Interrelationships between skeletal muscle adaptations and performance as studied by detraining and retraining

The effects of 15 days of detraining and 15 days of retraining were studied in 6 well-trained runners. Detraining resulted in significant decreases in the mean activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH) of 24 % and 13 %, respectively, but no significant increases in these enzyme activities occurred with retraining. Maximal oxygen uptake (VO₂ max) decreased by 4% with detraining (p < 0.05), and increased by a similar amount with retraining. Performance time in an intense submaximal run decreased by 25% (p < 0.05) with inactivity, but still averaged 9% below the initial level after retraining. Maximal heart rate and peak heart rate during the performance run were higher after detraining by 4 and 9 beats per min, respectively (p < 0.05). With retraining, these heart rate values were decreased by 7 and 9 beats per min (p < 0.05). Blood lactate concentrations after the VO₂ max and performance run were approximately 20% lower after detraining and retraining (p < 0.05). Muscle fibre areas for three subjects tended to be larger in biopsy samples taken after detraining and retraining. These data suggest that even short periods of detraining result in significant changes in indices of physiological capacity and function in subjects near their upper limit of adaptation, and that a longer period of retraining is necessary for muscle to re-adapt to its original trained state.     

Beta-adrenergic blockade and training in healthy men--effects on central circulation

The effect of chronic beta-adrenergic blockade on central circulatory adaptations to physical training was investigated. 16 healthy sedentary males (20-31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks at a work load that during the last 5 weeks corresponded to 75% of the pretraining VO2 max. In a single blind way, 8 subjects were during the training period treated with the beta-adrenergic receptor blocker propranolol (160 mg/day), while the remaining 8 received placebo tablets. Pretraining tests were performed before the start of medication and posttraining tests were performed 6 days after the last day of training and medication. The training program resulted in a similar increase (8%) in VO2 max in both groups (p less than 0.01). The resting heart rate (-4 beats/min; p less than 0.05) as well as the exercise heart rate at a moderate work load (120 W: -11 beats/min; p less than 0.01) decreased with training, and no significant difference was seen between the 2 groups. At a high work load (180 W), however, the heart rate decreased significantly more with training in the placebo group as compared with the beta-blockade group (-19 vs. -7 beats/min; p less than 0.05). The oxygen pulse (VO2/HR) increased in both groups at 120 W (+6%; p less than 0.01). At 180 W the oxygen pulse increased only in the placebo group (+8%; p less than 0.05). The estimated stroke volume at 120 and 180 W, as determined by impedance cardiography, did not change significantly with training although there was a tendency towards an increase in the placebo group only. The resting left ventricular wall thickness and diameter, as determined by echocardiography, did not change significantly with training in either group.--In conclusion, the present study indicates that a moderate degree of beta-adrenergic blockade does not prevent or impair the training-induced increase in the maximal oxygen uptake. During submaximal work, however, the circulatory adaptation may be less apparent if training has been performed during partial blockade of the sympatho-adrenal system.     

Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise

Five subjects cycled on an ergometer at power outputs corresponding to 20, 40, 60 and 80% of their maximal oxygen uptake (VO2 max). On one occasion the transition from rest to work was direct (D), while on the other occasion the power output was increased slowly (S) in a stepwise manner for 6-15 min prior to exercise at the predetermined intensity. Oxygen uptake (VO2) was measured, and O2 deficit and O2 debt were calculated. Oxygen deficit increased with the exercise intensities, the peak values being 2.1 +/- 0.2 and 1.9 +/- 0.1 litres (mean +/- SEM) at 80% of VO2 max after D and S respectively. No significant difference was observed in O2 deficit or O2 debt between D and S at any exercise intensity (P less than 0.05). The O2 debt was similar to the O2 deficit at 20, 40 and 60% of VO2 max but lower than the O2 deficit (P less than 0.05) at 80% of VO2 max. Femoral venous blood lactate remained unchanged at 20% of VO2 max but increased at the higher exercise intensities, reaching peak values of 7.6 +/- 0.6 and 7.4 +/- 1.1 mmol l-1 at 80% of VO2 max after D and S respectively. Blood lactate was not significantly different between D and S at any exercise intensity (P greater than 0.05). It is concluded that O2 deficit, O2 debt and blood lactate are not affected by the rate of transition from rest to submaximal exercise. The data contradict the hypothesis that O2 deficit is caused by an inadequate O2 transport at the onset of exercise.     

