Determining the Arterial Occlusion Pressure for Blood Flow Restriction: Pulse Oximeter as a New Method Compared With a Handheld Doppler.

ABSTRACT: Lima-Soares, F, Pessoa, KA, Torres Cabido, CE, Lauver, J, Cholewa, J, Rossi, FE, and Zanchi, NE. Determining the arterial occlusion pressure for blood flow restriction: Pulse oximeter as a new method compared with a handheld Doppler. J Strength Cond Res 36(4): 1120-1124, 2022-In laboratorial and clinical settings, the use of Doppler ultrasound equipment has been considered the gold standard method to determine arterial occlusion pressure (AOP). However, the use of Doppler equipment is inherently limited to the technical expertise needed to perform AOP measurements. To overcome the technical difficulties of the use of Doppler equipment use in the determination of AOP, a simpler and less subjective methodology would be helpful for blood flow restriction (BFR) practitioners. In this regard, portable pulse oximetry has been largely used in clinical practice for measuring systolic pressures, as well as loss or recovery of pulse, with results similar to those observed with the use of Doppler equipment. For such purposes, the AOP from young male and female subjects was evaluated after different body positions (standing, seated, and supine positions). Loss of capillary blood flow or AOP was readily determined by simple visual inspection for the pulse oximeter and loss of sound for the Doppler equipment. The results presented herein strongly suggest the use of the portable pulse oximetry equipment as reliable, when compared with the handheld Doppler (seated k = 0.962, standing k = 0.845, and supine k = 0.963 and seated rs = 0.980, standing rs = 0.958, and supine rs = 0.955). Because AOP measurement by pulse oximetry is relatively easier to perform and financially more accessible than handheld Doppler equipment, BFR practitioners may benefit from this new methodology to measure AOP, thus determining individualized restriction pressures.

Acute Responses to Cycling Exercise With Blood Flow Restriction During Various Intensities.

ABSTRACT: Lauver, JD, Moran, A, Guilkey, JP, Johnson, KE, Zanchi, NE, and Rotarius, TR. Acute responses to cycling exercise with blood flow restriction during various intensities. J Strength Cond Res 36(12): 3366-3373, 2022-The purpose of this study was to investigate the acute physiological responses during cycling at various intensities with blood flow restriction (BFR). Subjects ( N = 9; V̇ o2 peak = 36.09 ± 5.80 ml·kg -1 ·min -1 ) performed 5 protocols: high-intensity (HIGH), control (CON-90), 90% of ventilatory threshold (VT) work rate with BFR (90-BFR), 70% of VT with BFR (70-BFR), and 30% V̇ o2 peak with BFR (30-BFR). Protocols consisted of five 2-minute work intervals interspersed with 1-minute recovery intervals. Blood flow restriction pressure was 80% of limb occlusion pressure. V̇ o2 , muscle excitation, tissue oxygen saturation (StO 2 ), discomfort, and level of perceived exertion (RPE) were assessed. Muscle excitation was higher during HIGH (302.9 ± 159.9 %BSL [baseline]) compared with 70-BFR (99.7 ± 76.4 %BSL) and 30-BFR (98.2 ± 70.5 %BSL). StO 2 was greater during 90-BFR (40.7 ± 12.5 ∆BSL), 70-BFR (34.4 ± 15.2 ∆BSL), and 30-BFR (31.9 ± 18.7 ∆BSL) compared with CON-90 (4.4 ± 11.5 ∆BSL). 90-BFR (39.6 ± 12.0 ∆BSL) resulted in a greater StO 2 -Avg compared with HIGH (20.5 ± 13.8 ∆BSL). Also, HIGH (23.68 ± 5.31 ml·kg -1 ·min -1 ) resulted in a greater V̇ o2 compared with 30-BFR (15.43 ± 3.19 ml·kg -1 ·min -1 ), 70-BFR (16.65 ± 3.26 ml·kg -1 ·min -1 ), and 90-BFR (18.28 ± 3.89 ml·kg -1 ·min -1 ); 90-BFR (intervals: 4 = 15.9 ± 2.3; intervals: 5 = 16.4 ± 2.5) resulted in a greater RPE compared with 30-BFR (intervals: 4 = 13.3 ± 1.4; intervals: 5 = 13.7 ± 1.7) during intervals 4 and 5. These results suggest that when adding BFR to various intensities of aerobic exercise, consideration should be given to peak work and VT to provide a balance between high local physiological stress and perceptual responses.

