Physiological effects of endurance training

Contents

  1. Introduction
  2. 1. Molecular and Metabolic changes
    1. 1.1 General metabolic change
    2. 1.2 Changes in enzymes and proteins
    3. 1.3 Changes in hormonal activity
  3. 2. Effects of physical training on skeletal muscles metabolism
    1. 2.1 Physiology of endurance training in skeletal muscles
    2. 2.2 Aerobic pathway
    3. 2.3 Type of muscle fibers
    4. 2.4 Effects
  4. 3. Cardiovascular adaptation
    1. 3.1 Central adaptations
    2. 3.2 Blood volume and blood pressure responses
    3. 3.3 Arterial remodelling
    4. 3.4 Peripheral adaptation
  5. Conclusions
  6. Sources

Introduction

Endurance training can be described as repeated isotonic contractions, aerobic exercises at submaximal intensity, with the objective of having better cardiovascular and metabolic effects, and to increase the anaerobic threshold. This can be achieved by, for example: running, swimming, and for humans, cycling. As with any type of physical exercise, the short term and long term effects are different. In this student essay we will be focused on the long term effects, with three main aspects in mind: the molecular and metabolic changes, the skeletal muscles changes and the cardiovascular changes. We will also be mentioning the eventual negative side effects that don’t necessarily come from the physical changes induced by a prolonged endurance training.

1. Molecular and Metabolic changes

1.1 General metabolic change

The carbohydrate metabolism is affected by long term endurance training, more precisely the blood glucose level, the insulin sensitivity and the glycated haemoglobin. The insulin sensitivity is increased and the blood glucose level is decreased: this is important for individuals suffering from type 2 diabetes. The glycated haemoglobin level thus also decreases. These effects have been shown by a study called Effects of Endurance Training on Lipid Metabolism and Glycosylated Hemoglobin Levels in Streptozotocin-induced Type 2 Diabetic Rats on a High-fat Diet (Heo et al, 2013), in which diabetic rats were the test subjects.
Concerning the lipid metabolism, in the same study, it has been shown that the total cholesterol level and triglyceride level of the blood plasma significantly decreases over time with endurance training, but high density lipoprotein (HDL) levels increase. A reminder that HDL carries cholesterol from the circulation to the liver to be reused or excreted, thus reducing the plaque formations of cholesterol in the circulation, and ultimately reducing the risk for heart diseases.
The cerebral metabolism is also affected: indeed, the oxygen-carbohydrate index, which is the molar uptake of oxygen over that of glucose (O2/(Glucose+1/2lactate)) increases as a result of regularly practiced endurance training. This result was observed in an experiment (Seifert et al, 2009), in which the subjects were tested for multiple cerebral parameters before the experiment, and after three months of regular endurance training. This translates as the metabolic activity of the brain decreases when subjected to submaximal endurance training, mostly by decreasing the carbohydrate uptake.

1.2 Changes in enzymes and proteins

When looking into studies concerning the enzymatic changes caused by endurance training, creatine kinase is a recurring subject. Indeed, it is a cause of concern, because it is secreted during exercise, and degrades the myocardium, so naturally there is a concern that high levels of exercise could cause, on the long term, myocardial damage. A study on dogs (Miller et al, 1989) proved that there is no significant difference in the quantity of myocardial creatine kinase secreted by sedentary dogs and that by regularly exercised ones. The higher level of myocardial creatine kinase can also only be observed in the left ventricle (Stuewe et al. 2001), and no damage to the heart is observable on the long term.

