Category: Diet

Injury prevention through proper protein intake

Injury prevention through proper protein intake

Alternative medicine practices Injury prevention through proper protein intake plays a role in tissue repair and prfvention of Injury prevention through proper protein intake. Possible mediators of anabolic resistance with muscle disuse include impaired protein digestion and throygh acid absorption preventionn 3738 ], altered microvascular perfusion and amino acid uptake into muscle [ 343940 ], and impaired intracellular molecular anabolic signalling [ 233441 ]. Furthermore, creatine supplementation has been shown to counteract disorders of muscle [ 89 ]. Article PubMed Central CAS PubMed Google Scholar Wall BT, Hamer HM, de Lange A, et al.

Injury prevention through proper protein intake -

Negative energy balance will interfere with wound healing [ 48 ] and exacerbate muscle loss [ 49 , 50 ]. MPS is an energetically expensive process. It has been estimated that a well-muscled male expends ~ kcal a day on MPS even without the consideration of physical activity [ 51 ].

Given that decreased synthesis of myofibrillar proteins is the major metabolic contributor to muscle loss, if sustained, this energy deficit will result in accelerated loss of muscle mass [ 49 ].

Moreover, impaired MPS and negative energy balance, per se, will slow wound healing. Much care should be taken to ensure that sufficient energy is consumed during recovery from an injury.

Whereas, negative energy balance is clearly to be avoided, a large positive energy balance also is undesirable for optimal healing and recovery. Positive energy balance results in increased lean body mass BM in healthy humans [ 54 ].

Thus, it may be appealing to suggest a positive energy balance during immobilization, even considering a small increase in body fat. However, there is evidence that a positive energy balance actually accelerates muscle loss during inactivity, most likely via activation of systemic inflammation [ 55 ].

However, these data stem from a bed rest study, and it is not clear how much systemic inflammation is increased with limb immobility. Moreover, excess energy with reduced activity leads to decreased insulin sensitivity and alterations in muscle and adipose metabolism [ 56 ].

Therefore, careful assessment of energy balance via techniques such as indirect calorimetry during both the period of inactivity and rehabilitation may be well worthwhile. It also is possible that energy, per se, may not be the most important factor to consider.

The macronutrient composition of the energy may be an operative factor. Recent evidence suggests that oversupply of lipids decreases insulin sensitivity and impairs the response of MPS to amino acids [ 57 ].

Thus, both energy and macronutrient intake must be considered very carefully. If reduced energy intake is warranted, factors promoting satiety despite a reduced energy intake, including protein dose and type, plus low energy density choices such as vegetables need to be considered [ 58 ].

The macronutrient most prominently associated with nutrition support for injuries involving immobility is protein. Given a reduction in overall energy intake, if protein intake is kept proportional, an absolute reduction in protein intake is likely.

Clearly, insufficient protein intake will impede wound healing and increase inflammation to possibly deleterious levels [ 59 , 60 ]. Given that muscle loss results from decreased synthesis of myofibrillar proteins [ 23 ], and that the healing processes are heavily reliant on synthesis of collagen and other proteins [ 15 ], the importance of protein should be obvious.

Moreover, the reduction in protein intake, per se, may have a detrimental impact on muscle metabolism—even if the overall intake remains at or near the recommended dietary allowance 0. This disruption may be particularly evident if habitual protein intake is high, e.

A drastic decrease in protein intake results in negative nitrogen balance [ 61 ]. During negative energy balance, this loss of nitrogen is almost certainly from muscle [ 52 ]. We recently demonstrated that athletes consuming relatively high protein intakes ~2.

Thus, it may be that relatively high protein intakes, i. However, it should be considered that no direct comparison of 1.

Consequently, it is not clear if the preservation of muscle in our study was due to increasing the protein intake from habitual ~1.

Moreover, during bed rest, increasing protein intake from 1. A potential contributor to the difference between these studies is that the participants in the bed rest study were female [ 62 ].

The influence of sex on the response of muscle to disuse and protein ingestion remains to be elucidated. Nevertheless, it seems clear that appropriate evaluation of habitual protein intake that helps inform recommendations for protein intake after injury should be made.

Other factors in relation to protein should be considered in addition to the absolute amount of protein intake. The pattern of protein intake in terms of timing and amount in each meal is an important factor. The importance of protein intake stems from the resulting hyperaminoacidaemia and increased MPS [ 63 , 64 ].

In healthy, active muscle ~20—25 g 0. However, given the onset of anabolic resistance with immobility and reduced activity [ 23 , 34 , 35 ], it is likely that the amount of protein in each dose necessary to maximally stimulate MPS in immobilized muscle will be increased [ 66 ].

