Strenuous Exertion Research Articles

Work at high altitude and oxidative stress: antioxidant nutrients

A significant portion of the world's geography lies above 10,000 feet elevation, an arbitrary designation that separates moderate and high altitude. Although the number of indigenous people living at these elevations is relatively small, many people travel to high altitude for work or recreation, exposing themselves to chronic or intermittent hypoxia and the associated risk of acute mountain sickness (AMS) and less frequently, high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The symptoms of AMS (headache, nausea, anorexia, fatigue, lassitude) occur in those who travel too high, too fast. Some investigators have linked the development of these symptoms with the condition of altered blood–brain barrier permeability, possibly related to hypoxia induced free radical formation. The burden of oxidative stress increases during the time spent at altitude and may even persist for some time upon return to sea level. The physiological and medical consequences of increased oxidative stress engendered by altitude is unclear; indeed, hypoxia is believed to be the trigger for the cascade of signaling events that ultimately leads to adaptation to altitude. These signaling events include the generation of reactive oxygen species (ROS) that may elicit important adaptive responses. If produced in excess, however, these ROS may contribute to impaired muscle function and reduced capillary perfusion at altitude or may even play a role in precipitating more serious neurological and pulmonary crisis. Oxidative stress can be observed at altitude without strenuous physical exertion; however, environmental factors other than hypoxia, such as exercise, UV light exposure and cold exposure, can also contribute to the burden. Providing antioxidant nutrients via the diet or supplements to the diet can reduce oxidative stress secondary to altitude exposure. In summary, the significant unanswered question concerning altitude exposure and antioxidant supplementation is when does oxidative stress become potentially damaging enough to merit antioxidant therapy and conversely, what degree of oxidative stress is necessary to foster the adaptive response of altitude exposure?

O desafio da altitude. Uma perspectiva fisiológica

The High-Altitude Challenge. A Physiological Point of View High-altitude physical activities have been widely performed in the later years. Activities like mountaineering, climbing and skiing, demanding short or prolonged high-altitude exposure, induce strenuous physiological exertion as a consequence of hypobaric hypoxic environmental conditions. The present work reviews the main acute and chronic physiological adaptations on (i) the respiratory and cardiovascular systems, (ii) hematological components and (iii) muscular morphology and metabolism, allowing the maintenance of life and practice of physical activities on high-altitude hostile regions. Finally, is briefly reviewed the state of the art on altitude training concerning the physiological and sports benefits to perform at sea level.

Nutritional strategies to minimise exercise-induced immunosuppression in athletes.

Strenuous prolonged exertion and heavy training are associated with depressed immune function. Furthermore, improper nutrition can compound the negative influence of heavy exertion on immunocompetence. Dietary deficiencies of protein and specific micronutrients have long been associated with immune dysfunction. An adequate intake of iron, zinc, and vitamins A, E, B6 and B12 is particularly important but excess intakes can also impair immune function. Immune system impairment has also been associated with excess intake of fat. To maintain immune function, athletes should eat a well balanced diet sufficient to meet their energy requirements. An athlete exercising in a carbohydrate-depleted state experiences larger increases in circulating stress hormones and a greater perturbation of several immune function indices. Conversely, consuming carbohydrate during exercise attenuates rises in stress hormones such as cortisol and appears to limit the degree of exercise-induced immunosuppression, at least for non-fatiguing bouts of exercise. Strong evidence that high doses of antioxidant vitamins, glutamine supplementation or echinacea extracts can prevent exercise-induced immunosuppression is lacking.

Effect of marathon running on inflammatory and hemostatic markers

Although increasing levels of regular physical activity are incrementally cardioprotective,1,2 prolonged strenuous exercise such as marathon running may trigger acute myocardial infarction3 and sudden cardiac death.4,5 The mechanism of such events is not well understood but may be due to hemodynamic, vasoconstrictive, and prothrombotic effects with disruption of unstable coronary plaques leading to acute coronary thrombosis.6,7 Although several studies have demonstrated exercise-induced activation of fibrinolysis and coagulation,8 the effect of marathon running on hemostatic balance has not been well studied. We therefore measured changes in C-reactive protein (CRP), von Willebrand factor (vWF), D-dimer, fibrinogen, fibrinolytic activity, white blood cell (WBC) counts, and platelet activation in middle-aged runners before and after the Boston Marathon. An imbalance in prothrombotic and fibrinolytic factors after strenuous physical exertion may transiently increase the risk for intravascular—including coronary—thrombosis and trigger acute ischemic events.