Physiological adaptation during short distance triathlon swimming and cycling sectors simulation

The aim of this study was to typify cardiorespiratory and metabolic adaptation capacity at race pace of high-level triathletes during simulations of short distance triathlon swimming sector, first transition and cycling sector. Six national and international-level triathletes performed a 1500 m swimming trial followed by a transition and one hour on ergocycle at race pace, with sequenced measures of blood lactate concentration, gas exchange and heart rate recording. The mean speed obtained in the swimming sector was 1.29+/-0.07 m s(-1), matching 98+/-2% of MAS (Maximal Aerobic Speed), lactate concentration 6.8+/-2.1 mM and heart rate 162+/-15 beats min(-1). In the cycling sector, the mean power was 266+/-34 W, matching 77+/-10% of MAP (Maximal Aerobic Power), oxygen uptake 3788+/-327 mL min(-1) (82.8% of VO2max), heart rate 162+/-13 beats min(-1) (92% of maximal HR) and ventilation 112.8+/-20.8 L min(-1). MAS was correlated with performance in swimming sector (r = 0.944; P < 0.05). Despite intake 1.08+/-0.44 L of a solution with 8% of sugars, a significant loss of body weight (2.80%; P < 0.01) was observed. Changes in cycling power, speed and frequency, especially towards the end of the effort, were also found. By contrast, differences in lactate concentration and in cardiorespiratory or metabolic variables between the end of the swimming sector and the end of the first transition did not appear. In conclusion, this study remarks different relative intensities in cycling and swimming sectors. The observed loss of body weight does not modify pedalling economy in national and international-level athletes during the cycling sector, where effort intensity adapts itself to the one found in individual lactate threshold. However, changes in competition tactics and other effects, such as drafting in swimming and cycling, could alter the intensities established in this study for each sector.     

Comparison of male and female thermal, cardiac, and muscular responses induced by a prolonged run undertaken in a hot environment.]

The aim of this study was to compare male and female thermal, cardiac, and muscular responses induced by a prolonged run undertaken in a hot environment. Twelve volunteers participated in this study. The first group consisted of 6 men and the second one consisted of 6 women. After determination of their VO(2)max and maximal aerobic velocity (MAV), each athlete completed a 40-min run at 65% MAV in a hot and dry environment (temperature 31-33 degrees C, relative humidity 30%). Immediately before and after the run, each subject performed two different vertical jumps, i.e., a squat jump (SJ) and a counter-movement jump (CMJ) on a force platform. Force, velocity, power, and jump height were measured during each jump. The completion of the run was associated with a significant loss (p < 0.001) of body mass (BM) and significant increases (p < 0.001) in heart rate, tympanic temperature, and lactate concentration ([La]). Muscle power was significantly improved (+9%, p < 0.05) during the SJ only in the women. A significant enhancement of this parameter was also demonstrated during the CMJ in both groups (men: +10%, p < 0.05; women: +8%, p < 0.01). Surprisingly, a comparison of thermal, cardiac, and muscular responses did not reveal any significant differences between the sexes. Moderate dehydration (-2.0 to -2.3% of BM) and a rise in core temperature (above 39.2 degrees C) induced by the 40-min run led to an improvement of muscular strength in both men and women. However, the results of this study did not reveal any significant between-sex differences in thermal, cardiac, and muscular responses after exercising in the heat.     

Effect of high-intensity interval training and detraining on extra {\dot{{V}}\hbox{O}_{2}} and on the {\dot{{V}}\hbox{O}_{2}} slow component

