Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Effect of endurance training on muscle TCA cycle metabolism during exercise in humans.

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 +/- 1 yr) cycled at approximately 80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 +/- 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 +/- 6 min). In addition to improved performance, training increased (P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 +/- 0.2 vs. 4.3 +/- 0.2 mmol/kg dry wt (P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 +/- 0.2 vs. pretraining: 3.5 +/- 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 +/- 0.7 vs. pretraining: 7.7 +/- 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 +/- 0.2 vs. pretraining: 5.6 +/- 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].     

Effect of gestational stage on uterine artery blood flow during exercise in rabbits.

We tested the hypothesis that the uterine artery vasoconstrictor response to graded exercise during early gestation would be similar to the nonpregnant (NP) state and would be attenuated at mid and term gestation. Responses to graded treadmill exercise were measured in six female New Zealand White rabbits in the NP state and at day 10, day 20, and day 28 (term) of gestation. Uterine artery blood flow (UtBF) was measured continuously with a Transonic flow probe. Rabbits performed a graded exercise test to voluntary exhaustion (maximal exercise) starting at 7 m/min, 7% grade. UtBF and uterine artery conductance (UtC) decreased similarly during graded exercise (P < 0.01) in the NP state [at maximal exercise: -40% (SD 20) for UtBF and -45% (SD 14) for UtC] and at day 10 of gestation [at maximal exercise: -48% (SD 17) for UtBF; -56% (SD 14) for UtC]. In contrast, there was little change in UtBF or UtC during graded exercise at day 20 [at maximal exercise: -4% (SD 17) for UtBF, P < 0.05 vs. NP; -16% (SD 12) for UtC, P < 0.01 vs. NP] and at day 28 [At maximal exercise: +7% (SD 15) for UtBF, P < 0.01 vs. NP; -2% (SD 24) for UtC, P < 0.01 vs. NP], indicating substantial attenuation of the uterine artery vasoconstrictor response to exercise. At rest, UtC responses to graded doses of intravenous phenylephrine were unaffected by the stage of gestation, which suggests that uterine artery responsiveness to alpha(1)-adrenoreceptor stimulation is preserved through gestation. Normal pregnancy in the rabbit is associated with attenuation of the uterine artery vasoconstrictor response to graded exercise that develops by mid gestation.     

Relationship between local perfusion and FFA uptake in human skeletal muscle-no effect of increased physical activity and aerobic fitness.

We investigated heredity-independent effects of increased physical activity and aerobic fitness on skeletal muscle free fatty acid (FFA) uptake, perfusion, and their heterogeneity at rest and during exercise. Also, the relationship between local skeletal muscle FFA uptake and perfusion was studied. Nine young adult male monozygotic twin pairs with significant difference in physical activity [229 min (SD 156) average time spent for conditioning exercise per week in more and 98 min (SD 71) in less active twins, P = 0.013] and aerobic fitness [18% (SD 10) difference in maximum O2 uptake] between brothers were studied using positron emission tomography. Submaximal knee-extension exercise increased perfusion, FFA uptake, and oxygen uptake in quadriceps femoris muscles 6-10 times compared with resting values (P < 0.001). More active twins tended to utilize more oxygen, while no differences were found in muscle perfusion or FFA uptake between groups. Mean perfusion and FFA uptake correlated strongly at a whole muscle level, both at rest (r = 0.97, P = 0.03 in more and r = 0.98, P = 0.02 in less active twins) and during exercise (r = 0.99, P = 0.01 and r = 0.94, P = 0.06), but at the voxel level (87 mm3) correlation was only moderate during exercise [r = 0.73 (SD 0.08) vs. r = 0.74 (SD 0.10), P = 0.92] and weak at rest [r = 0.28 (SD 0.13) vs. r = 0.33 (SD 0.21), P = 0.58]. Exercise decreased both perfusion and FFA uptake heterogeneity within the muscles (P < 0.001) similarly in both groups. In conclusion, long-term history of moderately increased physical activity tends to enhance muscle oxidative metabolism, but it does not have any significant influence on the FFA uptake or perfusion rates or their heterogeneity in skeletal muscle. Submaximal knee-extension exercise decreases heterogeneity of muscle FFA uptake and perfusion and improves matching between local muscle perfusion and FFA uptake. Thus it seems that the genetic influence is more important to determine the heterogeneity of perfusion and FFA uptake in skeletal muscle than exercise training.     