EXERCISE AND THROMBOSIS

Long-term moderate or strenuous physical activity is associated with a considerable reduction in cardiovascular morbidity and mortality in primary and secondary prevention. Various mechanisms, including changes in lipids, lifestyle habits, and other positive physiologic effects, have been suggested to mediate these beneficial effects. In addition, the hemostatic and fibrinolytic systems appear to play an important role. Fibrinogen has been convincingly shown to be an independent cardiovascular risk factor. Other hemostatic and fibrinolytic parameters that are predictive of coronary events include factor VII, platelet hyperreactivity, plasminogen-activator inhibitor 1 (PAI-1), and tissue-plasminogen activator. The effects of exercise on fibrinogen have been intensively studied. Several randomized controlled trials, various other intervention studies and a large number of population-based cross-sectional studies all found an inverse relationship between measures of sport activity or leisure activity and plasma fibrinogen. The magnitude of the effect reported might be associated with a sizeable reduction in major coronary events. Relatively few data are available on the effects of endurance exercise on markers of the fibrinolytic system, with inconsistent results. Acute exercise leads to a transient activation of the coagulation system, which is accompanied by an increase in the fibrinolytic capacity in healthy subjects. Patients with ischemic heart disease, who cannot increase their fibrinolytic potential, however, may be at considerable risk for acute ischemic events if they are exposed to unaccustomed strenuous physical exertion.

Use of aspirin, epistaxis, and untreated hypertension as risk factors for primary intracerebral hemorrhage in middle-aged and elderly people.

The incidence of primary intracerebral hemorrhage (ICH) increases exponentially with age, but the risk factors are not well known. We investigated lifestyle factors, previous diseases, and medications as risk factors for ICH in middle-aged and elderly people. We compared 98 consecutive patients with primary ICH between 36 and 90 years of age with 206 community-based control subjects matched for age and sex. Odds ratios (ORs) and 95% confidence intervals (CIs) after adjustment for possible confounding variables were calculated by logistic regression. The independent risk factors for ICH were untreated hypertension (OR, 6.95; 95% CI, 3.06 to 15.8), previous ischemic stroke (OR, 3.83; 95% CI, 1.70 to 8.63), epilepsy (OR, 13.8; 95% CI, 2.49 to 76.6), recent strenuous physical exertion (OR, 3.97; 95% CI, 1.95 to 8.10), and a history of epistaxis (OR, 2.92; 95% CI, 1.28 to 6.62). In men, treated hypertension (OR, 2.67; 95% CI, 1.03 to 6.93) was also a significant risk factor. Patients with a history of epistaxis who had used nonsteroidal anti-inflammatory drugs, especially aspirin in high doses, had an increased risk for ICH (adjusted OR of epistaxis, 2.75; 95% CI, 1.11 to 6.81; adjusted OR of aspirin use, 14.7; 95% CI, 2.03 to 106). In addition, there was a significant (P:<0.01) positive interaction between the history of epistaxis and the use of aspirin on the risk for ICH. Epistaxis is a risk factor for ICH in middle-aged and elderly people, both independently and combined with the use of aspirin. Other independent risk factors are untreated hypertension, previous ischemic stroke, epilepsy, and recent strenuous physical exertion. Epistaxis may be a warning sign of an increased risk for ICH in subjects using aspirin.