1.3 Changes in hormonal activity

It has been shown that prolonged endurance training can reduce the risk of ventricular fibrillation by decreasing the cardiac sympathetic activity, which in turn decreases the beta-2-adrenergic receptor (ADRB2) responsiveness. ADRB2 can bind epinephrine and results in smooth muscle relaxation and bronchodilation. an increased ADRB2 responsiveness can cause sudden death in susceptible animals. According to a study (Billman et al, 2006) , endurance training on the long term can reduce the risk of sudden death and cardiac fibrillations.
Endurance training increases fibroblast growth factor 21, which partakes in embryo development, cell growth, tissue damage repair, and reduces inflammation. During exercise, muscles are constantly getting damaged when used, so FGF21 is necessary to promote repairing. (released from bone marrow, (Bonsignore et al, 2010))

2. Effects of physical training on skeletal muscles metabolism

Intracelular pathways: Regular / long term exercise positively influence skeletal muscle energy metabolism and function.Endurance training leads to an increase in mitochondrial volume density as well as the muscular capillarization.Regarding the intracellular pathway, PGC-1alpha plays a role in regulating mitochondrial biogenesis in skeletal muscle endurance training. In addition, proteins that are involved in mitochondrial dynamics correlate with PGC-1alpha.There is also a link between the activation of the calcineurin, and the expression of PGC-1alpha. As a result, the changes in intracellular calcium levels potentially regulate this metabolic transcriptional co-activator.Besides, there are other pathways are involved in the control of muscle oxidative pathways such as the MAPK and CaMKs pathways. (Ventura-Clapier, Mettauer, Bigard, 2007).

2.1 Physiology of endurance training in skeletal muscles

ATP synthesis during an endurance training: During an endurance training, skeletal muscles need a huge amount of energy. The source of energy is the ATP which gives ADP and Pi.ATP + H2O + ADP + Pi + H+ + energy There are 3 metabolic ways of ATP production during endurance training.
- Anaerobic alactic way
- Anaerobic lactic way
- Aerobic way
The first one aims to produce energy very quickly for short and intense activities such as races for quarter horses or jumping. The second one produces ATP for longer efforts but less intense such as races of 1km for example. ATP is created by degrading glucose that comes from intramuscular glycogen or glucose in the blood. The Aerobic way is mostly used by trotters and horses of endurance (thoroughbreds) for long efforts. In this case, ATP is produced by degrading fatty acids present in the muscular cells or by degrading the intramuscular glucose. Besides, the metabolic reactions in aerobic pathways occur in presence of oxygen in the mitochondria.

2.2 Aerobic pathway

In the beginning of every training, the three pathways are used in the same time in order to produce energy. Then, depending on the activity, intensity and length of the exercise, the proportions of each way differ.

2.3 Type of muscle fibers

(according to the University of Veterinary Medicine, Budapest)

Phasic type Fast twitch

Tonic type Slow twitch

Muscle types

Pink = IIa e.g. m.pectoralis

White = Type IIb e.g. m.gastrocnemius

Red e.g. m. long. dorsi

1)

ATPase type

Fast

Fast

Slow

2)

SR pump

Fast

Fast

Slow

3)

Junction / fibre

1:1

1:1

„en grappe”-type

4)

T-system

Developed

Very developed

Not developed

5)

Muscle AP/neural AP

Exists/very frequent

Exists/very frequent

No/rare

6)

Contraction time (ms)

20

10

200

7)

Metabolism

Mixed

Anaerobic

Oxidative

8)

Fatigue

Slow

Fast

No

9)

Fibre length

Intermediate

Very long

Very short


Figure 1.Types of muscle fibers and their role in endurance training

Muscles fibers play an important role in endurance training. Indeed, there are three different muscle fiber types that can be described: The pink muscle (type IIa) fibers, the white muscle fibers (type IIb) and the red muscle fibers. Pink muscle fibers and white fibers are also called fast twitch fibers. They are capable of powerful contractions. While White muscle fibers work thanks to the anaerobic metabolism, the pink muscle fibers use a mixed metabolism. Besides, the third type of fiber is the red type fiber, also referred as slow twitch. They maintain a durable work and gain energy thanks to the oxidative metabolism. After a regular training, some fibres will be modified and allow a better endurance capacity.

