Effects of Performance Enhancing Drugs
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ADHD Medications[edit | edit source]
Alcohol[edit | edit source]
Alcohol is a mind-altering drug that reduces thinking ability, distorts judgment, and acts as a depressant on the body. Research has suggested that alcohol leads to increased dopamine release in the human brain, bringing on feelings of relaxation and happiness.[1] Although this drug is often used during recreation for the purpose of feeling good, it should not be used in combination with exercise because of the serious negative physiological effects that it has on the body.
One of the most easily observable effects of alcohol on the body is dehydration. When alcohol is consumed, anti-diuretic hormone (ADH) is inhibited, causing less water to be absorbed back into the nephrons in the kidneys when urine is cycling through. This causes urine levels to increase, in turn increasing the frequency of urination. With higher levels of water exiting the body, dehydration is likely to occur. This is especially a problem during exercise, when the body is expelling water in the form of sweat as well. It is important to be fully hydrated for a workout; therefore it is dangerous to consume alcohol before or during exercise. Research has suggested that beverages containing up to 4% alcohol can delay the recovery process from dehydration to rehydration. [2] Alcohol not only leads to dehydration; it also prevents humans from reaching rehydration in a timely manner, which could be deadly in a situation regarding exercise.
Another important physiological effect that alcohol has on the body deals with blood pressure. Alcohol consumption increases blood and plasma volume, which in turn increases blood pressure. Exercise has a similar effect; the sympathetic immune system is stimulated, leading to vasoconstriction and ultimately increasing blood pressure. To practice safe exercise, it is important not to elevate blood pressure too high beforehand. Research has recommended that alcohol consumption be reduced in order to maintain healthy and safe blood pressure levels.[3] Likewise, it is unsafe to consume alcohol before or during exercise because blood pressure levels may rise to dangerous levels.
Perhaps the most important physiological effect that alcohol has on the body is that which concerns the heart. Research has shown that intoxication by alcohol directly relates to impairment of cardiac contractility. Depending on how much alcohol was consumed, cardiac contractility was impaired at varying levels; a lighter intoxication lead to less impairment while a heavier intoxication lead to greater impairment.[4] Exercise causes heart rate to increase, requiring a great deal of cardiac contractility. If the heart is impaired by because of alcohol intoxication, blood may not be pumped sufficiently throughout the body during exercise. Therefore, if a person plans on exercising, they should either drink lightly or not at all in an attempt to keep their heart working properly.
Anabolic Steroids[edit | edit source]
Anabolic steroids are drugs that have many neuropsychiatric effects in addition to the more commonly known effects they have on skeletal muscles. Anabolic steroids cause not only negative feelings like intense anger, but also some positive moods. Some of the negative feelings people have resulting from the use of anabolic steroids include irritability, mood swings, violent feelings, anger, and hostility [5]. Among the positive feelings related to steroid use include euphoria, increased energy, and sexual arousal [5]. Steroids are also linked to other cognitive symptoms like distractibility, forgetfulness, and confusion [5]. All of these effects result from steroid use alone, without exercise. These impacts on mood could have either positive or negative effects on exercise, depending on feelings of the person exercising.
Steroids have not been shown to increase creatine concentrations in the muscle, red blood cell concentration, or serum liver enzyme concentrations as some have postulated [6]. In addition one study found that injection of 600 mg of testoterone in adult males who did not exercise, resulted in more fat free mass and a greater increase in strength than individuals who did incorporate resistance training but only took a placebo.[6]. Some commonly reported side effects of steroid use, such as acne and breast tenderness resulted in some of the subjects as well, but most did not[6]. This would seem to indicate that individual physiological differences have a profound impact on how a person reacts to steroids.