To examine the effect of 6-week of high-intensity interval training (HIT) and of 6-week of detraining on the VO2/Work Rate (WR) relationship and on the slow component of VO2, nine young male adults performed on cycle ergometer, before, after training and after detraining, an incremental exercise (IE), and a 6-min constant work rate exercise (CWRE) above the first ventilatory threshold (VT1). For each IE, the slope and the intercept of the VO2/WR relationship were calculated with linear regression using data before VT1. The difference between VO2max measured and VO2max expected using the pre-VT1 slope was calculated (extra VO2). The difference between VO2 at 6th min and VO2 at 3rd min during CWRE (DeltaVO2(6'-3')) was also determined. HIT induced significant improvement of most of the aerobic fitness parameters while most of these parameters returned to their pre-training level after detraining. Extra VO2 during IE was reduced after training (130 +/- 100 vs. -29 +/- 175 ml min(-1), P = 0.04) and was not altered after detraining compared to post-training. DeltaVO2(6'-3') during CWRE was unchanged by training and by detraining. We found a significant correlation (r2 = 0.575, P = 0.02) between extra VO2 and DeltaVO2(6'-3') before training. These results show that an alteration of extra VO2 can occur without any change in the VO2 slow component, suggesting a possible dissociation of the two phenomena. Moreover, the fact that extra VO2 did not change after detraining could indicate that this improvement may remain after the loss of other adaptations.     

Dissociation of training effects on skeletal muscle mitochondrial enzymes and myoglobin in man

The effect of endurance training on skeletal muscle myoglobin concentration in man was investigated. 8 healthy sedentary males (20-31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks. The work consisted of continuous exercise at a work load that during the last 5 weeks corresponded to 75% of the pretraining maximal oxygen uptake (VO2 max). The training program resulted in a 7% increase in VO2 max (p less than 0.01). The activities of the mitochondrial enzymes citrate synthase (CS), succinate dehydrogenase (SDH) and cytochrome c oxidase (Cyt-c-ox) in the quadriceps femoris muscle, as indicators of muscle respiratory capacity, increased by 62-82% (p less than 0.01). The metabolic adaptation of skeletal muscle was further indicated by a 17% increase in the work load corresponding to a blood lactate concentration of 4 mmol/l, as determined by a progressive exercise test (p less than 0.05). There was, however, no change in the myoglobin concentration of the thigh muscle with training (-1%, NS). It is suggested that endurance exercise in man at 75% of the maximal oxygen uptake does not severely tax the functions of myoglobin in skeletal muscle.     

VO2 responses to different intermittent runs at velocity associated with VO2max.

The purposes of this study were (1) to determine the time sustained above 90% of VO2max in different intermittent running sessions having the same overall time run at the velocity (vVO2max) associated with VO2max, and (2) to test whether the use of a fixed-fraction (50%) of the time to exhaustion at vVO2max (Tlim) leads to longer time spent at a high percentage of VO2max. Subjects were 8 triathletes who, after determination of their track vVO2max and Tlim, performed three intermittent running sessions alternating the velocity between 100% and 50% of vVO2max, termed 30 s-30 s, 60 s-30 s, and 1/2 Tlim, where the overall time at vVO2max was similar (= 3 x Tlim). VO2max achieved in the incremental test was 71.1 +/- 3.9 ml.min-1.kg-1 and Tlim was 236 +/- 49 s. VO2peak and peak heart rate were lower in 30 s-30 s than in the other intermittent runs. The time spent above 90% of VO2max was significantly (p < 0.001) longer either in 60 s-30 s (531 +/- 187 s) or in 1/2 Tlim-1/2 Tlim (487 +/- 176 s) than in 30 s-30 s (149 +/- 33 s). Tlim was negatively correlated with the time (in % of Tlim) spent above 90% of VO2max in 30 s-30 s (r = -0.75, p < 0.05). Tlim was also correlated with the difference of time spent over 90% of VO2max between 60 s-30 s and 30 s-30 s (r = 0.77, p < 0.05), or between 1/2 Tlim-1/2 Tlim and 30 s-30 s (r = 0.97, p < 0.001). The results confirm that vVO2max and Tlim are useful for setting interval-training sessions. However, the use of an individualized fixed-fraction of Tlim did not lead to longer time spent at a high percentage of VO2max compared to when using a fixed work-interval duration.     

