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ScienceWeek
EVOLUTION: PHYSICAL PERFORMANCE AND DARWINIAN FITNESS
The following points are made by J-F. Le Galliard et al (Nature 2004 432:502):
1) Strong evidence for a genetic basis of variation in physical performance has accumulated(1,2). Considering one of the basic tenets of evolutionary physiology -- that physical performance and darwinian fitness are tightly linked(3) -- one may expect phenotypes with exceptional physiological capacities to be promoted by natural selection. Why then does physical performance remain considerably variable in human and other animal populations(1,2,4)?
2) Sporting events would be exceedingly boring were there no variation in human performance; fortunately, this is not the case. For example, the distribution of finish times at international marathons has a large variance and a long tail(1), due to a variety of factors affecting the performance of individual runners(5). Although genetic variation in locomotor performance has been documented in human and other animal populations(1,2), questions remain as to how genetic and non-genetic factors would interact with each other and what effect selection has on the resulting individual variation(1).
3) The authors addressed these two questions using ground-dwelling lizards, a popular model system for studies of locomotor performance(2,4). The focus of the authors is on the endurance capacity as assayed in the laboratory. In lizards, endurance shows considerable interindividual variation that reflects differences in tight muscle mass, heart mass, and aerobic metabolism The study species is the common lizard (Lacerta vivipara Jacquin 1787) for which locomotor performance and life-history traits have been routinely studied. The authors took advantage of the populations established at the Ecological Research Station of Foljuif (Nemours, France) in the semi-natural conditions of outdoor enclosures to measure the heritability of initial endurance and the age-specific strength of natural selection on this trait.
4) In summary: The analysis by the authors of locomotor performance in the common lizard (Lacerta vivipara) demonstrates that initial endurance (running time to exhaustion measured at birth) is indeed highly heritable, but natural selection in favor of this trait can be unexpectedly weak. A manipulation of dietary conditions unravels a proximate mechanism explaining this pattern. Fully fed individuals experience a marked reversal of performance within only one month after birth: juveniles with low endurance catch up, whereas individuals with high endurance lose their advantage. In contrast, dietary restriction allows highly endurant neonates to retain their locomotor superiority as they age. Thus, the expression of a genetic predisposition to high physical performance strongly depends on the environment experienced early in life.
References (abridged):
1. Rupert, J. L. The search for genotypes that underlie human performance phenotypes. Comp. Biochem. Physiol. A 136, 191-203 (2003)
2. Garland, T. J. & Losos, J. in Ecological Morphology: Integrative Organismal Biology (eds Wainwright, P. C. & Reilly, S. M.) 240-302 (Univ. Chicago Press, Chicago, 1994)
3. Arnold, S. J. Morphology, performance and fitness. Am. Zool. 23, 347-361 (1983)
4. Bennett, A. F. & Huey, R. B. in Oxford Surveys in Evolutionary Biology (eds Futuyma, D. J. & Antonovics, J.) 251-284, (1990)
5. Bouchard, C., Malina, R. M. & PÚrusse, L. Human Kinetics 408 (Champaign, Illinois, 1997)
Nature http://www.nature.com/nature
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Related Material:
ON FITNESS AND SURVIVAL
The following points are made by Gary J. Balady (New Engl. J. Med. 2002 346:852):
1) In 1859, Charles Darwin published his theory of evolution as an incessant struggle among individuals with different degrees of fitness within a species. Although at that time, his explanations created remarkable controversy, they were to revolutionize the course of science. Darwin's writings reflected conclusions drawn from years of study and observation. Now, nearly 150 years later, in the era of evidence-based medicine and rigorous scientific method, when fitness is quantitatively measured and study subjects are followed for years, the data supporting the concept of survival of the fittest are strong and compelling. During the past 15 years, many long-term epidemiologic studies have shown an unequivocal and robust relation of fitness, physical activity, and exercise to reduced mortality overall, to reduced mortality from cardiovascular causes, and to reduced cardiovascular risk.
2) Cardiorespiratory fitness, or physical fitness, is a set of attributes that enables a person to perform physical activity. It is determined, in part, by habitual physical activity and is also influenced by several other factors, including age, sex, heredity, and medical status. Physical fitness is best assessed by a measure of maximal or peak oxygen uptake (volume of oxygen consumed, measured in milliliters of oxygen per kilogram of body weight per minute), which is viewed as an index of energy expenditure.
3) It is now becoming clear that exercise modulates many biologic mechanisms to confer cardioprotection. Exercise improves the lipid profile and glucose tolerance, reduces obesity, and lowers blood pressure. However, modification of atherosclerotic risk factors does not fully explain the benefits that have been observed. Positive effects of exercise on vascular function, autonomic tone, blood coagulation, and inflammation are likely to contribute to improved cardiovascular health and survival.
New Engl. J. Med. http://www.nejm.org
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ON THE PHYSIOLOGY OF EXERCISE
Notes by ScienceWeek:
Underlying the various beneficial effects of physical exercise on the health of the human body are a constellation of physical, biochemical, and physiological factors that have been intensively studied for more than a century. At present, maximal oxygen consumption is the primary measure of exercise capacity, and mechanisms related to the delivery of oxygen to the muscles are considered to be the main factors determining exercise capacity.
