Sustained maximal ventilation after endurance exercise in athletes

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.     

Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training

It is welldocumented that endurance exercise training results in a bluntednorepinephrine (NE) response to exercise of a given absolute exerciseintensity. However, it is not clear what effect traininghas on the catecholamine response to exercise of the same relativeintensity because previous studies have provided conflicting results.The purpose of the present study was, therefore, to determine thecatecholamine response to exercise of the same relative exerciseintensity before and after endurance exercise training. Six women andthree men [age 28 ± 8 (SD) yr] performed 10 wk oftraining. Maximal O₂ uptake(O_{2 max}) wasdetermined during treadmill exercise. Fifteen-minute treadmill exercisebouts were performed at 60, 65, 70, 75, 80, and 85% ofO_{2 max} before andafter training.O_{2 max} was increasedby 20% (from 39.2 ± 7.7 to 46.9 ± 8.1 ml · kg¹ · min¹;P < 0.05) in response to training.Plasma NE concentrations were higher(P < 0.05) during exercise at thesame relative intensity after, compared with before, training at65-85% ofO_{2 max.}Differences between heart rates and plasma epinephrine concentrationsafter, compared with before, training were not statisticallysignificant. These results provide evidence that the NE response toexercise is dependent on the absolute as well as the relative intensity of the exercise.     

Muscle power and metabolism in maximal intermittent exercise

Muscle power and the associated metabolic changes in muscle were investigated in eight male human subjects who performed four 30-s bouts of maximal isokinetic cycling at 100 rpm, with 4-min recovery intervals. In the first bout peak power and total work were (mean +/- SE) 1,626 +/- 102 W and 20.83 +/- 1.18 kJ, respectively; muscle glycogen decreased by 18.2 mmol/kg wet wt, lactate increased to 28.9 +/- 2.7 mmol/kg, and there were up to 10-fold increases in glycolytic intermediates. External power and work decreased by 20% in both the second and third exercise periods, but no further change occurred in the fourth bout. Muscle glycogen decreased by an additional 14.8 mmol/kg after the second exercise and thereafter remained constant. Muscle adenosine triphosphate (ATP) was reduced by 40% from resting after each exercise period; creatine phosphate (CP) decreased successively to less than 5% of resting; in the recovery periods ATP and CP increased to 76 and 95% of initial resting levels, respectively. Venous plasma glycerol increased linearly to 485% of resting; free fatty acids did not change. Changes in muscle glycogen, lactate, and glycolytic intermediates suggested rate limitation at phosphofructokinase during the first and second exercise periods, and phosphorylase in the third and fourth exercise periods. Despite minimal glycolytic flux in the third and fourth exercise periods, subjects generated 1,000 W peak power and sustained 400 W for 30 s, 60% of the values recorded in the first exercise period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantitative trait loci associated with maximal exercise endurance in mice.

The role of genetics in the determination of maximal exercise endurance is unclear. Six- to nine-week-old F2 mice (n = 99; 60 female, 39 male), derived from an intercross of two inbred strains that had previously been phenotyped as having high maximal exercise endurance (Balb/cJ) and low maximal exercise endurance (DBA/2J), were treadmill tested to estimate exercise endurance. Selective genotyping of the F2 cohort (n = 12 high exercise endurance; n = 12 low exercise endurance) identified a significant quantitative trait locus (QTL) on chromosome X (53.7 cM, DXMit121) in the entire cohort and a suggestive QTL on chromosome 8 (36.1 cM, D8Mit359) in the female mice. Fine mapping with the entire F2 cohort and additional informative markers confirmed and narrowed the QTLs. The chromosome 8 QTL (EE8(F)) is homologous with two suggestive human QTLs and one significant rat QTL previously linked with exercise endurance. No effect of sex (P = 0.33) or body weight (P = 0.79) on exercise endurance was found in the F2 cohort. These data indicate that genetic factors in distinct chromosomal regions may affect maximal exercise endurance in the inbred mouse. Whereas multiple genes are located in the identified QTL that could functionally affect exercise endurance, this study serves as a foundation for further investigations delineating the identity of genetic factors influencing maximum exercise endurance.     

