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.     

Influence of sodium bicarbonate ingestion on plasma ammonia accumulation during incremental exercise in man

Summary This investigation evaluated the influence of metabolic alkalosis on plasma ammonia (NH₃) accumulation during incremental exercise. On two occasions separated by at least 6 days, six healthy men cycled at 70, 80, and 90%g of maximum oxygen consumption ( ) for 5 min; each exercise period was followed by 5 min of seated recovery. Exercise was then performed at 100% until exhaustion. Beginning 3 h prior to exercise, subjects ingested 3.6 mmol · kg body mass^– NaHCO₃ (test, T) or 3.0 mmol · kg body mass^–1 CaCO₃ (placebo, P) (both equivalent to 0.3 g · kg^–1) over a 2-h period. Trials were performed after an overnight fast and the order of treatments was randomized. Arterialized venous blood samples for the determination of acid-base status, blood lactate and plasma NH₃ concentrations were obtained at rest before treatment, 15 s prior to each exercise bout (Pre 70%, Pre 80%, Pre 90%, and Pre 100%), and at 0, 5 (5Post), and 10 (10'Post) min after exhaustion. Additional samples for blood lactate and plasma NH₃ determination were obtained immediately after each exercise bout (Post 70%, Post 80%, Post 90%) and at 15 min after exercise (15Post). Time to exhaustion at 100% of was not significantly different between treatments [mean (SE): 173 (42) s and 184 (44) s for T and P respectively]. A significant treatment effect was observed for plasma pH with values being significantly higher on T than on P Pre 70% [7.461 (0.007) vs 7.398 (0.008)], Pre 90% [7.410 (0.010) vs 7.340 (0.016)], and 10'Post [7.317 (0.032) vs 7.242 (0.036)]. The change in plasma pH was significantly greater following the 90%g bout (Pre 100% Pre 90%) for T [–0.09 (0.02)] than for P [–0.06 (0.01)]. Blood base excess and plasma bicarbonate concentrations were significantly higher for T than P before each exercise bout but not at the point of exhaustion. During recovery, base excess was higher for T than P at 5Post and 10Post while the bicarbonate concentration was higher for T than P at 10Post. A significant treatment effect was observed for the blood lactate concentration with T on the average being higher than P [7.0 (1.0) and 6.3 (1.1) mmol · l^–1 for T and P averaged across the 12 sampling times]. Plasma NH₃ accumulation was not different between treatments at any point in time. In addition, no differences were observed between treatments in blood alanine accumulation. The results suggest that under the conditions of the present investigation metabolic alkalosis does not influence plasma NH₃ accumulation or endurance capacity during intense incremental exercise.     

Respiratory alkalosis: no effect on blood lactate decline or exercise performance

Summary It was the purpose of this study to determine the effects of respiratory alkalosis before and after high intensity exercise on recovery blood lactate concentration. Five subjects were studied under three different acid-base conditions before and after 45 s of maximal effort exercise: 1) hyperventilating room air before exercise (Respiratory Alkalosis Before=RALB, 2) hyperventilating room air during recovery (Respiratory Alkalosis After=RALA), and 3) breathing room air normally throughout rest and recovery (Control =C). RALB increased blood pH during rest to 7.65±0.03 while RALA increased blood pH to 7.57±0.03 by 40 min of recovery. Neither alkalosis treatment had a significant effect on blood lactate concentration during recovery. The peak lactate values of 12.3±1.2 mmol · L^–1 for C, 11.8±1.2 mmol · L^–1 for RALB, and 10.2±0.9 mmol · L^–1 for RALA were not significantly different, nor were the half-times (t _1/2) for the decline in blood lactate concentration; C=18.2 min, RALB=19.3 min, and RALA=18.2 min. In C, RALB and RALA, the change in base excess from rest to postexercise was greater than the concomitant increase in blood lactate concentration, suggesting the presence of a significant amount of acid in the blood in addition to lactic acid. There was no significant difference in either the total number of cycle revolutions (C=77±2, RALB=77±1) or power output at 5 s intervals between RALB and C during the 45 s. These results suggest that the possible range of respiratory alkalosis changes in intact humans may be insufficient 1) to affect recovery blood lactate concentrations, or 2) to affect intense, short-term exercise performance.     