PPARGC1A genotype (Gly482Ser) predicts exceptional endurance capacity in European men.

Animal and human data indicate a role for the peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PPARGC1A) gene product in the development of maximal oxygen uptake (V(O2 max)), a determinant of endurance capacity, diabetes, and early death. We tested the hypothesis that the frequency of the minor Ser482 allele at the PPARGC1A locus is lower in World-class Spanish male endurance athletes (cases) [n = 104; mean (SD) age: 26.8 (3.8) yr] than in unfit United Kingdom (UK) Caucasian male controls [n = 100; mean (SD) age: 49.3 (8.1) yr]. In cases and controls, the Gly482Ser genotype met Hardy-Weinberg expectations (P > 0.05 in both groups tested separately). Cases had significantly higher V(O2 max) [73.4 (5.7) vs. 29.4 ml x kg(-1) x min(-1) (3.8); P < 0.0001] and were leaner [body mass index: 20.6 (1.5) vs. 27.6 kg/m2 (3.9); P < 0.0001] than controls. In unadjusted chi2 analyses, the frequency of the minor Ser482 allele was significantly lower in cases than in controls (29.1 vs. 40.0%; P = 0.01). To assess the possibility that genetic stratification could confound these observations, we also compared Gly482Ser genotype frequencies in Spanish (n = 164) and UK Caucasian men (n = 381) who were unselected for their level of fitness. In these analyses, Ser482 allele frequencies were very similar (36.9% in Spanish vs. 37.5% in UK Caucasians, P = 0.83), suggesting that confounding by genetic stratification is unlikely to explain the association between Gly482Ser genotype and endurance capacity. In summary, our data indicate a role for the Gly482Ser genotype in determining aerobic fitness. This finding has relevance from the perspective of physical performance, but it may also be informative for the targeted prevention of diseases associated with low fitness such as Type 2 diabetes.     

Blood glucose responses in humans mirror lactate responses for individual anaerobic threshold and for lactate minimum in track tests

The equilibrium point between blood lactate production and removal (La-(min)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-]b, catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc]b, this study investigated the [Glc] and [La-]b responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum (Glc(min)) in addition to IAT and La-(min) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v3km); IAT and IGT - 8 x 800 m runs at velocities between 84% and 102% of v3km; La-(min) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 6 x 800 m at intensities between 87% and 97% of v3km; endurance test (ET) - 30 min at the velocity of IAT. Capillary blood (25 microl) was collected for [La-]b and [Glc]b measurements. The IAT and IGT were determined by [La-]b and [Glc]b kinetics during the second test. The La-(min) and Glc(min) were determined considering the lowest [La-] and [Glc]b during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21) m. x min(-1); r = 0.096; P < 0.001] and between La-(min) [285 (SD 21)] and Glc(min) [287 (SD 20) m. x min(-1) r = 0.77; P < 0.05]. During ET, the [La-]b reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol x l(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min) as well as by IAT and La-(min).     

Aerobic power and insulin action improve in response to endurance exercise training in healthy 77-87 yr olds.

Previous studies have demonstrated that frail octogenarians have an attenuated capacity for cardiovascular adaptations to endurance exercise training. In the present study, we determined the magnitude of cardiovascular and metabolic adaptations to high-intensity endurance exercise training in healthy, nonfrail elderly subjects. Ten subjects [8 men, 2 women, 80.3 yr (SD2.5)] completed 10-12 mo (108 exercise sessions) of a supervised endurance exercise training program consisting of 2.5 sessions/wk (SD 0.2), 58 min/session (SD 6), at an intensity of 83% (SD 5) of peak heart rate. Primary outcomes were maximal attainable aerobic power [peak aerobic capacity (Vo(2peak))]; serum lipids, oral glucose tolerance, and insulin action during a hyperglycemic clamp; body composition by dual-energy X-ray absorptiometry, and energy expenditure using doubly labeled water and indirect calorimetry. The training program resulted in an increase in Vo(2peak) of 15% (SD 7) [22.9 (SD 3.3) to 26.2 ml.kg(-1).min(-1) (SD 4.0); P < 0.0001]. Favorable lipid changes included reductions in total cholesterol (-8%; P = 0.002) and LDL cholesterol (-10%; P = 0.003), with no significant change in HDL cholesterol or triglycerides. Insulin action improved, as evidenced by a 29% increase in glucose disposal rate relative to insulin concentration during the hyperglycemic clamp. Fat mass decreased by 1.8 kg (SD 1.4) (P = 0.003); lean mass did not change. Total energy expenditure increased by 400 kcal/day because of an increase in physical activity. No change occurred in resting metabolism. In summary, healthy nonfrail octogenarians can adapt to high-intensity endurance exercise training with improvements in aerobic power, insulin action, and serum lipid and lipoprotein risk factors for coronary heart disease; however, the adaptations in aerobic power and insulin action are attenuated compared with middle-aged individuals.     

