Effects of Strength Training on the Physiological Determinants of Middle- and Long-Distance Running Performance: A Systematic Review

Skeletal muscle hypertrophy is defined as an increase in muscle mass, which in the adult animal comes as a result of an increase in the size, as opposed to the number, of pre-existing skeletal muscle fibers. The protein growth factor insulin-like growth factor 1 (IGF-1) has been demonstrated to be sufficient to induce skeletal muscle hypertrophy. Over the past few years, signaling pathways which are activated by IGF-1, and which are responsible for regulating protein synthesis pathways, have been defined. More recently, it has been show that IGF-1 can also block the transcriptional upregulation of key mediators of skeletal muscle atrophy, the ubiquitin-ligases MuRF1 and MAFbx (also called Atrogin-1). Further, it has been demonstrated recently that activation of the NF-kappaB transcription pathway, activated by cachectic factors such as TNFalpha, is sufficient to induce skeletal muscle atrophy, and this atrophy occurs in part via NF-kappaB-mediated upregulation of MuRF1. Further work has demonstrated a trigger for MAFbx expression upon treatment with TNFalpha--the p38 MAPK pathway. This review will focus on the recent progress in the understanding of molecular signalling, which governs skeletal muscle atrophy and hypertrophy, and the known instances of cross-regulation between the two systems.

Progression in resistance training is a dynamic process that requires an exercise prescription process, evaluation of training progress, and careful development of target goals. The process starts with the determination of individual needs and training goals. This involves decisions regarding questions as to what muscles must be trained, injury prevention sites, metabolic demands of target training goals, etc. The single workout must then be designed reflecting these targeted program goals including the choice of exercises, order of exercise, amount of rest used between sets and exercises, number of repetitions and sets used for each exercise, and the intensity of each exercise. For progression, these variables must then be varied over time and the exercise prescription altered to maintain or advance specific training goals and to avoid overtraining. A careful system of goal targeting, exercise testing, proper exercise technique, supervision, and optimal exercise prescription all contribute to the successful implementation of a resistance training program.

High-resistance strength training (HRST) is one of the most widely practiced forms of physical activity, which is used to enhance athletic performance, augment musculo-skeletal health and alter body aesthetics. Chronic exposure to this type of activity produces marked increases in muscular strength, which are attributed to a range of neurological and morphological adaptations. This review assesses the evidence for these adaptations, their interplay and contribution to enhanced strength and the methodologies employed. The primary morphological adaptations involve an increase in the cross-sectional area of the whole muscle and individual muscle fibres, which is due to an increase in myofibrillar size and number. Satellite cells are activated in the very early stages of training; their proliferation and later fusion with existing fibres appears to be intimately involved in the hypertrophy response. Other possible morphological adaptations include hyperplasia, changes in fibre type, muscle architecture, myofilament density and the structure of connective tissue and tendons. Indirect evidence for neurological adaptations, which encompasses learning and coordination, comes from the specificity of the training adaptation, transfer of unilateral training to the contralateral limb and imagined contractions. The apparent rise in whole-muscle specific tension has been primarily used as evidence for neurological adaptations; however, morphological factors (e.g. preferential hypertrophy of type 2 fibres, increased angle of fibre pennation, increase in radiological density) are also likely to contribute to this phenomenon. Changes in inter-muscular coordination appear critical. Adaptations in agonist muscle activation, as assessed by electromyography, tetanic stimulation and the twitch interpolation technique, suggest small, but significant increases. Enhanced firing frequency and spinal reflexes most likely explain this improvement, although there is contrary evidence suggesting no change in cortical or corticospinal excitability. The gains in strength with HRST are undoubtedly due to a wide combination of neurological and morphological factors. Whilst the neurological factors may make their greatest contribution during the early stages of a training programme, hypertrophic processes also commence at the onset of training.