A comparison of blood gases and acid-base measurements in arterial,arterialized venous,and venous blood during short-term maximal exercise

Summary The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test 11). During test 11 arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO₃ ^–), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P<0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r=0.83 [regression equation: BE_a=(0.84 BE_av)–0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3mmol · 1^–1) and higher than both venous and arterialized venous La at EE. At EE La concentration was 9.2, SD 2.0, 4.6, SD 0.4, and 5.1, SD 0.1 mmol · 1^–1 in arterial, venous, and arterialized venous blood respectively. It is concluded that except for base excess, blood gases and acid base measurements in venous and arterialized venous blood do not accurately reflect values found in arterial blood during short-term maximal exercise. We suggest that these differences may be due in part to clearance by inactive muscle near the sampling site or vasoconstriction at the inactive sampling site.     

Acute hormonal and neuromuscular responses to hypertrophy,strength and power type resistance exercise

The purpose of the current study was to determine the acute neuroendocrine response to hypertrophy (H), strength (S), and power (P) type resistance exercise (RE) equated for total volume. Ten male subjects completed three RE protocols and a rest day (R) using a randomized cross-over design. The protocols included (1) H: 4 sets of 10 repetitions in the squat at 75% of 1RM (90 s rest periods); (2) S: 11 sets of three repetitions at 90% of 1RM (5 min rest periods); and (3) P: 8 sets of 6 repetitions of jump squats at 0% of 1RM (3 min rest periods). Total testosterone (T), cortisol (C), and sex hormone binding globulin (SHBG) were determined prior to (PRE), immediately post (IP), 60 min post, 24 h post, and 48 h post exercise bout. Peak force, rate of force development, and muscle activity from the vastus medialis (VM) and biceps femoris (BF) were determined during a maximal isometric squat test. A unique pattern of response was observed in T, C, and SHBG for each RE protocol. The percent change in T, C, and SHBG from PRE to IP was significantly (p ≤ 0.05) greater in comparison to the R condition only after the H protocol. The percent of baseline muscle activity of the VM at IP was significantly greater following the H compared to the S protocol. These data indicate that significant acute increases in hormone concentrations are limited to H type protocols independent of the volume of work competed. In addition, it appears the H protocol also elicits a unique pattern of muscle activity as well. RE protocols of varying intensity and rest periods elicit strikingly different acute neuroendocrine responses which indicate a unique physiological stimulus.     

Effect of induced metabolic alkalosis on sweat composition in men

To determine whether induced metabolic alkalosis affects sweat composition, 10 males cycled for 90 min at 62.5 +/- 1.3% peak oxygen uptake, on two separate occasions. Subjects ingested either empty capsules (placebo) or capsules containing NaHCO3- (0.3 g kg-1 body mass; six equal doses) over a 2-h period, which commenced 3 h prior to exercise. Arterialized-venous blood samples were drawn prior to and after 15, 30, 60 and 90 min of exercise. Sweat was aspirated at the end of exercise from a patch located on the right scapula region. NaHCO3- ingestion elevated blood pH, [HCO3-] and serum [Na+], whereas serum [Cl-] and [K+] were reduced, both at rest and during exercise (P < 0.05). Sweat pH was greater in the NaHCO3- trial (6.24 +/- 0.18 vs. 6.38 +/- 0.18; P < 0.05), whereas sweat [Na+] (49.5 +/- 4.8 vs. 50.2 +/- 4.3 mEq L-1), [Cl-] (37.5 +/- 5.1 vs. 39.3 +/- 4.2 mEq L-1) and [K+] (4.66 +/- 0.19 vs. 4.64 +/- 0.34 mEq L-1) did not differ between trials (P > 0.05). Sweat [HCO3-] (2.49 +/- 0.58 vs. 3.73 +/- 1.10 mEq L-1) and [lactate] (8.92 +/- 0.79 vs. 10.51 +/- 0.32 mmol L-1) tended to be greater after NaHCO3- ingestion, although significance was not reached (P=0.07 and P=0.08, respectively). These data indicate that induced metabolic alkalosis can modify sweat composition, although it is unclear whether the secretory coil, reabsorptive duct, or both are responsible for this alteration.     