Human power output during repeated sprint cycle exercise: the influence of thermal stress

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) degrees C, 40 (7)% relative humidity (RH; mean SD)] and a hot environment [30.1 (0.5) degrees 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 < 0.01] and sprint II [907 (150) vs 646 (37) W; P < 0.05]. Mean power output was higher in the heat compared to the normal environment in both sprint I [634 (91) W vs 510 (59) W; P < 0.05] and sprint II [589 (70) W vs 482 (47) W; P < 0.05]. There was a faster rate of fatigue (P < 0.05) when exercise was performed in the heat compared to the normal environment. Arterialised-venous blood samples were taken for the determination of acid-base status and blood lactate and blood glucose before exercise, 2 min after sprint I, and at several time points after sprint II. Before exercise there was no difference in resting acid-base status or blood metabolites between environmental conditions. There was a decrease in blood pH, plasma bicarbonate and base excess after sprint I and after sprint II. The degree of post-exercise acidosis was similar when exercise was performed in either of the environmental conditions. The metabolic response to exercise was similar between environmental conditions; the concentration of blood lactate increased (P < 0.01) after sprint I and sprint II but there were no differences in lactate concentration when comparing the exercise bouts performed in a normal and a hot environment. These data demonstrate that when brief intense exercise is performed in the heat, peak power output increases by about 25% and mean power output increases by 15%; this was due to achieving a higher pedal cadence in the heat.     

Preexercise sodium loading aids fluid balance and endurance for women exercising in the heat.

This study was conducted during the high-hormone phase of both natural and oral contraceptive pill (OCP)-mediated menstrual cycles to determine whether preexercise ingestion of a concentrated sodium beverage would increase plasma volume (PV), reduce physiological strain, and aid endurance of moderately trained women cycling in warm conditions. Thirteen trained cyclists [peak O(2) uptake 52 ml x kg(-1) x min(-1) (SD 2), age 26 yr (SD 6), weight 60.8 kg (SD 5)] who were oral contraceptive users (n = 6) or not (n = 7) completed this double-blind, crossover experiment. Cyclists ingested a concentrated-sodium (High Na(+): 164 mmol Na(+)/l) or low-sodium (Low Na(+): 10 mmol Na(+)/l) beverage (10 ml/kg) before cycling to exhaustion at 70% Peak O(2) uptake in warm conditions (32 degrees C, 50% relative humidity, air velocity 4.5 m/s). Beverage (approximately 628 ml) was ingested in seven portions across 60 min beginning 105 min before exercise, with no additional fluid given until the end of the trial. Trials were separated by one to two menstrual cycles. High Na(+) increased PV (calculated from hematocrit and hemoglobin concentration) before exercise, whereas Low Na(+) did not [-4.4 (SD 1.1) vs. -1.9% (SD 1.3); 95% confidence interval: for the difference 5.20, 6.92; P < 0.0001], and it involved greater time to exhaustion [98.8 (SD 25.6) vs. 78.7 (SD 24.6) min; 95% confidence interval: 13.3, 26.8; P < 0.0001]. Core temperature rose more quickly with Low Na(+) [1.6 degrees C/h (SD 0.2)] than High Na(+) [1.2 degrees C/h (SD 0.2); P = 0.04]. Plasma [AVP], [Na(+)] concentration, and osmolality, and urine volume, [Na(+)], and osmolality decreased with sodium loading (P < 0.05) independent of pill usage. Thus preexercise ingestion of a concentrated sodium beverage increased PV, reduced thermoregulatory strain, and increased exercise capacity for women in the high-hormone phase of natural and oral contraceptive pill-mediated menstrual cycles, in warm conditions.     