Acute Capsaicin Analog Supplementation Improves 400 M and 3000 M Running Time-Trial Performance.

OBJECTIVES: Performance in running-based sport depends on the ability to perform repetitive high intensity muscle contractions. Previous studies have shown that capsaicin analog (CAP) (i.e. Capsiate) supplementation may improve this performance. The purpose of this study was to investigate the acute effect of CAP supplementation on short (400 m) and middle distance (3000 m) running time-trial performance, maximum heart rate (HR), and rate of perceived exertion (RPE). METHODS: Twelve physically active men completed four randomized, double-blind trials: CAP condition (12 mg) or a placebo condition. Forty-five minutes after supplementation, the participants performed a 400- or 3000-meter running time trial. Time (in seconds) was recorded. HR was analyzed at rest and immediately post-exercise, and RPE was collected immediately after exercise. RESULTS: For both the 400 m time-trial (CAP = 66.4 + 4.2 sec vs Placebo = 67.1 + 4.8 sec, p = 0.046) and the 3000 m time-trial (CAP = 893.9 ± 46.8 sec vs Placebo = 915.2 ± 67.6 sec, p = 0.015), the time in seconds was significantly less in the CAP compared to placebo conditions. There were no statistically significant differences for HR and RPE in any condition. CONCLUSION: In summary, acute CAP supplementation improved 400 m and 3000 m running time-trial performance in a distance-dependent way but without modifying the HR and RPE.

Aerobic exercise, but not metformin, prevents reduction of muscular performance by AMPk activation in mice on doxorubicin chemotherapy.

Doxorubicin (DOX) is a chemotherapy agent widely used in clinical practice, and it is very efficient in tumor suppression, but the use of DOX is limited by a strong association with the development of severe muscle atrophy and cardiotoxicity effects. Reversion or neutralization of the muscular atrophy can lead to a better prognosis. Recent studies have proposed that the negative effect of DOX on skeletal muscle is linked to its inhibition of AMP-activated protein kinase (AMPk), a key mediator of cellular metabolism. On the basis of this, our goal was to evaluate if aerobic exercise or metformin treatment, activators of AMPk, would be able to attenuate the deleterious effects on skeletal muscle induced by the DOX treatment. C57BL6 mice received either saline (control) or DOX (2.5 mg/kg body weight) intraperitoneally, twice a week. The animals on DOX were further divided into groups that received adjuvant treatment in the form of moderate aerobic physical exercise (DOX+T) or metformin gavage (300 mg/body weight/day). Body weight, metabolism, distance run, muscle fiber cross-sectional area (CSA), and protein synthesis and degradation were assessed. We demonstrated that aerobic training, but not metformin, associated with DOX increased the maximal aerobic capacity without changing muscle mass or fiber CSA, rescuing the muscle fatigue observed with DOX treatment alone. This improvement was associated with AMPk activation, thus surpassing the negative effects of DOX on muscle performance and bioenergetics. In conclusion, aerobic exercise increases AMPk activation and improved the skeletal muscle function, reducing the side effects of DOX.

Impact of Short and Moderate Rest Intervals on the Acute Immunometabolic Response to Exhaustive Strength Exercise: Part I.

The purpose of this study was to verify the influence of the short and moderate intervals of recovery in response to an acute bout of exhaustive strength exercise on performance, inflammatory, and metabolic responses in healthy adults. Eight healthy subjects (age = 24.6 ± 4.1 years) performed 2 randomized sequences: short = 70% of 1 repetition maximum (1RM) with 30 seconds of rest between sets; moderate = 70% of 1RM with 90 seconds of rest between sets. All sequences of exercises were performed over 4 sets until movement failure in the squat and bench press exercises, respectively. The total number of repetitions performed was recorded for each set of each exercise for all sequences. The percentages of fat mass and fat-free mass were estimated by dual-energy x-ray absorptiometry. Glucose, tumor necrosis factor-α, interleukin (IL)-6, IL-10, and nonester fatty acid were assessed, at baseline, immediately after exercise, after 15 and 30 minutes. When compared with the maximum number of repetitions and the total weight lifted, there was a statistically significant decrease after both intervals. The only statistically significant decreases over time occurred at the post-15 minutes assessment of the IL-6 and glucose when a moderate interval of recovery was performed. When comparing the alterations between the pools (the mean of the cluster of all periods in each variable), there was a statistically significant increase on the IL-6 and IL-10 when a moderate interval of recovery was performed again, however, not considering a statistical difference on the IL-10. Thus, we concluded that different interval of recovery in response to exhaustive strength exercise decreases performance but in only moderate intervals, it is associated with inflammatory and metabolic response.