Effects of a 5-h hilly running on ankle plantar and dorsal flexor force and fatigability

This study aimed to examine the effects of a 5-h hilly run on ankle plantar (PF) and dorsal flexor (DF) force and fatigability. It was hypothesised that DF fatigue/fatigability would be greater than PF fatigue/fatigability. Eight male trail long distance runners (42.5 ± 5.9 years) were tested for ankle PF and DF maximal voluntary isokinetic contraction strength and fatigue resistance tests (percent decrement score), maximal voluntary and electrically evoked isometric contraction strength before and after the run. Maximal EMG root mean square (RMS(max)) and mean power frequency (MPF) values of the tibialis anterior (TA), gastrocnemius lateralis (GL) and soleus (SOL) EMG activity were calculated. The peak torque of the potentiated high- and low-frequency doublets and the ratio of paired stimulation peak torques at 10 Hz over 100 Hz (Db10:100) were analysed for PF. Maximal voluntary isometric contraction strength of PF decreased from pre- to post-run (-17.0 ± 6.2%; P < 0.05), but no significant decrease was evident for DF (-7.9 ± 6.2%). Maximal voluntary isokinetic contraction strength and fatigue resistance remained unchanged for both PF and DF. RMS(max) SOL during maximal voluntary isometric contraction and RMS(max) TA during maximal voluntary isokinetic contraction were decreased (P < 0.05) after the run. For MPF, a significant decrease for TA (P < 0.05) was found and the ratio Db10:100 decreased for PF (-6.5 ± 6.0%; P < 0.05). In conclusion, significant isometric strength loss was only detected for PF after a 5-h hilly run and was partly due to low-frequency fatigue. This study contradicted the hypothesis that neuromuscular alterations due to prolonged hilly running are predominant for DF.     

Effect of 4 weeks of training on the limit time at VO2 max]

The purpose of this study was to examine the effect of 4 weeks training in running on the time spent at VO2max (tlim VO2max). Eight athletes carried out, before and after an aerobic training, an incremental and five exhaustive tests at 90, 95, 100, 115% vVO2max and at the critical power at VO2max (CV'; slope of the linear relation between the tlim VO2max and the distance limit at VO2max). This training did not significantly improve VO2max (p = 0.17) or tlim VO2max (p = 0.72). However, the "tlim VO2max-intensity" curve was shifted toward the right, meaning that the athlete had to run at a higher intensity after training to obtain the same tlim VO2max. Tlim VO2max at CV' before training was significantly higher than tlim VO2max at 90, 95, 100, and 115% vVO2max (p < 0.05). This training increased CV' in absolute value (13.9 +/- 1.3 vs. 14.9 +/- 1.2 km.h-1, p < 0.05; n = 6) but not in relative value (86 +/- 4 vs. 86 +/- 5% vVO2max; p = 0.9). In conclusion, in spite of the shift of the "tlim VO2max-intensity" curve, tlim VO2max was not significantly increased by this training. Furthermore, CV' allowed subjects to spend the longest time of exercise at VO2max during a continuous exercise with constant speed, but CV', expressed in % vVO2max, did not improve with this training.     

Physiological parameters determined at OBLA vs. a fixed heart rate of 175 beats x min-1 in an incremental test performed by amateur and professional cyclists

A blood lactate concentration of 4 mmol x l-1 (OBLA) is frequently used as an indicator of the maximal steady state of lactate (MLSS) for workload planning in training programs. The aim of the present investigation was to compare several metabolic parameters determined at OBLA and at a fixed heart rate of 175 beats x min-1 (HR175) in amateur cyclists (AC) and professional cyclists (PC). Sixteen AC and 22 PC performed an exercise test on a cycle ergometer following a ramp protocol (25 W x min-1, 70-80 rpm) to exhaustion. Gaseous exchange was monitored throughout the test. VO2, %VO2 max, and power output (W) corresponding to OBLA and HR175 were determined and mean values compared using a Student's t-test. Findings indicated higher VO2 max and W in general in PC (p<0.01), and higher VO2 and W at OBLA and HR175 in PC (p<0.01). No significant difference was found between values determined at OBLA and HR175 in the AC group, while in the PC group, VO2, %VO2 max, and W were higher at OBLA. These observations suggest the possible use of a fixed, reference HR of 175 beats x min-1 to determine the exercise intensity corresponding to OBLA in amateur cyclists. This was not the case for the professional cyclists.     