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and [Formula: see text] Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at [Formula: see text] (IHE group, SaO(2) at [Formula: see text] baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise [Formula: see text] Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamuM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of [Formula: see text] was reduced (-0.9 +/- 0.8 DeltamuM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged [Formula: see text] following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.     

The effect of normocapnic hypoxia and the duration of exposure to hypoxia on supramaximal exercise performance

Summary Two investigations were designed that (a) evaluated the effect of the respiratory alkalosis that accompanies breathing an hypoxic (H) gas mixture and (b) examined the influence of the duration of breathing this H mixture on the subsequent performance of 45 s supramaximal dynamic exercise. In experiment 1, 12 men performed a 45-s Wingate Test (WT) on three occasions breathing a normoxic (N; 20.9% 02), H (11.3% 02), or normocapnic hypoxic (H + CO₂; 11.5070 O₂, 2.25% CO₂) gas mixture for 20 min prior to performing the WT. For experiment 2, nine men performed a 20-min normoxic (N20) and three hypoxic WT trials which consisted of breathing an 11070 O₂ balance N₂ gas mixture for 10 min (H10), 20 min (H20) or 30 min (H30) prior to the WT. For experiment 1,VO₂ was significantly reduced during the 45-s H [mean (SD); 1.22 (0.23) 1] and H + CO₂ [1.12 (0.18)1] trials compared with the N trial [1.78 (0.18) 1]. Peak power output (W _peak) during WT was similar across trials. However, a small (less than 3070) but significant reduction in the mean power output (W) was observed in both the H and H + CO₂ trials [6.8 (0.6) W · kg^–1] compared with the N trial [7.0 (0.6) W · kg^–1]. Prior to performing the WT, blood pH andPCO₂ were similar [7.40 (0.02) and 5.3 (0.3) kPa, respectively] for the N and H + CO₂ trials. A respiratory alkalosis accompanied the H condition [7.46 (0.02) for pH and 4.6 (0.3) kPa forPCO₂. For experiment 2,VO₂ also was significantly lower during the 45-s WT for H10 [1.16 (0.16) 1], H2O [1.17 (0.16)1], and H30 [1.18 (0.26) 1] compared with N20 [1.84 (0.41) 1].W _peak was similar across trials but a significant reduction in meanW was observed again for the H trials [7.1 (0.4) W · kg^–1] compared with N20 [7.4 (0.4) W · kg^–1]. These data conflict with our previous findings and suggest that breathing an 11% H gas mixture will reduce the mean power produced during 45 s of supramaximal exercise.     

Gastroenteropancreatic hormonal changes during exercise

Peripheral plasma concentrations of gastroenteropancreatic peptides were measured during a 3-h period of bicycle exercise at 40% of maximal oxygen uptake in six normal men. Marked increases (P < 0.02) were found in vasoactive intestinal polypeptide (VIP) [1.8 +/- 0.7 (rest) vs. 22.3 +/- 5.4 pmol x l-1 (mean +/- SE) (3 h)], secretin (0.5 +/- 0.5 vs. 11.1 +/- 2.7 pmol x l-1), pancreatic polypeptide (PP) (4.0 +/- 1.5 vs. 46.3 +/- 11.5 pmol x l-1), somatostatin (SRIF) (12.8 +/- 1.2 vs. 17.7 +/- 0.6 pmol x l-1), whereas no changes occurred in gastric inhibitory polypeptide (37.3 +/- 5.9 vs. 39.2 +/- 9.8 pmol x l-1). Immunoreactive insulin and C-peptide decreased from 0.08 +/- 0.004 and 0.39 +/- 0.03 pmol x l-1, respectively, to 0.04 +/- 0.003 (P < 0.005) and 0.13 +/- 0.02 (P < 0.001). The significant decrease in C-peptide and in the C-peptide-to-insulin molar ratio indicate decreased insulin secretion and clearance, respectively, during exercise. Plasma glucose decreased [5.0 +/- 0.1 (rest) vs. 4.2 +/- 0.3 mmol.l-1 (3 h)] (P < 0.01). During 3 h of rest, none of the measured parameters had changed. The marked exercise-induced changes in plasma concentrations of PP, secretin, VIP, and SRIF are provocative. We know in detail neither the stimuli for the release of these peptides nor their physiological role during exercise.     

