Magnesium (Mg2+), to human knowledge, is the ninth most abundant mineral in the universe and the second most profuse cation within the intracellular compartments of the human body (19,29). In exercise physiology, Mg2+ has tended to be overlooked, with a variety of textbooks (8,20,23,27,28,43) lending only a few token sentences to its function and applicability to exercise, compared with other micronutrients including phosphorus and calcium. A recent generic search of PubMed, using the key words “magnesium” and “human” yielded 512 publications; when Mg2+ was substituted for calcium (Ca2+), 4977 hits were reported. The same search was narrowed to include “Muscle”, resulting in 15 and 187 publications, respectively. These numbers reflect an imbalance in Mg2+ research that may stem from a lack of scientific interest, driven by methodological difficulties in determining Mg2+ concentration within the human body (12,40). It is also probable that only recently because of the advances in technology, such as nuclear magnetic resonance (NMR) spectroscopy and florescent dye techniques, whole body processes and cellular interactions involving Mg2+ in vivo could be studied (36) because the majority of research has been on animal models in vitro, which do not give an overall indication of events (25).
Despite the previous difficulties encountered in assessing an individual's Mg2+ status, the role of Mg2+ within the body is of fundamental importance, involved with or linked to the promotion of Ca2+ transport in/out of the sarcoplasmic reticulum (SR) (39), regulation of glycolytic metabolic pathways (22), oxygen delivery and uptake (26), adenosine triphosphate (ATP) production (19), an activator and cofactor of > 300 enzymatic reactions (4), regulation of muscle contraction and nerve impulses (24), stability of the immune system (41), and recently, cellular division and aging (5). Magnesium is clearly one of the most important cations that has received little focus in comparison to other substances within the field of sport, exercise, and health physiology. Therefore, the aim of this literature review is to first increase the awareness of strength and conditioning coaches regarding the functional and biological roles of Mg2+ within the body by briefly introducing its importance in (a) regulation of muscle contraction, (b) regulation of energy production, and (c) other processes of interest to practitioners. This review will also discuss possible implications of Mg2+ deficiency in untrained and athletic populations regarding the role Mg2+ can play in exercise performance including future directions for research.
FUNCTIONAL AND BIOLOGICAL IMPORTANCE OF Mg2+
To gain a full appreciation of the importance of Mg2+ in human biological processes requires an in depth understanding of chemistry and cellular physiology, which is outside the scope of this article and interest of most of the readership. Nonetheless, coaches and athletes still need to understand the importance of this cation, so this article will aim to illustrate the role of Mg2+ in a number of processes that are of fundamental importance in optimizing physiological performance. For a more in depth discussion of these processes, the reader is directed to the articles of Killilea and Maier (21), Lukaski (25), Mclean (29) Potter et al. (33), and Swaminathan (40).
REGULATION OF MUSCLE CONTRACTION
To put the role of Mg2+ into context, a brief overview of the classical theory of muscle contraction will be provided, and for a more detailed review, the reader is referred to Gordon et al. (16). The excitation-contraction coupling (ECC) process is whereby an action potential triggers a muscle cell to contract, which comprises the following events (Figure 1).
Acetylcholine is released by the neuron at the neuromuscular junction, which then binds to a receptor in the synaptic cleft, with the aid of Mg2+. This results in a depolarization of the sarcolemma, through a sodium (Na+) and potassium (K+) flux. This action potential spreads along the sarcolemma and into the SR via the T-tubule system. In the SR, the change in cellular polarity causes a shift in Mg2+, which opens the ryanodine receptors (RyRs) within the SR, allowing calcium influx (4). Calcium concentration further increases whereby it binds to troponin in the thin actin filament, causing a structural alteration of the filament. This alteration exposes the actin binding site to the myosin head, creating a crossbridge; it is here that ATP acts to facilitate the “power stroke” of muscular contraction. Muscle relaxation occurs as the result of the pumping of Ca2+ back into the SR via specific pumping mechanisms (38,39).
Classical theory infers that muscle contraction is regulated predominantly by the divalent cations Na+, K+, and Ca2+ (38,39). However, because of multiple in vitro experiments in animals and several recent in vivo studies of humans, physiologists have determined that this is not the whole picture because Mg2+ is an integral component of muscle contraction, ultimately affecting performance, strength, and endurance capacity (4,6,7,31).
