HISTORY OF MARATHON
The origins of the modern marathon begin with the legend of Philipides and the battle on the plain of Marathon between the Athenian and Persian armies. According to the legend, in 490 BC the greatly outnumbered Athenian army prevailed and dispatched a messenger, Philipides, to Athens to bring news of the victory. Philipides ran the 40 km from Marathon to Athens, where he proclaimed the famous words “rejoice, we conquer,” after which he promptly dropped dead, making him the first anecdotal case of sudden cardiac death in a marathoner. In 1896 the first modern Olympic Marathon was run, commemorating Philipides’ feat. It was a distance of 40 km (24.8 miles), from Marathon to Athens. The rather arbitrary distance of 26.2 miles (42.195 km) dates from the 1908 London Olympics. The distance of the race was lengthened so the racecourse, which started at Windsor Castle, would finish in front of the Royal Box so the Queen could watch the finish. In 1921 this distance became the internationally accepted marathon distance.
The physical examination should focus on the cardiopulmonary examination. The most notable characteristic usually is a resting bradycardia, often with an associated sinus dysrhythmia. The resting heart rate in a well-trained runner is, on average, 15 beats/min lower than in the general population.
CARDIAC EFFECTS
Normal LV Contractile Function
In individuals with normal LV function, exercise-related cardiac effects may be subdivided into 3 entities: prevention of cardiac pathologies associated with aging; cardiac adaptation to strenuous regular exercise training resulting in physiological cardiac hypertrophy commonly known as athlete’s heart; and prevention of impaired systolic and/or diastolic cardiac function associated with short-term challenges (eg, ischemia/reperfusion [I/R]).
Left ventricle
The maintenance of left ventricular (LV) mass and function depends on regular exercise. Prolonged periods of physical inactivity, as studied in bed rest trials, lead to significant reductions in LV mass and impaired cardiac compliance, resulting in reduced upright stroke volume and orthostatic intolerance. In contrast, a group of bed rest subjects randomized to regular supine lower-body negative pressure treadmill exercise showed an increase in LV mass and a preserved LV stoke volume. In previously sedentary healthy subjects, a 12-week moderate exercise program induced a mild cardiac hypertrophic response as measured by cardiac magnetic resonance imaging. These findings highlight the plasticity of LV mass and function in relation to the current level of physical activity.
Athlete’sHeart
In normal individuals, regular high-intensity physical activity for up 5 to 6 hours per week may result in cardiac adaptations known as athlete’s heart, resulting in compensatory myocardial hypertrophy, which is more eccentric in endurance training and more concentric in resistance training. Endurance-trained athletes show mean LV end-diastolic diameters of 53.7 mm compared with 49.6 mm in normal subjects; however, 14% of 1309 athletes examined by Pelliccia et al showed LV end-diastolic diameters between 66 and 70 mm. The diagnostic strategies to distinguish normal LV hypertrophy from hypertrophic cardiomyopathy are a matter of continuing discussions.
Ischemia and riperfusion
Exercise training has the potential to prevent myocardial damage related to I/R injury. Exercise training induces an upregulation of key antioxidative enzymes such as MnSOD, glutathione peroxidase (GPX), and catalase. Opening the sarcolemmal (sarco) K+ATP channel accelerates cardiomyocyte repolarization by increasing K+ outflow. As a result of the shorter action potential, Ca2+ overloading is prevented by reducing opening rates of the L-type Ca2+ channel. Although not essential for I/R protection, increased levels of HSP72 were observed after training. HSP72 can prevent apoptotic cell death, likely by interaction with caspase-3.
Oxidative Stress
Regular physical exercise seems to delay the accumulation of ROS- mediated cell damage by improving the antioxidative protection in the myocardium.
Cardiac Fatigue
Prolonged strenuous activity, as in the Ironman Triathlon, can lead to transient reductions of LV systolic and diastolic function. Several mechanisms are involved in cardiac fatigue, including changes in preload conditions, myocardial stunning, α1-receptor desensitization, and altered cardiac autonomic regulation.
Preload conditions were highlighted as a potential mechanism by Dawson et al, who demonstrated the lack of changes in LV function when central venous pressure was well maintained. However, other researchers with different training protocols found depressed LV contractile function unrelated to preload conditions, which confirms the relevance of intrinsic myocardial damage. Prolonged strenuous exercise results in a 5-fold increase in circulating catecholamines with consecutive desensitization of α1-adrenoreceptors. This results in a blunted chronotropic and inotropic response to dobutamine.
Cardiovascular effects of exercise training: molecular mechanisms.