Threshold increases in plasma growth hormone in relation to plasma catecholamine and blood lactate concentrations during progressive exercise in endurance-trained athletes

Plasma human growth hormone ([HGH]), adrenaline ([A]), noradrenaline ([NA]) and blood lactate ([La^–]_b) concentrations were measured during progressive, multistage exercise on a cycle ergometer in 12 endurance-trained athletes [aged 32.0 (SEM 2.0) years]. Exercise intensities (3 min each) were increased by 50 W until the subjects felt exhausted. Venous blood samples were taken after each intensity. The [HGH] and catecholamine concentrations increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to the lactate threshold ([La^–]-T). Close correlations (P < 0.001) were found between [La^–]_b and plasma [HGH] (r = 0.64), [A] (r = 0.71) and [NA] (r = 0.81). The mean threshold exercise intensities for [HGH], [A] and [NA], detected by log-log transformation, [154 (SEM 19) W, 162 (SEM 15) W and 160 (SEM 17) W, respectively] were not significantly different from the [La^–]-T [161 (SEM 12) W]. The results indicated that the threshold rise in plasma [HGH] followed the patterns of plasma catecholamine and blood lactate accumulation during progressive exercise in the endurancetrained athletes.     

Glucose ingestion before and during exercise does not enhance performance of daily repeated endurance exercise

Summary The effect of glucose (Glc) ingestion before and during daily, repeated, prolonged exercise on metabolism and performance was tested. Seven young, healthy males performed cycling exercise in two series, with 1 month interval. Each exercise series consisted of 1 h/day on 3 successive days. On the 3rd day, exercise was continued until exhaustion. The intensity was 73.4 (7.7) % [mean (SD)] of maximal oxygen uptake ( ). Glucose (Glc) or placebo (P) drink was ingested 15 min before the start, and at 15 and 45 min of each daily exercise. The total amount of Glc ingested was 43.1 (4.2) g. During exercise, blood Glc concentrations were significantly higher (P<0.05) when Glc was ingested than when P was ingested [Glc 5.14 (0.32) and P 4.12 (4.17) mmol · 1^–1 at exhaustion]. However, Glc ingestion did not improve performance time to exhaustion [Glc 92.05 (29.55) and P 98.07 (27.33) min]. Free fatty acid concentrations were significantly lower when Glc was ingested than when P was ingested [Glc 0.63 (0.21) and P 1.39 (0.46) mmol · l^–1 at exhaustion]. There were no significant differences in exercise heart rate, , respiratory exchange ratio, blood lactate concentrations or rating of perceived exertion between the conditions nor were there any significant differences in these parameters on different days of exercise. It seems that ingestion of small amounts of Glc does not increase the metabolism of carbohydrate or improve the performance of intensive endurance exercise of poorly trained subjects, even when the exercise is repeated daily.     

Middle cerebral artery blood velocity during exercise in patients with atrial fibrillation.

Atrial fibrillation limits the ability to increase cardiac output during exercise and may, in turn, affect the exercise-associated elevation in cerebral perfusion. In nine patients with atrial fibrillation (AF) and in five age-matched healthy subjects, middle cerebral artery blood velocity (MCA Vmean) was measured during incremental exercise using the transcranial Doppler. The AF patient group exhibited a lower aerobic capacity than the control group [peak work rate: 106 W (71-153 W; median and range) vs. 129 W (118-1.9 W) and maximal oxygen uptake: 1.4 l min-1 (1.0-1.9 l min-1) vs. 1.7 l min-1 (1.4-2.2 l min-1); P = 0.05]. At rest, MCA Vmean was not significantly different between the two groups [43 cm s-1 (39-56 cm s-1) vs. 52 cm s-1 (40-68 cm s-1)]. During intense cycling, the increase in MCA Vmean was to 51 cm s-1 (40-78 cm s-1) (9%) in the AF group and lower than in the healthy subjects [to 62 cm s-1 (50-81 cm s-1) 23%; P < 0.05], which corresponded with the smaller than expected increase in cardiac output [156% (130-169%) vs. 180%]. Thus, there was a correlation between the increase in MCA Vmean and the ability to increase cardiac output (r2 = 0.55, P < 0.01). We suggest that, during exercise with a large muscle mass, atrial fibrillation affects the ability to elevate cerebral perfusion, and this results from an impaired ability to increase cardiac output.     