Magnesium is an important regulator of Ca2+ and cellular pH balance (15,30,35). Were it not for the role of Mg2+ as a natural calcium antagonist, regulator, and transporter, calcium overload would occur resulting in enzyme breakdown, acidosis, and cell death (37). Cellular homeostasis is maintained through Mg2+'s ability to activate key enzyme reactions (30), transport hydrogen ions (H+) (14), modulate ion channels and protein transporters (35), and trigger adaptive cellular reconfiguration, notably within ECC (24,33).
An early study into crossbridge formation in isolated rabbit fibers found Mg2+ to affect crossbridge rate of detachment and force production, which was hypothesized (but not confirmed because of limited technological capability) to be the result of Mg2+, regulating troponin expression through Ca2+ concentration gradients and transport (4). Mg2+ may also stabilize the structure of proteins such as actin (35). Each actin exists as a globular monomer, which is bound to an ATP and Mg2+ molecule that acts to affect and stabilize the chemical structure complex almost as a hinge, forming the backbone of the thin filament in the sarcomere (16). Without this ATP and Mg2+ binding, actin would denature before crossbridge formation (30). Furthermore, crucial to muscle contraction is the relaxation phase that is dependent on the pumping of Ca2+ back into the SR of the muscle fiber (16). As eluded earlier, this is dependent on specific pumping mechanisms, which require both ATP and Mg2+ (16,37), because Mg2+ acts to anchor cofactors for chemical reactions such as ATP and activate enzyme reactions (32). In a study of an isolated frog fiber, it was found that Ca2+ transport was increased by a factor of 1.6 in the presence of Mg2+ by examining the rate of Ca2+ disappearance (39). It is apparent that Mg2+ works on multiple components of muscle contraction and relaxation.
REGULATION OF ENERGY PRODUCTION
Energy production is influenced by the presence of Mg2+, facilitating the activation of key enzymes in the metabolic pathways (25), is a cofactor in ATP production (22), modulator of O2 transport via stabilization of the membranous structure of red blood cells (35), and regulator of energy in reaction sequences (19). Magnesium is required for many oxidation-reduction and phosphorylation reactions, such as creatine phosphokinase, which acts as an ATP regenerator through formation of phosphocreatine; pyruvate dehydrogenase that oxidizes pyruvate, facilitating pyruvate transformation into acetyl coenzyme A; and hexokinase, which is a main component of glucose metabolism (14,22). All these reactions are crucial to energy production (35). Magnesium achieves this through formation of ATP-Mg complexes that anchor substrates to the active site on enzymes, catalyzing the reaction and speeding up metabolic pathways (21). Through its regulatory role in ATP production and the creatine kinase reaction, Mg2+ is also thought to favorably influence (attenuate) adenine nucleotide degradation, believed to be a key contributory component in muscle fatigue. In a recent modeling study, it was shown that a decrease in pH accompanied by an increase in Mg2+ counteracted the rise in adenosine diphosphate associated with phosphocreatine depletion (30). In separate studies examining Mg2+ shifts during high-intensity exercise, it was found that because there was greater demand on anaerobic and glycolytic pathways, there was a greater movement and loss of Mg2+ through shifts in water compartments, increased metabolism, and sweat (14).
Recent observations examining Mg2+ transporters within the mitochondria have shown that mitochondria contain high amounts of Mg2+ that as well as influencing mitochondrial enzymes also activate and stabilize cytochrome c oxidase, which catalyzes the final stage in aerobic respiration, combining H+ to form water (35). These catalytic properties may explain the increase in O2 consumption reported in previous articles. Deuster et al. (14) found a correlation of r = 0.87, p < 0.0001, between an increase in O2 consumption during recovery and a decrease in Mg2+ concentration following high-intensity exercise (90% o2peak). Further investigations (11,26) have also suggested a relationship between Mg2+ status and maximal oxygen uptake, r = 0.43 and r = 0.46, which was shown to be reduced in states of Mg2+ deficiency (11). During exercise, there is an increase in hormones designed to regulate fluid levels, including vasopressin and aldosterone, which act to maintain homeostasis because electrolytes, including Mg2+, are lost through sweat, fluid regulation, increased metabolic activity, and lipolysis (9,31,34). Though, in athletes participating in endurance exercise, they would find that these hormones would lead to an increased Mg2+ reabsorption, essential for maintaining metabolic activity; during acute high-intensity work, hormones can reduce Mg2+ reabsorption in the tubular system because plasma levels of Mg2+ are temporarily higher because of shifts in concentrations from intracellular to extracellular compartments (34). In both endurance and high-intensity events, this leads to an imbalance in Mg2+ homeostasis after exercise; therefore, replacement of Mg2+ levels should be considered to reduce the chance of oxidative stress and facilitate energy regulation.
