***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: The aim was to investigate the effects of low-load resistant training combined with vascular occlusion or normobaric hypoxic exposure , on  neuromuscular function . In a r and omised controlled trial , well-trained athletes took part in a 5-week training of knee flexor/extensor muscles in which low-load resistant exercise ( 20 % of one repetition maximum , 1-RM ) was combined with either ( 1 ) an occlusion pressure of approximately 230 mmHg ( KT , n = 10 ) , ( 2 ) hypoxic air to generate an arterial blood oxygen saturation of ~80 % ( HT , n = 10 ) , or ( 3 ) with no additional stimulus ( CT , n = 10 ) . Before and after training , participants completed the following tests : 3-s maximal voluntary contraction ( MVC3 ) , 30-s MVC , and an endurance test ( maximal number of repetitions at 20 % 1-RM , Reps20 ) . Electromyographic activity ( root mean square , RMS ) was measured during tests and the cross-sectional area ( CSA ) of the quadriceps and hamstrings was measured pre- and post-training . Relative to CT , KT , and HT showed likely increases in MVC3 ( 11.0 ± 11.9 and 15.0 ± 13.1 % , mean ± 90 % confidence interval ) , MVC30 ( 10.2 ± 9.0 and 18.3 ± 17.4 % ) , and Reps20 ( 28.9 ± 23.7 and 23.3 ± 24.0 % ) . Compared to the CT group , CSA increased in the KT ( 7.6 ± 5.8 ) and HT groups ( 5.3 ± 3.0 ) . KT had a large effect on RMS during MVC3 , compared to CT ( effect size 0.8 ) and HT ( effect size 0.8 ) . We suspect hypoxic conditions created within the muscles during vascular occlusion and hypoxic training may play a key role in these performance enhancements Abstract This study aim ed to investigate the effects of a short-term period of intermittent hypoxic training ( IHT ) on  cycling performance in athletes . Nineteen participants were r and omly assigned to two groups :  normoxic ( NT , n = 9 ) and intermittent hypoxic training group ( IHT , n = 10 ) . A 3-week training program ( 5 × 1 h–1 h 30 min per week ) was completed . Training sessions were performed in normoxia ( ∼30 m ) or hypoxia ( simulated altitude of 3,000 m ) for NT and IHT group , respectively . Each subject performed before ( W0 ) and after ( W4 ) the training program , three cycling tests including an incremental test to exhaustion in normoxia and hypoxia for determination of maximal aerobic power $ $ ( \ifmmode\exp and after\dot\else\exp and after\.\fi{V}{\text{O}}_{{2\max } } ) $ $ and peak power output ( PPO ) as well as a 10-min cycle time trial in normoxia ( TT ) to measure the average power output ( Paver ) . No significant difference in $ $ \ifmmode\exp and after\dot\else\exp and after\.\fi{V}{\text{O}}_{{2\max } } $ $ was observed between the two training groups before or after the training period . When measured in normoxia , the PPO significantly increased ( P < 0.05 ) by 7.2 and 6.6 % in NT and IHT groups , respectively . However , only the IHT group significantly improved ( 11.3 % ; P < 0.05 ) PPO when measured in hypoxia . The NT group improved ( P < 0.05 ) Paver in TT by 8.1 % , whereas IHT group did not show any significant difference . Intermittent training performed in hypoxia was less efficient for improving endurance performance at sea level than similar training performed in normoxia . However , IHT has the potential to assist athletes in preparation for competition at altitude This study investigates whether a 6-wk intermittent hypoxia training ( IHT ) , design ed to avoid reductions in training loads and intensities , improves the endurance performance capacity of competitive distance runners . Eighteen athletes were r and omly assigned to train in  normoxia  [ Nor group ; n = 9 ; maximal oxygen uptake ( VO2 max ) = 61.5 + /- 1.1 ml x kg(-1 ) x min(-1 ) ] or intermittently in hypoxia  ( Hyp group ; n = 9 ; VO2 max = 64.2 + /- 1.2 ml x kg(-1 ) x min(-1 ) ) . Into their usual normoxic training schedule , athletes included two weekly high-intensity ( second ventilatory threshold ) and moderate- duration ( 24 - 40 min ) training sessions , performed either in normoxia [ inspired O2 fraction ( FiO2 ) = 20.9 % ] or in normobaric hypoxia ( FiO2 ) = 14.5 % ) . Before and after training , all athletes realized 1 ) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds ( first and second ventilatory threshold ) , and 2 ) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion ( T(lim ) ) and the parameters of O2 uptake ( VO2 ) kinetics . Only the Hyp group significantly improved VO2 max ( + 5 % at both FiO2 , P < 0.05 ) , without changes in blood O2-carrying capacity . Moreover , T(lim ) lengthened in the Hyp group only ( + 35 % , P < 0.001 ) , without significant modifications of VO2 kinetics . Despite similar training load , the Nor group displayed no such improvements , with unchanged VO2 max ( + 1 % , nonsignificant ) , T(lim ) ( + 10 % , nonsignificant ) , and VO2 kinetics . In addition , T(lim ) improvements in the Hyp group were not correlated with concomitant modifications of other parameters , including VO2 max or VO2 kinetics . The present IHT model , involving specific high-intensity and moderate- duration hypoxic sessions , may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations , result ing in increased endurance performance capacity We hypothesized that specific muscular transcript level adaptations participate in the improvement of endurance performances following intermittent hypoxia training  in endurance-trained subjects . Fifteen male high-level , long-distance runners integrated a modified  living low-training high program comprising two weekly controlled training sessions performed at the second ventilatory threshold for 6 wk into their normal training schedule . The athletes were r and omly assigned to either a normoxic ( Nor ) ( inspired O2 fraction = 20.9 % , n = 6 ) or a hypoxic group exercising under normobaric hypoxia ( Hyp ) ( inspired O2 fraction = 14.5 % , n = 9 ) . Oxygen uptake and speed at second ventilatory threshold , maximal oxygen uptake ( VO2 max ) , and time to exhaustion ( Tlim ) at constant load at VO2 max velocity in normoxia and muscular levels of selected mRNAs in biopsies were determined before and after training . VO2 max ( + 5 % ) and Tlim ( + 35 % ) increased specifically in the Hyp group . At the molecular level , mRNA concentrations of the hypoxia-inducible factor 1alpha ( + 104 % ) , glucose transporter-4 ( + 32 % ) , phosphofructokinase ( + 32 % ) , peroxisome proliferator-activated receptor gamma coactivator 1alpha ( + 60 % ) , citrate synthase ( + 28 % ) , cytochrome oxidase 1 ( + 74 % ) and 4 ( + 36 % ) , carbonic anhydrase-3 ( + 74 % ) , and manganese superoxide dismutase ( + 44 % ) were significantly augmented in muscle after exercise training in Hyp only . Significant correlations were noted between muscular mRNA levels of monocarboxylate transporter-1 , carbonic anhydrase-3 , glucose transporter-4 , and Tlim only in the group of athletes who trained in hypoxia ( P < 0.05 ) . Accordingly , the addition of short hypoxic stress to the regular endurance training protocol induces transcriptional adaptations in skeletal muscle of athletic subjects . Expressional adaptations involving redox regulation and glucose uptake are being recognized as a potential molecular pathway , result ing in improved endurance performance in hypoxia-trained subjects To test the hypothesis that severe hypoxia during low-resistance/high-repetition strength training promotes muscle hypertrophy , 19 untrained males were assigned r and omly to 4 weeks of low-resistance/high-repetition knee extension exercise in either normoxia or in normobaric hypoxia ( FiO2 0.12 ) with recovery in normoxia . Before and after the training period , isokinetic strength tests were performed , muscle cross-sectional area ( MCSA ) measured ( magnetic resonance imaging ) and muscle biopsies taken . The significant increase in strength endurance capacity observed in both training groups was not matched by changes in MCSA , fibre type distribution or fibre cross-sectional area . RT-PCR revealed considerable inter-individual variations with no significant differences in the mRNA levels of hypoxia markers , glycolytic enzymes