Elevated peak exercise systolic blood pressure is not associated with reduced exercise capacity in subjects with Type 2 diabetes.

Subjects with Type 2 diabetes without cardiovascular disease have a reduced exercise capacity compared with nondiabetic subjects. However, the mechanisms responsible for this phenomenon are unknown. The purpose of this study was to evaluate the impact of exercise systolic blood pressure (SBP) response on diverse exercise tolerance parameters in Type 2 diabetic subjects. Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. Subjects were treated with oral hypoglycemic agents and/or diet. Evaluation of glycemic control and peak exercise capacity were performed for each subject. The subjects were divided into two groups according to the median value of peak SBP (210 mmHg) measured in each subject. We observed a 13, 13, and 16% reduction in the relative peak oxygen uptake (V(O2 peak)), absolute V(O2 peak), and peak work rate in the low- compared with the high-peak SBP group [26.95 (SD 5.35) vs. 30.96 (SD 3.61) ml.kg(-1).min(-1), 2.5 (SD 0.4) vs. 2.8 (SD 0.6) l/min, and 169 (SD 34) vs. 202 (SD 32) W; all P < 0.05]. After adjusting for age, relative V(O2 peak) was still significantly different (P < 0.05). There were similar peak respiratory exchange ratio (RER) [1.20 (SD 0.08) vs. 1.16 (SD 0.07); P = 0.24] and peak heart rate [160 (SD 20) vs. 169 (SD 15) beats/min; P = 0.18] between the low- compared with the high-SBP group. No difference in glycemic control was observed between the two groups. The results reported in this study suggest that in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and its modulation is probably not related to glycemic control.     

Relationship between peripheral muscle structure and function in patients with chronic obstructive pulmonary disease with different nutritional status

The purpose of this study was to investigate the relationships between peripheral muscle structure (mass) and function (strength, endurance, and maximal aerobic capacity) in patients with chronic obstructive pulmonary disease (COPD) with different nutritional states. Thirty-nine patients (31 male) with moderate-severe COPD (63.5 ± 7.3 [SD] years) and 17 controls (14 male; 64.7 ± 5.5 [SD] years) underwent isokinetic (peak torque [PT]), isometric (isometric torque [IT]), and endurance strength (total work [TW]) measurements of the knee extensor muscles and a maximal cardiopulmonary exercise test to evaluate the maximal aerobic capacity (peak oxygen uptake [VO(2)] peak). Muscle mass (MM) was determined using dual-energy x-ray absorptiometry. Patients with COPD presented with reduced muscle function as compared with the healthy controls: PT (105.9 ± 33.9 vs. 134.3 ± 30.9, N·m(-1), respectively, p < 0.05), TW (1,446.3 ± 550.8 vs. 1,792.9 ± 469.1 kJ, respectively, p < 0.05), and VO(2)peak (68.1 ± 15.1 vs. 93.7 ± 14.5, % pred, respectively, p < 0.05). Significant relationships were found between muscle structure and function (strength and endurance) in the patient subgroup with preserved MM and in the control group: PT·MM(r(2) = 0.36; p = 0.01 vs. r(2) = 0.32; p = 0.01, respectively) and TW·MM (r(2) = 0.32; p = 0.01 vs. r(2) = 0.22; p = 0.05, respectively). Strength corrected for mass normalized this function in both patient subgroups, whereas endurance was normalized only in the patient subgroup without muscle depletion. Maximal aerobic capacity remained reduced, despite the correction, in both patient subgroups (depleted or nondepleted) compared with the healthy controls (VO(2)peak.MM: 9.1 ± 3.7 vs. 21.8 ± 4.9 vs. 28.5 ± 4.2 ml·min·kg, respectively, with p < 0.01 among groups). Muscle atrophy seems to be the main determinant of strength reduction among patients with moderate-severe COPD, whereas endurance reduction seems to be more related to imbalance between oxygen delivery and consumption than to the local muscle structure itself. Peripheral MM did not constitute a good predictor for maximal aerobic capacity in this population. The main practical application of this study is to point out a crucial role for the strategies able to ameliorate cardiorespiratory and muscular fitness in patients with COPD, even in those patients with preserved MM.     