Moreover, the overall response of MPS throughout the day is optimized when this amount of protein is spread equally over the day [ 67 , 68 ]. This evenly spaced protein intake pattern is markedly different from the pattern habitually used by most athletes [ 69 , 70 ].

Thus, whereas the impact of meal pattern on the response of MPS during reduced activity is unknown, it seems prudent to recommend that athletes should plan their meal pattern to optimize MPS and ameliorate the loss of muscle protein.

The response of MPS to protein ingestion stems from the EAA content of the protein i. nonessential amino acids are not necessary for maximal stimulation of MPS [ 71 , 72 ]. Thus, EAA supplementation has been recommended for amelioration of muscle loss during muscle disuse following injury.

During prolonged bed rest [ 73 ] and joint immobilization [ 74 ], EAA supplementation has been shown to reduce the loss of muscle mass and strength. However, the dose of EAA may be critical. Smaller doses of EAA failed to prevent muscle loss during bed rest [ 75 ].

The volunteers in that study were in negative energy balance. So, it is unclear if the smaller dose of EAA may have been more effective during energy balance.

Moreover, unlike many other proposed interventions, there has been direct measurement of muscle loss with EAA supplementation following an injury. Dreyer et al.

Of course, it is not certain that injured athletes would experience a similar response to EAA ingestion after injury. Thus, whereas there is not a complete lack of equivocation, there is at least some evidence of efficacy of EAA supplementation during immobilization. Moreover, it is not clear if EAA supplementation is more effective than consuming whole proteins containing the same amount of EAA.

Given the cost and taste of EAA supplements, intact proteins may be preferred. The potential for EAA supplementation to ameliorate muscle loss during disuse may be attributed to the branched-chain amino acid leucine, as it has long been known to increase protein synthesis in rodent and cell models [ 77 , 78 ].

Moreover, recent evidence suggests that leucine ingestion increases MPS in healthy humans [ 79 ]. Thus, the use of leucine to ameliorate muscle loss is often touted [ 80 ].

However, the impact of leucine on human MPS and muscle loss during disuse is less clear. Leucine has been shown to restore impaired MPS in rats [ 81 , 82 ] and ameliorates muscle loss in rats during immobilization [ 83 ]. Furthermore, supplementation of branched-chain amino acids attenuated the nitrogen loss during bed rest, but did not impact MPS [ 84 ].

However, it is possible that leucine may be more effective by overcoming the resistance of muscle to anabolic stimulation. MPS was measured in the fasting state in the bed rest study [ 84 ], so there was no assessment of the impact of leucine on anabolic resistance.

In older humans, increasing the amount of leucine restored the response of MPS to protein ingestion [ 85 , 86 ]. Moreover, leucine ingestion increases the utilization of ingested amino acids for MPS [ 87 ]. Thus, leucine could play an important role in situations with limited energy and protein intake, such as with injuries.

Nevertheless, to date no study has directly investigated the response of muscle to leucine or branched-chain amino acid ingestion during a period of muscle disuse following an injury in humans. There are also potential negative effects with use of high-dose leucine supplementation.

Thus, caution is warranted prior to making recommendations for leucine supplementation during muscle disuse. Clearly, the evidence is intriguing and this intervention should be attempted in future studies.

There is a theoretical rationale for the efficacy for increased consumption of a variety of nutrients other than protein and amino acids during immobilization or reduced activity following injury.

These nutrients include, but are not limited to, creatine, omega-3 fatty acids, and antioxidants. Again it must be emphasized that deficiencies of these nutrients, and others, will impair wound healing and slow recovery.

However, evidence that supplementation of nutrients on top of an ample supply will enhance recovery from injury is scarce. Creatine supplementation is widely used to enhance muscle gains during resistance exercise training [ 88 ].

Furthermore, creatine supplementation has been shown to counteract disorders of muscle [ 89 ]. However, the evidence for use of creatine to counter muscle loss during immobility is less clear. Creatine supplementation during 2 weeks of lower-limb immobility in otherwise healthy volunteers did not lessen the loss of muscle mass or strength in healthy volunteers during 2 weeks of casting [ 90 ].

Moreover, muscle strength was not improved by creatine supplementation following total knee arthroplasty [ 91 ]. On the other hand, muscle atrophy in immobilized arm muscle was decreased with creatine supplementation [ 92 ].

Thus, it could be that arm and leg muscles respond differently to creatine supplementation during immobility.

Moreover, creatine supplementation did prevent a decrease in GLUT4 content during immobilization but increased it to a greater extent than placebo during rehabilitation [ 44 ].