Physical fitness in aging men

Of 56 middle-aged male joggers (mean age 43.3 yr), 38 were measured for maximal oxygen uptake (VO2max) and 18 for cardiac output at a heart rate of 170 bpm (Q170). Each Q170 was divided by subject body surface area to yield cardiac index (CI170). A treadmill protocol was used to elicit maximal exercise during measurement of VO2max. The bicycle ergometer was employed when measuring Q170. For maximal exercise, termination was upon subject-declared fatigue. In subjects measured for VO2max, heart rate at 3.5 miles/h and 5% treadmill grade (HRsubmax) as well as heart rate at maximal exercise (HRmax) were noted. Heart rates were monitored electrocardiographically. A modified Douglas bag technique was applied when sampling expired air for determination of VO2max. Carbon dioxide rebreathing was used to estimate Q170. Data were grouped according to age (43 yr and older; 42 yr and younger). There were significant (P less than 0.05) positive relationships between VO2max and HRmax and between HRsubmax and age. Significant negative relationships existed between HRmax and HRsubmax, and between CI170 and 10 km running time. There were no significant differences (P greater than 0.05) between means achieved by the age groups. The overall mean for VO2max was 43.36 ml/kg per min and for Q170 33.53 1/min. Findings suggest that men who remain physically active retain youthful characteristics of cardiorespiratory function.     

Role of blood volume in the age-associated decline in peak oxygen uptake in humans.

It has been reported that maximal oxygen uptake (VO(2 max)) is linearly correlated with blood volume (BV) in young people and that there is a reduction in VO(2 max) with aging. To examine the involvement of BV in the reduction of VO(2 max), we used an incremental cycle ergometer protocol in a semi-recumbent position to determine the relationship between peak oxygen uptake (VO(2 peak)) and BV in older subjects (69.1 +/- 1.0 years; n = 22), then compared that relationship with that in young subjects (22.3 +/- 0.5 years; n = 31). In the present study, VO(2 peak) and BV were significantly lower in the older subjects, compared with those in the young subjects. A linear correlation was demonstrated between the VO(2 peak) and BV in both the older (r = 0.705; p < 0.001) and the young (r = 0.681; p < 0.001) subjects within the groups. However, an analysis of covariance with BV as a covariate revealed that VO(2 peak) at a given BV was smaller in the older subjects than in the young subjects (p < 0.001), i.e., graphically, the regression line determined for the older subjects showed a downward shift. The decreased peak heart rate as a result of aging (153 +/- 3 beats/min in the older vs. 189 +/- 2 beats/min in the young subjects) contributed partly to this downward shift. These results suggest that the BV is an important determinant factor for VO(2 peak), especially within an age group, and that the age-associated decline of VO(2 peak) is also, to a relatively larger degree, because of factors other than BV and heart rate.     

Effect of training and detraining on monocarboxylate transporter (MCT) 1 and MCT4 in Thoroughbred horses

The aim of this study was to investigate the effects of training and detraining on the monocarboxylate transporter (MCT) 1 and MCT4 levels in the gluteus medius muscle of Thoroughbred horses. Twelve Thoroughbred horses were used for the analysis. For 18 weeks, all the horses underwent high-intensity training (HIT), with running at 90-110% maximal oxygen consumption (VO2 max ) for 3 min, 5 days week(-1). Thereafter, the horses either underwent detraining for 6 weeks by either 3 min of moderate-intensity training (MIT) at 70% VO2 max, 5 days week(-1) (HIT-MIT group) or stall rest (HIT-SR group). The horses underwent an incremental exercise test, VO2 max was measured and resting muscle samples were obtained from the middle gluteus muscle at 0, 18 and 24 weeks. The content of MCT1 and MCT4 proteins increased after 18 weeks of HIT. At the end of this period, an increase was noted in the citrate synthase activity, while phosphofructokinase activity remained unchanged. After 6 weeks of detraining, all these indexes returned to the pretraining levels in the HIT-SR group. However, in the HIT-MIT group, the increase in the MCT1 protein content and citrate synthase activity was maintained after 6 weeks of MIT, while the MCT4 protein content decreased to the pretraining value. These results suggest that the content of MCT1 and MCT4 proteins increases after HIT in Thoroughbred horses. In addition, the increase in the MCT1 protein content and oxidative capacity induced by HIT can be maintained by MIT of 70% VO2 max, but the increase in the MCT4 protein content cannot be maintained by MIT.     