Analgesic Medication[edit | edit source]
Caffeine/Stimulants[edit | edit source]
Caffeine is the most widely used stimulant in the world. This is because caffeine consumption is completely legal, socially acceptable, and is consumed daily by a large majority of the world population. Daily morning staples, such as coffee and tea, as well as soda pop and energy drinks contain caffeine. Much research has been conducted to determine how caffeine consumption effects one’s body systems and processes during exercise. Many studies support the findings that caffeine enhances both physical and cognitive performances. Physically, caffeine specifically improves aerobic performance [7]—extending the time that an activity can be sustained prior to fatigue. Mixed results exist as to whether caffeine significantly improves performance in resistance training [7]. Several mechanisms work on different systems of the body to produce the overall enhancement of exercise performance that caffeine causes.
A neuromuscular mechanism that aides in causing caffeine’s ergogenic effects is its action on the ryanodine receptors in the sarcoplasmic reticulum of muscles [8]. The function of these receptors is to open and allow Ca2+ to flow out of the sarcoplasmic reticulum. Ca2+ facilitates the contraction of muscle fibers. Therefore, the effect that caffeine has on this system is to allow for stronger contractions of muscles than is typical at a given level of stimulation, because more Ca2+ is available to bind to troponin, which moves tropomyosin aside so that myosin can bind to the actin myofilaments and muscle contraction can occur.
Caffeine also acts on the nervous system. Specifically, it affects normal neurotransmitter release, increasing both the amount of noradrenaline (NA) and dopamine (DA) released in the brain during exercise [9]. Dopamine has widespread functions, but a few of these include influences on motivation, cognition, reward, motor control, and mood [9]. Many studies have shown that an increase in DA release results in enhanced endurance [9]. One such study showed that muscle pain perception and perceived exertion was much lower in a group that received caffeine prior to resistance training, as opposed to when those same subjects were administered a placebo on a separate date [7]. When the individuals ingested the caffeine, they performed significantly more repetitions before failure than when they were given the placebo [7].
Although research supports the ergogenic effects of caffeine on endurance, it has been less conclusive as to whether caffeine has the same type of effects on resistance training. Data from several studies supports an increase in resistance training performance following caffeine ingestion; however, researchers have been unable to isolate the exact physiological mechanism responsible for this. Therefore, the increased performance could potentially be due only to the decreased pain & exertion perception of the subject [as previously explained] [7].
One other substantial mechanism by which caffeine positively effects athletic performance is by increasing the rate that lipolysis occurs [8]. Lipolysis is the process human bodies use to break apart fats and produce ATP (our primary usable form of energy) to fuel our body. Each triglyceride (fat molecule) that is broken down produces approximately 300-400 ATP (depending on how many carbons form the specific fat being used). The increase in fats being used to produce energy results in a decrease in carbohydrates used for that same purpose. This greatly increases efficiency because carbohydrate molecules produce far fewer ATP than triglycerides.
There are many factors in the methods of caffeine studies that cause confounded results. One factor that must be considered is the dose of caffeine administered. The many studies used different doses when investigating the effects that caffeine has on exercise. Researchers use doses of anywhere from 2-8 mg/kg, but the methods of most studies call for doses of 5-6 mg/kg [10]. Doses as small as 6 mg/kg have been shown to increase endurance. However, that small of a dose does not have an effect on shorter, higher intensity exercise performance [8]. Other factors include the form of caffeine used, other ingredients in the caffeine source and their possible physiological effects, diet, and length of time prior to exercise that the caffeine is administered [10]. These variables, in addition to many others, increase the complexity of research of caffeine and exercise performance.
Creatine[edit | edit source]
Human Growth Hormone (HGH)[edit | edit source]
Marijuana[edit | edit source]
Marijuana use affects various physiologic processes through its most active substance, tetrahydrocannabinol, otherwise known as THC. Marijuana use has a direct effect on the central nervous system because it contains the receptor sites for THC[11]. Although marijuana does possess some ergogenic effects in certain situations, it impacts the body oppositely during exercise. The drug has a sedative effect during exercise, resulting in decreased exercise and psychomotor performance like slower reaction time[11]. In terms of the cardiovascular system, marijuana has been shown to increase heart rate and blood pressure while decreasing overall cardiac output[11]. This is important for clinicians to consider when treating patients who use marijuana, as it is an ergolytic drug when used in combination with exercise that will negatively affect the patient’s exercise performance and overall health.