Thus, despite questions about the impact on muscle atrophy, creatine may have a positive impact on the muscle oxidative impairments observed during muscle disuse [ 31 , 42 — 44 ]. During rehabilitation after immobility, creatine supplementation resulted in an increased rate of muscle growth and strength gains compared with placebo [ 90 ].

Thus, the efficacy of creatine supplementation for augmentation of muscle hypertrophy seems to be a consistent finding, but results of investigations on creatine and muscle atrophy are more equivocal.

Omega-3 fatty acids n-3FA also have received considerable attention in the context of nutritional support for injuries. In many cases, this attention is related to the anti-inflammatory and immunomodulatory properties of n-3FA [ 93 , 94 ].

High levels of n-3FA are found in many foods, particularly some cold-water dwelling fish e. mackerel, salmon. Thus, fish oil supplementation is often touted for reduction of inflammation. Supplementation with n-3FA certainly may be important if inflammation is excessive or prolonged [ 93 ].

However, as mentioned previously, careful consideration of the use of anti-inflammatory nutrients or drugs is necessary given the importance of the inflammatory response for wound healing [ 18 — 20 ]. There is evidence of impaired wound healing with n-3FA supplementation [ 95 , 96 ].

Thus, an automatic recommendation of n-3FA supplementation for all injuries does not seem wise. Another potential property of n-3FA that may have relevance for injuries resulting in immobilization or reduced activity has recently been investigated.

Rats fed high amounts of fish oil during hind limb immobilization demonstrated less muscle loss than those rats on high corn oil diets [ 97 ]. Moreover, 8 weeks of fish oil supplementation increased the response of MPS to hyperaminoacidaemia and hyperinsulinaemia in both older [ 98 ] and younger volunteers [ 99 ].

The efficacy for fish oil in this context is thought to be due to changes in the muscle membrane lipid composition in relation to intracellular anabolic signalling [ 98 — ]. This preliminary evidence suggests that fish oil supplementation could play a role in the amelioration of muscle loss with disuse.

Then again, high fish oil diets inhibited recovery of muscle mass during recovery from hind limb suspension in rodents [ ]. Taken together, it seems that whereas high fish oil n-3FA consumption may ameliorate muscle loss during a catabolic situation, it does not seem to be effective to enhance muscle hypertrophy.

Moreover, the appropriate dose for injured humans has not been established. Thus, wholesale recommendations for fish oil supplementation during immobilization must be considered premature and caution is warranted.

There is a clear association of many micronutrients, such as zinc, vitamin C, vitamin A and others , with various aspects of wound healing and recovery from injury, including muscle disuse.

For example, vitamin C is associated with hydroxyproline synthesis necessary for collagen formation. For most micronutrients the story is similar, i.

deficiencies should be avoided, but supplementation above sufficiency does not appear warranted. Sufficient calcium and vitamin D during healing from fractures is important for optimal bone formation.

Moreover, there is an association of low vitamin D status with impaired recovery from knee surgery [ ]. However, there is no clear evidence for the necessity of supranormal micronutrient intakes during recovery from injury [ 59 ].

Oxidative damage is often a concern immediately following an injury. Oxidative damage is thought to be a contributing factor for muscle loss, primarily by increasing MPB [ ]. Thus, antioxidant compounds, including n-3FA, have been commonly recommended to improve healing and recovery [ 60 , ].

Antioxidant supplementation in rodent models results in decreased oxidative stress, but equivocal results in terms of muscle loss with immobility [ ]. In high doses, there does seem to be some impact of antioxidant supplementation on muscle loss in rodents. However, equivalent doses likely would be problematic and potentially toxic if taken by humans [ ].

Lower doses that might be better tolerated tend not to be as effective. In one human study, vitamin C and E supplementation failed to influence recovery of muscle dysfunction following knee surgery [ ]. However, vitamin C status prior to supplementation was correlated with improvements in muscle function.

Thus, taken together, these results suggest that sufficient antioxidant intake is important for optimal recovery, but supplementation on top of sufficiency is unnecessary if nutrient status is adequate.

Not all injuries require limb immobilization. So, even if training is curtailed or reduced, muscle loss may be less and the metabolic consequences might not be as severe.

There is also evidence that some injuries might have particular nutritional requirements. Thus, a brief discussion of what little is known about nutrition to support a few selected types of injuries seems warranted.

Traumatic brain injuries TBI in athletes are attracting an increasing amount of attention and scrutiny. In contact sports, such as rugby and American football, these injuries are increasingly common. TBI also are common in other contact sports and in military personnel.

