Adaptations to endurance training

Adaptations to endurance training.

Signalling pathways of adaptations to endurance training

What adaptations to endurance training can be expected? Regular, training-induced stimuli improve various components of endurance capacity. These adaptations take place centrally (improvement of cardiac output and/or improvement of stroke volume) and peripherally in the working muscles (muscle fibre distribution, mitochondrial density, capillarisation). It is particularly important to note that the central adaptations improve regardless of the chosen training method, whereas the peripheral adaptations take place predominantly in the endurance-trained muscles. For this reason, the choice of training method should be well considered and, above all, adapted to the individual goal.
How specific adaptations arise from the different types of endurance training and how these can, in part, be deliberately controlled through a suitable choice of training method is part of sports physiology research and is summarised here in a brief overview, for a basic understanding.

No. 1 of the adaptations to endurance training - athlete's heart or pathological cardiac hypertrophy

The main component of the central adaptation through endurance training is a predominantly structural change in the heart muscle. These changes can turn out positive (athlete's heart) or negative (hypertrophic cardiomyopathy). In the athlete's heart, the left ventricle predominantly enlarges and the heart muscle wall thickens in proportion, which net leads to an increased stroke volume (the heart can eject more blood volume per beat).(1) In heart patients, on the other hand (e.g. due to aortic stenosis or long-standing hypertension), wall thickness increases sharply at the expense of ventricular volume (2), which ultimately leads to a reduced stroke volume and, after usually long-standing heart failure due to failure of the heart muscle, ends in cardiac death.
As expected, two different molecular signalling pathways lead to the mentioned adaptations in the heart muscle. Above all, repeated intervals of intense endurance loads lead to physiological hypertrophy of the heart muscle cells by increasing the concentrations of PI3K and subsequently PKB/Akt(3,4) and decreasing the C/EBPbeta signalling pathway(5). Pathological cardiac hypertrophy, on the other hand, is predominantly based on increased calcineurin signalling.(6)
Perhaps it will become possible sooner or later to exert a direct influence on these signalling pathways by means of medication or genetic methods. What is certain, however, is the possibility of influencing them through repeated intense endurance training or by addressing the factors that promote hypertrophic cardiomyopathy (blood pressure regulation, aortic stenosis surgery, etc.)

No. 2 of the adaptations to endurance training - adaptations in muscle fibre distribution

An important structural component at muscle level for endurance performance is muscle fibre distribution. Basically, human skeletal muscle fibres can be divided into slow-contracting type 1 fibres and fast-contracting type 2a (fast) and type 2x (very fast) fibres. The names of this classification are based on the heavy myosin chains, which are expressed mainly in skeletal muscle fibres. Type 2x fibres, for example, mainly express heavy myosin chains of the 2x type.
In this regard, it has been shown that in type 1 muscle fibres the calcineurin-NFAT signalling pathway is predominantly induced. If this signal is weakened by a specific inhibitor, the ratio of type 1 to type 2 fibres decreases.(7) This signal is also increased by long-lasting electrical stimulation in model organisms, which indicates a link between muscle fibre distribution and physical training. Regarding type 2 fibres, a switch from type 2x to type 2a fibres induced by endurance training has been found, which suggests a slight slowing at fibre level. Overall, the muscle does of course not become slower through training-induced stimuli. A switch from type 1 to type 2 fibres and vice versa may theoretically be promoted by years of training, but the evidence for this is very limited, so no definitive statement is possible.(8)
What, on the other hand, has been shown with certainty is the mutual suppression of gene expression of the individual heavy myosin chain types. This explains the fact that in a given muscle fibre type only one type of heavy myosin chain is expressed and all others are suppressed.(9)

No. 3 of the adaptations to endurance training - training-induced mitochondrial biogenesis

Regular endurance training leads over time to an increase in the density of mitochondria in the muscle. This adaptation is called mitochondrial biogenesis and can in principle be explained by two signalling pathways. Long-lasting, slow endurance training leads to activation of CaMK through the release of calcium.(10–12) During high-intensity interval training (HIIT), on the other hand, AMPK registers the low concentrations of AMP and ADP. It also registers the drop in glycogen.(13
AMPK and CaMK increase the expression of the transcription factor PGC-1alpha, which in turn improves mitochondrial biogenesis by increasing expression of nuclear and mitochondrial DNA.(14)

No. 4 of the adaptations to endurance training - training-induced angiogenesis

As already described, a performance-limiting factor in endurance sports is, in addition to maximum oxygen uptake, also peripheral oxygen utilisation. In this respect, the density of the muscular capillary network is of central importance.
Via the CaMK/AMPK-PGC-1alpha signalling pathway, hypoxia-induced HIF-1 and shear-stress-induced NO, angiogenic growth factors (which promote capillary growth) are upregulated. One of the most important of these factors is VEGF (vascular endothelial growth factor).
In addition, endurance training increases the expression of metalloproteinases, which prepare the extracellular matrix for the sprouting of capillaries by forming tunnels.(15)

Step on the gas and get the adaptations to endurance training!

Sources:

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