Effect of exercise training on total daily physical activity in elderly humans

This study examined the effect of 12 weeks of exercise training on daily physical activity in elderly humans. Training consisted of a weekly group session and an individual session with cardio- and weight-stack machines. A group of 15 subjects served as the exercise group [EXER mean age 59 (SD 4) years], and 7 subjects as the controls [CONT mean age 57 (SD 3) years]. Physical activity and physical fitness were measured before the start of training (T), at week 6 and week 12 (T0, T6, T12 respectively) in EXER, and at T0 and T12 in CONT. Physical activity over 14 days was measured using a tri-axial accelerometer and physical fitness was measured during an incremental exercise test. At T12, mean maximal power output had significantly increased in EXER compared to CONT 8 (SD 12) vs -5 (SD 9) W; P < 0.02] and mean submaximal heart rate (at 100 W) had reduced [-10 (SD 7) vs -2 (SD 6) beats x min(-1); P < 0.05]. No differences or changes in physical activity were observed between EXER and CONT. At T6, physical activity on training days was significantly higher than on non-training days (P < 0.001). When the accelerometer output of the training session was subtracted from the accelerometer output on training days, at T12 non-training physical activity was significantly lower than on non-training days (P < 0.004). Accelerometer output of the individual training session at T12 had significantly increased compared to T6 (P < 0.05), whereas, accelerometer output of the group training session had remained unchanged. In conclusion, in elderly subjects an exercise training programme of moderate intensity resulted in an improved physical fitness but had no effect on total daily physical activity. Training activity was compensated for by a decrease in non-training physical activity.     

Prior exercise delays the onset of acidosis during incremental exercise.

The effects of prior moderate- and prior heavy-intensity exercise on the subsequent metabolic response to incremental exercise were examined. Healthy, young adult subjects (n = 8) performed three randomized plantar-flexion exercise tests: 1) an incremental exercise test (approximately 0.6 W/min) to volitional fatigue (Ramp); 2) Ramp preceded by 6 min of moderate-intensity, constant-load exercise below the intracellular pH threshold (pHT; Mod-Ramp); and 3) Ramp preceded by 6 min of heavy-intensity, constant-load exercise above pHT (Hvy-Ramp); the constant-load and incremental exercise periods were separated by 6 min of rest. (31)P-magnetic resonance spectroscopy was used to continuously monitor intracellular pH, phosphocreatine concentration ([PCr]), and inorganic phosphate concentration ([P(i)]). No differences in exercise performance or the metabolic response to exercise were observed between Ramp and Mod-Ramp. However, compared with Ramp, a 14% (SD 10) increase (P < 0.01) in peak power output (PPO) was observed in Hvy-Ramp. The improved exercise performance in Hvy-Ramp was accompanied by a delayed (P = 0.01) onset of intracellular acidosis [Hvy-Ramp 60.4% PPO (SD 11.7) vs. Ramp 45.8% PPO (SD 9.4)] and a delayed (P < 0.01) onset of rapid increases in [P(i)]/[PCr] [Hvy-Ramp 61.5% PPO (SD 12.0) vs. Ramp 45.1% PPO (SD 9.1)]. In conclusion, prior heavy-intensity exercise delayed the onset of intracellular acidosis and enhanced exercise performance during a subsequent incremental exercise test.     

NaHCO3-induced alkalosis reduces the phosphocreatine slow component during heavy-intensity forearm exercise.

During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-]. Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05) intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.     