ß-Hydroxy-ß-methylbutyrate free acid reduces markers of exercise-induced muscle damage and improves recovery in resistance-trained men.

The purpose of the present study was to determine the effects of short-term supplementation with the free acid form of b-hydroxyb-methylbutyrate (HMB-FA) on indices of muscle damage, protein breakdown, recovery and hormone status following a high-volume resistance training session in trained athletes. A total of twenty resistance-trained males were recruited to participate in a high-volume resistance training session centred on full squats, bench presses and dead lifts. Subjects were randomly assigned to receive either 3 g/d of HMB-FA or a placebo. Immediately before the exercise session and 48 h post-exercise, serum creatine kinase (CK), urinary 3-methylhistadine (3-MH), testosterone, cortisol and perceived recovery status (PRS) scale measurements were taken. The results showed that CK increased to a greater extent in the placebo (329%) than in the HMB-FA group (104%) (P»0·004, d » 1·6). There was also a significant change for PRS, which decreased to a greater extent in the placebo (9·1 (SEM 0·4) to 4·6 (SEM 0·5)) than in the HMB-FA group (9·1 (SEM 0·3) to 6·3 (SEM 0·3)) (P»0·005, d » 20·48). Muscle protein breakdown, measured by 3-MH analysis, numerically decreased with HMB-FA supplementation and approached significance (P»0·08, d » 0·12). There were no acute changes in plasma total or free testosterone, cortisol or C-reactive protein. In conclusion, these results suggest that an HMB-FA supplement given to trained athletes before exercise can blunt increases in muscle damage and prevent declines in perceived readiness to train following a high-volume, muscle-damaging resistance-training session.

Exercise intensity modulation of hepatic lipid metabolism.

Lipid metabolism in the liver is complex and involves the synthesis and secretion of very low density lipoproteins (VLDL), ketone bodies, and high rates of fatty acid oxidation, synthesis, and esterification. Exercise training induces several changes in lipid metabolism in the liver and affects VLDL secretion and fatty acid oxidation. These alterations are even more conspicuous in disease, as in obesity, and cancer cachexia. Our understanding of the mechanisms leading to metabolic adaptations in the liver as induced by exercise training has advanced considerably in the recent years, but much remains to be addressed. More recently, the adoption of high intensity exercise training has been put forward as a means of modulating hepatic metabolism. The purpose of the present paper is to summarise and discuss the merit of such new knowledge.

Effects of leucine supplementation and resistance exercise on dexamethasone-induced muscle atrophy and insulin resistance in rats.

OBJECTIVE: We aimed to evaluate the effects of resistance exercise (RE) and leucine (LEU) supplementation on dexamethasone (DEXA)-induced muscle atrophy and insulin resistance. METHODS: Male Wistar rats were randomly divided into DEXA (DEX), DEXA + RE (DEX-RE), DEXA + LEU (DEX-LEU), and DEXA + RE + LEU (DEX-RE-LEU) groups. Each group received DEXA 5 mg · kg(-1) · d(-1) for 7 d from drinking water and were pair-fed to the DEX group; LEU-supplemented groups received 0.135 g · kg(-1) · d(-1) through gavage for 7 d; the RE protocol was based on three sessions of squat-type exercise composed by three sets of 10 repetitions at 70% of maximal voluntary strength capacity. RESULTS: The plantaris mass was significantly greater in both trained groups compared with the non-trained groups. Muscle cross-sectional area and fiber areas did not differ between groups. Both trained groups displayed significant increases in the number of intermediated fibers (IIa/IIx), a decreased number of fast-twitch fibers (IIb), an increased ratio of the proteins phospho(Ser2448)/total mammalian target of rapamycin and phospho(Thr389)/total 70-kDa ribosomal protein S6 kinase, and a decreased ratio of phospho(Ser253)/total Forkhead box protein-3a. Plasma glucose was significantly increased in the DEX-LEU group compared with the DEX group and RE significantly decreased hyperglycemia. The DEX-LEU group displayed decreased glucose transporter-4 translocation compared with the DEX group and RE restored this response. LEU supplementation worsened insulin sensitivity and did not attenuate muscle wasting in rats treated with DEXA. Conversely, RE modulated glucose homeostasis and fiber type transition in the plantaris muscle. CONCLUSION: Resistance exercise but not LEU supplementation promoted fiber type transition and improved glucose homeostasis in DEXA-treated rats.