It has been demonstrated that Mg2+ regulates immune function because it is a cofactor for immunoglobulin synthesis (41). In presence of low Mg2+ concentrations, there are increased levels of interleukin 6 and tumor necrosis factor alpha, substances that lead to cellular degradation and decreased cell proliferation (21). This may also affect aging and senescence cells. It has been speculated that the accumulation of senescence (aging) cells in humans contributes to the aging phenotype by a degeneration of regenerative ability and cell creation, via a shortening of telomeres that act to protect chromosomes in DNA from damage (21). Low levels of Mg2+ have also been shown to induce oxidative stress because Mg2+ plays a role in mitochondrial aerobic metabolism, and as a result, this may induce premature senescence and cellular aging, through shortening of telomeres (5,41). It is clear that levels of Mg2+ need to be maintained within the body to facilitate efficient functioning and to protect the body against injury and illness.
MAGNESIUM DEFICIENCY AND CONSEQUENCES
The recommended daily intake for Mg2+ is 300-400 mg·d−1 for women and men (25). However, the Western diet tends to lack natural sources of Mg2+, leading to a growing deficiency within the population, including athletes (34). The standard test for Mg2+ concentration is a serum total Mg2+ test (2); however, this is not representative of the whole body distribution because most of Mg2+ is stored in intracellular compartments, including bone, which can be only partially assessed by NMR scans (40). During bouts of exercise, consumption of food and water, and thermoregulatory responses, Mg2+ is displaced into blood plasma through a shift from the intracellular compartments into blood, affecting test interpretations (14). Therefore, care should be taken in obtaining a resting fasted blood sample. Another noninvasive approach is to conduct a dietary analysis of an individual over a 7-day period and analyze mineral intakes, combined with serum concentrations; this may provide a more realistic and field test applicable approach for athletic testing because NMR scans are impractical outside of the laboratory environment. For additional information on sampling methods, the reader is directed to the article of Swaminathan (40).
Imbalances in Mg2+ can result from a number of mechanisms discussed previously including diuretics, decreased dietary intake, sweat loss, and high-intensity and endurance-based events (39). Magnesium can also be affected by ingestion of common substances including caffeine, which increases adrenaline secretion, while acting as a diuretic affecting the Mg2+ tubular absorption, and alcohol, which augments urinary excretion of Mg2+, which over a sustained period leads to Mg2+ depletion (17). In athletes, lower than required Mg2+ levels are common. Exercise enhances Mg2+ usage through increased muscle contraction, metabolic activity, and sweat loss (9). Low Mg2+ concentrations can lead to injury and illness (41), muscle weakness and cramps (34), hypocalcemia (37), reduced glucose breakdown (18), decreased bone remodeling (34), and increased blood pressure (36) through decreased enzyme efficiency and cellular instability (3,16). In those with severe Mg2+ deficiencies, a supplemental dose of 5 mg·kg body weight·day−1 can be administered orally, resulting in rapid symptom reversal (16,24). However, it should be emphasized that the aim of Mg2+ supplementation is to obtain homeostasis, not to overdose because this can lead to negative health consequences (40). Hypermagnesemia is rare because excess Mg2+ is usually filtered by the kidneys; however, if kidney function is impaired or high supplemental doses are used, symptoms (hypotension and irregular nerve transmission) may present and supplementation should be ceased (16,34).
Magnesium can be acquired through diet (Table 1); however, the demands on athletes, especially in weight classification sports such as boxing, gymnastics, and dance, can lead to calorific restriction and altered or disturbed eating habits, and in female athletes and dancers, disturbances in menstrual function and decreased bone density (13,43). All of these can contribute to Mg2+ deficiency and negative health consequences. Also worthy of consideration is that typical recommended daily intakes of micronutrients including Mg2+ may be insufficient for those expending more energy through training and recovery. It has been suggested that athletes may require up to 20% more than their sedentary counterparts; however, testing should be performed prior to serious supplementation (34). It may be inferred that a supplemental dose of near 100 mg·d−1 in athletes may prove beneficial to accommodate for deficits incurred during performance and training while reducing the chance of overdosing.