Influence of the menstrual cycle on proenkephalin peptide F responses to maximal cycle exercise

Proenkephalin peptide F [107–140] is an enkephalin-containing peptide found predominantly within the adrenal medulla and is co-packaged with epinephrine within adrenal medullary chromaffin granules. Peptide F has been shown to have the classic opioid analgesia effects along with immune cell interactions. This is only the second peptide F study in women, and in it we compare the responses of peptide F to a maximal cycle exercise test and recovery values over the follicular and luteal phases of the menstrual cycle. Eight untrained (directly documented in this study) women who were eumenorrheic performed a progressive maximal exercise test to volitional exhaustion on a cycle ergometer, once during the follicular phase, and once during the luteal phases of the menstrual cycle. Blood was obtained pre-exercise, immediately post-exercise and at 0, 15, and 30 min into recovery. Typical exercise changes in response to the cycle tests were observed with blood lactate increases that remained elevated 30 min into recovery. No significant exercise-induced elevations were observed for peptide F concentrations with exercise nor were any differences observed between the two menstrual phases. Thus, the effects of the menstrual cycle on peptide F concentrations appear to be minimal under the conditions of this investigation. With high concentrations of peptide F observed at rest (approx. 0.2–0.3 pmol ml⁻¹) pre-exercise arousal mechanisms may have obviated any exercise-induced response. In addition, inhibition via elevated epinephrine may have inhibited any post-exercise increases and finally adrenal medullary capacity for circulatory concentrations of peptide F may have been reached in such untrained women. Pre-exercise arousal mechanisms potentially related to analgesia may also be involved to prepare untrained women for the stress of maximal exercise.     

Response of left ventricular diastolic filling to graded exercise relative to the lactate threshold

Summary During incremental exercise, the left ventricular ejection fraction increases up to the intensity of the anaerobic threshold and tends to level off at higher exercise intensities. Since there is a correlation between the response of peak filling rate and ejection fraction to exercise, this study was conducted to determine whether the response of left ventricular diastolic function is similar to the response of systolic function relative to lactate threshold. Twelve healthy men performed two exercise tests on a cycle ergometer. In the first test, lactate threshold and maximal power output were determined. In the second exercise test, gated radionuclide ventriculography was performed at rest, at the lactate threshold intensity, and at peak exercise to measure ejection fraction and peak filling rate. Ejection fraction increased significantly from rest [mean (SD): 62 (5)%] to lactate threshold [76 (7) %] and did not change significantly from lactate threshold to peak exercise [77 (7)%]. Likewise, peak filling rate (normalized for stroke counts) increased from resting [6.1 (0.9)V _s · s^–1] to lactate threshold [9.4 (1.8)V _s · s^–1] and did not change significantly from lactate threshold to peak exercise [9.6 (2.9)V _s · s^–1]. There was no correlation between the change in peak filling rate and the change in ejection fraction from rest to lactate threshold. Thus, during incremental exercise, left ventricular diastolic function responds qualitatively similar to systolic function.     

Testosterone, dehydroepiandrosterone, insulin-like growth factor 1, and insulin in sedentary and physically trained aged men