Diagnosis of TBI is being treated much more seriously than in earlier times. Moreover, increasing awareness of long-term consequences of TBI, particularly if there are repetitive incidences, is forthcoming.

Significant brain abnormalities were reported in a group of retired American football players [ ]. In addition, retired American football players over the age of 50 with a history of repetitive TBI demonstrated rates of cognitive impairment five times that of retirees without a history of TBI [ ].

The pathogenic process leading to these problems is related to the secondary phase of recovery following TBI, which includes processes such as neuroinflammation, increased excitatory amino acids, free radicals and ion imbalances that lead to axonal and neuronal damage [ ].

However, there still are no approved therapies to treat TBI or the underlying processes of TBI and enhance recovery from TBI [ ]. Thus, it seems clear that a nutritional intervention that could ameliorate the consequences of TBI and improve cognitive and neuromuscular function would be valuable for active and retired athletes.

Nutritional treatments for TBI-related problems centre around antioxidants and anti-inflammatory agents. Virtually all of the research to date is based on rodent models.

One study showed that rats eating a diet supplemented with curcumin, an anti-inflammatory compound, had decreased levels of factors found to increase following TBI. These factors include oxidized proteins, normalized brain-derived neurotrophic factor BDNF , and molecules in the pathogenic pathway downstream of BDNF [ ].

Moreover, cognitive function was improved in the rats consuming supplemental curcumin. The efficacy of n-3FA for amelioration of TBI-related damage also has been investigated. Animal studies consistently demonstrated that both prophylactic and therapeutic use of n-3FA decreases axonal and neuronal damage, inflammation, and apoptosis and normalizes BDNF and neurotransmitter levels [ — ].

Moreover, these changes lead to improved cognitive function. Thus, there seems to be promising evidence of the efficacy of curcumin and, especially, n-3FA for recovery from TBI in rodents. However, it is not clear if the efficacy of n-3FA for TBI in rodents can be generalized to humans.

The promising nature of data generated from animal studies suggests that n-3FA may be an effective nutrient to counter the negative long-term effects of TBI. To date, no study has been published examining this question in humans.

However, clinical trials are under way after the US Institute of Medicine recommended further investigation in There have been a small number of case studies suggesting that high-dose n-3FA may improve acute outcomes after TBI [ , ].

Moreover, an open-design study demonstrated that a nutritional intervention, including n-3FA, improved cognitive function in retired American football players with a history of TBI [ ]. However, the players in this study participated in lifestyle interventions in addition to consuming a supplement that contained n-3FA and several other ingredients.

Thus, the contribution of the n-3FA, other nutrients, or the lifestyle intervention to the improvement in cognitive function cannot be definitively identified. A follow-up, double-blind, placebo-controlled study determined that nutritional supplementation, including n-3FA, resulted in improved neuropsychological function in healthy volunteers [ ].

Again, determination of the precise role of n-3FA in this improvement is not possible given the large number of nutrients consumed in the supplement. Therefore, whereas preclinical and preliminary data on the impact of n-3FA for recovery from TBI are promising, solid recommendations to include n-3FA in a treatment regimen cannot be made, at least until the results of the ongoing clinical trials are reported.

Common exercise-induced injuries include those with damaged muscle and other soft tissues. These injuries likely will not necessarily result in immobilization of the limb, but will require a reduction in activity of the injured limb—if for no other reason than that the injury is painful.

A common model used to examine muscle injuries is an eccentric exercise model. In this model, the volunteers perform a number of eccentric—force production during muscle lengthening—contractions.

Loss of muscle function, increases in blood proteins associated with muscle damage, and increased pain result from these types of situations [ — ].

Several methods have been used to perform the eccentric contractions, including eccentric resistance exercise, dynamometers, stepping down from a bench or block and downhill running [ ]. Many investigations have focused on nutrients that may be useful in recovery from these intense exercise situations.

Many nutrients have been touted to alleviate symptoms associated with muscular injuries using these eccentric exercise models. A complete examination of this literature is beyond the scope of this review. Interested readers are referred to recent reviews [ , — ].

Overall, the nutrients most often associated with alleviation of pain and increased recovery from eccentric exercise include protein and amino acids, anti-inflammatory compounds and antioxidants. The available information does not readily lend itself to a solid conclusion for any of these nutritional countermeasures to the deleterious effects of muscle injury.

Moreover, it is not certain that this eccentric exercise model is an appropriate way to evaluate soft tissue injuries in exercisers. Nonetheless, many studies have attempted to assess nutritional interventions to enhance recovery after exercise-induced muscle damage and many recommendations are commonly made.

