Jay R. Hoffman, Ph.D., FACSM, CSCS,*D 
Department of Health and Exercise Science 
The College of New Jersey 
Ewing, NJ 

 

There is a great deal of plasticity within the neuromuscular system. Improvements in muscle size or performance are seen following participation in physical conditioning programs. In addition to the individual's training status, the type of training program also impacts the physiological adaptations that occur. For example, strength training results in specific muscle adaptations; aerobic endurance training on the other hand causes completely different types of adaptations. Likewise, if the training stimulus is removed, muscle tends to revert back to its pretraining state. An understanding of the type of alterations seen with a given training program allows the strength and conditioning professional or personal trainer to develop the most appropriate training program and set the most realistic training goals. This review focuses on the neurological and skeletal muscle adaptations that are seen following resistance training, aerobic endurance training, and combined aerobic endurance and resistance training programs. 

 

Neural Adaptation

Maximal strength expression is not determined solely by the quantity and quality of the muscle mass but also the extent to which that muscle mass is activated (29). Maximal strength is achieved when the primary muscle group is fully activated, and the synergists and antagonists are appropriately activated or inhibited (29). Efficient coordination in the activation of these muscle groups allows for a better expression of strength. Muscle activation is best described as neural activity, and it is the adaptation of the neural system that is thought to provide the initial increases in strength following resistance training (28). 

 

Electromyographic (EMG) Changes

The most common method for assessing neural activity of the muscle is through EMG recordings. The EMG measures the electrical activity within the muscle and nerves, and indicates the neural drive to a muscle. An EMG recording is generally performed with surface electrodes on a muscle. Recording the EMG activity of that muscle prior to and following a resistance training program provides information concerning the neural adaptation resulting from a resistance training program. Resistance training has been demonstrated to increase EMG activity in both trained and untrained populations (12,28). Significant correlations between EMG and increases in strength have been reported following strength training (13,14). These findings support the idea that strength trained subjects may be more capable in fully activating their primary muscles during maximal performance than untrained subjects. Further findings have shown that EMG activity will be significantly increased during the initial stages of a resistance training program but as training duration progresses the rate of increase in EMG activity will diminish or plateau. It is during these latter stages of training that gains in strength become more attributable to muscle hypertrophy. 

 

Recruitment Patterns

Neural adaptations may also be recognized by a decrease in the electrical activity in the muscle with corresponding increase in force output (29). The reduced EMG responses that may be seen with an increase in muscle strength may reflect a more efficient recruitment pattern of the muscles responsible for the force production, i.e., the athlete/client is able to selectively fire the muscle(s) needed to perform a given task. In addition, trained individuals may be able to recruit additional motor units as an adaptation seen consequent to training programs (22). 

 

Synchronization

Further neural adaptations that contribute to increased force production include an increased synchronization‹ activation pattern of the motor units‹of motor unit firing (27). That is, as synchronization increases, more motor units fire at any one time. However, there has been little research in the last 30 years to support this synchronization concept. Although its role remains unclear, it may contribute to the rate of force development (29). 

 

Inhibitory Mechanisms

Within the muscle and tendon there are sensory receptors (e.g., muscle spindles and Golgi tendon organs‹GTOs) that provide feedback to the central nervous system concerning the stretch and tension of the muscle. These sensory receptors are referred to as muscle proprioceptors and serve primarily as a protective mechanism within the muscle and tendon to reduce the risk of injury. When muscle spindles sense a rapid stretch, the agonist muscle becomes active. When the GTO senses excessive tension development, it will activate the antagonistic muscle group(s) to limit force production. Whereas muscle spindles are active with rapid movements, GTOs are primarily active when maximal muscle actions are performed at slow speeds (7,36). Resistance training is thought to cause an inhibition of these protective mechanisms. When the antagonistic muscle group is contracted immediately prior to a lift, it is thought that this will partially inhibit the neural self-protective mechanism, and allow for a more forceful contraction (6). 

 

Time Course of Neural Activation

The quick strength gains seen during the initial phases of a resistance training program are accomplished without any noticeable increase in muscle mass. This indicates that the initial strength changes result primarily from neural adaptations. Moritani and deVries suggest that these neural adaptations are the predominant cause of strength increases for the first three to five weeks of training (28). Following this period, increases in muscle cross-sectional area becomes the predominant factor. 

 

Skeletal Muscle Adaptation

Skeletal muscle adapts to a variety of functional demands. When skeletal muscle works at intensities exceeding 60% of its maximal force generating capacity, adaptations occur that result in increased muscle size and strength (24). The initial strength increases following resistance training have been attributed primarily to the neurological adaptations discussed earlier. Further strength gains are largely the result of increased muscle size. Skeletal muscle grows by either increasing the size of pre-existing muscle fibers (muscle hypertrophy) or by increasing the number of fibers within the muscle (muscle hyperplasia). 