The influence of physical activity on dehydroepiandrosterone sulfate (DHEAS), total and free testosterone (TT and FT, respectively), insulin-like growth factor I (IGF-1), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and insulin concentrations in aging men was investigated. Eight trained and nine sedentary men aged 60–65 years volunteered to participate in this study. Physical activity was determined during an effort test and evaluated by the measure of the maximal aerobic power ( ). In the trained aging men, the was higher than in the sedentary group of matching age [mean (SD) 206.8 (17.1) W versus 136.6 (12.3) W; P<0.0001]. The fat percentage was higher in the sedentary (n=9) than in the trained (n=8) group [23.9 (3.2)% versus 14.6 (3.7)%; P<0.0001]. DHEAS and IGF-1 levels were higher in trained than in sedentary subjects, respectively 2.04 (1) μmol/l versus 1.01 (0.68) μmol/l (P=0.02) and 192.1 (40.1) ng/ml versus 132.8 (31.2) ng/ml (P=0.003). Insulin levels were higher in sedentary subjects [11.2 (3.5) mIU/l versus 7.6 (2.2) mIU/l, P=0.03]. No statistical difference was observed between both groups for FT and total TT values, FSH values and LH values. IGF-1 was correlated with (r=0.64, P=0.003), and DHEAS was correlated with IGF-1 (r=0.59, P=0.01). We observed a relationship between fat percentage and each of the following hormones: IGF-1 (r=–0.50, P=0.03), FT (r=–0.66, P=0.002), TT (r=–0.54, P=0.02) and insulin (r=0.63, P=0.004). Insulin was inversely correlated with FT (r=–0.66, P=0.002) and TT (r=–0.47, P=0.05). These results suggest that regular physical activity could maintain higher DHEAS and IGF-1 and lean body mass levels in elderly men, and participate in general well being in older age. Electronic Publication     

Effects of exercise training on plasma catecholamines and blood pressure in labile hypertensive subjects

Summary Plasma catecholamine concentrations (norepinephrine, NE; epinephrine, E) were measured along with heart rate (HR) and blood pressure (BP) at rest in supine (20 min) and standing (10 min) positions and in response to cycle ergometer exercise (5 min; 60% estimated maximal aerobic power) in 12 hypertensive patients before and after 20 weeks of aerobic training on cycle ergometer (six males, one female) or by jogging (five males). In a control group of labile hypertensive patients (five males, two females), estimated maximal aerobic power as well as HR and BP at rest in the supine and standing positions and in response to exercise were not modified from the first to the second evaluation (43±4 vs 43±5 ml·kg^–1·min^–1). In comparison estimated maximal aerobic power significantly increased in both training groups (cycle: 38±4 to 43±4; jogging: 38±3 to 46±4 ml·kg^–1·min^–1). However HR and BP were not modified following training, except for small reductions in systolic (18.9 to 18 kPa: 142 to 135 mmHg) and diastolic pressures (13.3 to 12 kPa: 100 to 90 mmHg) (p<0.05) at standing rest in the cycle group. Changes in plasma E and NE concentrations at rest and in response to exercise were small and not consistent: plasma NE was lower at standing rest following cycle training, (559±95 vs 462±108 pg·ml^–1) but a similar reduction was observed in the control group (428±45 vs 321±28 pg·ml^–1); plasma E was lower at rest following cycle training (29±7 vs 12±8 pg·ml^–1), but was higher in response to exercise (137±24 vs 419±113 pg·ml^–1). These results are in accordance with previous reports which do not clearly demonstrate that physical training in hypertensive patients lowers BP and the activity or reactivity of the sympathetic system.     

Oxidation of [13C]glucose ingested before and/or during prolonged exercise

Ingestion of glucose before exercise results in a transient increase in plasma insulin concentrations. We hypothesized that if glucose was also ingested during the exercise period the elevated plasma insulin concentration could increase exogenous glucose oxidation. The oxidation rate of glucose ingested 30 min before (50 g) and/or during (110 or 160 g in fractionated doses) exercise [120 min; 67.3 (1.2)% maximal O₂ uptake] was studied on six young male subjects, using ¹³C-labelling. Ingestion of glucose before exercise significantly increased plasma insulin concentration [from 196 (45) to 415 (57) pmol l^–1] but the value returned to pre-exercise level within the first 30 min of exercise in spite of a continuous increase in plasma glucose concentration. Ingestion of glucose 30 min before exercise did not increase the oxidation of exogenous glucose between minutes 30 and 60 during the exercise period [0.36 (0.03) vs 0.30 (0.02) g min^–1, when placebo or unlabelled glucose was ingested respectively]. Over the last 90 min of exercise, when glucose was ingested only during exercise, 49.2 (3.1) g [0.55 (0.04) g min^–1) was oxidized, while when it was ingested both before and during exercise, 65.7 (4.6) g [0.73 (0.05) g min^–1] was oxidized [26.7 (2.1) g of the 50 g ingested before exercise but only 39.0 (2.4) g of the 110 g ingested during the exercise period]. Thus, ingestion of glucose 30 min before the beginning of exercise did not enhance the oxidation rate of exogenous glucose ingested during the exercise period, although the total amount of exogenous glucose oxidized was larger than when ingested only during the exercise period.     