Water immersion delays the oxygen uptake response to sitting arm-cranking in humans

We investigated the effect of central hypervolaemia during water immersion up to the xiphoid process on the oxygen uptake (VO2) and heart rate (HR) response to arm cranking. Seven men performed a 6-min arm-cranking exercise at an intensity requiring a VO2 at 80% ventilatory threshold both in air [C trial, 29 (SD 9) W] and immersed in water [WI trial, 29 (SD 11) W] after 6 min of sitting. The VO2 (phase 2) and HR responses to exercise were obtained from a mono-exponential fit [f(t) = baseline + gain x (1 - e(-(t-TD)/tau))]. The response was evaluated by the mean response time [MRT; sum of time constant (tau) and time delay (TD)]. No significant difference in VO2 and HR gains between the C and WI trials was observed [VO2 0.78 (SD 0.1) vs 0.80 (SD 0.2) l x min(-1), HR 36 (SD 7) vs 37 (SD 8) beats x min(-1), respectively]. Although the HR MRT was not significantly different between the C and WI trials [17 (SD 3), 19 (SD 8) s, respectively), VO2 MRT was greater in the WI trial than in the C trial [40 (SD 6), 45 (SD 6) s, respectively; P < 0.05]. Assuming no difference in VO2 in active muscle between the two trials, these results would indicate that an increased oxygen store and/or an altered response in muscle blood distribution delayed the VO2 response to exercise.     

The respiratory system as an exercise limiting factor in normal sedentary subjects.

The present study was undertaken to investigate the respiratory system as an exercise limiting factor. Breathing and cycle endurance (i.e. the time until exhaustion at a given performance level) as well as physical working capacity 170 (i.e. the exercise intensity corresponding to a heart rate of 170 beats.min-1 on a cycle ergometer) were determined in four healthy sedentary subjects. Subsequently, the subjects trained their respiratory system for 4 weeks by breathing daily about 90 l.min-1 for 30 min. Otherwise they continued their sedentary lifestyle. Immediately after the respiratory training and 18 months later, all performance tests carried out at the beginning of the study were repeated. The respiratory training increased breathing endurance from 4.2 (SD 1.9) min to 15.3 (SD 3.8) min. Cycle endurance was improved from 26.8 (SD 5.9) min to 40.2 (SD 9.2) min whereas physical working capacity 170 remained essentially the same. During the endurance cycling test in the respiratory untrained state, the subjects continuously increased their ventilation up to hyperventilation [ventilation at exhaustion = 96.9 (SD 23.6) l.min-1] while after the respiratory training they reached a respiratory steady-state without hyperventilation [ventilation at exhaustion = 63.3 (SD 14.5) l.min-1]. The absence of this marked hyperventilation was the cause of the impressive increase of cycle endurance in normal sedentary subjects after respiratory training. The effects gained by the respiratory training were completely lost after 18 months. Our results indicated that the respiratory system was an exercise limiting factor during an endurance test in normal sedentary subjects.     

Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans

Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training "specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia [fraction of inspired oxygen (Fi(O(2))) = 21% or 13.5%]. Biopsies were taken from the musculus vastus lateralis, and cycle-ergometric incremental maximum oxygen uptake (VO(2max)) exercise tests were performed under normoxia, before and after the 10-wk training program. The main finding was a significant increase (P < 0.05) of fatty acid oxidation capacity per muscle mass, after endurance and strength training under normoxia [2.6- and 2.4-fold for endurance training normoxia group (ET(N)) and strength training normoxia group (ST(N)); n = 8 and 3] and hypoxia [2.0-fold for the endurance training hypoxia group (ET(H)) and strength training hypoxia group (ST(H)); n = 7 and 7], and higher coupling control of oxidative phosphorylation. The enhanced lipid oxidative phosphorylation (OXPHOS) capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P < 0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in muscle mass-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, and octanoylcarnitine). No significant increase was observed in mitochondrial DNA (mtDNA) content. Physiological OXPHOS capacity increased significantly in ET(N) (P < 0.01), with the same trend in ET(H) and ST(H) (P < 0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active lifestyle induced muscular changes of mitochondrial quality representative of mitochondrial health.     

Exercise can be pyrogenic in humans

Exercise increases mean body temperature (T(body)) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE(2) can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T(body) in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), Vo(2 max): 53 ml x kg(-1) x min(-1) (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running ( approximately 75% Vo(2 max)) followed by 45-min cycling and 60-min seated recovery (28 degrees C, 50% relative humidity). Plasma cytokine (TNF-alpha, IL-10) concentrations were measured at rest and 30-min recovery. T(body) was similar at rest in PLAC (35.59 degrees C) and NSAID (35.53 degrees C) and increased similarly during running, but became 0.33 degrees C (SD 0.26) lower in NSAID during cycling (37.39 degrees C vs. 37.07 degrees C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at T(body) of approximately 35.6 degrees C in both conditions but ceased at higher T(body) in PLAC than NSAID during recovery [36.66 degrees C (SD 0.36) vs. 36.39 degrees C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6 x min(-1) higher in PLAC (P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W x m(-2); P = 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.     

