Substantial research has been completed examining the impact of carbohydrate (CHO) intake on endurance exercise, whereas its role in resistance-based exercise performance, adaptation and cell signalling has yet to be fully characterised. This empirical shortcoming has precluded the ability to establish specific CHO recommendations for resistance exercise. This results in recommendations largely stemming from findings based on endurance exercise and/or anecdotal evidence despite the distinct energetic demands and molecular responses mediating adaptation from endurance- and resistance-based exercise. Moreover, the topic of CHO and exercise has become one of polarising nature with divergent views – some substantiated, others lacking evidence. Current literature suggests a moderately high daily CHO intake (3–7 g/kg per d) for resistance training, which is thought to prevent glycogen depletion and facilitate performance and adaptation. However, contemporary investigation, along with an emerging understanding of the molecular underpinnings of resistance exercise adaptation, may suggest that such an intake may not be necessary. In addition to the low likelihood of true glycogen depletion occurring in response to resistance exercise, a diet restrictive in CHO may not be detrimental to acute resistance exercise performance or the cellular signalling activity responsible for adaptation, even when muscle glycogen stores are reduced. Current evidence suggests that signalling of the mammalian target of rapamycin complex 1, the key regulatory kinase for gene translation (protein synthesis), is unaffected by CHO restriction or low muscular glycogen concentrations. Such findings may call into question the current view and subsequent recommendations of CHO intake with regard to resistance-based exercise.

Recruitment determines the profile of fibre-type-specific genes expressed across the range of muscle fibres associated with slow, fast fatigue-resistant and fast fatiguable motor units. Downstream signalling pathways activated by neural signalling and mechanical load have been the focus of intensive research in past years. It is now known that Ca2+-dependent calcineurin–nuclear factor of activated T cells and insulin-like growth factor 1 pathways and their downstream mediators contribute to these adaptive responses. These pathways regulate gene expression through muscle-specific (myocyte-enhancing factor 2, myoblast determination protein) and non-specific (nuclear factor of activated T cell 2, GATA-2) transcription factors. Transcriptional signals activated with increased contractile activity result in altered expression of fibre-type specific genes, including the myosin heavy chain isoforms and oxidative and glycolytic enzymes and a net change in muscle fibre-type composition. In contrast, transcriptional signals activated by increased load bearing result in hypertrophy or a growth response, a component of which involves satellite cell recruitment and fusion with existing adult myofibres. Calcineurin has been identified as a key mediator in the hypertrophic response, and the current challenge has been to determine the downstream target genes of this pathway. Exciting new data have emerged, showing that myostatin, a negative regulator of muscle growth, and utrophin, a cytoskeletal protein important in maintaining membrane integrity, are downstream targets of calcineurin signalling. Increased understanding of these mediators of muscle growth may provide strategies for the development of effective therapeutics to counter muscle weakness and muscular dystrophy.