Protein and amino acids probably have been the most widely studied nutrients in the context of muscle injuries. Any positive impact on recovery may be due to the branched-chain amino acid content of the protein [ , ]. The impact of protein has been attributed to increased MPS to enhance repair [ ].

However, changes in indices of muscle damage occur in the order of hours [ , , ]. Given that the turnover of structural muscle proteins is quite slow [ 26 , ], it is difficult to accept this attribution. Moreover, other studies do not report an effect of protein or amino acids [ , ].

The variable results are likely due to varying supplementation patterns, types of exercise, and other design considerations [ ]. Finally, many of the volunteers in the studies were untrained and generalizability of the results to an athletic population may be questioned.

Thus, this equivocality makes it difficult to conclude that protein or amino acid supplementation enhances recovery from muscle injury, particularly for injured athletes.

In fact, a recent systematic review concluded that the evidence for alleviation of symptoms of muscle injury by protein and amino acids is lacking [ ]. Provision of antioxidants and anti-inflammatory agents to alleviate symptoms of muscle damage also has been a popular strategy.

However, at best, as with protein, the literature can only be considered equivocal. The interested reader is referred to recent reviews [ , ] for a more detailed examination of these studies.

Clearly, given the disparity in the types of exercise, supplementation patterns, and other methodological issues, very little insight into nutrition for muscle injuries can be gleaned from exercise-induced muscle damage studies.

Hence, it is not possible to make solid recommendations regarding nutritional countermeasures to exercise-induced muscle damage and injuries. Thus far, the focus of the discussion has been on what nutrients to consume. However, consideration of what to avoid also should be made.

As mentioned above, the most obvious nutrition consideration is to avoid nutrient deficiencies. This consideration was discussed earlier in the context of inactivity and immobilization and should be the number one overriding priority for nutrition related to injury.

Additionally, nutrient excess should be avoided. Excess energy could lead to increased total and fat mass, particularly if activity is dramatically reduced. In light of the preliminary evidence for the efficacy of n-3FA in the context of several different injuries that has been discussed, careful consideration of the dose should be made before advising an injured athlete.

Excess n-3FA consumption could excessively depress the inflammatory response leading to impaired wound healing [ 95 , 96 ]. However, studies determining the appropriate or excessive doses in humans have not been conducted.

Thus, caution is justified. One obvious nutrient that is best avoided or at least ingested in only small amounts is alcohol.

Alcohol ingestion impairs MPS in rats [ ], as well as the response of MPS to exercise in humans [ ]. Moreover, it is clear that alcohol impairs wound healing, likely by reducing the inflammatory response [ ], and increases muscle loss during immobilization in rats [ ].

Thus, whereas it may be self-evident, it is worth emphasizing that limited alcohol ingestion during recovery is important. So, as tempting as it may be to indulge in alcohol to drown sorrows or diminish pain, only small amounts, if any, should be imbibed.

In summary, there is much still to be learned about the best nutritional strategy to enhance recovery from exercise-induced injuries. There are claims for the efficacy of many nutrients, yet direct evidence is sorely lacking. Nutritional status and energy requirements should be assessed throughout recovery and nutrient intake adjusted accordingly.

Deficiencies, particularly those of energy, protein, and micronutrients, must be avoided. Higher protein intakes ~2—2. There is promising—albeit it must be considered preliminary—evidence for the efficacy of other nutrients in certain situations. Leucine, n-3FA, curcumin, and others have been demonstrated to be beneficial in rodent studies, but information from studies on injured humans is yet forthcoming.

In some situations, higher intakes of these nutrients may do harm. Moreover, even if they are efficacious for injured humans, there is no information regarding the optimal dose of these nutrients.

Thus, caution is warranted before recommendations for wholesale use of these nutrients by injured athletes are made. Even if the benefit is uncertain, it may be worth trying if no risks can be identified.

Otherwise, if there is a risk of doing harm with use of a particular nutrient, then perhaps that nutrient should be avoided. As always, the basis of nutritional strategy for an injured exerciser should be a well-balanced diet based on a diet of whole foods from nature or foods made from ingredients from those foods that are minimally processed [ ].

Whereas this advice may be considered mundane, boring, and lacking insight, it seems still to be the best course of action.

Jacobsson J, Timpka T, Kowalski J, et al. Subsequent injury during injury recovery in elite athletics: cohort study in Swedish male and female athletes.

Br J Sports Med. Article Google Scholar. Tipton KD. Nutrition for acute exercise-induced injuries. Ann Nutr Metab. Article CAS Google Scholar. Dietary strategies to attenuate muscle loss during recovery from injury.