 

Muscle Hypertrophy

Hypertrophy, or increases in muscle cross-sectional area, is generally seen following six to eight weeks of heavy resistance training. However, some evidence suggests that muscle growth may occur even earlier (32,34). These size increases appear to be the result of increases to the size and number of actin and myosin filaments, and to the addition of sarcomeres within the fiber (3,9). The growth of these contractile elements may be related to the repeated trauma to the fibers from high intensity resistance training causing cellular damage. During recovery from such training, an overcompensation of protein synthesis may occur resulting in the noted size increase (5). 

Muscle hypertrophy occurs in both Type I and Type II fibers following high intensity resistance training programs. However, Type II fibers appear to hypertrophy to a greater degree (31). Since both Type I and Type II fibers are recruited during maximal contractions, the greater hypertrophy seen in the Type II fiber may be related to the greater activation of high threshold units than normally activated during daily activity (24). The magnitude of these increases varies considerably and is dependent upon several factors including the individual's response to training mode and intensity, duration of the training program, and the training status. 

Increases of 15.6 % (Type I), 17.3% (Type IIa), and 28.1% (Type IIb) have been reported in novice female subjects following 6 weeks of high intensity resistance training (32). As the length of the resistance training program increases (20 weeks), further increases in muscle size may be seen (15%, 45% and 57% in Type I, Type IIa and Type IIb muscle fibers, respectively) (33). Similar increases in muscle hypertrophy have been seen in untrained male subjects as well (1,17). Although gender differences in muscle growth do exist, these differences become apparent after longer periods of training. 

The training status of the individual does have an important impact on the morphological changes seen in the muscle following resistance training. Experienced body builders, both male and female, were examined during 24 weeks of training. No significant improvements in muscle cross-sectional area were noted over the training period (4). This is consistent with what has been reported in the literature concerning muscle growth in highly trained experienced body builders (15,16). It should be understood however, that there might be a large difference between statistical significance versus practical significance in understanding muscle growth. Generally, studies examining muscle morphological changes do not have a large sample number. Thus, they need a great difference in order to achieve statistical significance. Alway and colleagues (4) reported a 3.6% increase in the cross-sectional area of the biceps in five experienced male body builders following 24 weeks of training. Although, this was not statistically significant it may represent an important component for success during competition. 

Fewer studies have compared muscle fiber size changes to strength, aerobic endurance, and a combined strength and aerobic endurance training program. Kraemer and colleagues (22) examined muscle fiber morphological changes in untrained subjects that exercised for 3 months, 4 days a week, in either a high intensity resistance training program, an aerobic endurance training program or a combined strength/aerobic endurance training program. All training programs were periodized to enhance recovery from exercise and prevent overtraining. Both the strength and the combined strength and aerobic endurance training programs resulted in significant muscle fiber hypertrophy. However, the inclusion of aerobic endurance training stunted the growth in both Type I and IIc fibers. Aerobic endurance training alone caused a decrease in fiber size in the more oxidative fibers (Type I and IIc). Interestingly, Kraemer and colleagues (22) also included a study group that performed, in addition to the aerobic endurance training program, an upper body only resistance training program. Those subjects were able to lessen the decreases in fiber size of the legs through upper body training. This may have been caused by isometric contractions of the leg musculature during upper body exercise. 

Increases in fiber size do not appear to be accompanied by a concomitant increase in mitochondrial number, or in the capillary to fiber ratio. Therefore, increases in the cross-sectional area of the muscle are associated decreased mitochondrial and capillary volume densities within the fibers. Although this may not significantly effect strength or power development, it may have important implications for endurance capability in those muscles. It is possible that such adaptations could alter the oxygen kinetics within the muscle by delaying transport of oxygen from the vasculature to the exercising muscle. It is noteworthy that aerobic endurance training does decrease fiber size while increasing both mitochondrial and capillary density, thus potentially improving the muscles' aerobic capability. However, muscle hypertrophy does appear to be accompanied with a proportional increase in sarcoplasmic reticulum and transverse tubule volume density, thereby maintaining or improving contraction capabilities of the muscle (2). 

 

Muscle Hyperplasia

It has been generally understood that muscle fiber number is fixed from birth and that skeletal muscle growth is a result of hypertrophy of existing muscle fibers. However, a number of studies have suggested that high intensity resistance training may increase the number of muscle fibers, i.e., hyperplasia (10,18). Because most of these early studies used muscle ablation in an animal model to cause overload, a concern arose regarding whether humans adapt to an exercise stimulus in a similar fashion as that used in those animal models. However, later studies using methods that better simulated an exercise stress also demonstrated hyperplasia of skeletal muscle subsequent to muscle overload (3,11). Additional criticism was directed at the use of an animal model. The magnitude of muscle hypertrophy seen in humans does not occur in many animal species. Thus, muscle hyperplasia may be the primary compensatory mechanism in animals to combat muscle overload. Interestingly, MacDougall et al. (25) and Tesch and Larson (35) reported that elite bodybuilders had a greater number of muscle fibers than trained control subjects. These investigators suggested that the greater fiber numbers seen in the bodybuilders were attributable to the years of high intensity resistance training. However, subsequent research was unable to replicate their findings (26). 

