By I. Makas. Medical College of Wisconsin.
The influence of exercise on strength and endurance at any Whether or not exercise can improve sleep in patients age is dramatic purchase fucidin 10gm antibiotics bad taste in mouth. In fact buy fucidin 10 gm low price antibiotics for sinus infection if allergic to penicillin, a highly active 70-year-old, Whether acute or chronic exercise can help relieve depres- otherwise healthy, will typically display an absolute exer- sion remains unproven. The two most prominent biological cise capacity greater than a sedentary 20-year-old. Aging theories of depression—the dysregulation of central affects all the links in the chain of oxygen transport and use, monoamine activity and dysfunction of the hypothalamic- so aging-induced declines in lung elasticity, lung diffusing pituitary-adrenal axis—have received almost no study with capacity, cardiac output, and muscle metabolic potential regard to the impact of exercise. Consequently, the physiological Panic disorder patients, often characterized by agora- mechanisms underlying fatigue are similar at all ages. Although sodium Regular dynamic exercise, compared with inactivity, in- lactate infusion does provoke panic in these patients, the creases longevity in rats and humans. In descriptive terms, anxiety mediator appears to be hypernatremia, not lactate; the effects of exercise are modest; all-cause mortality is re- even strenuous exercise with substantial lactic acidosis will duced, but only in amounts sufficient to increase longevity not trigger panic attacks in these individuals. CHAPTER 30 Exercise Physiology 563 REVIEW QUESTIONS DIRECTIONS: Each of the numbered (E) Will be balanced by local dilation (D) Reduce risk of myocardial items or incomplete statements in this in these vascular beds infarction despite elevated total section is followed by answers or by 5. A young, healthy, highly trained cholesterol levels completions of the statement. Select the individual enters a marathon (40 km) (E) Elevate HDL and lower LDL ONE lettered answer or completion that is run on a warm, humid day (32 C, 70% 9. The best medical advice for completes a 500 m freestyle swim this individual is to be concerned about at an age-group competition. In an effort to strengthen selected the possibility for Breathing hard after the race, she muscles after surgery and (A) Heat exhaustion explains that her increased immobilization has led to muscle (B) Coronary ischemia ventilation is a normal response to atrophy, isometric exercise is (C) Renal ischemia and anoxia heavy, dynamic exercise. The intensity of (D) Hypertension increased ventilation results in isometric exercise is best quantified (E) Gastric mucosal ischemia and (A) Clinically significant systemic (A) Relative to the maximal oxygen increased risk for gastric ulceration arterial hypoxemia uptake 6. An individual with hypertension has (B) Normal or reduced arterial PCO2 (B) As mild, moderate, or strenuous been advised to increase physical (C) Respiratory alkalosis (C) As percentage of the maximum activity. At the same time, this person (D) Respiratory acidosis voluntary contraction has been counseled to avoid activities (E) Dizziness and decreased cerebral (D) In terms of anaerobic metabolism that substantially increase the systemic blood flow (E) On the basis of the total muscle arterial blood pressure. A 33-year-old woman embarks on an mass involved dynamic exercise, this individual extensive program of daily exercise, 2. Two people, one highly trained and should avoid exercise that with both strenuous dynamic and one not, each exercising at 75% of the (A) Causes fatigue isometric exercise included. After two maximal oxygen uptake, become (B) Is prolonged years, her maximal voluntary fatigued (C) Uses untrained muscle groups contraction of many major muscle (A) For similar physiological reasons (D) Is substituted for isometric exercise groups and her maximal oxygen (B) Very slowly (E) Involves an intermediate muscle mass uptake, are both increased 30%. In a patient with heart disease, a Predictably, pulmonary function tests (D) While performing equally well for treadmill test involving graded show at least a short period of time dynamic exercise results in falling (A) A 30% rise in vital capacity (E) Despite much higher circulating blood pressure at each exercise level. These vital capacity exercise test on a treadmill while results arise from inadequate cardiac (C) An increase in resting pulmonary showing a modest rise (25%) in mean output during exercise because the diffusing capacity of 30 to 50% arterial