Tetrahydrocannabinol is the primary constituent of marijuana that binds to G-Protein-Coupled CB1 receptors which are found throughout the brain in the frontal and and medial temporal lobe.[12] Marijuana is one of the most frequently used drugs among young adults. Marijuana induces tachycardia which can decrease the maximal work capacity after smoking this drug. [13] Marijuana creates an increase in carboxyhemoglobin concentration of blood due to large amount of carbon monoxide created from the smoking of this drug. [13] Some other factors that coudl affect the maximal work capacity after smoking marijuana are bronchodilation, decrease in perception of dyspnea, and increase blood flow to exercising muscles. [13] The utilization of marijuana with exercise has a negative correlation that affects their overall health greatly.
Methamphetamine[edit | edit source]
Amphetamines are a group of drugs with mind-altering capabilites. Methamphetamines are the most potent of the amphetamine group of drugs. [14] Methamphetamine falls under the classification of a stimulant. Typically, stimulants will increases and individuals sensations such as mental awareness while also increasing one's ability to respond to the environment[15]. Users of stimulants may also find an increase in energy levels. The effects that users feel while on methamphetamine (METH) causes this drug to be highly addictive. The physiological effect of METH is achieved by increasing the quantitiy and release of stimulatory neurotransmitters dopamine, noradrenaline and serotonin and decreasing their synaptic breakdown. [14]
A primary clinical consideration for methamphetamine is its use with other medications. Acute use of METH with other stimulants can overstimulate the sympathetic nervous system, potenitally resulting in cardiac arrythmia, seizures, cardiovascular collapse, and death. [14] Therefore, physical therapists should take special consideration when prescribing exercise to patients who present with signs suggestive of use. Characteristic presentation of METH use includes restlessness, weight loss, heightened alertness, violent behavior, and pupillary dilation. [14]
An acute response to METH use is hyperthermia. [16] Although the exact mechanism though which this is achieved is unknown, literature suggests that methamphetamine-induced hyperthermia results from heat generation as well as an inhibition in heat loss. [16] One study conducted in 2009 aimed to explore the effects of brain hyperthermia brought on by METH. The reaserachers of this study injected rodents with differing amounts of METH, and then proceeded to measure how dosages and enviromental factors impacted brain hyperthermia [17]. METH, especially in large doses, influences the metabolic activity of the brain due to oxidative stress which is what occurs when the body is unable to rid itself of free radicals at a rate to maintain a homeostatic balance [17]. Temperatures inside of the brain also increase due to "enhanced release of meluiple neuroactive substance, lipid peroxidation.... and numerous changes combined as oxidative stress" [17]. Increases in the metabolic brain activation paried with internal head production by the brain cells seem to be the driving force behind brain hyperthermia [17]. Ingesting METH at increased tempertures or during social gatherings when an individual is more likely to be active such as with exercise only exacerbates this increase in core body temperture. Even slight increases in cell tempertures can cause denaturation, which can then lead to impaired cell function or ultimately death of the cell.
Thus, combining therapeutic exercise when an individual is experiencing methamphetamine-induced hyperthermia could result in serious harm. The current practice for cooling methamphetamine-induced hyperthermia is placing the individual in a cool environment to try to bring that person back into a homeostatic balance [16].
Chronic METH use results in a range of physiologic disturbances. An adaptation with the greatest relevance to physical therapists is the presence of congestive heart failure in chronic users. [18] Impaired oxygen delivery to tissues would result in an inability to safely engage in treatment on the part of the patient. Moreover, attempting to engage in such an activtiy could result in cardiogenic shock. If the practitioner engages the patient in these activities without knowing about METH use, the outcome could be fatal. Another clinical implication is that chronic METH use can break down the blood-brain barrier (BBB) over time, and it has been shown that increased permeability in the BBB can lead to damage of myelin [17]. Without myelin, the nervous system is unable to communicate effectively to different systems, including muscular, which could have an impact on exercise prescriptions and individual expectations.