Effect of muscle glycogen availability on maximal exercise performance

This investigation determined the influence of pre-exercise muscle glycogen availability on performance during high intensity exercise. Nine trained male cyclists were studied during 75 s of all-out exercise on an air-braked cycle ergometer following muscle glycogen-lowering exercise and consumption of diets (energy content approximately 14 MJ) that were either high (HCHO – 80% CHO) or low (LCHO – 25% CHO) in carbohydrate content. The exercise-diet regimen was successful in producing differences in pre-exercise muscle glycogen contents [HCHO: 578(SEM?55) mmol?·?kg^?1 dry mass; LCHO: 364 (SEM 58) P??1 dry mass]. Despite this difference in muscle glycogen availability, there were no between trial differences for peak power [HCHO 1185 (SEM 50)W, LCHO 1179 (SEM?48)W], mean power [HCHO 547 (SEM?5)W, LCHO 554 (SEM ?8)W] and maximal accumulated oxygen deficit [HCHO 54.4 (SEM?2.3)?ml?·?kg^?1, LCHO 54.6 (SEM?2.0) ml?·?kg^?1]. Postexercise muscle lactate contents (HCHO 95.9 (SEM?4.6)?mmol?·?kg^?1 dry mass, LCHO 82.7 (SEM?12.3) mmol?·?kg^?1 dry mass, n?=?8] were no different between the two trials, nor were venous blood lactate concentrations immediately after and during recovery from exercise. These results would indicate that increased muscle glycogen availability has no direct effect on performance during all-out high intensity exercise.     

Effects of centrifuging at 2g on rat long bone metaphyses

Thermal stress is known to impair endurance capacity during moderate prolonged exercise. However, there is relatively little available information concerning the effects of thermal stress on the performance of high-intensity short-duration exercise. The present experiment examined human power output during repeated bouts of short-term maximal exercise. On two separate occasions, seven healthy males performed two 30-s bouts of sprint exercise (sprints I and II), with 4?min of passive recovery in between, on a cycle ergometer. The sprints were performed in both a normal environment [18.7?(1.5)°C, 40 (7)% relative humidity (RH; mean SD)] and a hot environment [30.1?(0.5)°C, 55 (9)% RH]. The order of exercise trials was randomised and separated by a minimum of 4 days. Mean power, peak power and decline in power output were calculated from the flywheel velocity after correction for flywheel acceleration. Peak power output was higher when exercise was performed in the heat compared to the normal environment in both sprint I [910 (172)?W vs 656?(58)?W; P?P?P?P?P?P?相似文献   

Accounting for flow dependence of respiratory resistance during exercise

Studies of airway function during exercise have produced conflicting results both in healthy and diseased subjects. Respiratory resistance (Rrs) was measured using an impulse oscillation technique. A flow/resistance curve was established for each of 16 healthy males during voluntary hyperventilation (VHV) at rest. Then, Rrs and flow were measured immediately (t(0)) and 90 sec (t(90)) after exercise on a cycle ergometer at 60, 70, and 80% of maximal aerobic power. The flow/resistance relationship at rest during VHV was used to assess the flow dependence of Rrs. Rrs at t(0) was higher than at rest (P <0.01) but lower than Rrs obtained at matched flow during VHV (P <0.05). In healthy subjects, the linear increase in Rrs with VHV indicates airflow dependency of Rrs following Rohrer's equation. The relative decrease in Rrs with exercise suggests bronchodilation. The bronchodilating effect disappeared promptly when exercise was stopped suggesting that it may have been related to a reflex mechanism.