Exercise in Cardiovascular Disease
VASCULAR EFFECTS
Aorta and other main Arteries
Among healthy individuals, high-intensity exercise led to vascular remodeling with up to 51% enlarged brachial conduit artery area and reduced distal aortic cross-sectional areas (up to 8%), whereas aortic distensibility remained un- changed. However, endurance and strength training have opposite effects on aortic compliance and vascular stiffness; in an elegant study, Otsuki et al measured plasma endothelin-1, nitric oxide (NO), and arterial stiffness in young, healthy endurance-trained versus strength-trained men. They demonstrated that aortic pulse-wave velocity as an established index of vascular stiffness was significantly increased in strength athletes and reduced in endurance athletes versus healthy controls. Strength athletes displayed elevated endothelin-1 levels that correlated with aortic pulse-wave velocity. Reductions of aortic stiffness after endurance training were confirmed in patients with hypertension and coronary artery disease.
Cardiovascular effects of exercise training: molecular mechanisms.
Exercise in Cardiovascular Disease
PULMONARY EFFECTS
When compared to spontaneously breathing exercise, cycle ergometry exercise with a similar reduction in breathing frequency (10 breaths per minute) is associated with a lower VE by a magnitude of 25% to 49%. Even greater reductions (55%) have been observed in the swimming literature where breathing frequency is reduced from breathing every second stroke cycle to breathing every sixth or every eight stroke cycle. As a reduction in VE is unlikely to be beneficial for exercise performance, it follows that an increase in VE (via VT) would be advantageous. Our results indicate that Reduced Breathing Frequency (RBF) training does increase VT during incremental exercise with RBF i.e. training reduced breathing restriction. Specifically, VT increased by 41 ± 19% following RBF and exercise training. It is interesting that there were no significant differences between pre- and post-training VT measured at submaximal work stages. It seemed that the obtained levels of VT were sufficient to enable successful regulation of blood gases during submaximal exercise with RBF. In addition, these results indicated that the ventilatory level reached with RBF was a limiting factor only for maximal performance. Due to the prescribed and unchanged breathing frequency in the present study, an increase in VT was the only mechanism available for increasing VE. This is consistent with reports that VT increases in proportion to the magnitude of breathing frequency restriction as well as exercise intensity.
Adaptation of Endurance Training with a Reduced Breathing Frequency
MUSCOLAR EFFECTS
HSP and αB-crystallin
Fibre type–specific expression of αB-crystallin, HSP27 and HSP70 in resting human skeletal muscle. Interestingly, the fibre type–specific basal expression of these HSPs can be influenced by different training regimens. Was observed significantly higher protein levels of αB-crystallin in endurance-trained subjects compared with untrained subjects in muscle samples from human vastus lateralis. the higher αB-crystallin content was due to an assumed greater proportion of oxidative type I fibres in the endurance-trained subjects. αB-crystallin has been hypothesized to be an important factor in protecting the cytoskeleton and contractile machinery during high-force eccentric contractions and also to be involved in the remodelling of contractile structures following high-force eccentric contractions.
The elevated levels of αB-crystallin are explained by an extended need of a molecular chaperone during the remodelling of type II muscle fibres in order to adapt to more aerobic metabolism. Further, αB-crystallin may also be required in type II fibres, which are adapted to an oxidative workload in endurance athletes.
Research about fiber type adaptation
High-intensity interval training (HIIT) forms an important component of endurance athletes’ training, but little is known on intramuscular metabolic and fiber type adaptations. This study investigated physiological and skeletal muscle adaptations in endurance runners subjected to 6 weeks HIIT. Eighteen well-trained endurance athletes were subjected to 6 weeks HIIT. Maximal and sub- maximal exercise tests and muscle biopsies were performed before and after training. Results indicated that peak treadmill speed (PTS) increased (21.0 +/- 0.8 vs 22.1 +/- 1.2 km/h, Po0.001) and plasma lactate decreased at 64% and 80% PTS (Po0.05) after HIIT. Cross-sectional area of type II fibers tended to have decreased (P 5 0.06). No changes were observed in maximal oxygen consumption, muscle fiber type, capillary supply, citrate synthase and 3-hydroxyacetyl CoA dehydrogenase activities. Lactate dehydrogenase (LDH) activity increased in homogenate (Po0.05) and type IIa fiber pools (9.3%, Po0.05). The change in the latter correlated with an absolute interval training speed (r 5 0.65; Po0.05). In conclusion, HIIT in trained endurance runners causes no adaptations in muscle oxidative capacity but increased LDH activity, especially in type IIa fibers and in relation to absolute HIIT speed.
In well- trained endurance runners, adaptations to HIIT are not to further increase oxidative enzyme activities as is the case in less-trained individuals, but rather to enhance the activity of the enzyme central to intra- cellular lactate metabolism (LDH). This was apparent only in fast twitch fibers and more apparent at a high interval speed. Therefore, whether or not acute exercise or longer term-training studies are undertaken, the analysis should include fiber type-specific responses.