Muscle Relaxants[edit | edit source]
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)[edit | edit source]
Smoking
[edit | edit source]
Aerobic exercise challenges the body's ability to supply and handle oxygen. For example, when performing high-intensity aerobic exercise, mitochondrial reactice oxygen species' (ROS) grow in number. ROS, is left unchecked, have have the ability to cause genetic mutations. However, several enzymes -- including superoxide dismutase -- are present to handle this oxidatve stress caused by ROS.The body responds to chronic aerobic exercise by enhancing its ability to cope with ROS. [19]
Smoking also induces an oxidative stress; however, smoking-induced oxidative stress also inhibits the body's abiltiy to cope by suppressing the genes responsible for antioxidant production. [20] The net result of smoking-induced oxidative stress is vascular and arteriolar inflammation -- further impairing the oxygen-delivering capabilties of the body. [20] Clearly, by limiting oxygen delivery, cigarette smoking impairs the ability to generate energy through the oxidative energy system. However, literature also suggests that smoking impairs anaerobic energy provision by altering contractile proteins, creatine kinase, and other glycolytic enzymes.[21] With this in mind, therapists should be weary of setting unrealistic goals for patients who are smokers.
Smoking is a huge risk factor coronary artery disease and many other complications such as myocardial infarction and sudden death. [22]Smoking is one of the biggest cause of death in the world. Smoking is also associated with marked, acute, and increase in blood pressure, systemic vascular resistance, and heart rate. [22] Nicotine is one factor that stimulates epinephrine and norepinephrine release from the sympathetic nerve terminals and adrenal glands, which explains that acute cardiovascular effects may be due to adrenergic stimulation at the peripheral levels. [22]Acute cigarette smoking is associated with a significant decrease in vagal cardiac modulations which may increase the risk of complications during daily exercise or intense physical activity. [22]Acute smoking affects the cardiorespiratory responses to both submaximal and maximal exercise, which can result in an increase of sympathetic dominance at lower levels of submaimal work.[22] Clinicians should be considerate of all options and treatment plans for patients who are avid smokers.
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Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
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- ↑ Boileau I, Assaad J, Pihl R, Benkelfat C, Leyton M, Diksic M, et al. Alcohol promotes dopamine release in the human nucleus accumbens. Synapse 2003;49:226-31. http://www.readcube.com/articles/10.1002%2Fsyn.10226?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER (accessed 15 Sep 2015).
- ↑ Shirreffs S, Maughan R. Restoration of fluid balance after exercise-induced dehydration: Effects of alcohol consumption. Journal of Applied Physiology 1997;83:1152-8. http://jap.physiology.org/content/83/4/1152 (accessed 15 Sep 2015).
- ↑ Xin X, He J, Frontini M, Ogden L, Motsamai O, Whelton P. Effects of alcohol reduction on blood pressure: A meta-analysis of randomized controlled trials. Hypertension 2001; 38:1112-7. http://hyper.ahajournals.org/content/38/5/1112.long (accessed 15 Sep 2015).
- ↑ Kelbaek H, Gjørup T, Brynjolf I, Christensen N, Godtfredsen J. Acute effects of alcohol on left ventricular function in healthy subjects at rest and during upright exercise. The American Journal of Cardiology 1985;55:164-7. http://www.sciencedirect.com/science/article/pii/0002914985903200 (accessed 15 Sep 2015).
- ↑ 5.0 5.1 5.2 Su, T., Pagliaro, M., Schmidt, P., Pickar, D., Wolkowitz, O., & Rubinow, D. Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA The Journal of the American Medical Association 1993;269:2760-4. http://ovidsp.tx.ovid.com.ezproxy.lib.ou.edu/sp-3.16.0b/ovidweb (accessed 22 Sept 2015).
- ↑ 6.0 6.1 6.2 Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, et al. The Effects of Supraphysiologic Doses of Testosterone on Muscle Size and Strength in Normal Men.Abridged version: NEJM 1996;335:1–7.Full version: http://www.nejm.org/doi/pdf/10.1056/nejm199607043350101 (accessed 28 Oct 2015).
