 (SEM 18.60) ng · ml⁻¹], the increase was suppressed by the administration of either atropine [mean peak GH concentration 8.64 (SEM 7.47)  ng · ml⁻¹] or yohimbine [mean peak GH concentration 17.50 (SEM 7.89) ng · ml⁻¹]. The area under the curve of serum GH concentration against time was significantly lower in the experiment using these drugs [with atropine, mean area 458 (SEM 409) ng · ml⁻¹ · min], with yohimbine mean area 946 (SEM 435) ng · ml⁻¹ · min] than in the control experiment [mean area 3135 (SEM 1098) ng · ml⁻¹ · min]. These results suggest that muscarinic cholinergic and α₂-adrenergic mechanisms are involved in GH secretion during exercise in humans. Accepted: 9 March 2000     

Haematological and serum biochemical profile of the upside-down catfish, Synodontis membranacea Geoffroy Saint Hilaire from Jebba Lake, Nigeria

Haematological and serum biochemical studies of natural population of Synodontis membranacea from Jebba Lake, North Central Nigeria were investigated in order to establish their mean and reference values. Bi-monthly collection of 1,408 live fish samples was carried out between April 2002 and March 2004, using gill nets of various mesh sizes ranging from 5.08 to 10.16 cm. The mean baseline value established for species-specific haematological and serum biochemical parameters were red blood cell (RBC) 3.83 ± 1.49 × 10¹² l⁻¹, haemoglobin (HB) 8.38 ± 1.96 g dl⁻¹, and packed cell volume (PCV) 25.65 ± 5.89%; mean cell volume 78.25 ± 37.90 fl; mean cell haemoglobin (MCH) 33.04 ± 12.50 pg; mean cell haemoglobin concentration 26.53 ± 15.18 g dl⁻¹; white blood cell (WBC) 315.65 ± 95.37 × 10⁻⁹; agranulocytes (Agr) 82.07 ± 11.38%; monocytes (Mon) 6.37 ± 3.01%; lymphocytes (Lym) 76.49 ± 10.81%; granulocytes (Gran) 40.28 ± 17.48%; neutrophils (Neut) 24.42 ± 10.68%; eosinophils (Eos) 16.14 ± 8.25%; basophils 0.09 ± 0.04%; protein 40.19 ± 7.45 g l⁻¹; albumin 19.78 ± 5.67 g l⁻¹; creatinine 49.71 ± 16.15 μmol l⁻¹; urea 3.05 ± 0.67 nmol l⁻¹; uric acid 0.76 ± 0.33 nmol l⁻¹; glucose 4.24 ± 1.74 mmol l⁻¹; cholesterol 8.46 ± 2.27 mmol l⁻¹; calcium 2.35 ± 0.94 mmol l⁻¹; potassium 13.36 ± 4.45 mmol l⁻¹; sodium 139.39 ± 23.19 mmol l⁻¹; alanine aminotransferase (ALT) 11.79 ± 2.67 U l⁻¹; aspartate aminotransferase 16.80 ± 4.73 U l⁻¹; and alkaline phosphatase 63.01 ± 20.44 U l⁻¹. Only three of these parameters (i.e. neutrophil, glucose and potassium) differed significantly (P > 0.05) on gender basis. Pearson’s correlation coefficients indicated significant relationship of standard length and total weight with RBC, PCV, HB, WBC, Agr, Mon, Lym, Gran, Neut, Eos, sodium, and ALT only. The study has provided baseline haematological and biochemical data for use in health monitoring and productivity of S. membranacea, which would be of great value for future comparative surveys in this era of increased fish culture in Nigeria.     