Effects of training in modifying working methods during common patient-handling activities

It is commonly recommended that those who must perform strenuous physical exertions be given training in proper techniques, and that musculoskeletal risks are thereby minimized. In the present study, the effects of training were examined at a behavioral level, and it was assumed that any long-term reduction in injuries must be preceded by measurable changes in how exertions are performed. Because of high injury incidence rates among nurses, common patient-handling tasks were the basis of the study. Participants performed several such tasks and sub-groups received training that consisted of either a commercial video or combined lecture and practice sessions. Compared to a control group, several perceptual, postural, and biomechanical measures were significantly altered following training. Specifically, training was associated with the adoption of a more upright lifting posture, and this change was retained in follow-up measures obtained after 4–6 weeks. While substantial inter-subject variability was present, the results suggest that training can modify behaviors in an intended direction. This observation provides support for the use of training as potential control measure, however more information is needed regarding retention and the relationship between trained behaviors and long-term injury risk. Relevance to industry Numerous training techniques have been recommended as ergonomic controls, yet there is mixed evidence regarding their efficacy. This study evaluates the potential of training to modify behaviors, and thus potentially reduce injury risk, in a setting of patient handling.

Exercise and thrombosis.

Long-term moderate or strenuous physical activity is associated with a considerable reduction in cardiovascular morbidity and mortality. This article reviews the evidence to suggest that part of the effect is mediated through the effects on thrombogenic factors. Fibrinogen has been convincingly shown to be an independent cardiovascular risk factor. Other hemostatic and fibrinolytic parameters that are predictive of coronary events include factor VII, platelet hyperreactivity, plasminogen activator inhibitor-1, and tissue-plasminogen activator. The effects of exercise on fibrinogen have been studied intensively. One randomized, controlled trial, two other intervention studies and a large number of population-based cross-sectional studies have consistently found an inverse relationship between various measures of sport activity or leisure activity and plasma levels of fibrinogen. The magnitude of the effect might be associated with a sizeable reduction in major coronary events. Relatively few data are available on endurance exercise and markers of the fibrinolytic system. Acute exercise leads to a transient activation of the coagulation system, which is accompanied by an increase in the fibrinolytic capacity in healthy subjects. However, patients with ischemic heart disease, who cannot increase their fibrinolytic potential, may be at considerable risk for acute ischemic events if they are exposed to unaccustomed strenuous physical exertion. It is concluded that physical activity has profound effects on thrombogenic factors and that these mechanisms could contribute to its beneficial cardiovascular effects.

EXERTIONAL FATIGUE ALTERS COLD-INDUCED VASODILATION

894 When fingers are exposed to cold, oscillations in finger blood flow and skin temperature (cold-induced vasodilation, CIVD) occur, which may be modulated by the sympathetic nervous system. Chronic fatigue, due to repeated strenuous physical exertion with insufficient recovery, results in increased basal circulating norepinephrine and may reduce effector sensitivity to sympathetic stimulation. Thus, fatigue could alter vasomotor and skin temperature responses to cold. This study compared CIVD in 6 subjects to determine if any systematic variation due to fatigue could be detected. Nailbed skin temperature (Tf) was measured 15 min before and during 30 min immersion of the middle finger in cold (4°C) water. This test was completed before (CONTROL) and after (FATIGUE) 5 days of physically exhausting exercise (∼4 h/d). The time to reach the first Tf apex was shorter (P<0.05) during FATIGUE (10.79±2.12 min), versus CONTROL (11.98±2.13 min). As a group, fatigue had no effect on mean Tf during immersion. However, 4 leaner subjects (13.7±4.5% body fat) displayed higher (P<0.05) Tf apex during FATIGUE (8.99±1.17°C), compared to CONTROL (7.53±0.51°C), while 2 fatter subjects (25.7±2.1 % fat) showed no change (P>0.05). These findings suggest that fatigue results in more rapid CIVD, possibly due to blunted cold-induced vasoconstriction. Leaner subjects also experienced more pronounced CIVD with fatigue. Greater tissue insulation in fatter subjects may habituate them to tolerate cold without eliciting the same degree of vasoconstriction as leaner subjects, thus fatigue-related blunting of vasoconstriction would be less apparent.

Arrhythmias in the Athlete With Congenital Heart Disease: Guidelines For Participation

Advances in the diagnosis and early management of congenital heart disease in recent decades have led to increasing numbers of individuals being sufficiently well to participate in social as well as truly competitive sports. Physicians are increasingly asked whether such participation is safe, advisable, and efficacious, yet few guidelines exist to help them make these decisions. There are three apparent subgroups of patients: (a) those with mild or repaired problems, who function normally or nearly so and may fully participate; (b) those with severe functional deficit or known high risk, for whom strenuous exertion must be strictly proscribed; and (c) those who fall in between, with some limitations and some risk--these patients present a great challenge to the wisdom and clinical skill of the physician.

