Effect of NaHCO3 on lactate kinetics in forearm muscles during leg exercise in man

We investigated NaHCO3 infusion effects on plasma lactate removal by forearm muscles and performance during intensive leg exercise. Seven subjects performed the force-velocity (FV) test with placebo and NaHCO3 (2 mEq.min-1) with a double-blind crossover protocol. Blood samples for arterial ([LA]A) and venous ([LA]V) lactate determinations were taken 1) at rest before infusion, and 2, 6, 10, 14, 18, and 22 min following its start; and 2) at the end of each exercise bout. The arteriovenous difference ([LA]A-V) was determined for each sampling. NaHCO3 significantly increased arterial bicarbonate concentration and pH during rest (P < 0.001; P < 0.001) and the FV test (P < 0.001; P < 0.05). During the test, [LA]A and [LA]V were significantly higher with NaHCO3 (P < 0.05, P < 0.001). At test onset, [LA]A-V became positive and increased until the braking force of 6 kg, with NaHCO3 and placebo, with values significantly lower for NaHCO3 (P < 0.001). Peak anaerobic power (Wanae, peak) and the corresponding braking force (Fmax) were also determined. Fmax was significantly increased with NaHCO3 (P < 0.001). In conclusion, the increasing rise in [LA]A and [LA]V induced by NaHCO3 may be partly explained by a decreased rate of lactate uptake by forearm skeletal muscles. NaHCO3 did not improve Wanae, peak, but improved Fmax, thus increasing FV duration.     

Prediction of blood lactate accumulation from excess CO2 output during constant exercise

To determine the predictability of blood lactate accumulation from excess CO2 output derived from bicarbonate buffering of lactic acid during constant exercise, eight normal active volunteers were studied during three stages of constant exercise on a cycle ergometer. Three work rates consisted of 100% (stage I), 120% (stage II) and 150% (stage III) of each subject's anaerobic threshold (AT), each of which was lasted for 4 min. Excess CO2 output (Ex CO2, ml) at each stage of constant exercise was estimated form the integral of difference between total VCO2 and aerobic VCO2 (from regression line for VCO2 and VO2 at exercise intensities below the AT obtained in incremental exercise test). Ex CO2 per body mass (Ex CO2-mass-1) was increased progressively with blood lactate (La) accumulation from rest to each stage of constant exercise. Mean values (+/-SD) in the measured La accumulation (delta La,measured) and predicted La accumulation (delta La,predicted) at three stages of constant exercise were 1.82 +/- 0.83 vs 3.19 +/- 1.70 for stage 1, 5.58 +/- 3.47 vs 7.09 +/- 3.28 for stage II and 12.19 +/- 2.36 vs 12.74 +/- 1.83 mmol.l-1 for stage III, respectively. There was a significant difference between delta La,measured and delta La,predicted at stage I (p < 0.05), but no significant differences between these two variables at stage II and III. The averaged difference from delta La,predicted to delta La,measured at stage III (0.55 mmol.l-1) showed a tendency to be smaller than stage I (1.38 mmol.l-1) and II (1.50 mmol.l-1). On the other hand, delta La,predicted was found to correlate very closely with delta La,measured (r = 0.954, P < 0.001, n = 20). The results of this study suggest that the changes of La accumulation could be predicted from excess CO2 output generated in constant exercises above the AT.     

Effects of exercise on fluid exchange and body composition in man during 14-day bed rest

To determine the cause of the body weight loss during bed rest (BR), fluid balance and anthropometric measurements were taken from seven men (19-21 yr) during three 2-wk BR periods which were separated by 3-wk ambulatory recovery periods. Caloric intake was 3,073 +/- 155 (SD) kcal/day. During two of the three BR periods they performed supine isotonic exercise at 68% of VO2max on the ergometer for 1 h/day; or supine isometric exercise at 21% of maximal leg extension force for 1 min followed by a 1-min rest for 1 h/day. No prescribed exercise was given during the other BR period. During BR, body weight decreased slightly with no exercise (-0.43 kg, NS), but decreased significantly (P less than 0.05) by -0.91 kg with isometric and by -1.77 kg with isotonic exercise. About one-third of the weight reduction with isotonic exercise was due to fat loss (-0.69 kg) and, the remainder, to loss of lean body mass (-0.98 kg). It is concluded that the reduction in body weight during bed rest has two major components: First, a loss of lean body mass caused by assumption of the horizontal body position that is independent of the metabolic rate. Second, a loss of body fat content that is proportional to the metabolic rate.     

Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?

OBJECTIVE: To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure. DESIGN: Muscle biopsy study. PATIENTS: Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1). RESULTS: Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure. CONCLUSIONS: It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.     

The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95 percent of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8) percent protein (Pro), 37.5 (2.2) percent fat (Fat) and 47.5 (2.1) percent carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3) percent Pro, 64.4 (1.5) percent Fat and 2.2 (0.4) percent CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO(3) or CaCO(3) (3.6 and 3.0 mmol*kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO(3). Blood pH, bicarbonate (HCO-(3)) and base excess (BE) were higher following NaHCO(3) ingestion after the normal diet than all of the other experimental conditions (P <0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P <0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO-(3); and BE were higher following the ingestion of NaHCO(3) irrespective of the pre-exercise diet (P <0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO(3) when compared to the low-CHO diets with either NaHCO(3) or placebo (P <0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.     

Muscle glycogen accumulation after endurance exercise in trained and untrained individuals

Muscle glycogen accumulation was determined in six trained cyclists (Trn) and six untrained subjects (UT) at 6 and either 48 or 72 h after 2 h of cycling exercise at approximately 75% peak O2 uptake (VO2 peak), which terminated with five 1-min sprints. Subjects ate 10 g carbohydrate . kg-1 . day-1 for 48-72 h postexercise. Muscle glycogen accumulation averaged 71 +/- 9 (SE) mmol/kg (Trn) and 31 +/- 9 mmol/kg (UT) during the first 6 h postexercise (P < 0.01) and 79 +/- 22 mmol/kg (Trn) and 60 +/- 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogen concentration was 164 +/- 21 mmol/kg (Trn) and 99 +/- 16 mmol/kg (UT) 48-72 h postexercise (P < 0.05). Muscle GLUT-4 content immediately postexercise was threefold higher in Trn than in UT (P < 0.05) and correlated with glycogen accumulation rates (r = 0.66, P < 0.05). Glycogen synthase in the active I form was 2.5 +/- 0.5, 3.3 +/- 0.5, and 1.0 +/- 0.3 micromol . g-1 . min-1 in Trn at 0, 6, and 48 or 72 h postexercise, respectively; corresponding values were 1.2 +/- 0.3, 2.7 +/- 0.5, and 1.6 +/- 0.3 micromol . g-1 . min-1 in UT (P < 0.05 at 0 h). Plasma insulin and plasma C-peptide area under the curve were lower in Trn than in UT over the first 6 h postexercise (P < 0.05). Plasma creatine kinase concentrations were 125 +/- 25 IU/l (Trn) and 91 +/- 9 IU/l (UT) preexercise and 112 +/- 14 IU/l (Trn) and 144 +/- 22 IU/l (UT; P < 0.05 vs. preexercise) at 48-72 h postexercise (normal: 30-200 IU/l). We conclude that endurance exercise training results in an increased ability to accumulate muscle glycogen after exercise.     