It is evident that Mg2+ plays a substantial role in the modulation of homeostasis and cellular function within the body. However, there remain only a handful of studies that have investigated the potential for monitoring or supplementing Mg2+ in athletes to improve performance, and of those, there is a severe lack of integrated and multidimensional experimental designs (31). One study found that in sedentary and actively trained individuals, there was a decrease in lactate production after exhaustive exercise; however, there was a lack of report as to whether these measures improved performance ability (10). A previous meta-analysis conducted on Mg2+ supplementation highlighted that in previous literature, there were severe differences in supplementation methodologies and a lack of crossover designs between studies that made inferences as to the effects of supplementation difficult (31). It was also noted that few studies utilized any method for determining Mg2+ status prior to supplementation and even fewer looked at the effects in women, who are at a higher risk of developing Mg2+ depletion.
Magnesium deficiency has been linked to reduced strength through disrupted metabolic pathways and neuromuscular contractility (9,19), decreased blood glucose clearance via disrupted ion channels and transport proteins (18), and reduced ability to sustain high oxygen consumption levels via disruption of the enzymes responsible for transphosphorylation, aerobic metabolism, and oxygen transportation (26). Research should expand upon these areas to determine how Mg2+ concentration or supplementation can affect them.
Any study aiming to explore supplementation should look to obtain premeasures prior to commencement because it has been shown that in those with optimal levels of Mg2+, short-term Mg2+ has little effect (13). This can be achieved either through a dietary analysis or blood serum Mg2+ levels. A placebo-controlled crossover design should also be used to increase reliability of assertions made from trials, as well as a homogenous sample because many previous studies have used individuals with varying degrees of fitness (10). Other important areas that should be investigated are the effects of supplementation on maximal voluntary contraction (MVC) and rapid force development (RFD) because these could have implications not just for athletes but for age-associated losses in MVC and RFD abilities, linked to an increased risk of falls in aging population as a result of sarcopenia (1). A previous 7-week research study (7), using a placebo-controlled supplementation program, on strength training parameters in untrained individuals found a significantly higher increase in peak quadriceps torque with Mg2+ supplementation versus placebo (211 versus 174 N m). These findings could be further investigated in trained individuals to ascertain whether it is the training status that influences strength gains or the supplement. The effects of Mg2+ status on oxygen kinetics could also be assessed, investigating whether supplementation could increase maximal oxygen uptake, could decrease oxidative stress, or whether it could reduce oxygen debt accumulated during exercise, facilitating enhanced endurance capacity.
Magnesium has also been shown to interact with several medications in the clinical setting (40); it would therefore benefit exercise physiologists to know if there are additional interactional effects with common sports aids, such as creatine monohydrate, which may be augmented by enhanced Mg2+ status; as eluded to earlier, Mg2+ plays a key role in the activation of creatine phosphokinase and deficiencies may explain why some individuals do not respond to supplementation. Similar trials should also be conducted on emerging ergogenic aids, such as β-alanine and sodium bicarbonate, as well as caffeine, to see if a combined magnesium-caffeine supplementation would prove superior because it may attenuate the decline in Mg2+ loss associated with caffeine alone. The supplement zinc magnesium aspartate should also be investigated further because 2 previous studies, looking at strength parameters, produced conflicting results (6,42). This may be because of differences in study design because the first was during the off-season of soccer players, while the other examined active resistance-trained individuals. It may also be because of interactions between those minerals or an insufficient dose of Mg2+. Regardless, further investigation is warranted.
Finally, it should be investigated as to whether Mg2+ can influence glucose kinetics and decrease circulating blood glucose in normal and trained populations, as high circulating levels can lead to diabetes. Several clinical studies in patients have been undertaken previously, but it remains unseen as to whether supplementation could act as a countermeasure to hyperglycemic states through regulation of glucose metabolism (18).
Magnesium is one of the most important divalent cations within the human body. In short, it regulates muscle function, neural networks, energy production, and enzyme reactions; facilitates transport of other nutrients; and affects cellular integrity (Figure 2). However, there remains a lack of acknowledgment and research in sport and exercise science as to the importance of Mg2+. From this review of existing literature, it is clear that there is a large scope for further research in this field for both athletes and clinical populations, but care should be taken in interpretation of results because of its numerous affects within the body. Future experimental designs should try to incorporate techniques to validate the importance of this substance and potential impact on training and sporting performance.