Effect of training on the activity of five muscle enzymes studied on elite cross-country skiers

This study examines the effect of training intensity on the activity of enzymes in m. vastus lateralis. Elite junior cross-country skiers of both sexes trained 12-15 h weeks-1 for 5 months at either moderate (60-70% of VO2max, MIG) or high training intensity (80-90% of the VO2max, close to the lactate threshold; HIG). Muscle biopsies for enzyme analyses and fibre typing were taken before and after the training period. Histochemical analyses on single fibres were done for three enzymes (succinate dehydrogenase [SDH], hydroxybutyrate dehydrogenase [HBDH], glycerol-3-phosphate dehydrogenase [GPDH]), while the activity of citrate synthase [CS] and phosphofructokinase [PFK] was measured on whole biopsies. The activity of GPDH was low in ST fibres and high in FT fibres. The activity of SDH and HBDH was high in both ST and FTa fibres but low in the FTb fibres. The HIG increased their performance more than the MIG did during the training period as judged from scores on a 20-min run test. The SDH activity rose by 6% for the HIG (P < 0.02). No effects of training were found in the activities of CS, HBDH or GPDH, neither in the two training groups nor for the two genders (P > or = 0.16). The PFK activity fell by 10% for the HIG (P=0.02), while no change was found for the MIG. For GPDH, CS and SDH the women's activity was approximately 20% less than the value for the men (P < 0.03). For PFK and HBDH there was no sex difference (P > or = 0.27). There were positive correlations between the activity of three of the enzymes (CS, SDH and GPDH) and the performance parameters (VO2max, cross-country skiing and running performance; r > or = 0.6, P < 0.01). No correlations were found between the PFK or HBDH activities and the performance parameters (r < or = 0.16, P > 0.05). This study suggests that intensities near the lactate threshold affect biochemical and physiological parameters examined in this study as well as the performance of elite skiers, and that the rate-limiting enzymes may be more sensitive to training than non-rate-limiting enzymes.     

Exercise performance of subjects with ankylosing spondylitis and limited chest expansion

To examine the mechanism of exercise limitation associated with chest wall restriction (CWR), we compared the ramp (1 W/3 s) exercise performance of six untrained subjects with ankylosing spondylitis (AS) and six healthy subjects matched for age and body size. Subjects with AS had CWR (maximum rib cage expansion : 1.4 +/- 0.2 cm; means +/- sem). The maximum oxygen uptake (VO2max) of AS subjects (2.15 +/- 0.2 1-stpd) was less than their predicted VO2max (2.68 +/- 0.13 1-stpd; p less than 0.03) and the measured VO2max of matched healthy subjects (2.78 +/- 0.22 1-stpd; p less than 0.03). Subjects with AS achieved 95 percent of predicted maximum heart rate, and their maximum voluntary ventilation exceeded their maximum exercise ventilation by at least 15 l X min-1 unless parenchymal pulmonary disease was present. We conclude that maximum ramp exercise performance of AS subjects with CWR is decreased. Deconditioning or cardiovascular impairment rather than ventilatory impairment appears responsible for the observed reduction of VO2max.     

Improvement of $$\dot{V}\hbox{O}_{2 \max},$$ by cardiac output and oxygen extraction adaptation during intermittent versus continuous endurance training

Improvement of exercise capacity by continuous (CT) versus interval training (IT) remains debated. We tested the hypothesis that CT and IT might improve peripheral and/or central adaptations, respectively, by randomly assigning 10 healthy subjects to two periods of 24 trainings sessions over 8 weeks in a cross-over design, separated by 12 weeks of detraining. Maximal oxygen uptake (VO2max), cardiac output (Qmax) and maximal arteriovenous oxygen difference (Da-vO2max) were obtained during an exhaustive incremental test before and after each training period. VO2max and Qmax increased only after IT (from 26.3 +/- 1.6 to 35.2 +/- 3.8 ml min(-1) kg(-1) and from 17.5 +/- 1.3 to 19.5 +/- 1.8 l min(-1), respectively; P < 0.01). Da-vO2max increased after both protocols (from 11.0 +/- 0.8 to 12.7 +/- 1.0; P < 0.01 and from 11.0 +/- 0.8 to 12.1 +/- 1.0 ml 100 ml(-1), P < 0.05 in CT and IT, respectively). At submaximal intensity a significant rightward shift of the Q/Da-vO2 relationship appeared only after CT. These results suggest that in isoenergetic training, central and peripheral adaptations in oxygen transport and utilization are training-modality dependant. IT improves both central and peripheral components of Da-vO2max whereas CT is mainly associated with greater oxygen extraction.     