Potential therapeutic effects of branched-chain amino acids supplementation on resistance exercise-based muscle damage in humans.

Branched-chain amino acids (BCAA) supplementation has been considered an interesting nutritional strategy to improve skeletal muscle protein turnover in several conditions. In this context, there is evidence that resistance exercise (RE)-derived biochemical markers of muscle soreness (creatine kinase (CK), aldolase, myoglobin), soreness, and functional strength may be modulated by BCAA supplementation in order to favor of muscle adaptation. However, few studies have investigated such effects in well-controlled conditions in humans. Therefore, the aim of this short report is to describe the potential therapeutic effects of BCAA supplementation on RE-based muscle damage in humans. The main point is that BCAA supplementation may decrease some biochemical markers related with muscle soreness but this does not necessarily reflect on muscle functionality.

Acute exhaustive exercise regulates IL-2, IL-4 and MyoD in skeletal muscle but not adipose tissue in rats.

BACKGROUND: The purpose of this study was to evaluate the effect of exhaustive exercise on proteins associated with muscle damage and regeneration, including IL-2, IL-4 and MyoD, in extensor digitorum longus (EDL) and soleus muscles and mesenteric (MEAT) and retroperitoneal adipose tissues (RPAT). METHODS: Rats were killed by decapitation immediately (E0 group, n = 6), 2 (E2 group, n = 6) or 6 (E6 group, n = 6) hours after the exhaustion protocol, which consisted of running on a treadmill at approximately 70% of VO(2max) for fifty minutes and then at an elevated rate that increased at one m/min every minute, until exhaustion. RESULTS: The control group (C group, n = 6) was not subjected to exercise. IL-2 protein expression increased at E0 in the soleus and EDL; at E2, this cytokine returned to control levels in both tissues. In the soleus, IL-2 protein expression was lower than that in the control at E6. IL-4 protein levels increased in EDL at E6, but the opposite result was observed in the soleus. MyoD expression increased at E6 in EDL. CONCLUSION: Exhaustive exercise was unable to modify IL-2 and IL-4 levels in MEAT and RPAT. The results show that exhaustive exercise has different effects depending on which muscle is analysed.

ß-Hydroxy-ß-methylbutyrate (HMß) supplementation stimulates skeletal muscle hypertrophy in rats via the mTOR pathway.

ß-Hydroxy-ß-methylbutyrate (HMß) supplementation is used to treat cancer, sepsis and exercise-induced muscle damage. However, its effects on animal and human health and the consequences of this treatment in other tissues (e.g., fat and liver) have not been examined. The purpose of this study was to evaluate the effects of HMß supplementation on skeletal muscle hypertrophy and the expression of proteins involved in insulin signalling. Rats were treated with HMß (320 mg/kg body weight) or saline for one month. The skeletal muscle hypertrophy and insulin signalling were evaluated by western blotting, and hormonal concentrations were evaluated using ELISAs. HMß supplementation induced muscle hypertrophy in the extensor digitorum longus (EDL) and soleus muscles and increased serum insulin levels, the expression of the mammalian target of rapamycin (mTOR) and phosphorylation of p70S6K in the EDL muscle. Expression of the insulin receptor was increased only in liver. Thus, our results suggest that HMß supplementation can be used to increase muscle mass without adverse health effects.

Low and moderate, rather than high intensity strength exercise induces benefit regarding plasma lipid profile.

