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AbstractSkeletal muscle fibres. What types have we got? Can we change them and does it matter?Stephen D.R. Harridge, Division of Applied Biomedical Research, King’s College LondonOur muscles are machines that allow us to convert the chemical energy stored in food into mechanical work, enabling us to undertake all the necessary activities for daily living. Our muscles are made up of hundreds and thousands of long cells, our fibres, and nature has produced a system by which differences in these fibres allow us to produce great feats of strength and power on the one hand and great feats of endurance on the other. Fibres can crudely be classified on their basis of their colour (red or white), or on the basis of twitch contraction time (slow twitch and fast-twitch). There are however, traditionally considered to be three types of fibre which can be identified on the basis of their ATPase activity (type 1, type IIa and type IIx), their metabolic properties (slow oxidative, fast oxidative or fast glycolytic) or different isoforms of myosin, the molecular motors, (myosin heavy chain (MHC)-I, MHC-IIa and MHC-IIx). Whilst the nomenclature of these classifications is based on the specific characteristic measured, there is a general agreement between classifications. For example, slow oxidative fibres are those that normally contain MHC-I isoforms and are classified as type I by ATPase histochemistry. However, it should be noted that even these classifications are somewhat crude, in that fibres can also represent a continuum between types, with some containing more than one type of MHC isosform (i.e. they are hybrid). In contrast to type I fibres, type II fibres have a higher velocity of shortening and as a consequence have a greater potential for power generation than type I fibres. However, the compromise is the lesser ability of type II (particularly type IIx fibres) to sustain power over a prolonged period of time. In other words they fatigue more easily. Type I fibres are slow to contract, but are highly resistant to fatigue. Unlike some animal muscles, human muscles are not made up of exclusively one or other type, but are mixed with varying proportions of fast and slow fibres. However, it makes sense that muscles with a postural function, such as the soleus, are dominated by type I, fatigue-resistant fibres. It also comes as little surprise that athletes who excel in different events have muscles with compositions that reflect the demands of particular events. Sprinters tend to have a high proportion of high-power generating type II fibres, whilst endurance runners tend to have with a higher proportion of fatigue resistant type I fibres. The question is to what extent can, through changes in activity, a fibre be switched? We know from animal studies, that have used cross-innervation or chronic low-frequency stimulation techniques, that it is possible to effectively change fast muscles into slow muscles. However, under more normal physiological conditions, such as voluntary exercise, such a switch is difficult to demonstrate. This is the case in both humans and animals. In contrast to increased activity, we know that disuse, associated with prolonged bed rest or cast immobilisation, results not only in fibre atrophy, but also a switch towards the fast type. This is exemplified in the muscles of spinal chord injured individuals who demonstrate a dominance of type II fibres in the affected muscles distal to the sire of lesion. This lecture will address the extent to which human muscles can alter their type within the context of athletic performance, rehabilitation and ageing. It will also address the question as to whether a drive towards making fibres become “type I”, is a desirable outcome. Indeed it may be preferable for fast fibres to be conditioned so as to increase their fatigue resistance, but retain their ability to generate power. |