Cardiorespiratory drift during exercise in the horse

The purpose of the present study was to measure the time-course and degree of cardiovascular and respiratory 'drift' during constant submaximal exercise in the horse. One Thoroughbred and four Morgan mares were instrumented for simultaneous measurement of respiratory and blood gases which also enabled cardiac output (Q) to be calculated. Data were collected at rest, and at 10, 20 and 30 mins during a constant workload which elicited an initial exercising heart rate (HR) of 150 beats/min, and an approximate 15-fold increase in oxygen consumption (VO2). Significant cardiac and respiratory drift during exercise were observed over time so that ventilation increased from 750 +/- 58 to 910 +/- 49 litres/min (21 per cent increase) from the 10 to 30 min time-point (P < 0.05) and HR went from 154 +/- 4 to 173 +/- 9 beats/min (mean +/- se) over the same time period (P < 0.05). Q also rose from 142 +/- 5 to 177 +/- 17 litres/min (P < 0.05) during the same interval while stroke volume (SV) was maintained. Rectal temperature (TR) and mixed venous lactate (LA) also showed significant increases during exercise while PaO2 and PaCO2 remained constant. The results indicate a significant degree of cardiac and respiratory drift in the horse in response to strenuous submaximal exercise. At the constant exercise work rate chosen, a levelling off, or plateauing of the selected parameters of interest was not observed. Therefore if a true exercising 'steady-state' was achieved, it must have occurred very early in the exercise bout.     

Glucose kinetics during exercise in trained men

The effects of a novel bradycardic agent Zeneca ZM 227189 (4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) triazinium iodide) were tested on the inward rectifying properties of guinea-pig substantia nigra pas compacta (SNC) and guinea-pig olfactory cortical cells recorded in vitro. In SNC neurones, ZM 227189 (10-100 microM) produced a dose-dependent block of the slow anomalous rectifier; under voltage clamp, a clear reduction was seen in the amplitude of the slow inward current (Ih) relaxation evoked by negative voltage commands from a holding potential of -60 mV. ZM 227189 (50-100 microM) induced an irreversible block of the Ih current after 10-15 min exposure. A similar block of Ih was observed following application of 5 mM Cs+. ZM 227189 had little effect on other membrane properties. By contrast, in olfactory cortical neurones, ZM 227189 (100 microM) induced an increase in the input resistance (approximately 20%) and cell excitability, accompanied by a small (< 2 mV) hyperpolarization; these effects were also not reversible. Activation of the fast (K(+)-mediated) inward rectifier at negative membrane potentials remained unaffected. Lower concentrations (1-10 microM) of ZM 227189 had no obvious effect on cortical cell properties. Our data indicate that ZM 227189 is a potent and apparently selective blocker of Ih in substantia nigra neurones, but has no effect on the fast-type inward rectifier in olfactory cortical cells.     

Myocardial rupture during exercise ECG

We report a case of heart rupture in connection with a stress test performed nine days after an otherwise uncomplicated myocardial infarction. The Danish Association of Cardiologists recommend stress testing 5-20 days after myocardial infarction. We question whether this timing is appropriate considering the vulnerability of the myocardium at that time.     

Temperature regulation during exercise in water and air

Four healthy subjects were studied during exercise in water, using a swimming flume, and in air, on a stationary bicycle ergometer at mean skin temperatures of 30 and 33 degrees C, respectively. Measurements included rectal (Tre), esophageal (Tes), and mean skin (Ts) temperatures, metabolic energy liberation (M) and total heat production (H), maximal aerobic power output (Vo2 max), cardiac frequency and calculated peripheral tissue heat conductance (K). The results showed that for a given M and Ts, Tes and Tre were about 0.4 degree C lower and the K values were consistently higher in swimming than in bicycling. The intersubject variability in Tes and Tre was reduced by considering relative (expressed as %VO2max) rather than absolute work load, but the differences in the body temperatures between the two types of exercise remained. It was concluded that during exercise in water where the capacity for heat dissipation is increased, the body core temperature (Tc) is maintained at a lower level due to the higher forced convective and conductive heat transfer from the skin in water. This reduces the heat storage at the beginning of exercise compared with conditions in air. The lower Tc-Ts gradient for a given H in swimming, which results in higher K values implies a greater skin circulation than during cycling in air.     

