Long-term metabolic and skeletal muscle adaptations to short-sprint training: implications for sprint training and tapering.
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.
Ross
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School of Human Movement Studies, University of Queensland, St Lucia, Queensland, Australia. angur@hms.uq.edu.au
Leveritt
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D000222:Adaptation, Physiological / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000332:Aerobiosis / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D006019:Glycolysis / Q000502:physiology; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000145:classification / Q000502:physiology / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology; D010725:Phosphocreatine / Q000378:metabolism; D010806:Physical Education and Training / Q000379:methods*; D012146:Rest / Q000502:physiology; D012420:Running / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000502:physiology; D013995:Time
D010725:Phosphocreatine; D000255:Adenosine Triphosphate