The following points are made by N.L. Jones and K.J. Killian (New England J. Med. 2000 343:633):
1) A fit 25-year-old man can generate 650 watts while bicycling for a few seconds and can maintain a power of 400 watts while bicycling for 1 minute, 230 watts while bicycling for 10 minutes, and 175 watts while bicycling for 30 minutes. He is able to reach 275 watts in a progressive incremental (increasing at 16.7 watts per minute) test to capacity; this power represents peak exercise and is the power at which maximal oxygen consumption (3.3 liters per minute) is measured. To put these figures in perspective, brisk walking represents an output of approximately 50 watts of power and an oxygen intake of 0.8 liters per minute.
2) Exercise depends on the oxidation of carbohydrate and fat for the regeneration of adenosine triphosphate required to sustain muscular contraction. Ventilation, gas exchange, and the circulation are adjusted to meet the requirements for delivery of oxygen and removal of carbon dioxide. As the intensity of exercise increases, the concentration of intramuscular creatine phosphate decreases, and the concentrations of intramuscular adenosine diphosphate, adenosine monophosphate, and inorganic phosphate increase. Increases in the intramuscular lactate concentration and decreases in the intramuscular potassium concentration contribute to a marked decline in muscle pH to below 6.5.
3) With prolonged submaximal exercise, the changes in intramuscular metabolite concentrations are less marked, but intramuscular glycogen is progressively depleted. The ability to sustain exercise depends on the initial intramuscular glycogen concentration. Fat stores represent a huge reservoir of potential energy, but the rate at which fat can be oxidized is limited to approximately one-fourth of the rate at which glycogen can be oxidized. Thus, even with maximal utilization of fat, the ability to maintain exercise is dependent on the oxidation of glycogen, which eventually becomes depleted, leading to muscle fatigue.
4) In exercise lasting longer than a minute or two, the cardiac output and heart rate increase linearly with peripheral oxygen uptake. The mean systemic arterial pressure and the vascular resistance in active muscle falls, leading to a large increase in blood flow to the muscles. Blood is pumped back to the heart by muscular contraction, and the cardiac output is determined by the venous return.
5) Muscle contraction during exercise is initiated by a central command from the *motor cortex of the brain that leads to activation of *motor neurons, depolarization of *motor end plates, propagation of *muscle action potentials, calcium release, formation of *cross-bridges, and shortening of *myofibrils. The magnitude of the central motor command increases in parallel with the power output, but it also increases if the responsiveness of the motor neurons or muscles decreases during fatigue. A maximum voluntary command is capable of activating virtually 100 percent of the *motor units in a fresh muscle (i.e., a muscle that has not been exercised). The responsiveness of motor neurons may be decreased by central and peripheral factors acting through reflexes in the spinal cord and by stimulation of receptors in the muscles.
6) Among the changes that accompany increasing intensity of exercise is a large increase in the intramuscular hydrogen ion concentration from 100 nanomoles per liter (pH = 7.0) at rest to 400 nanomoles per liter (pH = 6.4) or more at exhaustion, leading to inhibition of *excitation-contraction coupling and thus reducing the responsiveness of the muscle to stimulation of motor units.
New Engl. J. Med. http://www.nejm.org
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Notes by ScienceWeek:
motor cortex of the brain: (cortex) The cerebral cortex is a thin surface layering of nerve cells of the brain, the region only several millimeters thick but covering all of the brain surface. This is the part of the central nervous system most intimately involved with the so-called "higher faculties", although the cortex operates in concert with other parts of the brain. The structure is primitive in lower mammals, and is found progressively more pronounced and with greater surface area in primates and man. The motor cortex is the region of the cortex involved in voluntary muscle movements.
motor neurons: In this context, motor neurons are neurons with cell bodies in the spinal cord and extensions that leave the spinal cord to terminate on muscle fibers. In this report, the general paradigm for activation of voluntary muscles is neurons in brain (motor cortex) to neurons in spinal cord (motor neurons) to peripheral muscle fibers.
motor end plates: The junctions between nerve fiber (axon) terminations and muscle fibers.
muscle action potentials: The muscle "action potential" is completely analogous to the nerve action potential and consists of a brief (approximately 1 millisecond) reversal of polarization that travels along the fiber. This electrical change initiates calcium movements that begin the contraction process.
cross-bridges: In general, connections between contractile elements of muscle fibers.
myofibrils: In general, any of the long cylindrical contractile elements, 1 to 2 microns in diameter, that constitute the major component of muscle fibers.
motor units: In general, a single motor neuron and all the muscle fibers that are innervated by it. (The axons of motor neurons branch to make contact with a number of muscle fibers.)
excitation-contraction coupling: In general, the coupling of an excitatory stimulus to the contraction of muscle; at the cellular level, the process by which muscle fibers are caused to contract by the stimulation of a neuron.
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