Anesthetic Implications of Laryngeal Trauma

Anesthetic Implications of Laryngeal Trauma

The Bench Press Mark Revisited

Extensive soft-tissue uptake after strenuous physical exercise and/or trauma has been observed with bone scanning agents. Reports since 1984 suggest that muscle damage secondary to strenuous exertion is more common than realized, an observation that has assumed an important role in the last decade because of the evolution of sports medicine practices. Furthermore, although localization of the phosphate bone scanning agents following exercise has been recognized since 1978, there is no one explanation for the exact mechanism by which these bone-seeking agents are concentrated in injured skeletal tissues and muscles.

Immune deficits induced by strenuous exertion under adverse environmental conditions: manifestations and countermeasures.

A brief description is given of the various laboratory and clinical manifestations of immune suppression that arise when strenuous exertion must be carried out in the face of a negative energy balance, shifts of circadian rhythm, sleep deprivation, psychological stressors, and exposure to hostile environments (extremes of heat or cold, high or low ambient pressures, and hyper- or hypo-gravity conditions). From the operational viewpoint, immune suppression could impair both physical and mental performance by increasing susceptibility to opportunistic microorganisms. It is also likely to increase susceptibility to sepsis following trauma or extensive burns, and has occasionally predisposed to fatal myocarditis. The effects of such challenges are complex, in part because of interactions between the various stressors. It is thus important to investigate the impact and to devise appropriate countermeasures with the full physical and intellectual resources of a defense environmental research laboratory. Existing knowledge of the topic is reviewed, and suggestions are made for research that may lead to new and more effective countermeasures.

Exercise-induced asthma.

Exercise-induced asthma (EIA) is characterised by transient airway obstruction occurring after strenuous exertion. A fall of 10% or more in the FEV1 after exercise is diagnostic. Inhalation of large volumes of dry, cold air during exercise leads to loss of heat and water from the bronchial mucosa and airway cooling and drying. Proposed mechanisms for bronchoconstriction include: (i) mucosal drying and increased osmolarity stimulating mast cell degranulation; and (ii) rapid airway rewarming after exercise causing vascular congestion, increased permeability and oedema leading to obstruction. EIA symptoms start after exercise, peak 8 to 15 minutes after exercise and spontaneously resolve in about 60 minutes. A refractory period of up to 3 hours after recovery, during which repeat exercise causes less bronchospasm, has been observed. The amount of ventilation and the temperature of inspired air are important factors in determining the severity of EIA. Greater ventilation and cold, dry air increase the risk for EIA. Education regarding the nature and management of EIA is important not only for asthmatics but also for their families and coaches. With the proper precautions and workout techniques, there is no limit to what individuals with asthma can achieve in sports. Prevention is the main objective in managing EIA. Nonpharmacological measures include warming up before vigorous exertion, covering the mouth and nose in cold weather, exercising in warm, humidified environments if possible and warming down after exercise. Aerobic fitness and good control of baseline bronchial reactivity also help to diminish the effects of EIA. Inhaled beta-agonists are the medications of choice in EIA prophylaxis. Inhaled sodium cromoglycate (cromolyn sodium) or nedocromil may also be used. Agents that may be added if inhaled beta-agonists or sodium cromoglycate are not adequate include anticholinergic agents (such as ipratropium bromide), theophylline, calcium channel blockers, alpha-agonists, antihistamines and oral beta-agonists. Newer agents include antileukotriene agents, inhaled heparin and inhaled furosemide (frusemide).