Nestle Nutr Inst Workshop Ser. Article PubMed Google Scholar. Wall BT, Morton JP, van Loon LJ. Strategies to maintain skeletal muscle mass in the injured athlete: nutritional considerations and exercise mimetics.

Eur J Sport Sci. Malliaropoulos N, Papacostas E, Kiritsi O, et al. Posterior thigh muscle injuries in elite track and field athletes. Am J Sports Med. Jones SW, Hill RJ, Krasney PA, et al. Disuse atrophy and exercise rehabilitation in humans profoundly affects the expression of genes associated with the regulation of skeletal muscle mass.

FASEB J. CAS PubMed Google Scholar. Bostick GP, Jomha NM, Suchak AA, et al. Factors associated with calf muscle endurance recovery 1 year after achilles tendon rupture repair. J Orthop Sports Phys Ther.

Silder A, Heiderscheit BC, Thelen DG, et al. MR observations of long-term musculotendon remodeling following a hamstring strain injury. Skeletal Radiol. Article PubMed Central PubMed Google Scholar.

Snow BJ, Wilcox JJ, Burks RT, et al. Evaluation of muscle size and fatty infiltration with MRI nine to eleven years following hamstring harvest for ACL reconstruction.

J Bone Joint Surg Am. Phillips SM. The science of muscle hypertrophy: making dietary protein count. Proc Nutr Soc. Article CAS PubMed Google Scholar. Phillips SM, Hartman JW, Wilkinson SB. Dietary protein to support anabolism with resistance exercise in young men.

J Am Coll Nutr. Tipton KD, Ferrando AA. Improving muscle mass: response of muscle metabolism to exercise, nutrition and anabolic agents. Essays Biochem. Tipton KD, Phillips SM.

Dietary protein for muscle hypertrophy. Tipton KD, Witard OC. Protein requirements and recommendations for athletes: relevance of ivory tower arguments for practical recommendations. Clin Sports Med. Lorenz HP, Longaker MT. Wounds: Biology, Pathology, and Management.

In: Norton JA, Barie PS, Bollinger RR, Chang AE, Lowry SF, Mulvhill SJ, et al. Surgery: basic science and clinical evidence.

New York: Spring Publishing Company; Chapter Google Scholar. Stechmiller JK. Understanding the role of nutrition and wound healing. Nutr Clin Pract. Lin E, Kotani JG, Lowry SF. Nutritional modulation of immunity and the inflammatory response.

Lopez HL. Nutritional interventions to prevent and treat osteoarthritis. Part II: focus on micronutrients and supportive nutraceuticals. Part I: focus on fatty acids and macronutrients.

Galland L. Diet and inflammation. Ferrando AA, Lane HW, Stuart CA, et al. Prolonged bed rest decreases skeletal muscle and whole body protein synthesis. Am J Physiol. Ferrando AA, Stuart CA, Brunder DG, et al. Magnetic resonance imaging quantitation of changes in muscle volume during 7 days of strict bed rest.

Aviat Space Environ Med. Glover EI, Phillips SM, Oates BR, et al. Immobilization induces anabolic resistance in human myofibrillar protein synthesis with low and high dose amino acid infusion. J Physiol. Article PubMed Central CAS PubMed Google Scholar. Wall BT, Dirks ML, Snijders T, et al.

Substantial skeletal muscle loss occurs during only 5 days of disuse. Acta Physiol. de Boer MD, Maganaris CN, Seynnes OR, et al. Time course of muscular, neural and tendinous adaptations to 23 day unilateral lower-limb suspension in young men.

Article PubMed Central PubMed CAS Google Scholar. Tipton KD, Borsheim E, Wolf SE, et al. Acute response of net muscle protein balance reflects h balance after exercise and amino acid ingestion. CAS Google Scholar. Reich KA, Chen YW, Thompson PD, et al.

Forty-eight hours of unloading and 24 h of reloading lead to changes in global gene expression patterns related to ubiquitination and oxidative stress in humans.

J Appl Physiol. Gibson JN, Halliday D, Morrison WL, et al. Decrease in human quadriceps muscle protein turnover consequent upon leg immobilization. Clin Sci. Tesch PA, von Walden F, Gustafsson T, et al.

Skeletal muscle proteolysis in response to short-term unloading in humans. Urso ML, Scrimgeour AG, Chen YW, et al. Analysis of human skeletal muscle after 48 h immobilization reveals alterations in mRNA and protein for extracellular matrix components. Abadi A, Glover EI, Isfort RJ, et al.

Limb immobilization induces a coordinate down-regulation of mitochondrial and other metabolic pathways in men and women.