and myosin heavy chain isoforms . We found significant correlations , in the hypoxia group only , for those hypoxia marker and glycolytic enzyme mRNAs that have previously been linked to hypoxia-specific muscle adaptations . This is interpreted as a small , otherwise undetectable adaptation to the hypoxia training condition . In terms of strength parameters , there were , however , no indications that low-resistance/high-repetition training in severe hypoxia is superior to equivalent normoxic training This study was performed to explore changes in gene expression as a consequence of exercise training at two levels of intensity under normoxic and normobaric hypoxic conditions ( corresponding to an altitude of 3,850 m ) . Four groups of human subjects trained five times a week  for a total of 6 wk on a bicycle ergometer . Muscle biopsies were taken , and performance tests were carried out before and after the training period . Similar increases in maximal O(2 ) uptake ( 8.3 - 13.1 % ) and maximal power output ( 11.4 - 20.8 % ) were found in all groups . RT-PCR revealed elevated mRNA concentrations of the alpha-subunit of hypoxia-inducible factor 1 ( HIF-1 ) after both high- ( + 82.4 % ) and low (+78.4%)-intensity training under hypoxic conditions . The mRNA of HIF-1alpha(736 ) , a splice variant of HIF-1alpha newly detected in human skeletal muscle , was shown to be changed in a similar pattern as HIF-1alpha . Increased mRNA contents of myoglobin ( + 72.2 % ) and vascular endothelial growth factor ( + 52.4 % ) were evoked only after high-intensity training in hypoxia . Augmented mRNA levels of oxidative enzymes , phosphofructokinase , and heat shock protein 70 were found after high-intensity training under both hypoxic and normoxic conditions . Our findings suggest that HIF-1 is specifically involved in the regulation of muscle adaptations after hypoxia training . Fine-tuning of the training response is recognized at the molecular level , and with less sensitivity also at the structural level , but not at global functional responses like maximal O(2 ) uptake or maximal power output The effects of concurrent hypoxic/endurance training on mitochondrial respiration in permeabilized fibers in trained athletes were investigated . Eighteen endurance athletes were divided into two training groups :  normoxic ( Nor , n = 8) and hypoxic  ( H , n = 10 ) . Three weeks ( W1-W3 ) of endurance training ( 5 sessions of 1 h to 1 h and 30 min per week ) were completed . All training sessions were performed under normoxic [ 160 Torr inspired Po(2 ) ( Pi(O(2 ) ) ) ] or hypoxic conditions ( approximately 100 Torr Pi(O(2 ) ) , approximately 3,000 m ) for Nor and H group , respectively , at the same relative intensity . Before and after the training period , an incremental test to exhaustion in normoxia was performed , muscle biopsy sample s were taken from the vastus lateralis , and mitochondrial respiration in permeabilized fibers was measured . Peak power output ( PPO ) increased by 7.2 % and 6.6 % ( P < 0.05 ) for Nor and H , respectively , whereas maximal O(2 ) uptake ( Vo(2 max ) ) remained unchanged : 58.1 + /- 0.8 vs. 61.0 + /- 1.2 ml.kg(-1).min(-1 ) and 58.5 + /- 0.7 vs. 58.3 + /- 0.6 ml.kg(-1).min(-1 ) for Nor and H , respectively , between pretraining ( W0 ) and posttraining ( W4 ) . Maximal ADP-stimulated mitochondrial respiration significantly increased for glutamate + malate ( 6.27 + /- 0.37 vs. 8.51 + /- 0.33 mumol O(2).min(-1).g dry weight(-1 ) ) and significantly decreased for palmitate + malate ( 3.88 + /- 0.23 vs. 2.77 + /- 0.08 m 
    Output:
    
Conclusion Four modes of LLTH are identified in the current literature ( CHT , IHT , RSH and RTH ) , with training mode and intensity appearing to be key factors in mediating subsequent performance responses in normoxia .
Improvements in normoxic performance appear most likely following high-intensity , short-term and intermittent training ( e.g. IHT , RSH ) .
For RTH , it is unclear whether the associated adaptations are greater than those of traditional ( maximal ) resistance training programmes