Determinants of time trial performance and maximal incremental exercise in highly trained endurance athletes

Human endurance performance can be predicted from maximal oxygen consumption (Vo(2max)), lactate threshold, and exercise efficiency. These physiological parameters, however, are not wholly exclusive from one another, and their interplay is complex. Accordingly, we sought to identify more specific measurements explaining the range of performance among athletes. Out of 150 separate variables we identified 10 principal factors responsible for hematological, cardiovascular, respiratory, musculoskeletal, and neurological variation in 16 highly trained cyclists. These principal factors were then correlated with a 26-km time trial and test of maximal incremental power output. Average power output during the 26-km time trial was attributed to, in order of importance, oxidative phosphorylation capacity of the vastus lateralis muscle (P = 0.0005), steady-state submaximal blood lactate concentrations (P = 0.0017), and maximal leg oxygenation (sO(2LEG)) (P = 0.0295), accounting for 78% of the variation in time trial performance. Variability in maximal power output, on the other hand, was attributed to total body hemoglobin mass (Hb(mass); P = 0.0038), Vo(2max) (P = 0.0213), and sO(2LEG) (P = 0.0463). In conclusion, 1) skeletal muscle oxidative capacity is the primary predictor of time trial performance in highly trained cyclists; 2) the strongest predictor for maximal incremental power output is Hb(mass); and 3) overall exercise performance (time trial performance + maximal incremental power output) correlates most strongly to measures regarding the capability for oxygen transport, high Vo(2max) and Hb(mass), in addition to measures of oxygen utilization, maximal oxidative phosphorylation, and electron transport system capacities in the skeletal muscle.     

Determination of maximal aerobic power during upper-body exercise

The purpose of this investigation was to evaluate four protocols for their effectiveness in eliciting maximal aerobic power (peak VO2) during arm-crank exercise. Comparisons were made 1) between a continuous (CON) and an intermittent (INT) protocol (both employed a crank rate of 50 rpm) and 2) among the CON protocols employing crank rates of 30, 50, or 70 rpm. For the first group of experiments no significant (P greater than 0.05) differences were found between the CON and INT protocols for peak VO2, maximal pulmonary ventilation (VEmax), maximal heart rate (HRmax), or maximal blood lactate (LAmax) responses. For the second group of experiments, the CON-50 was compared with the CON-30 and CON-70 protocols. In comparison to the CON-50, significantly higher peak VO2 (+10%) and VEmax (+14%) responses were elicited by the CON-70 protocol, whereas significantly lower peak VO2 (-11%), VEmax (-23%), HRmax (-8%), and LAmax (-29%) responses were elicited by the CON-30 protocol. Of the arm-crank protocols examined the combination of a continuous design and a crank rate of 70 rpm provided the most effective protocol to elicit peak VO2 values.     