2.4 Effects

Fiber type transition: According to American Journal of Veterinary Research, there is a modification of the type of muscular fibers in the case of Thoroughbred horses. Indeed, thoroughbred horses possess more oxidative fiber of type I and type IIa than the other breeds. These characteristics allow the thoroughbreds to adapt themselves better in endurance races for example. Regarding untrained horses, an increase of the muscular fibers type II is observed (Yamano et al., 2002). Trained thoroughbreds do not have an obvious change in fiber type due to endurance training.
How to measure a physiological muscular adaptation due to training? There are different ways to measure the endurance adaptation of horses. First, some parameters can be measured such as heart rate, speed of the animal and the level of lactic acid. Indeed, blood acid lactic is used to evaluate the aerobic capacity of exercise for training according to Mitsutoshi Kobayashi.Second, it is possible to measure the glycogen content as well as the enzyme activity in the skeletal muscles.

3. Cardiovascular adaptation

The heart can improve structurally and functionally engaging a larger muscle mass with regular exercise. Endurance training leads to cardiovascular adaptations that markedly increase aerobic power and improve performance. Adaptation is due to long term physiological changes in response to training that allows the body to meet new demands. Studies demonstrate that endurance training results in :
● Increased cardiac output
● Increased vascular conductance
● A greater perfusion capacity in muscle
● A greater oxygen extraction

3.1 Central adaptations

Cardiac output (beats per min) and Stroke volume (mL per min) increase in elite female and male athletes.According to several studies, we observe an increase in end-diastolic (end of filling) dimensions of the left(LV) and right(RV) ventricles, LV hypertrophy, and increased LV mass, and an increased volume of the left atrium (LA). LV end-diastolic diameter, LV wall thickness, and LV mass have been reported in endurance athletes. The dynamics of the blood changes that occur during exercise is the origin of cardiac remodelling as shown by the study Cardiovascular Adaptations to Exercise Training (Hellsten and Nyberg, 2016) 2 principals form of training :
● endurance exercise with an elevation in cardiac output with a reduced peripheral vascular resistance e.g long-distance running, cycling ==> LV enlargement
● strength training characterized by an increase of the peripheral vascular resistance and low cardiac output. ==> LV hypertrophy ( increased wall thickness/size) The increased wall thickness improves the heart's ability to circulate blood è it produces a more powerful contraction which helps to push the blood. Either endurance and strength training lead to adaptations in cardiac structure. However, endurance training induces enhanced diastolic LV filling and a faster filling of the heart during exercises. Another study states that the largest increase in LV has been reported after 6 months of training preparing for a marathon for one year(Arbab-Zadeh et al, 2014), while the Stroke Volume increase between the 6th and 9th months. They define two terms in their study:
● Eccentric hypertrophy: characterized by dilation of the LV chamber
● Concentric hypertrophy: associated with increased LV wall

The LV mass increased in a concentric way during between the 3 and 6 months, and then returned to a baseline, leading to classic eccentric hypertrophy. However, the RV in contrast changes in an eccentric pattern, and the mass-volume ratio does not change significantly.

3.2 Blood volume and blood pressure responses

Plasma volume is reduced proportionally to the metabolic and thermal demand during exercise. It results in a loss accompanied by increased electrolyte concentration and leads to the activation of the renin-angiotensin-aldosterone water retention. Endurance training leads to an expansion of blood volume (hypervolemia) via an aldosterone sodium retention with an increase in plasma albumin concentration. Data shows that trained and elite athletes have a higher blood volume than untrained individuals. The hypervolemia is also associated with a larger body water volume, which helps in the conductance of perfusion at the level of the skin, but also followed by a lower hematocrit value and blood viscosity.
This kind of training is also associated with an increased hemoglobin mass, which increases the buffer capacity of the blood. It facilitates the lactate release from active skeletal muscle. In their study titled Cardiac remodeling in response to 1 year of intensive endurance training (Arbab-Zadeh et al, 2014) they compared the pressure to the volumes changes during endurance training. When the influence of the pericardium was taken into account they could notice a right shift into the curve and conclude that together, these curves suggest a combination of reduced pericardial constraint and improvement of the myocardial compliance (the ability of the cardiac tissue to expand when filling with blood) occurred after training.

The blood pressure is controlled by a complex mixture between neural, hormonal and intrinsic factors involving brain, heart, and kidney (controls fluid balance). According to the pressure-volume changes, we notice an increase in the Stroke volume for any given filling pressure after 12 months of training (from the same study by Arbab-Zadeh et al., 2014).
It has been shown that endurance training reduces blood pressure at rest, due to vascular remodeling and changes in the peripheral vascular function.