Plasma catecholamine responses and neural adaptation during short-term resistance training

Low exercise-induced plasma adrenaline (A) responses have been reported in resistance-trained individuals. In the study reported here, we investigated the interaction between strength gain and neural adaptation of the muscles, and the plasma A response in eight healthy men during a short-term resistance-training period. The subjects performed 5 resistance exercises (E1–E5), consisting of 6 sets of 12 bilateral leg extensions performed at a 50% load, and with 2 days rest in between. Average electromyographic (EMG) signal amplitude was recorded before and after the exercises, from the knee extensor muscles in isometric maximal voluntary contraction (MVC) as well as during the exercises (aEMG_max and aEMG_exerc, respectively). Total oxygen consumed during the exercises (V˙O_2tot) was also measured. All of the exercises were exhaustive and caused significant decreases in MVC (34–36%, P < 0.001). As expected, the concentric one-repetition maximum (1-RM), MVC and aEMG_max were all higher before the last exercise (E5) than before the first exercise (E1; 7, 9 and 19%, respectively, P < 0.05). In addition, in E5 the aEMG_exerc:load and V˙O_2tot:load ratios were lower than in E1 (−5 and −14%, P < 0.05), indicating enhanced efficiency of the muscle contractions, However, the post-exercise plasma noradrenaline (NA) and A were not different in these two exercises [mean (SD) 10.2 (3.8) nmol · l⁻¹ vs 11.3 (6.0) nmol · l⁻¹, ns, and 1.2 (1.0) nmol · l⁻¹ vs 1.9 (1.1) nmol · l⁻¹, ns, respectively]. However, although NA increased similarly in every exercise (P < 0.01), the increase in A reached the level of statistical significance only in E1 (P < 0.05). The post-exercise A was also already lower in E2 [0.7 (0.7) nmol · l⁻¹, P < 0.05) than in E1, despite the higher post-exercise blood lactate concentration than in the other exercises [9.4 (1.1) mmol · l⁻¹, P < 0.05]. Thus, the results suggest that the observed attenuation in the A response can not be explained by reduced exercise-induced strain due to the strength gain and neural adaptation of the muscles. Correlation analysis actually revealed that those individuals who had the highest strength gain during the training period even tended to have an increased post-exercise A concentration in the last exercise as compared to first one (r=0.76, P < 0.05). Accepted: 10 February 2000     

Cortisol and testosterone concentrations in wheelchair athletes during submaximal wheelchair ergometry

It is yet unknown how upper body exercise combined with high ambient temperatures affects plasma testosterone and cortisol concentrations and furthermore, how these hormones respond to exercise in people suffering spinal cord injuries. The purpose of this study was to characterize plasma testosterone and cortisol responses to upper body exercise in wheelchair athletes (WA) compared to able-bodied individuals (AB) at two ambient temperatures. Four WA [mean age 36 (SEM 13) years, mean body mass 66.9 (SEM 11.8) kg, injury level T₇–T₁₁], matched with five AB [mean age 33.4 (SEM 8.9) years, mean body mass 72.5 (SEM 13.1) kg] exercised (cross-over design) for 20 min on a wheelchair ergometer (0.03 kg resistance · kg⁻¹ body mass) at 25 °C and 32 °C. Blood samples were obtained before (PRE), at min 10 (MID), and min 20 (END) of exercise. No differences were found between results obtained at 25 °C and 32 °C for any physiological variable studied and therefore these data were combined. Pre-exercise testosterone concentration was lower (P < 0.05) in WA [18.3 (SEM 0.9) nmol · l⁻¹] compared to AB [21.9 (SEM 3.6) nmol · l⁻¹], and increased PRE to END only in WA. Cortisol concentrations were similar between groups before and during exercise, despite higher rectal temperatures in WA compared to AB, at MID [37.21 (SEM  0.14) and 37.02 (SEM  0.08)°C, respectively] and END [37.36 (SEM 0.16) and 37.19 (SEM 0.10)°C, respectively]. Plasma norepinephrine responses were similar between groups. In conclusion, there were no differences in plasma cortisol concentrations, which may have been due to the low relative exercise intensities employed. The greater exercise response in WA for plasma testosterone should be confirmed on a larger population. It could have been the result of the lower plasma testosterone concentrations at rest in our group. Accepted: 4 September 2000