ISSN:0112-1642    

DOI:10.2165/00007256-199111060-00001

出版商:Springer International Publishing    

年代:2012

数据来源: ADIS

ISSN:0112-1642    

DOI:10.2165/00007256-199111060-00002

出版商:Springer International Publishing    

年代:2012

数据来源: ADIS

摘要:

SummaryRecreational and job requirements have increased the incidence in which humans exercise in cold environments. Understanding the physiological responses while exposed to cold entails knowledge of how exercise and cold interact on metabolic, cardiopulmonary, muscle and thermal aspects of human performance. Where possible, distinctions are made between responses in cold air and cold water.While there is no consensus for diets most appropriate for working cold exposures, the evidence is strong that adequate amounts of carbohydrate are necessary. Carbohydrate loading appears to be efficacious, as it is for other athletic endeavours.Contrary to conventional wisdom, the combination of exercise and cold exposure does not act synergistically to enhance metabolism of fats. Free fatty acid (FFA) levels are not higher, and may be lower, with exercise in cold air or water when compared to corresponding warmer conditions. Glycerol, a good indicator of lipid mobilisation, is likewise reduced in the cold, suggesting impaired mobilisation from adipose tissue.Catecholamines, which promote lipolysis, are higher during exercise in cold air and water, indicating that the reduced lipid metabolism is not due to a lack of adequate hormonal stimulation. It is proposed that cold-induced vasoconstriction of peripheral adipose tissue may account, in part, for the decrease in lipid mobilisation. The respiratory exchange ratio (RER) is often similar for exercise conducted in warm and cold climates, suggesting FFA utilisation is equivalent between warm and cold exposures. The fractional portion of oxygen consumption (V̇O2) used for FFA combustion may decrease slightly during exercise in the cold. This decrease may be related to a relative decrease in oxygen delivery (i.e. muscle blood flow) or to impaired lipid mobilisation.Venous glucose is not substantially altered during exercise in the cold, but lactate levels are generally higher than with work in milder conditions. The time lag between production of lactate within the muscle and its release into the venous circulation may be increased by cold exposure.Minute ventilation is substantially increased upon initial exposure to cold, and a relative hyperventilation may persist throughout exercise. With prolonged exercise, though, ventilation may return to values comparable to exercise in warmer conditions. Exercise V̇O2is generally higher in the cold, but the difference between warm and cold environments becomes less as workload increases. Increases in oxygen uptake may be due to persistence of shivering during exercise, to an increase in muscle tonus in the absence of overshivering, or to nonshivering thermogenesis.Heart rate is often, but not always, lower during exercise in the cold. The linear relationship between heart rate and oxygen consumption is displaced such that at a given rate oxygen uptake is higher. Cardiac arrhythmias are more frequent in the cold. Stroke volume tends to be higher than under warmer control conditions, but may decline sooner or at a rate equivalent to warm controls at heavy workloads. Cardiac output is similar to the same work done in temperature environments.Cold-induced vasoconstriction occurs both in cutaneous and resting skeletal muscle beds, but inactive muscle provides most of the passive body insulation. With exercise insulation provided by muscle decreases as blood flow increases. Relative to warmer conditions, muscle blood flow at a given workload may be reduced if deep muscle temperature is below normal (i.e. 39°C optimum).Respiratory heat loss is often assumed to represent 8% of the total metabolic heat production. However, during exercise this value will increase as minute ventilation increases. Loss of significant amounts of heat from the distal extremities can limit performance, even though the area is not directly involved with exercise.Cooled muscle has a decreased capacity to generate force expressed on cross-sectional area. As a consequence, it may be necessary to recruit more fast twitch motor units. Glycolysis is higher in cooled muscle, which may account for higher lactate levels and greater rates of muscle glycogen depletion. Brief intense exercise will not raise cooled muscle temperature to normal limits, but mild exercise can maintain normal temperatures if exercise begins before the muscles become cooled.Regional heat flux increases with exercise in the cold in direct proportion to the workload. Differing rates of heat loss can occur between active and inactive limbs, and individual rates are not constant throughout steady-state exercise. Peak rates of heat flux for inactive limbs occur during exercise, but peak flux for active limbs occurs in the postexercise period. At equal metabolic rates, more heat is lost with arm than with leg exercise.Most of the heat generated by exercising muscle is transferred convectively to the core via the venous circulation. The amount of heat lost conductively to the environment through tissue depends upon factors such as subcutaneous fat. Thus, individuals with higher levels of fat (e.g. skinfold thickness) generally are better able to maintain their core temperature in cold environments.Steady-state exercise V̇O2values of approximately 2.0 L/min have been shown to prevent falls in core temperature in water as low as 15°C. Warmer temperatures are required in order to maintain core homeostasis during intermittent exercise.Predicting an individual’s response to exercise in the cold is quite difficult because of the interplay of many factors. Using existing data, responses to some forms of exercise and environmental stress can be estimated with reasonable accuracy. However, the number of these type responses is small compared to the total number of possible permutations, showing that much is yet to be learned.

