Regardless of the “stigmata” of the champion (i.e., the genetic heritage), it is evident how a good training program can determine a substantial increase in athletic ability. It is a common experience that the more you train in a particular sport, the less effort you have to make to do the same work or, alternatively, the more work you would be able to do with the same effort. Trivializing, if a sedentary subject can cover an average of 5 km after 30 min of running (therefore, running at 10 km/h), the same subject, after a few weeks of constant training on the same distance, would be able to run much faster (e.g., at 15 km/h), to cover the same distance in less time (e.g., in 20 min) or covering a greater distance (e.g., 7.5 km) in the same time. This favorable evolution results from a well-defined biological principle named “adaptation” and involves almost all systems, organs, and apparatuses, as briefly summarized in Table 1.

Table1. Organic adaptations to physical activity

Of particular interest in this context are undoubtedly the adaptations of the muscular tissue, which are essentially implemented by three mechanisms: (a) an increase in muscular mass (the transverse diameter of the muscle can increase by up to 30%); (b) an increase in vascularization (capillarization can increase by up to 25%); and (c) neuro logical mechanisms, which allow the muscle to contract more intensely (the coordination of impulses to the muscles improves, and the contraction becomes more “ordered” and practical). Concerning the first adaptation (an increase in mass), it has long been debated whether it is a consequence of hyperplasia (an increase in the size of the muscle fibers), hypertrophy (an increase in the number of cells), fibrosis (deposition of scar tissue), or a combination of all the three previous phenomena. The most accredited hypothesis is precisely the last one, involving a co-participation of all three mechanisms. If, on the one hand, it is indisputable how the continuous stimulus of a muscle determines a hypertrophic process, then it is equally clear that a muscle contraction determines an increased production of growth factors (some, such as insulin-like growth factor (IGF) and IGF-1, also pro duced as a result of a “physiological” muscle microtrauma, which determines the necrosis of some myocytes), which leads to the recruitment of muscle stem cells, thus promoting their subsequent differentiation into myocytes. Also not to be underestimated is the muscular enlargement linked to the progressive accumulation of the fibrotic tissue, consequent to repeated muscular microtrauma, especially in certain types of sports in which the muscular work becomes extreme (in weightlifting, for example). In these cases, although muscle regeneration is usually completed in 30–40 days, with restitutio ad integrum of the damaged muscle parenchyma, the deposition of the scar tissue is completed within 2–3 weeks. However, the reabsorption of the newly deposited fibrotic tissue is never complete, leaving more or less voluminous residues, which will amplify the muscle size as a whole. When following the decrease in the intensity of physical exercise (especially in old age), hyperplasia and hypertrophy will physiologically tend to regress and the fibrotic tissue will constitute part of the residual muscle volume.

Concerning circulatory changes within muscle tissue, blood flow at rest is approximately 3–4 mL/min/100 g. During intense exercise, the oxygen demand increases up to 20-fold and is associated with increased blood flow of up to 25-fold in exercising muscle (50–80 mL/min/100 g). This increase is not only unparalleled in other districts of the human body but also paradoxically involves the diversion of most of the blood flow in the muscle, increasing the irroration from 20% at rest up to 85–90% under conditions of maximal effort. Since most of the blood is then diverted to the muscle during exercise, the blood flow in other organs and systems decreases at the same time, contracting up to almost 90% (compared to the resting condition) in the kidneys, spleen, and digestive system. It is well documented that during a run at high intensity, the urination stimulus tends to stop progressively, only to resume at the end of the physical activity. This is a reflection of glomerular filtration, which tends to drastically decrease during physical activity (due to reduced vascularization of the renal parenchyma) and then gradually return to normal conditions at the end of training.

An increase in the oxygen-carrying capacity of the blood is a further adaptation to exercise. In individuals who regularly exercise in a moderate-to-intensive manner, the total blood volume (blood volume) and the amount of hemoglobin in the blood simultaneously increase with the training load. This has obvious logical assumptions (adaptive), when a greater blood mass (hypervolemia) allows the heart to reach a greater cardiac output, facilitating the transfer of oxygen to the tissues and also giving a thermoregulatory advantage (better cooling of the body), whereas a more significant amount of hemoglobin (due to the increased bone marrow synthesis of red blood cells) promotes a greater transport of oxygen to the muscle in exercise. However, in this context, it should be mentioned that hypervolemia and an increase in the amount of hemoglobin in the blood are rarely of equal magnitude since the former is greater than the latter. In summary, an aerobic training program can promote an increase in plasma volume by up to 25% (usually from about 5.2 to about 6.5 liters), at the same time as increasing the amount of hemoglobin in the blood by 20% (for example, from 800 to 950 g). Transforming these values into hemoglobin concentration in the blood, the balance appears paradoxically negative (from −1% to −2%). Despite the increase in total quantity, it is always physiological to record a progressive decrease in hemoglobin concentration in the blood in parallel with the increase in workload. Therefore, the rule is that when athletes start a 3-week cycling stage race (the Giro d’Italia, for example), the hemoglobin concentration always tends to be higher than the value recorded at the end. When this does not happen, it is reasonable to assume that the athlete has used some technique (more or less legitimate) to further increase the total amount of circulating hemoglobin, which will be discussed in a later section of this chapter.