Regulation of ventilatory capacity during exercise in asthmatics

In asthmatic and control subjects, we examined the changes in ventilatory capacity (VECap), end-expiratory lung volume (EELV), and degree of flow limitation during three types of exercise: 1) incremental, 2) constant load (50% of maximal exercise capacity; 36 min), and 3) interval (alternating between 60 and 40% of maximal exercise capacity; 6-min workloads for 36 min). The VECap and degree of flow limitation at rest and during the various stages of exercise were estimated by aligning the tidal breathing flow-volume (F-V) loops within the maximal expiratory F-V (MEFV) envelope using the measured EELV. In contrast to more usual estimates of VECap (i.e., maximal voluntary ventilation and forced expiratory volume in 1 s x 40), the calculated VECap depended on the existing bronchomotor tone, the lung volume at which the subjects breathed (i.e., EELV), and the tidal volume. During interval and constant-load exercise, asthmatic subjects experienced reduced ventilatory reserve, higher degrees of flow limitation, and had higher EELVs compared with nonasthmatic subjects. During interval exercise, the VECap of the asthmatic subjects increased and decreased with variations in minute ventilation, due in part to alterations in their MEFV curve as exercise intensity varied between 60 and 49% of maximal capacity. In conclusion, asthmatic subjects have a more variable VECap and reduced ventilatory reserve during exercise compared with nonasthmatic subjects. The variations in VECap are due in part to a more labile MEFV curve secondary to changes in bronchomotor tone. Asthmatics defend VECap and minimize flow limitation by increasing EELV.     

Expiratory flow limitation during exercise in competition cyclists

In some trained athletes, maximal exercise ventilation is believed to be constrained by expiratory flow limitation (FL). Using the negative expiratory pressure method, we assessed whether FL was reached during a progressive maximal exercise test in 10 male competition cyclists. The cyclists reached an average maximal O2 consumption of 72 ml. kg-1. min-1 (range: 67-82 ml. kg-1. min-1) and ventilation of 147 l/min (range: 122-180 l/min) (88% of preexercise maximal voluntary ventilation in 15 s). In nine subjects, FL was absent at all levels of exercise (i.e., expiratory flow increased with negative expiratory pressure over the entire tidal volume range). One subject, the oldest in the group, exhibited FL during peak exercise. The group end-expiratory lung volume (EELV) decreased during light-to-moderate exercise by 13% (range: 5-33%) of forced vital capacity but increased as maximal exercise was approached. EELV at peak exercise and at rest were not significantly different. The end-inspiratory lung volume increased progressively throughout the exercise test. The conclusions reached are as follows: 1) most well-trained young cyclists do not reach FL even during maximal exercise, and, hence, mechanical ventilatory constraint does not limit their aerobic exercise capacity, and 2) in absence of FL, EELV decreases initially but increases during heavy exercise.     

Role of vagus during exercise in thermal panting

In dogs anaesthetised with pentobarbitone sodium raising the body temperature from 37 degrees C during mild exercise increased the rate of respiration and pulmonary ventilation but decreased the tidal volume. Cold blocking the vagi during the exercise resulted in decrease in respiration rate and minute ventilation, but increase in tidal volume. At 40 degrees C body temperature vagal block was not effective in decreasing the respiration rate and minute ventilation, which may be due to stimulation of lung irritant receptors through hyperthermia.     

Heat storage regulation in exercise during thermal transients

The operating principles of the CentrifiChem are briefly described and the results of the evaluation are summarised. The pipettor, the temperature control unit, and the photometer were tested separately, but the remainder of the instrument is interdependent. Up to 10 different tests were used to measure within-batch and between-day precision, and accuracy. Carryover was found to be small, and for the six tests investigated the linearity was good. Estimates are given of the running costs, and also included are sections on the reliability and safety of the instrument. Since it requires only a small volume of serum, it is ideally suited to paediatric requirements. When used as an enzyme analyser it can work at about 200 specimens per hour.     

Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man

Eight healthy males performed four rides to exhaustion at approximately 70% of their VO2max obtained in a neutral environment. Subjects cycled at ambient temperatures (Ta) of 3.6 +/- 0.3 (SD), 10.5 +/- 0.5, 20.6 +/- 0.2, and 30.5 +/- 0.2 degrees C with a relative humidity of 70 +/- 2% and an air velocity of approximately 0.7 m.s-1. Weighted mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were recorded at rest, during exercise and at exhaustion. Venous samples were drawn before and during exercise and at exhaustion for determination of hemoglobin, hematocrit, blood metabolites, and serum electrolytes and osmolality. Expired air was collected for calculation of VO2 and R which were used to estimate rates of fuel oxidation. Ratings of perceived exertion (RPE) were also obtained. Time to exhaustion was significantly influenced by Ta (P = 0.001): exercise duration was shortest at 30.5 degrees C (51.6 +/- 3.7 min) and longest at 10.5 degrees C (93.5 +/- 6.2 min). Significant effects of Ta were also observed on VE, VO2, R, estimated fuel oxidation, HR, Tre, Tsk, sweat rate, and RPE. This study demonstrates that there is a clear effect of temperature on exercise capacity which appears to follow an inverted U relationship.     

Thermogenesis during rest and exercise in cold air

Nine non-cold-acclimated subjects (5 female, 4 male, mean age 22.5 years) were studied to determine whether nonshivering thermogenesis contributes to cold-induced metabolic heat production during rest (50 min standing) and exercise (40 min treadmill walking) in 5 degrees C. Propranolol was administered orally (females, 60 mg, 1.12 mg.kg-1; males, 80 mg, 0.96 mg.kg-1) to block nonshivering thermogenesis. Measurements were taken at both 25 degrees C, 13.1 Torr (water vapor pressure; 1 Torr = 133.3 Pa) and 5 degrees C, 3.6 Torr, with sessions randomly assigned to be drug-neutral (DN), drug-cold (DC), placebo-neutral (PN), and placebo-cold (PC). Body core temperature was not different between any of the experimental conditions. Mean body temperature (5 degrees C, 32.2 +/- 0.20 degrees C (+/- SEM); 25 degrees C, 35.3 +/- 0.20 degrees C) and mean skin temperature (5 degrees C, 22.4 +/- 0.70 degrees C; 25 degrees C, 31.4 +/- 0.60 degrees C) were lower (p < 0.05) in the 5 degrees C than 25 degrees C environment (rest, exercise, drug (D), placebo (P), combined); while shivering (EMG) was higher (16.5 +/- 3.9% above baseline) at 5 degrees C than 25 degrees C (15 +/- 2.1% below baseline) (p < 0.05). The greater VO2 in 5 degrees C compared with 25 degrees C for the same condition is the thermoregulatory VO2 (TVO2). TVO2 (mL.min-1) was lower (p < 0.05) on the D (mean = 189.5 +/- 17.7) than on the P (mean = 238.1 +/- 20.2) during rest and during exercise (D, 206.1 +/- 63.7; P, 338.4 +/- 46.7). The EMG was 21% above baseline in the DC, and 12% above baseline for PC (p > 0.05). These results suggest a nonshivering component to heat production during acute cold exposure, which can be blocked with propranolol.     

Lactate distribution in the blood during steady-state exercise

PURPOSE: The purpose of this investigation was to examine the plasma to red blood cell (RBC) lactate concentration ([La]) gradient and RBC:plasma [La] ratio during 30 min of steady-state cycle ergometer exercise at work rates below lactate threshold ( LT. Blood samples were taken from a heated forearm vein, immediately cooled to 4 degrees C in a dry-ice ethanol slurry, and centrifuged at 4 degrees C to separate plasma and RBCs. RESULTS: During >LT, plasma [La] rose to 8.8+/-1.1 mM after 10 min and remained above 6 mM. RBC [La] (4.9+/-0.7 mM) was significantly lower than plasma [La] at 10 min and remained lower throughout exercise. As a result, there was a sizable [La] gradient (approximately 3.5 mM) from plasma to RBC during most of >LT. In LT, the ratio of RBC [La]:plasma [La] was the same for both (0.58+/-0.02) and not significantly different from rest. CONCLUSIONS: These results refuted our hypothesis that the RBC:plasma [La] ratio would decrease at the onset of >LT exercise because of muscle lactate release exceeding the ability of RBCs to take up the lactate. Instead, there appears to be an equilibrium between plasma [La] and RBC [La] in arterialized venous blood from a resting muscle group as evidenced by the constant RBC [La]:plasma [La] ratio.