PLoS One. Glover EI, Yasuda N, Tarnopolsky MA, et al. Little change in markers of protein breakdown and oxidative stress in humans in immobilization-induced skeletal muscle atrophy. Appl Physiol Nutr Metab.

Greenhaff PL, Karagounis LG, Peirce N, et al. Disassociation between the effects of amino acids and insulin on signaling, ubiquitin ligases, and protein turnover in human muscle. Drummond MJ, Dickinson JM, Fry CS, et al. Bed rest impairs skeletal muscle amino acid transporter expression, mTORC1 signaling, and protein synthesis in response to essential amino acids in older adults.

Wall BT, Snijders T, Senden JM, et al. Disuse impairs the muscle protein synthetic response to protein ingestion in healthy men. J Clin Endocrinol Metab. Breen L, Stokes KA, Churchward-Venne TA, et al. Pennings B, Boirie Y, Senden JM, et al. Whey protein stimulates postprandial muscle protein accretion more effectively than do casein and casein hydrolysate in older men.

Am J Clin Nutr. Pennings B, Koopman R, Beelen M, et al. Exercising before protein intake allows for greater use of dietary protein-derived amino acids for de novo muscle protein synthesis in both young and elderly men. Rasmussen BB, Fujita S, Wolfe RR, et al. Insulin resistance of muscle protein metabolism in aging.

PubMed Central CAS PubMed Google Scholar. Timmerman KL, Lee JL, Dreyer HC, et al. Insulin stimulates human skeletal muscle protein synthesis via an indirect mechanism involving endothelial-dependent vasodilation and mammalian target of rapamycin complex 1 signaling.

Cuthbertson D, Smith K, Babraj J, et al. Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle.

Richter EA, Kiens B, Mizuno M, et al. Insulin action in human thighs after one-legged immobilization. Stuart CA, Shangraw RE, Prince MJ, et al.

Bed-rest-induced insulin resistance occurs primarily in muscle. Effect of oral creatine supplementation on human muscle GLUT4 protein content after immobilization. Bergouignan A, Momken I, Schoeller DA, et al. Regulation of energy balance during long-term physical inactivity induced by bed rest with and without exercise training.

McBeath AA, Bahrke M, Balke B. Efficiency of assisted ambulation determined by oxygen consumption measurement. Waters RL, Campbell J, Perry J. Energy cost of three-point crutch ambulation in fracture patients.

J Orthop Trauma. Frankenfield D. Energy expenditure and protein requirements after traumatic injury. Biolo G, Ciocchi B, Stulle M, et al. Calorie restriction accelerates the catabolism of lean body mass during 2 wk of bed rest. Mettler S, Mitchell N, Tipton KD.

Increased protein intake reduces lean body mass loss during weight loss in athletes. Med Sci Sports Exerc. Wolfe RR. The underappreciated role of muscle in health and disease. Pasiakos SM, Vislocky LM, Carbone JW, et al.

Acute energy deprivation affects skeletal muscle protein synthesis and associated intracellular signaling proteins in physically active adults. J Nutr. Areta JL, Burke LM, Camera DM, et al.

Reduced resting skeletal muscle protein synthesis is rescued by resistance exercise and protein ingestion following short-term energy deficit. Forbes GB, Brown MR, Welle SL, et al. Deliberate overfeeding in women and men: energy cost and composition of the weight gain. Br J Nutr.

Biolo G, Agostini F, Simunic B, et al. Positive energy balance is associated with accelerated muscle atrophy and increased erythrocyte glutathione turnover during 5 wk of bed rest. Walhin JP, Richardson JD, Betts JA, et al.

Exercise counteracts the effects of short-term overfeeding and reduced physical activity independent of energy imbalance in healthy young men. Stephens FB, Chee C, Wall BT, et al. Lipid induced insulin resistance is associated with an impaired skeletal muscle protein synthetic response to amino acid ingestion in healthy young men.

Rebello CJ, Liu AG, Greenway FL, et al. Dietary strategies to increase satiety. Adv Food Nutr Res. Arnold M, Barbul A. Nutrition and wound healing. Plast Reconstr Surg. Demling RH. Nutrition, anabolism, and the wound healing process: an overview.

PubMed Central PubMed Google Scholar. Quevedo MR, Price GM, Halliday D, et al. Nitrogen homoeostasis in man: diurnal changes in nitrogen excretion, leucine oxidation and whole body leucine kinetics during a reduction from a high to a moderate protein intake.

Trappe TA, Burd NA, Louis ES, et al. Influence of concurrent exercise or nutrition countermeasures on thigh and calf muscle size and function during 60 days of bed rest in women. Biolo G, Tipton KD, Klein S, et al. An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein.

