Conventional resistance training typically involves the controlled movement of weighted devices such as barbells, dumbbells and machines (with fulcrums and loaded weight stacks) where muscles undergo concentric (shortening), isometric (static) and eccentric (lengthening) actions against a constant external load — the magnitude of which is limited by the individual’s concentric strength.[1,2] Effective resistance training should involve the use of progressively heavier loads lifted in sets of maximum-effort repetitions. Although this form of exercise has been studied quite intensively over the last 25 years, it’s use as a “tool” to build muscle (hypertrophy), functional ability and offset age-related changes in body composition, is poorly understood. The link between effective training and achieving bigger, stronger muscles is anything but clear.
The functional adaptations from resistance training are typically interpreted within the context of two components; changes that occur at the level of the muscle tissue itself (peripheral)[5] and a central component that accounts for training-induced changes in motor-neural unit recruitment [4]. This article will focus on the peripheral morphology that responsible for strength development and possibly, hypertrophy.
The value of resistance training for increasing functional strength and muscle mass became a topic of increasing interest within the scientific community once DeLorme and Watkins demonstrated the importance of progressive loading for the rehabilitation of injured World War II military personnel. A major reason for this interest is the remarkable plasticity of this tissue. Muscle responds specifically to current functional demands; fibers can undergo extensive remodeling within their contractile apparatus to meet new functional requirements. These adaptations can occur before or after hypertrophy becomes evident.
Improvements in strength and ultimately muscle mass are the result of this remodeling process which involves transformations at the molecular level. For example, fiber type classifications can be based on the concentration of myosin ATPase (a muscle-specific enzyme) that is the study of histochemistry. These muscle fiber classifications represent a continuum that spans the functional demands of the entire muscular system.[6,7,8]. That is muscle fibers are classified from type-I (slow twitch), Ic, IIc, IIac, IIa, IIab, IIb (fast twitch).[7] During contractile activity muscle fibers are always recruited from slow twitch first, and the type-II fibers only come into play during heavy loads. And only the heaviest loads recruit all fibers. Lighter loads recruit a limited number of fibers, no matter how many repetitions are completed.
We know that to lift a heavy weight, large amounts of muscle fibers have to contract. However, the shortening velocity is actually slow. Therefore, even though the lifter might attempt to move a heavy weight explosively, the initial adaptations that occur in strength development are via the expression of slower, (not faster) contractile protein isoforms. [9,10]
Of the contractile proteins within the muscle, the myosin heavy chains (MHCs) are the largest subunits. The MHCs make up the majority of the myosin filament that forms the cross bridge according to the sliding filament theory and is the site of mATPase activity. [8] The MHC isoform expressed within a muscle fiber reflect the contractile properties of the fiber type. [10] At least nine different MHC isoforms have been identified in mammalian muscle; four of which are expressed in adult rodent muscle (MHC type-I, IIa, IIx, and IIb). [11] Three, (type-I, IIa, and IIx) are expressed in most human adult muscle. [12] (A gene for a type-IIb MHC has not been identified in humans. Fibers that have been classified as type-IIb express the type-IIx isoform rather than type-IIb. Therefore, human muscle fibers are often classified as type-I, IIa, and IIx).[13]
The differing isoforms with their unique mATPase activity reflect the fiber type and correlate with the speed of contraction; MHC type-I being the slowest and MHC type-IIx the fastest and most powerful. [14,15]
Strength and (possibly hypertrophy) adaptations appear to reside in the ability of the fibers to transcribe different isoforms of MHC protein in response to exercise. It is these alterations in the phenotypic expression of the MHCs that provide the main mechanism of adaptation to stresses (overload) placed upon the muscle. And remember, these changes in MHC expression occur in response to activity (as in exercise) but also, inactivity. [16] The polymorphism of the MHCs play a major role in the adaptability and contractile efforts necessary for various types of exercise.[17] So the type of MHC isoforms your muscles express is a direct response to the type of exercise you perform.
Fibers contain the capacity to express all MHC isoforms, but each fiber has predominant MHCs they are most capable of expressing in response to exercise. While MHC isoform (and subsequent fiber type) transitions tend to go in the direction from type-IIx to type-IIa, there is little or no change to type-I regardless of the modality of exercise. [10,14,16] That is, with consistent training, fibers can (and do) assume the contractile properties of other fiber types – thanks primarily to MHC isoform expression. However, a type-1 muscle fiber cannot be “turned into” a type-II fiber, no matter how long you train. But the range of type-II fibers is such that they can remodel themselves to mimic the ideal fiber types ideally suited to whatever training demands are placed upon them. For example, with consistent high-overload training, most type-II fibers readily convert to type-IIa.[10,14,16]- this subunit of type-II is most conducive to strength and hypertrophy development. Furthermore, chronic resistance exercise does appear to change MHC isoform expression along with the fiber type transitions. [14,16]
The way you train (the intensity – load used and speed of contraction) does play an important role in dictating adaptations at the molecular level. The type proteins expressed is influenced by the type of training performed. That is, the correct type of training can speed favorable adaptations. Whereas the wrong type can hinder the polymorphism of MHC isoform composition most conducive to optimizing strength development. [14,15,18] Of all the variables involved in resistance training (sets, reps, tempo, exercise selection and sequence) it is pertinent to note that the amount of overload used is the primary determinant of the adaptations that occur at the molecular level. That is, a program structured for progressive overload appears to be the fastest way to express the MHC isoforms that are most conducive to strength development.
Does training status (training age) affect the capacity to induce these changes? Yes, it can. An individual that has undertaking consistent weight training for a number of years will express different MHC isoforms in response to a workout compared to a novice that has just commenced training. Changes in the relative abundance or rate of translation of the mRNAs encoding the different MHC isoforms precedes major changes in the protein isoform, and this does take several weeks.[10,17] This is due to the slow turnover of MHC in human muscle. This delay between exercise-induced changes in MHC mRNA isoform expression and alterations in protein isoform distribution is the basis for mismatches between mRNA and protein expression in individual fibers during training.[19] This might sound a little confusing but the important point to remember here is MHC protein isoform gene expression early in a training program may not be the same as those expressed later throughout a training program.
Having said that, in my clinical work, analyzing the muscle fiber types of bodybuilders before and after training programs, I consistent viewed large (statically significant) shifts in fiber type in experienced bodybuilders during a 12-week program. Even in bodybuilders that had been training for up to 10 years, I still observed changes in the expression of the more favorable MHC type-IIa isoforms during a structured program I’d designed for them. Therefore, in my mind at least (after analyzing around 10,000 muscle samples), I believe there is always the capacity to induce significant changes. And these changes can occur simply by utilizing a better program.
Strength improvements are the result of functional changes within the muscle, and these peripheral adaptations involve extensive remodeling of qualitative or intrinsic contractile properties such as MHC isoform composition and alterations in fiber type distribution. One exciting question is, can nutrition or supplements affect (speed) this adaptation process?
The topic of nutritional interventions to speed muscle adaptations during resistance training was a major focus of my Ph.D. But even after 6 years of study, I was just scratching the surface. I will say that the most effective nutrient (supplement) for speeding the molecular adaptations that result in greater muscle size and strength is creatine monohydrate. Turbo-charged is the more likely term when the effects of this supplement come to mind – but that’s the topic of another article.
References
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