Physical characteristics that predict functional performance in Division I college football players

Strength and conditioning professionals who work with collegiate football players focus much of their time and effort on developing programs to enhance athletic performance. Although there has been much speculation, there is little scientific evidence to suggest which combination of physical characteristics best predicts athletic performance in this population. The purpose of this investigation was to examine the relationship among 6 physical characteristics and 3 functional measures in college football players. Data were gathered on 46 NCAA Division I college football players. The 3 response variables were 36.6-m sprint, 18.3-m shuttle run, and vertical jump. The 6 regressor variables were height, weight, percentage of body fat, hamstring length, bench press, and hang clean. A stepwise multiple regression analysis was performed to screen for variables that predict physical performance. Regression analysis revealed clear prediction models for the 36.6-m sprint and 18.3-m shuttle run. The results of this investigation will help strength and conditioning specialists better understand the variables that predict athletic performance in Division I college football players.     

The normalization of explosive functional movements in a diverse population of elite American football players

The objective of this study was to investigate the need to normalize, for body mass, explosive functional tasks in a population exhibiting diverse body masses. Measures investigated in elite college American football players attending the National Football League's annual combine (n = 1,136) were the 9.1-, 18.3-, and 36.6-m sprints, vertical and horizontal jumps, 18.3-m shuttle, and 3-cone drill. To determine the relationship between body mass and performance outcomes, Pearson's correlation coefficients (r) were generated using log-transformed data. Task-specific allometric exponents, accounting for body mass, were also determined. The strength of the correlations suggests that sprint and jump abilities are associated with body mass, whereas change-of-direction ability is not. The determined allometric exponents range between 0.296 and -0.463 for the sprint and jump tasks and are -0.022 and -0.006 for the 18.3-m shuttle and the 3-cone drill, respectively. In populations exhibiting relatively large variations in body mass, normalization of sprint and jump abilities is recommended, whereas normalization of change-of-direction ability is unwarranted. Novel suggestions derived from the present research are that sprint and jump abilities in diverse populations warrant normalization and that physical attributes associated with explosive functional movements deserve attribute-specific consideration when contemplating normalization.     

Head impact exposure in collegiate football players

In American football, impacts to the helmet and the resulting head accelerations are the primary cause of concussion injury and potentially chronic brain injury. The purpose of this study was to quantify exposures to impacts to the head (frequency, location and magnitude) for individual collegiate football players and to investigate differences in head impact exposure by player position. A total of 314 players were enrolled at three institutions and 286,636 head impacts were recorded over three seasons. The 95th percentile peak linear and rotational acceleration and HITsp (a composite severity measure) were 62.7g, 4378rad/s(2) and 32.6, respectively. These exposure measures as well as the frequency of impacts varied significantly by player position and by helmet impact location. Running backs (RB) and quarter backs (QB) received the greatest magnitude head impacts, while defensive line (DL), offensive line (OL) and line backers (LB) received the most frequent head impacts (more than twice as many than any other position). Impacts to the top of the helmet had the lowest peak rotational acceleration (2387rad/s(2)), but the greatest peak linear acceleration (72.4g), and were the least frequent of all locations (13.7%) among all positions. OL and QB had the highest (49.2%) and the lowest (23.7%) frequency, respectively, of front impacts. QB received the greatest magnitude (70.8g and 5428rad/s(2)) and the most frequent (44% and 38.9%) impacts to the back of the helmet. This study quantified head impact exposure in collegiate football, providing data that is critical to advancing the understanding of the biomechanics of concussive injuries and sub-concussive head impacts.     

Variation in the uncoupling protein 2 and 3 genes and human performance

Uncoupling proteins 2 and 3 (UCP2 and UCP3) may negatively regulate mitochondrial ATP synthesis and, through this, influence human physical performance. However, human data relating to both these issues remain sparse. Examining the association of common variants in the UCP3/2 locus with performance phenotypes offers one means of investigation. The efficiency of skeletal muscle contraction, delta efficiency (DE), was assessed by cycle ergometry in 85 young, healthy, sedentary adults both before and after a period of endurance training. Of these, 58 were successfully genotyped for the UCP3-55C>T (rs1800849) and 61 for the UCP2-866G>A (rs659366) variant. At baseline, UCP genotype was unrelated to any physical characteristic, including DE. However, the UCP2-866G>A variant was independently and strongly associated with the DE response to physical training, with UCP2-866A allele carriers exhibiting a greater increase in DE with training (absolute change in DE of -0.2 ± 3.6% vs. 1.7 ± 2.8% vs. 2.3 ± 3.7% for GG vs. GA vs. AA, respectively; P = 0.02 for A allele carriers vs. GG homozygotes). In multivariate analysis, there was a significant interaction between UCP2-866G>A and UCP3-55C>T genotypes in determining changes in DE (adjusted R(2) = 0.137; P value for interaction = 0.003), which was independent of the effect of either single polymorphism or baseline characteristics. In conclusion, common genetic variation at the UCP3/2 gene locus is associated with training-related improvements in DE, an index of skeletal muscle performance. Such effects may be mediated through differences in the coupling of mitochondrial energy transduction in human skeletal muscle, but further mechanistic studies are required to delineate this potential role.     