Extract from “The effects of strenuous exertion on women”—Practitioner, 1956

Extract from “The effects of strenuous exertion on women”—Practitioner, 1956

Unbalanced haemostatic changes following strenuous physical exercise

During acute exercise both coagulant and fibrinolytic potential increase. Since strenuous exertion is associated with an enhanced risk for cardiac events, especially in untrained individuals, it is important to determine whether the initial haemostatic balance is maintained during exercise. Twenty-nine sedentary males (20-30 years) were subjected to a standardized cycle ergometer test. Blood samples were obtained at two exercise levels, 70% VO2max (submaximal), 100% VO2max (maximal) and during 25 min recovery. Both during submaximal and maximal performance, tissue type plasminogen activator antigen, urokinase plasminogen activator antigen and tissue type plasminogen activator activity were increased. A concomitant enhancement of clotting activity of factors VII, VIII, IX, XII and fibrinogen resulted in a shortening of clotting times. Following correction for changes in plasma volume, the results for factor VII:c were reversed, and factor XII:c and fibrinogen no longer demonstrated exercise-related changes. Increases in coagulant (activated partial thromboplastin time) and fibrinolytic (tissue type plasminogen activator activity) potential proceeded in parallel during exercise. However, during recovery while there was a sustained increase in coagulant potential, fibrinolytic potential demonstrated a sharp fall. We conclude that during physical activity, while parallel changes in coagulant and fibrinolytic activity occur, this haemostatic balance is not maintained during recovery. This phenomenon could constitute an enhanced risk for coronary artery thrombosis which may contribute to exercise-related cardiovascular events.

Hypokalemic thyrotoxic periodic paralysis in a Caucasian male with Graves’ disease

The case of a 34-yr-old Caucasian male with Graves' disease presenting with a flaccid quadriplegia and severe hypokalemia is reported. The weakness was prevalent at the lower extremities and began during nocturnal sleep, after a strenuous physical exertion performed during the day. Correction of hypokalemia promptly reversed the quadriplegia. The occurrence of hypokalemic thyrotoxic periodic paralysis several months after the beginning of thyrotoxic symptoms, and the normal insulin serum levels on admission differentiate this patient from most of the previously reported cases.

Rhabdomyolysis and acute encephalopathy in late onset medium chain acyl-CoA dehydrogenase deficiency.

A previously asymptomatic 30 year old man presented with rhabdomyolysis, muscle weakness, and acute encephalopathy after strenuous exertion in the cold without adequate food intake. Serum and muscle carnitine concentrations were decreased. Urinary excretion of carnitine and glycine esters and biochemical examination of skeletal muscle and fibroblasts led to the diagnosis of medium chain acyl-CoA dehydrogenase (MCAD) deficiency. A point mutation at nucleotide position 985 of the coding region of the MCAD gene was found. The MCAD protein was synthesised in the patient's fibroblasts at a normal rate, but was unstable. In general, patients in whom the 985 point mutation has been established show much more severe clinical symptoms and other symptoms than those seen in this patient. The relation of the 985 point mutation and the residual MACD activity to the symptoms is not as straightforward as previously thought.

Exercise-induced diarrhea

Exercise-associated lower gastrointestinal symptoms seem to be a fairly common clinical finding occurring in anywhere from 10-50% of runners. However, it is unclear what percentage of those affected may have discrete medical conditions that are exacerbated by strenuous physical exertion. Perhaps, difficult physical training sessions function as a "stress test" for the colon. A case report of exercise induced diarrhea is presented with a discussion of the current medical literature and proposed management for the primary care sports physician.

Infection in athletes.

Coaches and athletic team physicians have provided anecdotal information and case studies to support their beliefs that athletes may be unusually prone to illness during strenuous training or competition. Many athletes, in contrast, believe that physical activity improves their resistance to infectious disease. However, it is generally agreed that the stress of competition may make athletes temporarily more susceptible to infectious illness. A review of the literature shows that upper respiratory tract infections and skin infections are more prevalent in top level athletes than in the general population, particularly during periods of intensive training. Exercise induced changes occur in both the innate and adaptive components of the immune system; however, the relative importance of each component is unknown. Strenuous exertion and contact sports may compromise host defence both by reducing physical protection and by impairing immunosurveillance. Skin lacerations, vigorous sweating and maceration of the dermis impair the defence normally provided by the skin surface. In addition, adverse changes in soluble and cellular components of the immune system can increase susceptibility to infection. Persistence with strenuous training during an infectious illness can have deleterious effects; not only is athletic performance impaired, but the severity of the disease process can be augmented.