blood pressure. In contrast, baroreceptors, during exercise, (D) A 25% increase in maximal forced during the highest level of exercise at (A) Reset blood pressure to a lower expiratory flow rate the end of the test, an indirect method level (E) Decreases in residual volume and shows that cardiac output has risen (B) Are “turned off” airways resistance at rest 300% from rest. In older adults at risk for falls, that during graded, dynamic exercise training osteoporosis, and fractures, a program to exhaustion, systemic vascular (D) Are decreased in sensitivity by of weight-bearing exercise resistance training (A) Increases the risk of hip fracture (A) Is constant (E) Reset blood pressure to a higher (B) Decreases bone mineral density (B) Rises slightly level (C) Leaves gait, coordination, (C) Falls only if work is prolonged 8. A man with a family history of heart proprioception, and reaction time (D) Falls dramatically disease has both diabetes and unaltered (E) Cannot be measured hypertension. In addition, falls, and fractures disease and compromised kidney his LDL cholesterol is elevated and his (E) Is less valuable than dynamic function asks if exercise will alter blood HDL cholesterol is reduced, compared exercise during water immersion flow to either the gastrointestinal tract with individuals with low 12. When at risk for osteoporosis, starts an vasoconstriction in both the renal and exercise and diet are recommended, exercise class that emphasizes weight- splanchnic vascular beds during this individual asks what effect a long- bearing activities and development of exercise term exercise program will have on the muscle strength. The answer is that extensive muscle soreness after the first (B) Occurs only after prolonged exercise, over time, will two sessions, indicating that the training (A) Have no independent effect on exercise that she performed (C) Helps maintain arterial blood blood cholesterol levels (A) Involved isometric contractions pressure (B) Elevate both HDL and LDL (B) Produced muscle ischemia (D) Allows renal and splanchnic flows (C) Lower HDL and LDL, thereby (C) Was actually most effective for to parallel cerebral blood flow lowering total cholesterol increasing muscle endurance (continued) 564 PART VIII TEMPERATURE REGULATION AND EXERCISE PHYSIOLOGY (D) Involved eccentric contractions His specific concern is the impact that ity, and disease. Physiol Rev (E) Required at least 50% of the an acute episode of exercise will have 2000;80:1215–1265. He is correctly informed Waging war on modern chronic dis- knee early in the season. The knee that during exercise, an important eases: Primary prevention through ex- requires immobilization for six weeks, factor to consider is that ercise biology. J Appl Physiol after which time the athlete undergoes (A) Muscle glucose uptake decreases in 2000;88:774–787.
Thus animals with MPTP-induced Parkinsonism not only show extensive gliosis in the substantia nigra (like humans) in which the glial cells produce NO fucidin 10gm low price antibiotics for neck acne, but Liberatore and colleagues have found that in iNOS (inducible nitric oxide synthase) knock-out mice the toxicity of MPTP is halved generic fucidin 10gm without prescription antimicrobial plastic. Since NO releases iron from ferritin and produces toxic peroxinitrate in the presence of superoxide radicals it could accelerate, even if it does not initiate, dopaminergic cell death (see Hirsch and Hunot 2000 for further details). It is an inherited autosomal dominant disease with the child of an affected parent having a 50% chance of inheriting the gene and then unavoidably suffering from the disease. It is characterised by choreas (dyskinesias) which start in the extremities (fingers) but spread to the face, limbs and whole body even though they disappear during sleep. Akinesia develops as in PD and like that disease HC is initially a disorder of the basal ganglia but starts earlier (30±45 years). It is more progressive, invariably resulting in death within 20 years, as motor impairment makes any function difficult and emotional disturbances and dementia develop. Early neuron loss occurs in the striatum and especially of the GABA/ENK neurons which project to the GPext (Fig. This would leave the GABA/DYN neurons and the direct pathway dominant, which appears to be the requirement for dyskinesia (Fig. Thus, unlike PD, there is no loss of neuronal input to the striatum or of DA levels but a marked reduction in striatal GABA as well as its co-transmitting peptides, especially metenkephalin but also dynorphin and substance P. It is not possible to replace adequately the lost GABA but the early dyskinesias can be reduced by using DA antagonists which would primarily block the D2 inhibitory effect on the remaining GABA/ENK neurons and so help to restore balance. Whether adenosine A1 agonists or opiate antagonists (see above) could usefully reduce the activity of those neurons remains to be evaluated. Unfortunately any process reducing dyskinesias could encourage akinesia. This is the opposite problem to that in PD but a reminder of the pivotal role of the striatum and DA in movement control (see Fig. Since HC is such a progressive disorder with clear neuronal loss, it is not surprising that NT manipulation has been of little value in therapy and that there is no drug treatment of any significance. More hope rests on a genetic approach and the mutated gene has in fact been identified and cloned but its precise role remains uncertain. For details of its structure, possible actions and appropriate models see Reddy, Williams and Tagle (1999). ADDENDUM The first proper double blind trial of embryonic implants in 40 PD patients (20 undergoing just surgery without any implant), has shown no improvement in patients over 60 years but some clinical benefit (fewer symptoms between levodopa dosing) in those below that age. Unfortunately some of these responders eventually developed dyskinesias, a sign of too much dopamine, and further implants were halted until the technique has been re-evaluated, see Freed, CR et al. Chesselet, M-F and Delfs, JM (1996) Basal ganglia and movement disorders. Chiara, G, Morelli, M and Consolo, S (1994) Modulatory function of neurotransmitters in the striatum: ACh/dopamine/NMDA interactions. Cotzias, GC, von Woert, MH and Schiffer, LM (1967) Aromatic amino acids and modification of Parkinsonism. Ehringer, H and Hornykiewicz, O (1960) Verteilung von Noradrenalin and Dopamin im Gehirn des Menschen und ihr Verholten bei Erkrankungen des Extrapyramidalen systems. Ferre, S, Fredholm, BB, Morelli, M, Popoli, P and Fuxe, K (1997) Adenosine±dopamine receptor±receptor interaction as an integrative mechanism in the basal ganglia. Hirsch, EC and Hunot, S (2000) Nitric oxide, glial cells and neuronal degeneration in Parkinsonism. Jolkkonen, J, Jenner, P and Marsden, CD (1995) L-Dopa reverses altered gene expression of substance P but not enkephalin in the caudate-putamen of common marmosets treated with MPTP. Kawaguchi, Y, Wilson, CJ, Augood, ST and Emson, PC (1995) Striatal interneurones: chemical physiological and morphological characterization. Maneuf, YP, Mitchell, IJ, Crossman, AR, Woodruff, GN and Brotchis, JM (1995) Functional implications of Kappa opioid receptor mediated modulation of glutamate transmission in the output regions of the basal ganglia in rodent and primate models. Mercuri, NB, Bonci, A and Bernardi, G (1997) Electrophysiological pharmacology of the autoreceptor mediated responses of dopaminergic cells to antiparkinsonian drugs.
In view of the opposingexcitatory and inhibitory effects of ACh and DA in the striatum and the known loss of striatal DA in Parkinsonism (see Chapter 15) it is perhaps not surprisingthat antimuscarinic agents have been of some value in the treatment of that condition buy fucidin 10gm on line the infection 0 origins movie, especially in controllingtremor buy 10gm fucidin mastercard bacteria labeled, and that certain muscarinic agonists, like oxotremorine, produce tremor in animals. CORTEX Cholinergic neurotransmission has been most thoroughly studied in the cortex where the role of ACh as a mediator of some afferent input is indicated by the findingthat undercuttingthe cortex leads to the virtual loss of cortical ACh, ChAT and cholinesterase. That it is not the mediator of the primary afferent input has been shown by the inability of atropine to block the excitatory effect of stimulatingthose pathways and the fact that such stimulation causes a release of ACh over a wide area of the cortex and not just localised to the area of their cortical representation (see Collier and Mitchell 1967). Indeed there have been many experiments which show that the release of ACh in the cortex is proportional to the level of cortical excitability, being increased by a variety of convulsants and decreased by anaesthesia (Fig. The origins of this diffuse cholinergic input have been traced in the rat to the magnocellular forebrain nuclei (MFN) by mappingchanges in cortical cholinesterase and ChAT after lesioningspecific subcortical nuclei. The most important of them appears to be the nucleus basalis magnocellularis, similar to the nucleus of Maynert in humans, which projects predominantly to the frontal and parietal cortex and is thought to be affected ACETYLCHOLINE 133 Figure 6. Correlation between acetylcholine release and EEG activity after injections of leptazol (LEP mgkgÀ1 intravenously) into the urethane anaesthetised rat. ACh was collected in a cortical cup incorporatingEEG recordingelectrodes. This nucleus, together with the diagonal band, forms the sub- stantia innominata and the dorsal neurons of this band also join with those in the medial septum to provide a distinct cholinergic input to the hippocampus (Fig. There is a second group of cholinergic neurons more caudally in the pontine teg- mentum, the pendunculo pontine tegmental nucleus (PPPTN) and a smaller laterodorsal tegmental nucleus (LDTN). Despite the excitatory effect of ACh in the cortex and its increased release during convulsive activity, antimuscarinic agents have only a slight sedative action (indeed, as emphasised above, atropine may cause excitation) and no anticonvulsant activity, except possibly in reducingsome forms of experimentally induced kindling. ACh appears to exert a background excitatory effect on cortical function and while it may not directly stimulate the firingof pyramidal cells it will sensitise them to other excitatory inputs through its muscarinic activity. If this pathway is lesioned the cortical EEG becomes quiescent but when stimulated it produces a high-frequency low-voltage desynchronised (aroused) EEG, which can be countered by antimuscarinic and potentiated by anticholinesterase drugs. Unfortunately this does not seem to apply to the actual behavioural arousal produced by such stimulation and suggests that ACh does not have a primary and certainly not a unique role in the maintenance of consciousness or sleep, although the firingof forebrain cholinergic neurons increases duringthe transition from sleep to waking. ACh does, however, feature prominently in one aspect of sleep behaviour. This so-called slow-wave sleep is interrupted at intervals of some 1±2 h by the break-up and desynchronisation of the EEG into an awake-like pattern. Since this is accompanied by rapid eye movements, even though sleep persists and can be deeper, the phase is known as rapid eye movement, REM or paradoxical, sleep. More importantly, for this discussion, it can be intensified by anticholinesterases and reduced by antimuscarinics and it is accompanied, and in fact preceded, by burst firing of a group of cholinergic neurons in the pedunculo pontine tegmental nucleus (PPTN). Neurons from this nucleus, which is quite distinct from the nucleus basalis, project to the paramedian pontine reticular formation, the thalamic lateral geniculate body and thus to the occipital cortex, all of which show increased activity during REM sleep to give PGO (ponto±geniculo±occipital) waves. Clearly sleep is not just a passive event and while cholinergic activity may be important in the production of REM sleep it does not appear to be responsible for turningit off or for actually inducingsleep. COGNITION AND REWARD Not only is REM sleep a time for dreamingbut it is also believed to be a time for the layingdown (consolidation) of memory. This is only one observation amongmany that implicates ACh in the memory process. Certainly antimuscarinic drugs like atropine are well known to impair cognitive function in both animals and humans. In the former antimuscarinic drugs appear to impair both the acquisition and retention of some learned tasks, as in the Morris water maze. This involves placinga rat in a circular tank of water containinga stand with a platform just below the surface but which is not clearly visible because the vessel walls or water have been made opaque. Generally the rat quickly learns (2±3 trials) to identify the position of and swims to the platform. That ability is impaired by pretreatment with antimuscarinics which increase the number of ACETYLCHOLINE 135 trials (possibly tenfold) required before the animal swims directly to the platform and can increase the time to achieve it if given after the task has been learnt. How cholinergic function can facilitate the memory process is uncertain. It is generally thought that the laying down of memory is in some way dependent on the high-frequency discharge of hippo- campal neurons in which long-term potentiation or LTP (the persisting potentiated response to a normal afferent input after a prior and short intense activation) plays an important part (see Chapter 18). Unfortunately while NMDA antagonists impair LTP, antimuscarinics do not.
Talar osteochon- fragment is consistent with healing and stability generic fucidin 10gm on line antibiotic resistance is caused by, while a dral fractures commonly occur in the medial or lateral high signal intensity interface on fat-suppressed post-in- corners of the dome buy 10gm fucidin otc antimicrobial toilet seats, although central lesions have been tra-articular contrast T1-weighted images indicates a also sporadically described. Partial detachment is in- more common than lateral lesions in most series. The pres- cation of the lesion is related to the mechanism of trau- ence of cyst underneath an osteochondral lesion indicates ma. Medial osteochondral fracture frequently results instability whether the rim appears complete or not. Medial osteo- Inaccurate staging of type II-IV osteochondral lesions chondral fragments usually remain in situ, causing fewer has been reported to be as high as 50% using conven- symptoms. This low diagnostic yield is probably inversion injuries with dorsiflexion of the foot, causing secondary to the inability to discriminate between fluid impaction of the fibula against the middle third of the ta- and granulation tissue on T2-weighted images. Lateral collateral ligament injury may be asso- cases, the use of MR arthrography greatly increases the ciated with both types of fractures, more commonly with accuracy of MRI. Hyperintense signal on T2-weighted or STIR on the integrity of the articular cartilage and the degree images reflects viable bone marrow, while low signal in- of attachment and displacement of the subchondral frag- tensity on all pulse sequences suggests necrosis. Stage I lesions present as intact articular cartilage Additional evaluation may be obtained using post-intra- with signal changes of the subchondral bone. Stage II venous gadolinium fat-suppressed T1-weighted images, represents partial detachment of the cartilage and sub- which demonstrate enhancement of the marrow in viable chondral fragment. Stage III implies a completely de- bone and the lack of enhancement in necrotic fragments. Stage IV is a detached and displaced osteochondral fragment located away from the crater site. Treatment and prognosis depend to a great Sesamoid Dysfunction extent on the accurate evaluation of the overlying articu- lar cartilage and the stability of the osteochondral frag- The sesamoid bones of the first metatarsal can undergo a ment. Stages I and II and medial stage III lesions are number of pathologic processes, including osteoarthritis, treated conservatively, while surgical intervention is indi- fracture, osteonecrosis and sesamoiditis. Acute fractures cated for lateral stages III and medial and lateral stage IV. Osteonecrosis is thought to be Imaging of the Foot and Ankle 41 traumatic but the exact etiology is not fully known. Increased signal abnormality on T2-weighted im- Sesamoiditis is a painful inflammatory condition sec- ages are noted when significant intrasubstance degenera- ondary to repetitive injury to the plantar soft tissues of tion is present. Surgical removal of the sesamoids may be con- is complicated by the magic-angle artifact, which affects sidered in refractory cases. The signal increase routine plain radiographs due to overlap of the sesamoids on MR images with short TEs (under 37ms) depends on on the first metatarsal head and on each other on the AP the orientation of the fibers and on the main magnetic view and lateral views, respectively. The maximum signal increase is observed at a modality for appreciating fragmentation of the sesamoids magic angle of 55° relatively to the orientation of B0. In but, unlike MRI, is inadequate for assessing marrow ab- the standard supine body position with neutral position of normalities and soft-tissue disease around the sesamoids. Magic-angle artifacts in the ankle Involvement of two sesamoids is usually reflective of ei- tendons are almost absent when the patient is scanned in ther osteoarthritis or sesamoiditis while a fracture and os- the prone body position with plantar flexion of the foot. In This position should be considered for assessment of the general, the medial (tibial) sesamoid is most frequently ankle tendons. The anterior group consists of the an- phytosis of the first metatarsal head and both sesamoids terior tibial tendon, extensor hallucis longus tendon and without marrow signal alterations. The medial group in- fracture line, best noted on sagittal views, are required for cludes the posterior tibial tendon, flexor digitorum longus establishing the diagnosis of a fracture. The peroneus sesamoid can usually be differentiated from a fracture brevis and peroneus longus tendons form the lateral group. Osteonecrosis of a sesamoid is diagnosed when The anterior tibial tendon is usually exposed only to mi- fragmentation and low signal on all pulse sequences are nor mechanical stress due to its relatively straight course. However, since the signal characteristics of Consequently, abnormalities are less common than in osteonecrosis can be variable on T2 weighted images and other tendons. Nevertheless, hypoxic degenerative tendi- since the osteonecrosis is often advanced by the time it is nosis or mucoid degeneration occur and may lead to a imaged, it may be difficult to differentiate it from os- partial or complete tear of the anterior tibial tendon. Sesamoiditis may depict signal alterations in tears occur without a trauma.
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