The adaptation process now appears to result from a series of individual variables linked to the intensity of the exercise, its duration, and the character and duration of recovery intervals between one exercise and another. Programming adequate recovery allows the body to progressively raise the bar of performance (a phenomenon known as “supercompensation”), up to a hypothetical maximum defined by the theo retical limit of the athletic ability. Interspersing a series of exercises with an excessive recovery period (e.g., running only once a month) effectively nullifies the potential benefit of supercompensation. Conversely, continuing to perform highly intense exercise series without adequate recovery not only can negate the potential benefits of supercompensation but can also lead to negative consequences such as overreaching or overtraining. These three possibilities are summarized in Fig. 1. It is clear from the figure that, in the first case, adequate recovery allows a progressive increase in athletic performance. In the second case, where recovery is excessive compared to the load, athletic performance will remain unchanged. In the third case, on the other hand, characterized by too little or no recovery, fatigue will prevail over supercompensation, to the point of determining a paradoxical decline in athletic performance: the fateful, much-feared by professional athletes (and others), “overtraining syndrome.”

Fig1. Effects of the different cadences of workload and recovery on the progression of athletic performance (at the top, corrected program; in the middle, interval of excessive recovery, and at the bottom, interval of insufficient recovery). (Copyright EDISES 2021. Reproduced with permission)

The importance of adaptations, besides the practical effects on athletic performance, involves a real biochemical revolution. So much so that, after the Sydney Olympics, the debate arose as to whether medium/high-level athletes should be considered “normal” people because by doing a higher-than-normal physical activity, they may instead mani fest many biochemical parameters that place them well outside the normal reference ranges, mostly established using sedentary or only moderately active populations. While not wishing to be all-inclusive, since the biochemical parameters that can be measured in the laboratory are almost infinite, the main biochemical alterations that occur as workloads (especially aerobic) progressively increase are summarized in Table 2.

Table2. Biochemical adaptations to physical activity

All these biochemical alterations should be considered strictly “physiological,” normal consequences of an adaptive metabolic process, which has progressively promoted a com plex physical and biochemical change in the subject devoted to regular moderate/intense physical activity compared to a sedentary individual. The correct interpretation of these changes is essential for laboratory medicine professionals, sports physicians, and athletic trainers to be able to fully discern the concept of “pathological abnormality” from that of “physiological variation.” For example, it should not be surprising to find significantly elevated creatine kinase (CK) and cardiac troponin (T or I) values after a marathon. This is in line with the physiological release during a relatively intense and prolonged physical activity. It becomes essential to know the behavior of the various laboratory parameters in athletes, since abnormalities of their kinetics instead represent highly sensitive spies of potential pathological processes (e.g., muscle damage). The variables that should therefore be considered include:

• Demographics (age, sex, ethnicity)

 • Type of athletic performance (endurance, power or mixed sports)

 • Workload (type of training and context, e.g., competitions or rest)

• Contingent situations (diet, hydration)

• Intake of drugs or nutritional supplements

A final consideration should be reserved for the clinical molecular biology of exercise. Reliable scientific evidence shows that specific genes’ polymorphisms can significantly influence athletic performance. These genes mainly encode proteins and enzymes involved in determining the efficiency of muscle metabolism (e.g., oxidative and glycolytic enzymes), muscle performance (e.g., contractile proteins), tendon and ligament apparatus (tendon proteins), and psychological inclination. In the future, the role of laboratory medicine will be to demonstrate whether a panel integrating the most significant polymorphisms can help predict success in different sports disciplines.

اخر الاخبار

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المزيد

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"أوميغا 3" صديق القلب.. هل يربك سكر الدم؟

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دراسة: محاولة متعمدة لنشر الإنفلونزا تنتهي بـ"مفاجأة"

المزيد

الآخبار التكنلوجية

سلامة الأطفال: سبع قواعد ذهبية للركوب الآمن بالسيارة

توقع خطير لماسك: الروبوتات ستتفوق على البشر من حيث العدد

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"ميتا" توقف وصول المراهقين إلى شخصيات الذكاء الاصطناعي ؟

المزيد

مواضيع ذات صلة

Iron is Strictly Conserved

Haptoglobin Protects the Kidneys

The Levels of Certain Plasma Proteins Increase During Inflammation or Following Tissue Damage

Albumin is the Most Abundant Protein in Human Plasma

Biochemical Parameters for Assessing Athletic Performance

Clinical Biochemistry of Metabolic Substrates

Generalities on the Structure and Biochemistry of the Skeletal Muscle

Plasma Contains A Complex Mixture of Proteins

Intermediate Filaments Differ From Microfilaments & Microtubules

Microtubules Contain α- & β-Tubulins

Muscle Tissue are The Target of Several Genetic Disorders

Skeletal Muscle Contains Slow (Red) & Fast (White) Twitch Fibers