Joint-specific power production and fatigue during maximal cycling

Cycling power decreases substantially during a maximal cycling trial of just 30 s. It is not known whether movement patterns and joint powers produced at each joint decrease to a similar extent or if each joint exhibits an individual fatigue profile. Changes in movement patterns and/or joint powers associated with overall task fatigue could arise from several different mechanisms or from a complex interplay of these mechanisms. The purpose of this investigation was to determine the changes in movement and power at each joint during a fatiguing cycling trial. Thirteen trained cyclists performed a 30 s maximal cycling trial on an isokinetic cycle ergometer at 120 rpm. Pedal forces and limb kinematics were recorded. Joint powers were calculated using a sagittal plane inverse dynamics model and averaged for the initial, middle, and final three second intervals of the trial, and normalized to initial values. Relative ankle plantar flexion power was significantly less than all other joint actions at the middle interval (51±5% of initial power; p=0.013). Relative ankle plantar flexion power for the final interval (37±3%) was significantly less than the relative knee flexion and hip extension power (p=0.010). Relative knee extension power (41±5%) was significantly less than relative hip extension power (55±4%) during the final three second interval (p=0.045). Knee flexion power (47±5%) did not differ from relative hip extension power (p=0.06). These changes in power were accompanied by a decrease in time spent extending by each joint with fatigue (i.e., decreased duty cycle, p<0.03). While central mechanisms may have played a role across all joints, because the ankle fatigued more than the hip and knee joints, either peripheral muscle fatigue or changes in motor control strategies were identified as the potential mechanisms for joint-specific fatigue during a maximal 30 s cycling trial.     

Effects of short-period exercise training and orlistat therapy on body composition and maximal power production capacity in obese patients

We examined the effects of weight loss induced by diet-orlistat (DO) and diet-orlistat combined with exercise (DOE) on maximal work rate production (Wmax) capacity in obese patients. Total of 24 obese patients were involved in this study. Twelve of them were subjected to DO therapy only and the remaining 12 patients participated in a regular aerobic exercise-training program in addition to DO therapy (DOE). Each patient performed two incremental ramp exercise tests up to exhaustion using an electromagnetically-braked cycle ergometer: one at the onset and one at the end of the 4th week. DOE therapy caused a significant decrease in total body weight: 101.5+/-17.4 kg (basal) vs 96.3+/-17.3 kg (4 wk) associated with a significant decrease in body fat mass: 45.0+/-10.5 kg (basal) vs 40.9+/-9.8 kg (4 wk). DO therapy also resulted in a significant decrease of total body weight 94.9+/-14.9 kg (basal) vs 91.6+/-13.5 kg (4 wk) associated with small but significant decreases in body fat mass: 37.7+/-5.6 kg (basal) to 36.0+/-6.2 kg (4 wk). Weight reduction achieved during DO therapy was not associated with increased Wmax capacity: 106+/-32 W (basal) vs 106+/-33 W (4 wk), while DOE therapy resulted in a markedly increased Wmax capacity: 109+/-39 W (basal) vs 138+/-30 W (4 wk). DO therapy combined with aerobic exercise training resulted in a significant reduction of fat mass tissue and markedly improved the aerobic fitness and Wmax capacities of obese patients. Considering this improvement within such a short period, physicians should consider applying an aerobic exercise-training program to sedentary obese patients for improving their physical fitness and thereby reduce the negative outcomes of obesity.     

Cardiac adaptation to endurance exercise in rats

Endurance exercise is widely assumed to improve cardiac function in humans. This project has determined cardiac function following endurance exercise for 6 (n = 30) or 12 (n = 25) weeks in male Wistar rats (8 weeks old). The exercise protocol was 30 min/day at 0.8 km/h for 5 days/week with an endurance test on the 6th day by running at 1.2 km/h until exhaustion. Exercise endurance increased by 318% after 6 weeks and 609% after 12 weeks. Heart weight/kg body weight increased by 10.2% after 6 weeks and 24.1% after 12 weeks. Echocardiography after 12 weeks showed increases in left ventricular internal diameter in diastole (6.39 ± 0.32 to 7.90 ± 0.17 mm), systolic volume (49 ± 7 to 83 ± 11 μl) and cardiac output (75 ± 3 to 107 ± 8 ml/min) but not left wall thickness in diastole (1.74 ± 0.07 to 1.80 ± 0.06 mm). Isolated Langendorff hearts from trained rats displayed decreased left ventricular myocardial stiffness (22 ± 1.1 to 19.1 ± 0.3) and reduced purine efflux during pacing-induced workload increases. 31P-NMR spectroscopy in isolated hearts from trained rats showed decreased PCr and PCr/ATP ratios with increased creatine, AMP and ADP concentrations. Thus, this endurance exercise protocol resulted in physiological hypertrophy while maintaining or improving cardiac function. (Mol Cell Biochem 251: 51–59, 2003)     

