Adaptations in the structural and/or functional properties of cells, tissues and organ systems in the human body occurs when exposed to various stimuli. While there is unanimous agreement that regular physical activity is essential for optimal function of the human body, it is evident that extrinsic factors, such as diet, smoking, exercise habits, are reflected in the morbidity and mortality statistics of the population. Ageing is obligatorily associated with reduced maximal aerobic power and reduced muscle strength, i.e. with reduced physical fitness. As a consequence of diminished exercise tolerance, a large and increasing number of the aged population will be living below, at or just above ‘threshold’ of physical ability, needing only a minor illness to render them completely dependent. Physical training can readily produce a profound improvement of functions essential for physical fitness in old age. Adaptation to regular physical activity causes less disruption of the cells’ internal environment and minimises fatigue which enhances performances and the economy of energy output during daily physical activity. Regular physical exercise reduces the risk of premature mortality in general, and of coronary heart disease, hypertension and diabetes mellitus. Physical activity also improves mental health and is important for health and optimal function of muscles, bones and joints. The most recent recommendations advice the people of all ages to include a minimum of 30 minutes of physical activity of moderate intensity, such as brisk walking, on most, if not all, days of the week. Check out the latest glucofort reviews.
The reason we need to know the importance of exercise as a therapeutic agent is because exercise provides a unique opportunity to study how different functions are regulated and integrated. In fact, most functions and structures are in one way or another affected by acute and chronic exercises (like a regular training programme). Therefore, physiology of exercise is an integrated science that has the goal of identifying the mechanisms of overall bodily function and its regulation. Let me review some factors of key importance to exercise. Try out steel bite pro for tooth decay prevention.
For an individual’s aerobic performance, the maximal oxygen consumption or uptake is the decisive factor. However, as the exercise prolongs, the availability of substances for the exercising muscles is another factor to consider as well as the economy of movement. During the last century, much research has been done analysing which step in the oxygen cascade from the air to the mitochondria in the skeletal muscle is the limiting factor. Some of these factors include: pulmonary ventilation, pulmonary diffusing capacity, cardiac output, oxygen diffusion from blood to muscle and to mitochondria and oxidising enzymes in the mitochondria. To date, there is general agreement that the central circulation of the human limits the maximal oxygen uptake during exercise in which large muscle groups are involved (1).
A) Is maximal oxygen uptake trainable?
A simple answer is yes. A training programme including interval or continuous exercise, for 30–40 minutes three times per week, at 50% for beginners and up to 80% of maximal oxygen uptake or heart rate reserve can effectively increase stroke volume and, therefore, maximal cardiac output by about 15% or more, albeit with large individual variations (2, 3). The percentage improvement in maximal oxygen uptake for the same training programme is the same in young and old adults, in women and men (4).
Recent evidence shows that this cardiorespiratory fitness gains are similar when physical activity occurs in several short sessions (e.g. 10 minutes) as when the same total amount and intensity of activity occurs in one longer session (30 minutes) (5). Although, the health benefits of such intermittent activity have yet to be demonstrated, it is reasonable to expect them to be similar to those of continuous activity. Moreover, for people who are unable to set aside 30 minutes for physical activity, shorter exercise sessions are clearly better than none. This was shown in one study where there was greater adherence to a walking programme among those walking several times per day than among those walking once per day when the total amount of walking time was kept the same (5). Check out the most accurat one and done workout reviews.
From cross-sectional studies, it is concluded that there is a decline in maximal oxygen uptake amounting to 0.5 – 1.0% per year (1, 8). However, as has been reported, the degree of habitual physical activity undertaken and heredity can markedly affect this maximum oxygen uptake.
(C) Limiting factors for endurance
An untrained person with a maximal oxygen uptake of 2.5 L.min−1 may be able to exercise at 90% of the maximum for 20 minutes. If, after a period of training, this maximal oxygen uptake is raised to 3.0 L.min−1, the submaximal rate of oxygen uptake of 2.25 L.min−1 will only demand 75% of this new maximum. This trained person can tolerate this metabolic rate for 90 minutes, i.e. there is a 4.5 fold improvement of endurance that is most probably not limited by the oxygen transport system. It is more likely that the depletion of glycogen stores in the exercising muscles is the limiting factor. With a glycogen-saving, training-induced, and increased utilisation of free fatty acids as a substrate for exercising skeletal muscles, the performance time at 75% of maximal aerobic power will be longer than when a similar relative rate of exercise was maintained before training (7).
Numerous studies have demonstrated a significant increase in mitochondrial density as a consequence of aerobic training with a proportionate increase in mitochondrial enzymes (7, 8). If one expresses skeletal muscle’s oxidative capacity for a sedentary individual as one ‘unit’, then the endurance trained elite athletes will have 3 ‘units’ capacity. In a rabbit muscle, 3–5 week of chronic electrical stimulation with a frequency of 10 Hz can bring the capacity up to 6 ‘units’. If a leg is subjected to encasement in plaster for some weeks, the activity may drop to 0.7 ‘unit’ (7). From this data, we can conclude that with aerobic training, there is a shift in the trained skeletal muscle to greater muscle reliance on oxidative metabolism to provide energy for Adenosine Triphosphate (ATP) resynthesis.