Effects of detraining on enzymes of energy metabolism in individual human muscle fibers

Muscle biopsies were obtained from three cyclists and four runners at the end of 10-24 mo of intensive training and after intervals of detraining up to 12 wk. Control samples came from four untrained persons and four former athletes. Macro mixed fiber samples were assayed for lactate dehydrogenase, adenylate kinase, glycogen phosphorylase, citrate synthase, malate dehydrogenase, beta-hydroxyacyl-CoA dehydrogenase, succinate dehydrogenase, beta-hydroxybutyrate dehydrogenase, creatine kinase, hexokinase, 1-phosphofructokinase, fructosebisphosphatase, protein, and total creatine. In the case of three trained persons and two controls, the first six of the enzymes were also measured in individual fibers. Before detraining, enzymes of oxidative metabolism were substantially higher than in controls, and differences in levels between type I and type II fibers were smaller. During detraining, oxidative enzymes were decreased in both fiber types but the type II fibers did not fall to control levels even after 12 wk. Phosphorylase increased with detraining in both fiber types. The same is true for lactate dehydrogenase and adenylate kinase, except in the case of the type I fibers of one individual. Among the other six enzymes (measured in mixed fiber samples), only hexokinase was consistently affected (decreased) by detraining.     

Determinant factors of the decrease in aerobic performance in moderate acute hypoxia in women endurance athletes

The purpose of this study was to evaluate the limiting factors of maximal aerobic performance in endurance trained (TW) and sedentary (UW) women. Subjects performed four incremental tests on a cycle ergometer at sea level and in normobaric hypoxia corresponding to 1000, 2500 and 4500 m. Maximal oxygen uptake decrement (Delta VO2 max) was larger in TW at each altitude. Maximal heart rate and ventilation decreased at 4500 m in TW. Maximal cardiac output remained unchanged. In both groups, arterialized oxygen saturation (Sa'O2 max) decreased at and above 2500 m and maximal O2 transport (QaO2 max) decreased from 1000 m. At 4500 m, there was no more difference in QaO2 max between TW and UW. Mixed venous O2 pressure (PvO2 max) was lower and O2 extraction (O2ERmax) greater in TW at each altitude. The primary determinant factor of VO2 max decrement in moderate acute hypoxia in trained and untrained women is a reduced maximal O2 transport that cannot be compensate by tissue O2 extraction.     

NADH content and lactate production in the perfused rabbit heart

The influence of oxygen availability and absence of contractile activity on the NADH content and lactate production were investigated in the rabbit heart. Isolated hearts were perfused according to Langendorff with a modified Tyrode solution, saturated with a gas mixture containing either 95% O2:5% CO2 (control), 50% O2:5% CO2 in N2 (hypoxia), or 5% CO2 in N2 (anoxia). In another series of hearts cardiac arrest was induced by perfusion with Tyrode solution (95% O2:5% CO2) where the KCl concentration was increased to 15 mmol l-1 (hyperkalemia). Oxygen uptake (VO2) was similar in hypoxic and control hearts (P greater than 0.05), whereas lactate production was four-fold higher during hypoxia vs. control (P less than 0.01). Hyperkalemia resulted in a 60% decrease in VO2 (P less than 0.05), and no significant change in lactate production vs. control (P greater than 0.05). Both PCr and ATP were substantially decreased only during anoxia. Muscle NADH, whose changes reflect those within the mitochondria, averaged (+/- SE) 0.074 +/- 0.010, 0.153 +/- 0.016, 0.486 +/- 0.162 and 1.771 +/- 0.091 mmol kg-1 dry wt during control, hyperkalemia, hypoxia and anoxia, respectively. It is concluded that: muscle contraction during conditions of adequate oxygen supply results in an oxidation of mitochondrial NADH (presumably due to ADP stimulation of respiration), and a decreased oxygen availability results in an increase in NADH and an accelerated lactate production, although the VO2 is not affected.