Effects of endurance exercise on metabolic water production and plasma volume

Six endurance-trained and heat-acclimatized adult males ran for 1 h (or until exhaustion) at room temperature (23.8 degrees C) on three occasions. The work loads approximated 37, 56, and 74% of the subjects' aerobic capacities. Venous blood samples were drawn, and urine was collected before and immediately after each exercise bout. Metabolic cost was partitioned by energy substrate, and metabolic water production was quantified from urinary nitrogen, oxygen, and carbon dioxide production. Total body water loss was recorded as the decrease in body weight during the exercise. All subjects completed 1 h of exercise at the two lower exercise intensities but, due to exhaustion, averaged only 35.5 min at the highest work intensity. There were no significant changes in plasma volume after the exercise bouts. Metabolic water production increased with increasing work intensity as did the fraction of total caloric expenditure derived from carbohydrate metabolism. Plasma protein content significantly increased at all levels of exercise intensity. Metabolic water production alone would be of minimal help in plasma volume maintenance and thermoregulation during endurance exercise.     

Effect of prior exercise on maximal short-term power output in humans

The effect of prior exercise (PE) on subsequent maximal short-term power output (STPO) was examined during cycling exercise on an isokinetic ergometer. In the first series of experiments the duration of PE at a power output equivalent to 98% maximum O2 uptake (VO2max) was varied between 0.5 and 6 min before measurement of maximal STPO. As PE duration increased subsequent STPO fell to approximately 70% of control values after 3-6 min. In series ii the effect of varying the intensity of PE of fixed 6-min duration was studied in five subjects. After PE less than 60% VO2max there was an increase of 12% in STPO, but after greater than 60% VO2max there was a progressive fall in STPO as PE intensity increased, indicating a reduction of approximately 35% at 100% VO2max compared with control values. In series iii we examined the effect on STPO of allowing a recovery period after a fixed intensity (mean = 87% VO2max) of 6 min PE before measurement of STPO. This indicated a rapid recovery of dynamic function with a half time of approximately 32 s, which is similar to the kinetics of PC resynthesis and taken with the other findings suggests the dominant role that PC exerts on the STPO under these conditions.     

Effects of exercise on maximal instantaneous muscular power of humans

The maximal instantaneous anaerobic power (w), as determined during a high jump off both feet on a force platform, was measured on eight subjects starting from a resting base line; a base line of steady-state cycloergometric exercise requiring 30, 50, and 70% of individual maximum O2 consumption (VO2max); and a base line of maximal and supramaximal exercise (100 and 120% of VO2max). In addition, w was also measured during the VO2 transients from rest to each of the above work loads. Blood lactate concentration ([Lab]) was determined before and 8 min after the end of each priming load. After the onset of any priming load, w decreases with time reaching in 2 min a steady level that is lower the higher the VO2. For the three lowest work rates, the steady w level is unchanged by increasing the duration of the priming exercise up to 30 min. For low work levels, the decrease of w as a function of VO2 is essentially parallel to that of estimated muscle concentration of ATP ([ATP]). For work levels greater than 60% of VO2max involving a substantial accumulation of lactate, the decrease of w becomes smaller than the estimated drop of muscle [ATP]. This finding is tentatively attributed to an increase of either the mechanical equivalent or of the velocity constant of ATP splitting brought about by the lowering of intracellular muscle pH after lactate accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ultra short-term heart rate recovery after maximal exercise: relations to aerobic power in sportsmen