ISSN:0112-1642    

DOI:10.2165/00007256-199111060-00003

出版商:Springer International Publishing    

年代:2012

数据来源: ADIS

摘要:

SummaryThe concentrations of extracellular and intracellular potassium (K+) in skeletal muscle influence muscle cell function and are also important determinants of cardiovascular and respiratory function.Several studies over the years have shown that exercise results in a release of K+ions from contracting muscles which produces a decrease in intracellular K+concentrations and an increase in plasma K+concentrations. Following exercise there is a recovery of intracellular K+concentrations in previously contracting muscle and plasma K+concentrations rapidly return to resting values.The cardiovascular and respiratory responses to K+released by contracting muscle produce some changes which aid exercise performance. Increases in the interstitial K+concentrations of contracting muscles stimulate CIII and CIV afferents to directly stimulate heart rate and the rate of ventilation. Localised K+release causes a vasodilatation of the vascular bed within contracting muscle. This, together with the increase in cardiac output (through increased heart rate), results in an increase in blood flow to isometrically contracted muscle upon cessation of contraction and to dynamically contracting muscle. This exercise hyperaemia aids in the delivery of metabolic substrates to, and in the removal of metabolic endproducts from, contracting and recovering muscle tissues.In contrast to the beneficial respiratory and cardiovascular effects of elevations in interstitial and plasma K+concentrations, the responses of contracting muscle to decreases in intracellular K+concentrations and increases in intracellular Na+concentrations and extracellular K+concentrations contribute to a reduction in the strength of muscular contraction. Muscle K+loss has thus been cited as a major factor associated with or contributing to muscle fatigue.The sarcolemma, because of changes in intracellular and extracellular K+concentrations and Na+concentrations on the membrane potential and cell excitability, contributes to a fatigue ‘safety mechanism’. The purpose of this safety mechanism would be to prevent the muscle cell from the self-destruction which is evident upon overload (metabolic insufficiency) of the tissues. The net loss of K+and associated net gain of Na+by contracting muscles may contribute to the pain and degenerative changes seen with prolonged exercise.During exercise, mechanisms are brought into play which serve to regulate cellular and whole body K+homeostasis. Increased rates of uptake of K+by contracting muscles and inactive tissues through activation of the Na+-K+pump serve to restore active muscle intracellular K+concentrations towards precontraction levels and to prevent plasma K+concentrations from rising to toxic levels. These effects are at least partially mediated by exercise-induced increases in plasma catecholamines, particularly adrenaline. Upon cessation of exercise intracellular K+concentrations rapidly recover towards resting values, and this is associated with improvements in muscle contraction.Training may result in an increase in intracellular K+concentrations of resting muscle and relatively lower plasma K+concentrations compared to values reported in untrained individuals. Also, a blunting of the exercise-induced hyperkalaemia in trained individuals is associated with a decrease in the net loss of K+from contracting muscle; these observations have been attributed to an upregulation of Na+-K+pump activity in both inactive tissues and active muscle.

ISSN:0112-1642    

DOI:10.2165/00007256-199111060-00004

出版商:Springer International Publishing    

年代:2012

数据来源: ADIS

摘要:

SummaryRehabilitation is recognised as a critical component in the treatment of the anterior cruciate ligament (ACL) injured athlete, and has been the subject of intense research over the past decade. As a result, sound scientific principles have been applied to this realm of sports medicine, and have improved the outcome of both surgical and nonsurgical treatment. Possibly the most intriguing of these principles is the use of the kinetic chain concept in exercise prescription following ACL reconstruction.The hip, knee, and ankle joints when taken together, comprise the lower extremity kinetic chain. Kinetic chain exercises like the squat recruit all 3 links in unison while exercises such as seated quadriceps extensions isolate one link of the chain. Biomechanical assessment with force diagrams reveals that ACL strain is reduced during kinetic chain exercise by virtue of the axial orientation of the applied load and muscular co-contraction.Additionally, kinetic chain exercise through recruitment of all hip, knee, and ankle extensors in synchrony takes advantage of specificity of training principles. More importantly, however, it is the only way to reproduce the concurrent shift of ‘antagonistic’ biarticular muscle groups that occurs during simultaneous hip, knee, and ankle extension. Incoordination of the concurrent shift fostered by exercising each muscle group in isolation may ultimately hamper complete recovery. Modifying present day leg press and isokinetic equipment will allow clinicians to make better use of kinetic chain exercise and allow safe isokinetic testing of the ACL reconstructed knee. Reconstruction of the ACL with a strong well placed graft to restore joint kinematics, followed by scientifically sound rehabilitation to improve dynamic control of tibial translation, will improve the outcome after ACL injury.

ISSN:0112-1642    

DOI:10.2165/00007256-199111060-00005

出版商:Springer International Publishing    

年代:2012

数据来源: ADIS