BACKGROUND: The effects of chronic aerobic exercise upon lipid profile has been previously demonstrated, but few studies showed this effect under resistance exercise conditions. OBJECTIVE: The aim of this study was to examine the effects of different resistance exercise loads on blood lipids. METHODS: Thirty healthy, untrained male volunteers were allocated randomly into four groups based at different percentages of one repetition maximum (1 RM); 50%-1 RM, 75%-1 RM, 90%-1 RM, and 110%-1 RM. The total volume (sets x reps x load) of the exercise was equalized. The lipid profile (Triglycerides [TG], HDL-cholesterol [HDL-c], LDL-cholesterol, and Total cholesterol) was determined at rest and after 1, 24, 48 and 72 h of resistance exercise. RESULTS: The 75%-1 RM group demonstrated greater TG reduction when compared to other groups (p < 0.05). Additionally, the 110%-1 RM group presented an increased TG concentration when compared to 50% and 75% groups (p = 0.01, p = 0.01, respectively). HDL-c concentration was significantly greater after resistance exercise in 50%-1 RM and 75%-1 RM when compared to 110%-1 RM group (p = 0.004 and p = 0.03, respectively). Accordingly, the 50%-1 RM group had greater HDL-c concentration than 110%-1 RM group after 48 h (p = 0.05) and 72 h (p = 0.004), respectively. Finally, The 50% group has showed lesser LDL-c concentration than 110% group after 24 h (p = 0.007). No significant difference was found in Total Cholesterol concentrations. CONCLUSION: These results indicate that the acute resistance exercise may induce changes in lipid profile in a specific-intensity manner. Overall, low and moderate exercise intensities appear to be promoting more benefits on lipid profile than high intensity. Long term studies should confirm these findings.

Chronic exercise decreases cytokine production in healthy rat skeletal muscle.

Skeletal muscle is the source of pro- and anti-inflammatory cytokines, and recently, it has been recognized as an important source of interleukin-6 (IL-6). Acute physical exercise is known to induce a pro-inflammatory cytokine profile in the plasma. However, the effect of chronic physical exercise in the production of pro- and anti-inflammatory cytokines by the skeletal muscle has never been examined. We assessed IL-6, TNF-alpha, IL-1beta and IL-10 levels in the skeletal muscle of rats submitted to endurance training. Animals were randomly assigned to either a sedentary group (S, n = 7) or an endurance exercise trained group (T, n = 8). Trained rats ran on a treadmill for 5 days week(-1) for 8 weeks (60% VO(2max)). Detection of IL-6, TNF-alpha, IL-1beta and IL-10 protein expression was carried out by ELISA. We found decreased expression of IL-1beta, IL-6, TNF-alpha and IL-10 (28%, 27%, 32% and 37%, respectively, p < 0.05) in the extensor digital longus (EDL) from T, when compared with S. In the soleus, IL-1beta, TNF-alpha and IL-10 protein levels were similarly decreased (34%, 42% and 50%, respectively, p < 0.05) in T in relation to S, while IL-6 expression was not affected by the training protocol. In conclusion, exercise training induced decreased cytokine protein expression in the skeletal muscle. These data show that in healthy rats, 8-week moderate-intensity aerobic training down regulates skeletal muscle production of cytokines involved in the onset, maintenance and regulation of inflammation, and that the response is heterogeneous according to fibre composition.

Acute high-intensity exercise with low energy expenditure reduced LDL-c and total cholesterol in men.

A reduction in LDL cholesterol and an increase in HDL cholesterol levels are clinically relevant parameters for the treatment of dyslipidaemia, and exercise is often recommended as an intervention. This study aimed to examine the effects of acute, high-intensity exercise ( approximately 90% VO(2max)) and varying carbohydrate levels (control, low and high) on the blood lipid profile. Six male subjects were distributed randomly into exercise groups, based on the carbohydrate diets (control, low and high) to which the subjects were restricted before each exercise session. The lipid profile (triglycerides, VLDL, HDL cholesterol, LDL cholesterol and total cholesterol) was determined at rest, and immediately and 1 h after exercise bouts. There were no changes in the time exhaustion (8.00 +/- 1.83; 7.82 +/- 2.66; and 9.09 +/- 3.51 min) and energy expenditure (496.0 +/- 224.8; 411.5 +/- 223.1; and 592.1 +/- 369.9 kJ) parameters with the three varying carbohydrate intake (control, low and high). Glucose and insulin levels did not show time-dependent changes under the different conditions (P > 0.05). Total cholesterol and LDL cholesterol were reduced after the exhaustion and 1 h recovery periods when compared with rest periods only in the control carbohydrate intake group (P < 0.05), although this relation failed when the diet was manipulated. These results indicate that acute, high-intensity exercise with low energy expenditure induces changes in the cholesterol profile, and that influences of carbohydrate level corresponding to these modifications fail when carbohydrate (low and high) intake is manipulated.