The main aim of the study was to investigate whether different levels of aerobic power influence heart rate (HR) responses during the first minute of recovery following maximal exercise in athletes. Thirty-two young male soccer players were recruited for the study during the final week of their training prior to [corrected] the competition. Following the maximal exercise on treadmill the participants were placed supine for 60 s of HR recording. The time between exercise cessation and the recovery HR measurement was kept as short as possible. At the end of exercise (i.e., the start of recovery), HRs were [corrected] was similar in both trials. At both 10 s and 20 s of recovery period, the players characterized by high aerobic power (> 60 ml/kg/ min) revealed significantly lower HR as compared to their sub-elite counterparts (< 50 ml/kg/min; P < 0.05). No differences between the groups were found at later stages of the analyzed post-exercise HR. The data suggest that the athletes characterized by high aerobic capacity could be better adapted to maximal exercise with faster recovery HR immediately following an exercise test. These results generally suggest that the aerobic power along with autonomic modulation might have played a role in the ultra short-term cardiovascular responses to all-out exercise.     

Cerebral hemodynamic response to maximal exercise

The response of central and cerebral hemodynamics to a stepwise increase in dynamic exercise until failure was studied in healthy young men. Each subject was examined using Doppler ultrasound assessment of blood flow in the middle cerebral artery (MCA), Doppler echocardiography, and spiroergometry. Hemodynamic parameters were recorded before the study and during the last several seconds of each step of the dynamic exercise. The central hemodynamic and energy exchange parameters exhibited typical changes with increasing exercise intensity. The peak systolic blood flow velocity in the MCA increased only in response to exercise of a moderate intensity (1 W/kg body weight, 45% of the maximal oxygen uptake); the further increase in exercise intensity did not affect the blood flow velocity. The cerebral vascular resistance index at the last step of the exercise was 24% higher than at rest. The increase in the MCA resistance index during the exercise was moderately correlated with the increase in the pulse pressure and systolic blood pressure, whereas the increase in blood pressure was not related to the increase in the peak systolic blood flow velocity in the MCA in response to an exercise intensity at which the oxygen uptake was higher than 45% of its maximal value. The differences between the responses of central and cerebral hemodynamics to the stepwise increase in exercise intensity reflect the phenomenon of cerebral hemodynamic autoregulation.     

Water and carbohydrate ingestion during prolonged exercise increase maximal neuromuscular power.

This study investigated the individual and combined effects of water and carbohydrate ingestion during prolonged cycling on maximal neuromuscular power (P(max)), thermoregulation, cardiovascular function, and metabolism. Eight endurance-trained cyclists exercised for 122 min at 62% maximal oxygen uptake in a 35 degrees C environment (50% relative humidity, 2 m/s fan speed). P(max) was measured in triplicate during 6-min periods beginning at 26, 56, 86, and 116 min. On four different occasions, immediately before and during exercise, subjects ingested 1) 3.28 +/- 0.21 liters of water with no carbohydrate (W); 2) 3.39 +/- 0.23 liters of a solution containing 204 +/- 14 g of carbohydrate (W+C); 3) 204 +/- 14 g of carbohydrate in only 0.49 +/- 0.03 liter of solution (C); and 4) 0. 37 +/- 0.02 liter of water with no carbohydrate (placebo; Pl). These treatments were randomized, disguised, and presented double blind. At 26 min of exercise, P(max) was similar in all trials. From 26 to 116 min, P(max) declined 15.2 +/- 3.3 and 14.5 +/- 2.1% during C and Pl, respectively; 10.4 +/- 1.9% during W (W > C, W > Pl; P < 0.05); and 7.4 +/- 2.2% during W+C (W+C > W, W+C > C, and W+C > Pl; P < 0. 05). As an interesting secondary findings, we also observed that carbohydrate ingestion increased heat production, final core temperature, and whole body sweating rate. We conclude that, during prolonged moderate-intensity exercise in a warm environment, ingestion of W attenuates the decline in P(max). Furthermore, ingestion of W+C attenuates the decline in maximal power more than does W alone, and ingestion of C alone does not attenuate the decline in P(max) compared with Pl.