There does not appear to be any convincing support for the occurrence of muscle hyperplasia in humans. However, conflicting results still make this issue quite controversial, and its potential quite appealing. If hyperplasia does exist in humans, it most probably occurs in a small portion of Type II fibers when they reach their predetermined genetic growth limit (8). 

 

Fiber Type Conversions

The proportion of Type I to Type II muscle fibers appears to be genetically determined and their expression is set early in life. A number of studies have examined whether conditioning programs can alter the proportion of Type I to Type II muscle fibers. Some studies have suggested that aerobic training may increase the percentage of Type I fibers (19,30), while other studies have reported that sprint training may increase Type II fiber proportion (20,21). However, the overwhelming majority of investigations have been unable to see any alterations in fiber type composition following strength and conditioning programs. It is generally believed that only fiber type transformations within a fiber type can be accomplished through training (i.e., from one subtype to another‹e.g., IIb to IIa‹of the same fiber type). 

High intensity resistance training appears to be a potent stimulus in causing a transformation of the Type IIb to Type IIa fiber subtype. (23,31,32,34). Type IIb fiber types have been shown to convert to Type IIa fibers following 20 weeks of resistance training (32). This is similar to the Type II fiber conversions previously associated with aerobic exercise training. Kraemer and colleagues (23) have also demonstrated skeletal muscle fiber subtype transformations from IIb to IIa in subjects performing high intensity resistance training, and in subjects performing a combined high intensity resistance training and aerobic endurance training program. Subjects that were only performing aerobic endurance exercise also tended to increase the proportion of Type IIa fibers, but significantly elevated their Type IIc fibers. This would be expected as the Type IIc fibers are the most oxidative of the Type II subtypes. 

Fiber subtype transformations appear to occur quite rapidly (within two weeks) during participation in physical conditioning programs. These adaptations however may be transient. During periods of inactivity or detraining a transformation of fast twitch fiber subtypes from Type IIa back to Type IIb is observed (32). A resumption of training results in a fiber type transformation back to its trained state in a relatively shorter period of time. These studies highlight the dynamic nature of skeletal fiber transformations. 

 

Summary

Neuromuscular adaptations to training are specific to the type of training program (i.e., strength or aerobic endurance training) used. Initial improvements in strength are primarily associated with neurological adaptations, while further increases in strength are more dependent upon increases in the cross-sectional area of the muscle. These increases are thought to occur from either hypertrophy of existing muscle fibers or perhaps through muscle hyperplasia. Fiber type transformations may be possible within a subtype, but that it is not possible to convert between fiber types (i.e., Type I to a Type II). 

 

References

1. Adams, G.R., B.M. Hather, K.M. Baldwin, and G.A. Dudley. 1993. Skeletal muscle myosin heavy chain composition and resistance training. Journal of Applied Physiology. 74:911-915. 

2. Alway, S.E., J.D. MacDougall and D.G. Sale. 1989. Contractile adaptations in human triceps surae after isometric exercise. Journal of Applied Physiology. 66:2725-273. 

3. Alway, S.E., P.K. Winchester, M.E. Davis, and W.J. Gonyea. 1989. Regionalized adaptations and fiber proliferation in stretch-induced muscle enlargement. Journal Applied Physiology. 66:771-781. 

4. Alway, S.E., W.H. Grumbt, J. Stray-Gunderson, and W.J. Gonyea. 1992. Effects of resistance training on elbow flexors of highly competitive bodybuilders. Journal Applied Physiology 72:1512-1521. 

5. Antonio, J. and W.J. Gonyea. 1993. Skeletal muscle fiber hyperplasia. Medicine and Science in Sports and Exercise. 25:1333-1345. 

6. Caiozzo, V.J., T. Laird, K. Chow, C.A. Prietto, and W.C. McMaster. 1983. The use of precontractions to enhance the in-vivo force velocity relationship. Medicine and Science in Sports and Exercise. 14:162. 

7. Caizzo, V.J., J.J. Perrine and V.R. Edgerton. 1981. Training induced alterations of the in vivo force-velocity relationship of human muscle. Journal of Applied Physiology: Respiration Environmental Exercise Physiology. 51:750-754. 

8. Fleck, S.J. and W.J. Kraemer. 1997. Designing Resistance Training Programs. Champaign, Ill: Human Kinetics. 

9. Goldspink G. 1970. The proliferation of myofibrils during muscle fiber growth. Journal of Cell Science. 6:593-603. 

10. Gonyea, W.J. 1980. Role of exercise in inducing increases in skeletal muscle fiber number. Journal of Applied Physiology: Respiration Environmental Exercise Physiology. 48:421-426. 

11. Gonyea, W.J., D.G. Sale, F. Gonyea, and A. Mikesky. 1986. Exercise induced increases in muscle fiber number. European Journal of Applied Physiology. 55: