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Postgraduate Medicine. Primary Care: Clinics in Office Practice. Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training NCAA Publications.
National Collegiate Athletic Association. Retrieved 8 October British Journal of Pharmacology. Clinics in Sports Medicine.
In , Chandler and Blair 47 showed significant increases in knee extension strength, acceleration, anaerobic capacity, time to exhaustion during exercise, pre-exercise and maximum heart rates, and time to exhaustion during maximal oxygen consumption VO2 max testing after administration of 15 mg of dextroamphetamine versus placebo.
Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise.
Sports Medicine. In high-ambient temperatures, dopaminergic manipulations clearly improve performance. The distribution of the power output reveals that after dopamine reuptake inhibition, subjects are able to maintain a higher power output compared with placebo.
Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is 'off-limits' in a normal placebo situation.
Frontiers in Integrative Neuroscience. Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or "clock," activity.
For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing; Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing.
Frontiers in Physiology. Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash Chambers et al.
Dopamine stimulating drugs are known to enhance aspects of exercise performance Roelands et al. This indicates that subjects did not feel they were producing more power and consequently more heat.
The authors concluded that the "safety switch" or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration Roelands et al.
Taken together, these data indicate strong ergogenic effects of an increased DA concentration in the brain, without any change in the perception of effort.
Retrieved 22 December National Institute on Drug Abuse. Retrieved 7 May Retrieved 27 February Southern Medical Journal.
Rather they are intended to limit claims by pharmaceutical companies. Arbor Pharmaceuticals, LLC. International Programme on Chemical Safety.
Retrieved 24 June Journal of Affective Disorders. Tris Pharma, Inc. Retrieved 29 April Table 2.
Archived from the original on 25 August Retrieved 24 December New England Journal of Medicine. Archived from the original on 14 December Merck Manual for Health Care Professionals.
Retrieved 8 May Shoptaw SJ, Ali R ed. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals.
In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation.
Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis. BMC Psychiatry.
In these studies, amphetamine was given in consecutively higher doses until psychosis was precipitated, often after — mg of amphetamine Archived from the original PDF on 3 November Retrieved 2 November This study demonstrates that humans, like nonhumans, prefer a place associated with amphetamine administration.
These findings support the idea that subjective responses to a drug contribute to its ability to establish place conditioning.
Dialogues in Clinical Neuroscience. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction.
Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders DSM-5 referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home.
Depending on the level of severity, this disorder is classified as mild, moderate, or severe. Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug.
In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure.
Chronic exposure to psychostimulants increases glutamatergic [signaling] from the prefrontal cortex to the NAc. The Journal of General Physiology.
Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex PFC , as well as projections from midbrain dopamine neurons.
Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses Goto and Grace, KEGG Pathway.
Retrieved 31 October Most addictive drugs increase extracellular concentrations of dopamine DA in nucleus accumbens NAc and medial prefrontal cortex mPFC , projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit".
Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals.
Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
Molecular Neurobiology. Nature Reviews Neuroscience. The net result is gene activation and increased CDK5 expression. The net result is c-fos gene repression.
Clinical Psychopharmacology and Neuroscience. Such agents also have important therapeutic uses; cocaine, for example, is used as a local anesthetic Chapter 2 , and amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy Chapter Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction, especially when they are rapidly administered or when high-potency forms are given.
Current Medical Research and Opinion. When oral formulations of psychostimulants are used at recommended doses and frequencies, they are unlikely to yield effects consistent with abuse potential in patients with ADHD.
Magnesium Research. Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse Cosgrove et al.
There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers Daniel et al.
In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs.
This syndrome is characterized by a medication-induced increase in or compulsive engagement in non-drug rewards such as gambling, shopping, or sex Evans et al.
Exercise has been proposed as a treatment for drug addiction that may reduce drug craving and risk of relapse. Although few clinical studies have investigated the efficacy of exercise for preventing relapse, the few studies that have been conducted generally report a reduction in drug craving and better treatment outcomes Taken together, these data suggest that the potential benefits of exercise during relapse, particularly for relapse to psychostimulants, may be mediated via chromatin remodeling and possibly lead to greater treatment outcomes.
Frontiers in Neuroendocrinology. The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation.
The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to the scarce intervention trials to date, a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published.
Annual Review of Neuroscience. Progress in Neurobiology. Proceedings of the National Academy of Sciences. Bibcode : PNAS.. Annals of Agricultural and Environmental Medicine.
Nature Neuroscience. Nature Reviews. Journal of Psychoactive Drugs. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward.
Pitchers and colleagues reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus.
The Journal of Neuroscience. Pharmacologic treatment for psychostimulant addiction is generally unsatisfactory.
As previously discussed, cessation of cocaine use and the use of other psychostimulants in dependent individuals does not produce a physical withdrawal syndrome but may produce dysphoria, anhedonia, and an intense desire to reinitiate drug use.
Addiction Abingdon, England. Expert Review of Clinical Pharmacology. Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders, no widely effective medications have been approved.
Drug and Alcohol Dependence. When considered together with the rapidly growing literature in the field a compelling case emerges in support of developing TAAR1-selective agonists as medications for preventing relapse to psychostimulant abuse.
European Journal of Pharmacology. Existing data provided robust preclinical evidence supporting the development of TAAR1 agonists as potential treatment for psychostimulant abuse and addiction.
PLOS Medicine. Frontiers in Psychiatry. Physical Exercise There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse.
The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time.
Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon.
Merck Manual Home Edition. Archived from the original on 17 February Retrieved 28 February Shoptaw SJ ed. The prevalence of this withdrawal syndrome is extremely common Cantwell ; Gossop with The severity of withdrawal symptoms is greater in amphetamine dependent individuals who are older and who have more extensive amphetamine use disorders McGregor The first phase of this syndrome is the initial "crash" that resolves within about a week Gossop ;McGregor Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter DAT and less so the norepinephrine NET and serotonin transporter.
The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin.
The Lancet. Retrieved 3 March Amphetamine use disorders Emergency Medicine Australasia. Journal of Attention Disorders.
The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier BBB resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals.
In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus.
Direct toxic damage to vessels seems unlikely because of the dilution that occurs before the drug reaches the cerebral circulation.
Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons. Neurotoxicity Research.
Acta Medica Okayama. Expert Rev. Zinc binds at In this context, controlled double-blind studies in children are of interest, which showed positive effects of zinc [supplementation] on symptoms of ADHD [,].
It should be stated that at this time [supplementation] with zinc is not integrated in any ADHD treatment algorithm.
They did not confirm the predicted straightforward relationship between uptake and release, but rather that some compounds including AMPH were better releasers than substrates for uptake.
This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes. See Laboratory Report. Room temperature.
Reference ranges are provided as general guidance only. To interpret test results use the reference range in the laboratory report.
CPT coding is the sole responsibility of the billing party. If desired, you may sip liquid to help swallow the dissolved tablet. While using amphetamine, your doctor will need to check your progress at regular visits.
Tell any doctor who treats you that you are using this medicine. Store at room temperature away from moisture and heat. Keep the bottle tightly closed when not in use.
Keep track of your medicine. Amphetamine is a drug of abuse and you should be aware if anyone is using your medicine improperly or without a prescription.
Amphetamine dosage information in more detail. Take the missed dose as soon as you remember, but not late in the day.
Skip the missed dose if it is almost evening. Do not take extra medicine to make up the missed dose. Seek emergency medical attention or call the Poison Help line at An overdose of amphetamine could be fatal.
Overdose symptoms may include restlessness, tremor, muscle twitches, rapid breathing, hostility, violence, panic, muscle pain or weakness, and dark colored urine.
These symptoms may be followed by depression and tiredness. Overdose may also cause seizure or coma. Avoid drinking fruit juices or taking vitamin C at the same time you take amphetamine.
These can make your body absorb less of the medicine. Avoid driving or hazardous activity until you know how amphetamine will affect you.
Your reactions could be impaired. Get emergency medical help if you have signs of an allergic reaction to amphetamine: hives; difficult breathing; swelling of your face, lips, tongue, or throat.
Seek medical attention right away if you have symptoms of serotonin syndrome, such as: agitation, hallucinations, fever, sweating, shivering, fast heart rate, muscle stiffness, twitching, loss of coordination, nausea, vomiting, or diarrhea.
Amphetamine can affect growth in children. Tell your doctor if your child is not growing at a normal rate while using this medicine.
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. Amphetamine side effects in more detail.
Ask your doctor before using a stomach acid medicine including Alka-Seltzer or sodium bicarbonate. Some of these medicines can change the way your body absorbs amphetamine, and may increase side effects.
Many drugs can interact with amphetamine. This includes prescription and over-the-counter medicines, vitamins, and herbal products.
Tell your doctor if you are taking an anti-depressant or any other medication for mental illness; an antihistamine such as allergy medication; seizure drugs, or any over the counter medications.
Not all possible interactions are listed in this medication guide. Tell your doctor about all your current medicines and any medicine you start or stop using.
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