Evidence map›Paper›PMID 11735686›Full record

ReviewSports medicine (Auckland, N.Z.)2001

Long-term metabolic and skeletal muscle adaptations to short-sprint training: implications for sprint training and tapering.

A Ross, M Leveritt

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Sports medicine (Auckland, N.Z.), 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07319962 (Investigation of Arterial Stiffness, Intercostal Muscle Oxygenation, Aerobic and Anaerobic Exercise Capacity in Elite American Football Players), which is not on this map. Cited by 85 papers, 12 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 12 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07319962 completednot on this mapstarted 2024, after this paper: background citation

Investigation of Arterial Stiffness, Intercostal Muscle Oxygenation, Aerobic and Anaerobic Exercise Capacity in Elite American Football Players

TypeobservationalSponsorGazi UniversityRan2024 to 2025Enrolled30ConditionsArterial Stiffness, Football Players, Muscle Oxygenation
3 · Its place in the literature

Who cites it

85 citing papers in PubMed, 12 syntheses or guidelines pooled it.

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25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

A RossSchool of Human Movement Studies, University of Queensland, St Lucia, Queensland, Australia. angur@hms.uq.edu.au
M Leveritt

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (>10-second) or short (<10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus. Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type IIa muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca(2+). Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.

Indexed as

Adaptation, PhysiologicalAdenosine TriphosphateAerobiosisEnergy MetabolismExerciseGlycolysisHumansMuscle ContractionMuscle Fibers, SkeletalMuscle, SkeletalNeuromuscular JunctionPhosphocreatinePhysical Education and TrainingRestRunningSarcoplasmic ReticulumAdenosine TriphosphatePhosphocreatine

Identifiers

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Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.