Fibre Type Differences in Response to Resistance and Deficit

Skeletal Muscle Fibre Types: Characteristics and Distribution

Skeletal muscle is composed of heterogeneous populations of fibres with distinct morphological, metabolic, and contractile properties. The primary classification distinguishes two major fibre types based on myosin heavy chain (MHC) isoforms and oxidative capacity:

Type I (slow-twitch, oxidative): Express MHC I, have high mitochondrial density, high capillary supply, and rely primarily on oxidative metabolism. They are fatigue-resistant but generate low contractile force and have low basal protein synthesis rates.
Type II (fast-twitch, glycolytic): Express MHC II (further subdivided into IIa and IIx), have lower mitochondrial density, rely more on anaerobic glycolysis, generate high contractile force, and exhibit higher basal protein synthesis rates despite lower oxidative capacity.

In humans, the distribution of fibre types varies by muscle and individual factors. Postural muscles tend to be Type I dominant, whilst muscles involved in explosive movements are Type II rich. Most locomotor muscles contain a mixed population of both fibre types.

Type II Fibre Vulnerability During Energy Deficit

During energy restriction, Type II fibres are preferentially lost compared to Type I fibres. This selective vulnerability has several proposed mechanisms:

Lower oxidative capacity: Type II fibres depend more on anaerobic glycolysis and have lower mitochondrial density, making them less efficient at generating ATP in a restricted energy environment. This may render them more vulnerable to catabolic signals.
Lower constitutive protein synthesis: Paradoxically, while Type II fibres have higher basal protein synthesis rates under anabolic conditions, their protein synthesis becomes more severely depressed during energy deficit due to greater dependence on growth factor signalling.
Lower oxidative enzyme content: Type II fibres express lower levels of oxidative enzymes (citrate synthase, succinate dehydrogenase), reducing their capacity to extract energy from available fuels during restriction.
Greater glycolytic dependence: Type II fibres rely heavily on glucose and glycogen. During energy deficit, both circulating glucose and muscle glycogen are limiting, potentially creating metabolic stress in these fibres.

Cross-sectional studies and longitudinal biopsy data from individuals undergoing energy restriction without exercise show selective reductions in Type II fibre cross-sectional area, with Type I fibres relatively spared.

Mechanical Loading and Type II Fibre Recruitment

Resistance exercise preferentially recruits Type II fibres, particularly at high intensities and during rapid, forceful contractions. This is explained by Henneman's size principle: motor units are recruited in order of increasing size, and Type I motor units are smaller and recruited first. Type II fibres are only recruited when higher forces are demanded or when Type I recruitment is insufficient.

During resistance training, the mechanical loading experienced by Type II fibres is substantially greater than that experienced by Type I fibres or by non-exercised muscles. This heightened mechanical stimulus creates a potent anabolic signal localised to Type II fibres.

As discussed previously, this mechanical stimulus activates mTORC1 and Akt signalling within Type II fibres, enhancing their anabolic sensitivity and suppressing proteolytic pathways (FoxO/atrogin-1/MuRF1) locally. The result is substantial protection of Type II fibre size and myonuclear content.

Type II Fibre Preservation with Combined Resistance and Energy Restriction

Studies employing muscle biopsy and immunohistochemical analysis have demonstrated that when individuals undergo energy restriction combined with resistance training, Type II fibre cross-sectional area is substantially better preserved compared to restriction alone.

For example, longitudinal studies lasting 8–12 weeks of energy deficit show:

Deficit alone: Type II CSA declines by ~10–15%; Type I CSA relatively stable or declines slightly (~2–5%).
Deficit + resistance training: Type II CSA stable or declines only ~1–3%; Type I CSA stable or increases slightly (~1–3%).

Furthermore, myonuclear content—the number of nuclei within a given fibre, which correlates with protein synthetic capacity—is better preserved in Type II fibres with resistance training. This suggests that the protective effect operates at the level of the fibre's intrinsic anabolic capacity.

The preservation of Type II fibres is particularly important functionally, as these fibres are essential for generating maximal strength and power. Selective loss of Type II fibres during aging or energy restriction is associated with disproportionate losses in strength, whereas preservation of Type II content maintains functional capacity better.

Type I Fibres and Metabolic Flexibility

Type I fibres, whilst less preferentially affected by energy deficit, also benefit from resistance training. Type I fibres respond to mechanical loading by increasing oxidative enzyme content and mitochondrial density, adaptations that enhance their fatigue resistance and metabolic efficiency.

During energy restriction, Type I fibres may even increase slightly in proportion (as a fraction of total fibre population) due to greater atrophy of Type II, but absolute cross-sectional area of Type I is typically maintained or slightly reduced.