With training, there is also an increase in capillary density. An increase in capillary density reduces the distance between blood and cell interior, which enhances the exchange rate of gases, substances, and metabolites. The surface area available for this exchange also increases. With more capillaries in a given tissue volume, more blood can flow through the vascular bed per unit of time. The mean transit time in increased, which allows a more complete exchange of substrates. The primary advantage of a high capillary density in highly endurance trained muscle is probably that it allows for an adequate mean transit time at high flow rates, thereby promoting a more complete exchange of materials (9).
The physiological site of action of enzyme lipoprotein lipase (LPL) is in the luminar surfaces of the capillary endothelium. With an increased capillary bed, more binding sites for LPL will be available. This may favour the provision of free fatty acids to the muscle, because the degradation of triglyceride-rich particles depend largely on the activity of LPL. In addition, the activation of LPL also transfers more surface material into high density lipoproteins (HDL). This mechanism may explain the elevated HDL concentration seen in endurance-trained individuals, and may be one of the factors in the observation that habitual physical activity seems to reduce the risk for coronary heart disease.
(D) Limitation in strength – effects of training
With age, there is a decrease in muscle strength that seems to parallel the reduction in muscle mass. This age-associated loss of muscle fibres is related to a loss of alpha-motoneurons (12) without affecting the force-generating capacity of the residual contractile material. It is noted that there are normally no signs of degenerated fibres in ageing muscle and the fiber composition is relatively constant, i.e. independent of age. However, the muscle fibres per motor unit have been reported to increase, which is interpreted as a reduction in motoneurons. As such, the increase in muscular strength induced by training is therefore not due to an increase in the number of muscle fibres (13) but due to the facilitation of nerve fibre sprouting (14).
When starting a strength-training programme, a 20–40% increase in strength may occur during the first weeks of training, without a noticeable increase in cross-sectional area of the muscle involved. This suggests a more efficient activation of the muscle. With continued strength training, there is an adaptation hypertrophy exclusively achieved by an increase in fibre size without an increase in the number of muscle fibres (13). It is interesting to note that as little as a 6-seconds isometric contraction repeated five times, three times per week can prevent loss of muscle mass and muscle function during periods of recovery from injury with joint immobilisation (15).
Gains in strength and speed of muscle contraction was observed by Fiatarone et al. (16). He studied nine frail, 90 year-old (range 87–96 years) institutionalised volunteers who undertook 8 weeks of resistance training consisting of standard rehabilitation principles of progressive resistance training with concentric (lifting) and eccentric (lowering) activation of knee extensor muscles. The subjects performed three sets of eight repetitions with each leg 6 to 9 seconds per repetition, with a 1 to 2 minute rest period between sets, three times per week. Except for the first week, the load was 80% of one repetition maximum. Strength gain averaged 174 ± 31% (mean ± SEM). Midthigh muscle area increased by 9.0 ± 4.5%. Mean tandem gait speed improved by 48% after training. The activation of the muscles involved only lasted some 10 minutes per week. These findings suggest that age does not appear to affect the trainability of skeletal muscle.
(E) Specificity of training
Training adaptations, whether for strength or endurance, in the skeletal muscles are limited to the muscles actually engaged in training. Specificity in training is also obvious with the circulatory response to exercise. Saltin (9) reported that the heart rate was approximately 25 beats, min−1 higher at a given oxygen uptake when one leg, which had been inactivated by a cast for 4–6 weeks, was exercised on a cycle ergometer than when the other leg exercised on a cycle ergometer at the same oxygen uptake. Before the cast was put on, no differences in heart rate response was noted.
To maintain or improve both flexibility in joints and dexterity and endurance in technically demanding sports, the specific activities must be practised. It is generally thought that elderly persons cannot execute coordinated, quick, precise finger movements with age. However, it is surprising that many musicians can perform perfectly at an advanced age. For example, Arthur Rubinstein played a very demanding Chopin composition at the age of 88 years and Andres Segovia, at the age of 92 years, gave concerts on the classical guitar. Hours of daily ‘training’ were behind these achievements. Most likely, their fantastic performances were not only, question of talent but of continuous practice (exercise).
Since there is specificity in training effects, it is advisable that one understands variations in the type of habitual physical activity, i.e. a variety of activities should be practised throughout life.
Is physical inactivity a risk factor for cardiovascular disease?
During the 1987, coronary heart disease (CHD) accounted for 27.5% of the 2.1 million deaths in the United States. In 1998, nearly 30% of the deaths as a result of medical problems in Malaysia is caused by cardiovascular disease and of this, 20% is due to coronary heart disease (17). Well-documented risk factors for CHD are sedentary lifestyles, increases in triglycerides and low density lipoprotein levels in the blood, decreases in the high density lipoproteins level, cigarette smoking, hypertension, diabetes, obesity, post-prandial hyperinsulinemia and carbohydrate intolerance. During the last 10–15 years, there have been several reports showing a significant reduction in morbidity and mortality in CHD in physically active persons compared with sedentary control groups (5, 6, 12, 18–24). In a longitudinal study of approximately 17,000 Harvard alumni, it was found that men who expended more than 2000 kcal per week in walking, stair-climbing and participation in sports were at 39% lower risk of developing coronary heart diseases than less active counterparts (22). This study demonstrated that sedentary adults, who increase physical activity even relatively late in life, can reduce their relative risk of CHD and all-cause mortality to levels similar to those who were always physically active.