- ↑ 7.0 7.1 7.2 7.3 7.4 Duncan, M. J., & Hankey, J. (2013). The effect of a caffeinated energy drink on various psychological measures during submaximal cycling. Physiology & Behavior, 116, 60-65.
- ↑ 8.0 8.1 8.2 Tarnopolsky, M. (1994). Caffeine and Endurance Performance. Sports medicine, 18(2), 109-125. doi: 10.2165/00007256-199418020-00004
- ↑ 9.0 9.1 9.2 Zheng, X., Takatsu, S., Wang, H., & Hasegawa, H. (2014). Acute intraperitoneal injection of caffeine improves endurance exercise performance in association with increasing brain dopamine release during exercise. Pharmacology Biochemistry and Behavior, 122, 136-143.
- ↑ 10.0 10.1 Shearer, J., & Graham, T. E. (2014). Performance effects and metabolic consequences of caffeine and caffeinated energy drink consumption on glucose disposal. Nutrition Reviews, 72(suppl 1), 121-136. doi: 10.1111/nure.12124
- ↑ 11.0 11.1 11.2 Pesta, D. H., Angadi, S. S., Burtscher, M., & Roberts, C. K. (2013). The fckLReffects of caffeine, nicotine, ethanol, and tetrahydrocannabinol on exercise performance. Nutrition & Metabolism 2013;10:71. http://www.nutritionandmetabolism.com/content/10/1/71 (accessed 4 Oct 2015).
- ↑ Gevins A, Ilan A, Smith M. Effects of marijuana on neurophysiological signals of working and episodic memory. Psychopharmacology 2004;176:214-22
- ↑ 13.0 13.1 13.2 Cormier Y, Renaud A. Acute effects of marijuana smoking on maximal exercise performance. Medicine and Science in Sports and Exercise 1986;18:685-689
- ↑ 14.0 14.1 14.2 14.3 McAvoy, B. Methamphetamine -- what primary care practitioners need to know. J Primary Health Care. 2009;1(3): 170-176.
- ↑ National Institute on Drug Abuse. Prescription drug abuse. United States: NIH, 2014.
- ↑ 16.0 16.1 16.2 Matsumoto R, Seminerio M, Turner R, Robson M, Nguyen L, Miller D, O'Callaghan J. Methamphetamine-induced toxicity: an updated review on issues related to hyperthermia. Pharmacology & Therapeutics; 144: 28-40.
- ↑ 17.0 17.1 17.2 17.3 17.4 Kiyatkin EA, Sharma HS. Acute methamphetamine intoxication: Brain hyperthermia, blood-brain barrier and brain edema. International Review of Neurobiology 2009; 88: 65–100.
- ↑ Wijetunga M, Seto T, Lindsay J, Schatz I. Crystal methamphetamine-associated cardiomyopathy: tip of the iceberg? J Toxicology; 41: 981-986
- ↑ Vollaard, NB, Shearman, JP, Cooper, CE Exercise-induced oxidative stress. Sports Med 2005; 35: 1045-1062
- ↑ 20.0 20.1 Garbin U, Pasini AF, Stranieri C, Cominacini M, Pasini A, Manfro S, et al. Cigarette smoking blocks the protective expression of Nrf2/ARE pathway in peripheral mononuclear cells of young heavy smokers favouring inflammation. PLoS ONE 2009; 4: 1-12
- ↑ Barreiro E, Peinado VI, Galdiz JB, Ferrer E, Marin-Corral J, Sanchez F, et al. Cigarette smoking-induced oxidative stress: A role in chronic obstructive pulmonary disease skeletal muscle dysfunction. Am J Resp Crit Care Med 2010; 182: 477-488
- ↑ 22.0 22.1 22.2 22.3 22.4 Fernhall B, Mendonca G, Pereira F. Effects of cigarette smoking on cardiac autonomic function during dynamic exercise. Journal of Sports Science 2011;29:879-86