1. Aagaard P, Magnusson PS, Larsson B, Kjaer, M, and Krustrup P. Mechanical muscle function, morphology and fibre types in lifelong trained elderly. Med Sci Sports Exerc
39: 1989-1996, 2007.
2. Altura BM and Altura BT. New perspectives on the role of magnesium in the pathophysiology of the cardiovascular system: Experimental aspects. Magnesium
4: 245-271, 1985.
3. Altura BM, Zhang A, and Altura BT. Magnesium, hypertensive vascular diseases, atherogenesis, subcellular compartmentation of Ca2+
and vascular contractility. Miner Electrolyte Metab
19: 323-336, 1993.
4. Anderson ML and Schoenberg M. Possible cooperativity in crossbridge detachment in muscle fibres having magnesium pyrophosphate at the active site. Biophys J
52: 1077-1082, 1987.
5. Billard JM. Ageing, hippocampal synaptic activity and magnesium. Magnes Res
19: 199-215, 2006.
6. Brilla LR and Conte V. A novel zinc and magnesium formulation (ZMA) increases anabolic hormones and strength in athletes. Med Sci Sports Exerc
31: 483, 1999.
7. Brilla LR and Haley TF. Effect of magnesium supplementation on strength training in humans. J Am Coll Nutr
11: 326-329, 1992.
8. Brooks GA, Fahey TD, and Baldwin KM. The maintenance of ATP homeostasis in energetics and human movement. In: Exercise Physiology: Human Bioenergetics and its Applications
, Eds. Brooks, GA, Fahey, TD, and Baldwin, KM, (4th ed). London, United Kingdom: McGraw-Hill, 2005. pp. 31-42.
9. Buchman, AL, Keen, C, Commisso, J, Killip D, Ou C, Rognerud CI, Dennis K, and Dunn JK. The effect of a marathon run on plasma and urine mineral and metal concentrations. J Am Coll Nutr
17: 124-127, 1998.
10. Cinar V, Nizamlioglu M, and Mogulkoc R. The effect of magnesium supplementation on lactate levels of sportsmen and sedentary. Acta Physiol Hung
93: 137-144, 2006.
11. Conn CA, Schemmel RA, Smith BW, Ryder E, Heusner WW, and Ku PK. Plasma and erythrocyte magnesium concentrations and correlations with maximum oxygen consumption in nine- to twelve-year-old competitive swimmers. Magnesium
7: 27-36, 1988.
12. Coudray CF, Coudray C, Gueux E, Mazur A, and Rayssiguier Y. A new in vitro blood load test using a magnesium stable isotope for assessment of magnesium status. J Nutr
133: 1220-1223, 2003.
13. Coudray CF, Coudray C, Tressol JC, Pepin D, Mazur A, Abrams SA, and Rayssiguier Y. Exchangeable magnesium pool masses in healthy women: Effects of magnesium supplementation. Am J Clin Nutr
75: 72-78, 2002.
14. Deuster PA, Dolev E, Kyle SB, Anderson RA, and Schoomaker EB. Magnesium homeostasis during high-intensity anaerobic exercise in men. J Appl Physiol
62: 545-500, 1987.
15. Elsden S. Magnesium and muscle respiration. Biochem J
16. Gordon AM, Homsher E, and Regnier M. Regulation of contraction in striated muscle. Physiol Rev
80: 853-924, 2000.
17. Gullestad, L, Dolva LO, Søyland E, Manger AT, Falch D, and Kjekshus J. Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics. Alcohol Clin Exp Res
16: 986-990, 1992.
18. Haenni A, Reneland R, Anderson P, Lind I, and Lithell H. Skeletal muscle magnesium content is correlated with plasma glucose concentration in patients with essential hypertension treated with lisinopril or bendrofluazide. Am J Hypertens
15: 735-738, 2002.
19. Hasselbach W, Fassold E, Migala A, and Rauch B. Magnesium dependence of sarcoplasmic reticulum calcium
transport. Fed Proc
40: 2657-2661, 1981.
20. Houston ME. Energy systems and bioenergetics. In: Biochemistry Primer for Exercise Science
Eds. Houston, ME, (3rd ed). Champaign, IL: Human Kinetics, 2006. pp. 35-58.
21. Killilea DW and Maier JM. A connection between magnesium deficiency and aging: New insights into cellular studies. Magnes Res
21: 77-82, 2008.
22. Lawson RJW and Veech RL. Effects of pH and free Mg2+
on the Keq
of the creatine kinase reaction and other phosphate hydrolysis and phosphate transfer reactions. J Biol Chem
254: 6528-6537, 1979.
23. Lilly LS. The electrocardiogram. In: Pathophysiology of Heart Disease
Eds. Lilly LS (4th ed). Philadelphia, PA: Lippincott Williams and Wilkins, 2007. pp. 80-117.
24. Lotti S and Malucelli E. In vivo assessment of Mg2+
in human brain and skeletal muscle by 31
P-MRS. Magnes Res
21: 157-162, 2008.
25. Lukaski HC. Magnesium, zinc, and chromium nutrition and physical activity. Am J Clin Nutr
72: 585S-593S, 2000.
26. Lukaski HC, Bolonchuk WW, Klevay LM, Milne DB, and Sandstead HH. Maximal oxygen consumption as related to magnesium, copper and zinc nutriture. Am J Clin Nutr
37: 407-415, 1983.
27. Maughan RJ and Gleeson M. The weightlifter. In: The Biochemical Basis of Sports Performance
, Eds. RJ Maughan and M Gleeson. Oxford, NY: Oxford University Press, 2004. pp. 13-65.
28. McArdle WD, Katch FI, and Katch VL. Exercise Physiology: Energy, Nutrition, and Human Performance
(6th ed). Philadelphia, PA: Lippincott Williams and Wilkins, 2007. pp. 66-70.
29. Mclean RM. Magnesium and its therapeutic uses: A Review. Am J Med
96: 63-76, 1994.
30. Michailova A and McCulloch AD. Effects of Mg2+
, pH and PCr on cardiac excitation-metabolic coupling. Magnes Res
21: 16-28, 2008.
31. Newstead IJ and Finstad EW. The effects of magnesium supplementation on exercise performance. Clin J Sports Med
10: 195-200, 2000.
32. Potter JD and Gergely J. The calcium
and magnesium binding sites on troponin and their role in the regulation on myofibrillar adenosine triphosphatase. J Biol Chem
250: 4628-4633, 1975.
33. Potter JD, Robertson SP, and Johnson JD. Magnesium and the regulation of muscle contraction
. Fed Proc
40: 2653-2656, 1981.
34. Rayssiguier Y, Guezennec CY, and Durlach J. New experimental and clinical data on the relationship between magnesium and sport. Magnes Res
3: 93-102, 1990.
35. Schmitz C, Deason F, and Perraud A. Molecular components of vertebrate Mg2+
homeostasis regulation. Magnes Res
20: 6-18, 2007.
36. Selivanov VA, Krause S, Roca J, and Cascante M. Modelling of spatial metabolite distributions in the cardiac sarcomere. Biophys J
92: 3492-3500, 2007.
37. Skarikabad MN, Østybye KM, and BrØrs O. Increased Mg2+
influx and disruption of mitochondrial membrane potential during reoxygenation. Am J Physiol Heart Circ Physiol
281: 2113-2123, 2001.
38. Stephenson DG, Lamb GD, and Stephenson GM. Events of the excitation-contraction-relaxation (E-C-R) cycle in fast- and slow-twitch mammalian muscle fibres relevant to muscle fatigue. Acta Physiol Scand
162: 229-245, 1998.
39. Stephenson EW and Podolsky RJ. Regulation by magnesium of intracellular calcium
movement in skinned muscle fibres. J Gen Physiol
69: 1-16, 1977.
40. Swaminathan R. Magnesium metabolism and its disorders. Clin Biochem Rev
24: 27-66, 2003.
41. Tam M, Gomez S, Gonzalez-Gross M, and Marcos A. Possible roles of magnesium on the immune system. Euro J Clin Nutr
57: 1193-1197, 2003.
42. Wilborn CD, Kerksick CM, Campbell BI, Taylor LW, Marcello BM, Rasmussen CJ, Greenword MC, Almada A, and Kreider RB. Effects of zinc magnesium aspartate (ZMA) supplementation on training adaptations and markers of anabolism and catabolism. J Int Soc Sports Nutr
1: 12-20, 2004.
43. Willmore JH and Costill DL. Physiology of Sport and Exercise
(3rd ed). Champaign, IL; Human Kinetics, 2004. pp. 420-424, 456-467.