3.3 Arterial remodelling

Schrezenmaier exposed cat femoral arteries to an increased blood flow via the stimulation of the hindlimb nerve and observed a gradual increase of the diameter. That was the first study that proved the force changes caused by the circulating blood.
Endurance trained individuals display a reduced arterial wall thickness and an increased lumen diameter for the transport of blood from the heart to the different organs. Optimally, the diameter and the elastic properties of the arteries should be adequate for the blood flow. (from 6 to 12 weeks of training to increase the femoral artery).
Some studies showed that the coronary arteries enlargement might be induced by training, but a genetic contribution must be taken into consideration.
Athletes exhibit an enlargement located at the level of large peripheral arteries, this observation were found across canoeists, where they show larger brachial arteries providing evidence that endurance training could lead to localized diameter adaptation supplying the specific active limb as showed by an experiment called Exercise and arterial adaptation in humans: uncoupling localized and systemic effects (Rowley et al, 2011) .
However, the requirement for this enlargement is due to the relationship between blood flow and oxygen consumption. The increased diameter is accompanied by an increased volume of the muscle to facilitate the ability of aerobic work. Thus we can state that the arteries are constantly modified by their vasomotor tone.

3.4 Peripheral adaptation

During exercise, the blood flow increases to accommodate the increased demand for oxygen by the skeletal muscle. This elevation is achieved by the increased cardiac output with the improvement of vascular conductance in the active blood.
The increased cardiac output is originated by the sympathetic activity, which induces a vasoconstriction tone in organs and active muscles. Training induces the other adaptation that may influence the level of blood flow, it is the better distribution of the flow by capillarization and therefore increases the oxygen diffusion. This vascular distribution may originate from the nervous system.
Endurance training may also stimulate the thermoregulation at the level of the skin, which induces a vasodilatation remodeling at the level of the arteriole and the capillary bed density, as shown by a study from L. Gliemann (Gliemann et al, 2015). This cutaneous adaptation is the result of an efficient heat transfer.

Conclusions

Finally, we can demonstrate that through endurance training, which improved cardiac and arterial function and increases the number of microcirculation vessels in cardiac and skeletal muscles, the sedentary individuals susceptible to cardiovascular disfunctionment can improve their health by exercising regularly. Milder metabolic disorders such as insulin resistency and higher cholesterol levels can also be regulated by endurance training. Endurance training also reduces cardiac disfunctionnement by regulating the ADRB2 responsiveness.

Sources


Billman, G. E.; Kukielka, M.; Kelley, R.; Moustafa-Bayoumi, M.; Altschuld, R. A. (2006):


Gliemann, L.; Buess, R.; Nyberg, M.; Hoppeler, H.; Odriozola, A.; Thaning, P.; Hellsten, Y.; Baum, O.; Mortensen, S. P. (2015):


Hellsten, Y.; Nyberg, M. (2016).


Heo, M.; Kim, E. (2013):


Miller, T. D.; Rogers P. J.; Bauer B. A.; O’Brien J. F.; Squires R. W.; Bailey K. R.; Bove A. A. (1989):


Morici, G.; Gruttad’Auria, C. I.; Baiamonte, P.; Mazzuca, E.; Castrogiovanni, A.; Bonsignore, M. R. (2016):


Rowley, N. J.; Dawson, E. A.; Birk, G. K.; Cable, N. T.; George, K.; Whyte, G.; Thijssen, D. H. J.; Green, D. J. (2011):


Seifert, T.; Rasmussen, P.; Brassard, P.; Homann, P. H.; Wissenberg, M.; Nordby, P.; Stallknecht, B.; Secher, N. H.; Nielsen, H. B. (2009):


Stuewe, S. R.; Gwirtz, P. A.; Mallet, R. T. (2001):


Venturaclapier, R.; Mettauer, B.; Bigard, X. (2007):

Endurance_training (last edited 2020-05-03 19:50:36 by 3938E)