Strength training (ST) and endurance training (ET) are common modalities used in many sports and are known to alter the protein synthetic response. Repeated bouts of exercise results in morphological and molecular adaptations and are highly specific to the type of exercise performed. However, the concomitant ST and ET might interfere or inhibit training response leading to conflicting adaptations.
It is well established that ST induce neuromuscular and metabolic adaptations of skeletal muscle. Acute gains in ST are primarily related to neurological adaptations such as motor unit activation, firing rate, synchronization, agonist-antagonist interaction, increase rate-of-force-development and potential chronic changes at peripheral, supra and spinal level.
The primary morphological adaptation is the increase in the cross-sectional-area (CSA) as a result of the increase in myofibrillar size and number. Hypertrophy on type IIab fibres is more likely to occur as ST has the potential to decrease myosin heavy chain (MHC) IIb leading to a significant increase in MHC IIa resulting in fibre-type IIab conversion. This preferential hypertrophy of type II fibres is due to an increase in myosin-filament density and myofibrillar proliferation. As myofibrillar size increases, the arrays of the A and I bands causes the actin filaments to pull the Z-disks, while the myofibrillar size increases, a lateral displacement occurs initiating a ‘split’ (Figure 1) of the Z-disks leading to a longitudinal division of the myofibril, eventually resulting are two myofibrils. ST is also associated with tendon, connective tissue adaptations and increase in muscle stiffness as well as changes in pennation angle.
Figure 1: The oblique pull of the peripheral actin filaments resulting in myofibrillar splitting.
The molecular mechanism of ST is initiated by contractile activity that stimulates secretion of insulin-like growth factor (IGF-1) resulting in the initiation of a molecular cascade. The binding of IGF-1 leads to activation of intracellular signalling pathways of phosphatidylinositol 3-kinase (PI3-k)–Akt– mammalian target of rapamycin (mTOR) cascade. mTORC1 is regarded as a master controller of anabolic metabolism by promoting protein synthesis, lipid syntheses and nucleotide synthesis following both acute and chronic ST.
Conversely, ET predominantly activate type I muscle fibres which are associated with endurance performance. ET promotes a better utilization fuel and oxygen plus cardiovascular and pulmonary adaptations. ET has shown to increase mitochondrial level and the ability to oxidize pyruvate and conversion of type II to type I fibres as a result of high volume ET. Common cardiovascular adaptation after ET are an increase in the left ventricle, improved stroke volume, decrease in heart rate linked with better cardiac output, increase in capillarization, decrease in blood pressure, increase in red blood cell and volume. Respiratory adaptations relate to increase in ventilation, respiratory rate, increased pulmonary diffusion and the (a-v) O2 difference.
The molecular response to ET increases mRNA expression in a growing number of genes. Within these transcriptors co-activators are the Peroxisome proliferator receptor-1α (PGC-1α), known to rapidly increase after a bout of ET. Mitochondrial biogenesis transcription is mediated by (PGC-1α) and also regulates of conversion of fast-to-slow fibre type. Mitochondrial biogenesis elevates adenosine monophosphate (AMP) which activates the enzyme AMP-activated protein kinase (AMPK). A decreases in energy levels are likely to activate AMPK resulting in the activation of pathways involved in carbohydrate and fatty acid catabolism to restore ATP levels.
Figure 2: Cascade of intracellular signalling mediating exercise induced responses to ST and ET.
Concurrent training (CT) is the concomitant integration of ET and ST during a training program. CT has been used to enhance performance in aerobic sports and recovery or work capacity in anaerobic sports. Studies have shown that CT improves strength and endurance in untrained individuals and trained endurance runners. Conversely, for power sports, CT appears to attenuate power production. However, when physical components are stressed concurrently, improvements appear to be substantially lower when compared with training for either exercise mode alone. This incompatibility of strength and endurance is hypothesized to be acute or chronic. That means, CT is affected by fatigue or substrate depletion (acute hypothesis) or metabolic and molecular adaptations are attenuated (chronic hypothesis).
There has been little elucidation of the mechanisms underlying CT. CT has shown to attenuate strength, hypertrophy and power development. Other studies have found that resistance training has no effect on Vo2Max or either maximise endurance performance. Conversely, CT compromises aerobic capacity versus endurance training alone. The most compelling molecular mechanism proposed to mediate specificity of training and the subsequent interference effect comes from the work of Atherton et al. (2005) who attempted to determine the exercise signalling specific in rats and found that ST increase phosphorylation of the anabolic Akt-mTOR cascade and ET increase AMPK phosphorylation and PGC-1 protein levels. In addition, increases in AMPK-TSC2 activity, PGC1α gene expression elicit inhibition of mTOR. In human studies the result still elusive as the molecular responses reported present an unequal response to exercise because the variability on subjects background. However, it appears that muscle phenotype dictates the molecular response, rather than the mode of exercise. Due to the fact that increases in the myofibrillar content of actin and myosin is the result of ST, whereas the increase in mitochondrial proteins is the result of ET.
In summary, the molecular transcription of ST and ET seems incompatible attributable to their functional outcomes. Adaptations to training are the result of cumulative molecular signaling responses initiating gene expression after exercise bouts and eventually building specific proteins and shifting muscle phenotype.
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