Witard OC, Jackman SR, Breen L, et al. Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. Moore DR, Robinson MJ, Fry JL, et al. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men.

Article PubMed CAS Google Scholar. Yang Y, Breen L, Burd NA, et al. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men.

Areta JL, Burke LM, Ross ML, et al. Timing and distribution of protein ingestion during prolonged recovery from resistance exercise alters myofibrillar protein synthesis. Mamerow MM, Mettler JA, English KL, et al. Dietary protein distribution positively influences h muscle protein synthesis in healthy adults.

Burke LM, Slater G, Broad EM, et al. Eating patterns and meal frequency of elite Australian athletes. Int J Sport Nutr Exerc Metab. PubMed Google Scholar. Garcia-Roves PM, Fernandez S, Rodriguez M, et al. Eating pattern and nutritional status of international elite flatwater paddlers.

Tipton KD, Ferrando AA, Phillips SM, et al. Postexercise net protein synthesis in human muscle from orally administered amino acids. Tipton KD, Gurkin BE, Matin S, et al. Nonessential amino acids are not necessary to stimulate net muscle protein synthesis in healthy volunteers.

J Nutr Biochem. Paddon-Jones D, Sheffield-Moore M, Urban RJ, et al. Essential amino acid and carbohydrate supplementation ameliorates muscle protein loss in humans during 28 days bedrest. Bostock EL, Pheasey CM, Morse CI, et al. Effects of essential amino acid supplementation on muscular adaptations to 3 weeks of combined unilateral glenohumeral and radiohumeral joints immobilisation.

J Athl Enhanc. doi: Brooks N, Cloutier GJ, Cadena SM, et al. Resistance training and timed essential amino acids protect against the loss of muscle mass and strength during 28 days of bed rest and energy deficit.

Dreyer HC, Strycker LA, Senesac HA, et al. Essential amino acid supplementation in patients following total knee arthroplasty. J Clin Invest. Kimball SR. Regulation of global and specific mRNA translation by amino acids. Kimball SR, Jefferson LS. Role of amino acids in the translational control of protein synthesis in mammals.

Semin Cell Dev Biol. Wilkinson DJ, Hossain T, Hill DS, et al. To help prevent injury fuel up with both carbohydrate and protein hours before your workout and within 30 minutes after. Combination pre-workout meal may include a smoothie made with low fat milk and fruit. For a convenient recovery snack, chocolate milk fits the bill.

A dehydrated joint is more susceptible to tears and injuries. Dehydration creates added stress on the body including increased internal temperature, heart rate, sweat rate, early fatigue and loss of balance and mental focus. To help prevent dehydration you should practice drinking fluids before, during and after your exercise session.

Be sure to drink water throughout your day not just around physical activity! Water, fruit juice, smoothies and milk all count towards your fluid intake.

Preventing stress fractures are critical in preventing other exercise-related injuries. Getting adequate amounts of calcium and vitamin D every day helps develop and maintain strong bones.

Studies have shown that athletes who consume diets low in calcium tend to have lower bone mineral density BMD and increased risk for stress fractures. Great dietary sources of calcium and vitamin D are dairy products and fortified foods such as orange juice.

Dietary fats provide essential fatty acids that the body cannot make on its own. Essential fatty acids like omega-3 fatty acids are needed to make and repair cell membrane, and are good for the heart, a source of energy, lubricating joints and tissues and reducing inflammation in the body.

Cold water fish salmon, mackerel, and sardines , ground flaxseed and walnuts are a few good dietary sources to include in your daily training diet. Vitamin C plays a role in tissue repair and formation of collagen. Collagen provides strength and flexibility for ligaments, tendons and is necessary to hold bone together.

Vitamin E helps protect tissues and organs from damage caused by free radicals. The combination of these vitamins is thought to minimize damage from exercise and therefore help with recovery from your workout or training session.

Nutrition is one method to counter the negative Anti-inflammatory foods of an exercise-induced injury. Deficiencies of energy, prktein Injury prevention through proper protein intake throough nutrients should be avoided. Claims for the hhrough of Propsr other nutrients following injuries are rampant, but the evidence is equivocal. The results of an exercise-induced injury may vary widely depending on the nature of the injury and severity. Injuries typically result in cessation, or at least a reduction, in participation in sport and decreased physical activity. Limb immobility may be necessary with some injuries, contributing to reduced activity and training. Injury prevention through proper protein intake


Nutrition for Performance and Injury Prevention

Author: Bagrel

1 thoughts on “Injury prevention through proper protein intake

Leave a comment

Yours email will be published. Important fields a marked *

Design by