Specific muscle adaptations in type II fibers after high-intensity interval training of well-trained runners.
The expression of heat shock protein in human skeletal muscle: effects of muscle fibre phenotype and training background.
NEUROHORMONAL EFFECTS
An aerobic training program reduces the resting heart rate, which indicates a reduction in sympathoadrenergic drive. This has also been confirmed for serum catecholamine levels. This reduction in adrenergic tone was accompanied by an increase in heart rate variability. In addition to the reduction in circulating catecholamines, Braith et al described a 25% to 30% reduction of angiotensin II, aldosterone, arginine vasopeptide, and atrial natriuretic peptide after 4 months of walking training.
Xu and colleagues found a significant reduction of myocardial angiotensin-converting enzyme mRNA expression and AT1-receptor expression after 8 weeks of treadmill training. This finding is of special importance given the fact that up to 90% of angiotensin II is produced locally in the myocardium and implies that local angiotensin II levels are significantly reduced by training. This reduction also translates into reduced fibrogenesis, as indicated by reduced tissue inhibitor of metalloproteinase-1 expression with unchanged matrix metalloproteinase (MMP)-1 expression and reduced collagen volume fraction in the exercised animals.
Cardiovascular effects of exercise training: molecular mechanisms.
Exercise in Cardiovascular Disease
Melatonin
Depending on the time of the day, on the intensity of light, and on the proximity of the exercise to the onset or decline of the circadian production of melatonin, the consequence of exercise on the melatonin rhythm varies. Moreover, especially strenuous exercise per se induces an increased oxidative stress that in turn may affect melatonin levels in the peripheral circulation because indole is rapidly used to combat free radical damage. On the other hand, melatonin also may influence physical performance, and thus, there are mutually interactions between exercise and melatonin production which may be beneficial. Melatonin reduces oxidative stress and inflammation in cardiac and skeletal muscle induced by different conditions such as sepsis, aging, exercise, etc.. Thus, the levels of melatonin detected after exercise do not correspond to the melatonin produced by exercise itself, but also depend on the degree of utilization of melatonin in resisting oxidative damage.
Exercise and melatonin in humans: reciprocal benefits.
Brain Derived Neurotrophic Factor
Evidence has demonstrated positive effects of physical activity and exercise on brain structure and cognitive function in humans. Brain-derived neurotrophic factor (BDNF) is a crucial mediator of the benefits of exercise for brain health. Voluntary exercise increased levels of BDNF mRNA and protein in the hippocampus and other brain regions, whereas the beneficial effect of exercise on cognitive function was inhibited when blocking BDNF action in the hippocampus. BDNF is a member of the neurotrophin family, which includes nerve growth factor, neurotrophin-3, neurotrophin-4/5, and neurotrophin-6 . BDNF is broadly expressed in the developing and adult mammalian brain, as well as in several peripheral tissues, such as the muscle and adipose tissue. By activating its major tropomyosin receptor kinase B, BDNF plays an important role in various aspects of developmental and adult brain plastic- ity, including proliferation, differentiation, and survival of neurons, neurogenesis, synaptic plasticity, and cognitive function.
The results from most observational studies suggested an inverse relationship between the peripheral BDNF level and habitual physical activity or cardiorespiratory fitness.
Recent evidence has shown that BDNF signaling pathway in the hypothalamus had a potential to regulate energy homeostasis, body weight control, and feeding behavior. Besides, BDNF has been identified as a contraction-induced muscle cell-derived protein that can increase fat oxidation in skeletal muscle in an AMP- activated protein kinase-dependent signaling pathway.
It has been demonstrated that factors, such as age, gender, and weight status, have an influence on stored and circulating BDNF levels in humans. Recently, there has been a growing body of research that focused on the relationship between physical activity and BDNF levels in peripheral blood.
The effects of physical activity and exercise on brain-derived neurotrophic factor in healthy humans
Inquisitiveness
Since the 1968 Mexico City Olympics, Kenyan and Ethiopian runners have dominated
the middle- and long-distance events in athletics and have exhibited comparable
dominance in international cross-country and road-racing competition. Several
factors have been proposed to explain the extraordinary success of the Kenyan and
Ethiopian distance runners, including genetic predisposition, development
of a high maximal oxygen uptake as a result of extensive walking and running at
an early age, relatively high hemoglobin and hematocrit, development of
good metabolic "economy/efficiency" based on somatotype and lower limb
characteristics, favorable skeletal-muscle-fiber composition and oxidative
enzyme profile, traditional Kenyan/Ethiopian diet, living and training at
altitude, and motivation to achieve economic success.
Kenyan and Ethiopian distance runners: what makes them so good?
Aimar G. , Clemente A.