Exhaustive exercise causes an anti-inflammatory effect in skeletal muscle and a pro-inflammatory effect in adipose tissue in rats.

It is well known that exhaustive exercise increases serum and skeletal muscle IL-6 concentrations. However, the effect of exhaustive exercise on the concentrations of other cytokines in the muscle and in the adipose tissue is controversial. The purpose of this study was to evaluate the effect of exhaustive exercise on mRNA and protein expression of IL-10, TNF-alpha and IL-6 in different types of skeletal muscle (EDL, soleus) and in two different depots of white adipose tissue (mesenteric-MEAT and retroperitoneal-RPAT). Rats were killed by decapitation immediately (E0 group, n = 6), 2 (E2 group, n = 6) and 6 (E6 group, n = 6) hours after the exhaustion protocol, which consisted of running on a treadmill (approximately 70% VO(2max) for 50 min and then subsequently at an elevated rate that increased at 1 m/min every minute, until exhaustion). The control group (C group, n = 6) was not subjected to exercise. Cytokine protein expression increased in EDL, soleus, MEAT and RPAT from all exercised groups, as detected by ELISA. EDL IL-10 and TNF-alpha expression was higher than that of the soleus. The IL-10/TNF-alpha ratio was increased in the skeletal muscle, especially in EDL, but it was found to be decreased in the adipose tissue. These results show that exhaustive exercise presents a different effect depending on the tissue which is analysed: in the muscle, it induces an anti-inflammatory effect, especially in type 2 fibres, while the pro-inflammatory effect prevails in adipose tissue, possibly contributing to increased lipolysis to provide energy for the exercising muscle.

Regulation of inflammation in the adipose tissue in cancer cachexia: effect of exercise.

The paraneoplastic syndrome of cachexia is considered a degenerative chronic inflammatory disease, being deeply related to the increase of pro-inflammatory factors, especially tumour necrosis factor alpha (TNF-alpha). It is known that the adipose tissue is affected by cachexia and contributing with the secretion of pro-inflammatory factors which reach the adjacent tissues and the circulation. The effect of pro-inflammatory factors is balanced by the effect of anti-inflammatory factors, such as interleukin 10 (IL-10). The IL-10/TNF-alpha ratio has been recently postulated as a marker for the assessment of the degree of inflammation, which correlates with disease-associated morbidity and mortality. In order to counteract inflammation in chronic disease, our group has currently adopted chronic endurance exercise in models of cancer cachexia and chronic heart failure. Since it is clear that white adipose tissue is strongly implicated in the secretion of both pro- and anti-inflammatory factors in disease, we chose to address its contribution to cachexia-related inflammation and the effect of endurance training on the capacity of cytokine expression and secretion by this tissue. Our results show an enhancement of IL-10 adipose tissue content, and increased IL-10/TNF-alpha ratio induced by endurance training. The mechanisms are discussed.

Potential antiproteolytic effects of L-leucine: observations of in vitro and in vivo studies.

The purpose of present review is to describe the effect of leucine supplementation on skeletal muscle proteolysis suppression in both in vivo and in vitro studies. Most studies, using in vitro methodology, incubated skeletal muscles with leucine with different doses and the results suggests that there is a dose-dependent effect. The same responses can be observed in in vivo studies. Importantly, the leucine effects on skeletal muscle protein synthesis are not always connected to the inhibition of skeletal muscle proteolysis. As a matter of fact, high doses of leucine incubation can promote suppression of muscle proteolysis without additional effects on protein synthesis, and low leucine doses improve skeletal muscle protein ynthesis but have no effect on skeletal muscle proteolysis. These research findings may have an important clinical relevancy, because muscle loss in atrophic states would be reversed by specific leucine supplementation doses. Additionally, it has been clearly demonstrated that leucine administration suppresses skeletal muscle proteolysis in various catabolic states. Thus, if protein metabolism changes during different atrophic conditions, it is not surprising that the leucine dose-effect relationship must also change, according to atrophy or pathological state and catabolism magnitude. In conclusion, leucine has a potential role on attenuate skeletal muscle proteolysis. Future studies will help to sharpen the leucine efficacy on skeletal muscle protein degradation during several atrophic states.