Increased concentrations of interleukin 1-β in whole blood cultures supernatants after 12 weeks of moderate endurance exercise

The aim of the study was to investigate whether a regular moderate endurance exercise programme influenced the in vitro cytokine synthesis by stimulated whole blood cultures. To this end, eight healthy subjects exercised moderately by running for 3-5 h a week over a period of 12 weeks, whilst seven other healthy subjects served as the control group. The intensity of the exercise was determined by lactic acid concentrations in the blood which were maintained between 1.8 and 2.5 mmol x l(-1). Over the period of training the running velocity producing the 4 mmol x l(-1) lactic acid threshold increased from 2.86 (SD 0.83) m x s(-1) to 3.06+/-0.79 m x s(-1) (P < or = 0.008). Blood samples were taken at rest before and after the training programme. The following blood parameters were determined: leucocyte count, differential leucocyte count, lymphocyte subpopulations [CD14 positive (+)/CD45+, CD4+/ CD25+, CD8+, CD16+/CD122+]. Whole blood cultures were stimulated with lipopolysaccarides [interleukin (IL)-1 beta and IL-6] and staphylococcal enterotoxin B [IL-2, soluble interleukin 2 receptor (sIL2-R) and interferon (IFN)-gamma]. Cytokine concentrations in the supernatants were measured using an enzyme-linked immunosorbent assay. The white blood cell count, differential leucocyte count, lymphocyte subset distribution and the expression of the CD25 and CD122 antigen on lymphocytes were unchanged by training. After the training programme the IL-1 beta production changed significantly [1496 (SD 264) pg ml(-1) before, compared to 2127 (SD 672) pg ml(-1) after training, P < or = 0.008]. In the control group these parameters remained unchanged. With respect to changes in the values in both groups the syntheses of IL-1 beta (P < or = 0.023) and IL-6 (P < or = 0.021) were significantly higher after regular training. The syntheses of IL-2, sIL-2 and INF-gamma were not significantly influenced. Regular endurance exercise influenced the in vitro production of monocyte derived cytokines, while the effect of exercise on the cytokines synthesized by T-cells appeared to be of lesser importance.     

Effect of obesity on respiratory mechanics during rest and exercise in COPD

The presence of obesity in COPD appears not to be a disadvantage with respect to dyspnea and weight-supported cycle exercise performance. We hypothesized that one explanation for this might be that the volume-reducing effects of obesity convey mechanical and respiratory muscle function advantages. Twelve obese chronic obstructive pulmonary disease (COPD) (OB) [forced expiratory volume in 1 s (FEV(1)) = 60%predicted; body mass index (BMI) = 32 ± 1 kg/m(2); mean ± SD] and 12 age-matched, normal-weight COPD (NW) (FEV(1) = 59%predicted; BMI = 23 ± 2 kg/m(2)) subjects were compared at rest and during symptom-limited constant-work-rate exercise at 75% of their maximum. Measurements included pulmonary function tests, operating lung volumes, esophageal pressure, and gastric pressure. OB vs. NW had a reduced total lung capacity (109 vs. 124%predicted; P < 0.05) and resting end-expiratory lung volume (130 vs. 158%predicted; P < 0.05). At rest, there was no difference in respiratory muscle strength but OB had greater (P < 0.05) static recoil and intra-abdominal pressures than NW. Peak ventilation, oxygen consumption, and exercise endurance times were similar in OB and NW. Pulmonary resistance fell (P < 0.05) at the onset of exercise in OB but not in NW. Resting inspiratory capacity, dyspnea/ventilation plots, and the ratio of respiratory muscle effort to tidal volume displacement were similar, as was the dynamic performance of the respiratory muscles including the diaphragm. In conclusion, the lack of increase in dyspnea and exercise intolerance in OB vs. NW could not be attributed to improvement in respiratory muscle function. Potential contributory factors included alterations in the elastic properties of the lungs, raised intra-abdominal pressures, reduced lung hyperinflation, and preserved inspiratory capacity.