Association of the sirtuin and mitochondrial uncoupling protein genes with carotid plaque

Objective

Sirtuins (SIRTs) and mitochondrial uncoupling proteins (UCPs) have been implicated in cardiovascular diseases through the control of reactive oxygen species production. This study sought to investigate the association between genetic variants in the SIRT and UCP genes and carotid plaque.

Methods

In a group of 1018 stroke-free subjects from the Northern Manhattan Study with high-definition carotid ultrasonography and genotyping, we investigated the associations of 85 single nucleotide polymorphisms (SNPs) in the 11 SIRT and UCP genes with the presence and number of carotid plaques, and evaluated interactions of SNPs with sex, smoking, diabetes and hypertension as well as interactions between SNPs significantly associated with carotid plaque.

Results

Overall, 60% of subjects had carotid plaques. After adjustment for demographic and vascular risk factors, T-carriers of the SIRT6 SNP rs107251 had an increased risk for carotid plaque (odds ratio, OR = 1.71, 95% CI = 1.23–2.37, Bonferroni-corrected p = 0.03) and for a number of plaques (rate ratio, RR = 1.31, 1.18–1.45, Bonferroni-corrected p = 1.4×10⁻⁵), whereas T-carriers of the UCP5 SNP rs5977238 had an decreased risk for carotid plaque (OR = 0.49, 95% CI = 0.32–0.74, Bonferroni-corrected p = 0.02) and plaque number (RR = 0.64, 95% CI = 0.52–0.78, Bonferroni-corrected p = 4.9×10⁻⁴). Some interactions with a nominal p≤0.01 were found between sex and SNPs in the UCP1 and UCP3 gene; between smoking, diabetes, hypertension and SNPs in UCP5 and SIRT5; and between SNPs in the UCP5 gene and the UCP1, SIRT1, SIRT3, SIRT5, and SIRT6 genes in association with plaque phenotypes.

Conclusion

We observed significant associations between genetic variants in the SIRT6 and UCP5 genes and atherosclerotic plaque. We also found potential effect modifications by sex, smoking and vascular risk factors of the SIRT/UCP genes in the associations with atherosclerotic plaque. Further studies are needed to validate our observations.     

Endogenous mutations in human uncoupling protein 3 alter its functional properties

Human uncoupling protein (UCP3) is a mitochondrial transmembrane carrier that uncouples oxidative phosphorylation and is a candidate gene for obesity. Expression of native human UCP3 mutations in yeast showed complete loss (R70W), significant reduction (R143X), or no effect (V102I and IVS6+1G > A) on the uncoupling activity of UCP3. It is concluded that certain mutations in UCP3 alter its functional impact on membrane potential (deltaphi), possibly conferring susceptibility to develop metabolic diseases.     

Magnitude of head impact exposures in individual collegiate football players

The purpose of this study was to quantify the severity of head impacts sustained by individual collegiate football players and to investigate differences between impacts sustained during practice and game sessions, as well as by player position and impact location. Head impacts (N = 184,358) were analyzed for 254 collegiate players at three collegiate institutions. In practice, the 50th and 95th percentile values for individual players were 20.0 g and 49.5 g for peak linear acceleration, 1187 rad/s2 and 3147 rad/s2 for peak rotational acceleration, and 13.4 and 29.9 for HITsp, respectively. Only the 95th percentile HITsp increased significantly in games compared with practices (8.4%, p = .0002). Player position and impact location were the largest factors associated with differences in head impacts. Running backs consistently sustained the greatest impact magnitudes. Peak linear accelerations were greatest for impacts to the top of the helmet, whereas rotational accelerations were greatest for impacts to the front and back. The findings of this study provide essential data for future investigations that aim to establish the correlations between head impact exposure, acute brain injury, and long-term cognitive deficits.     

Postcompetition elevation of muscle enzyme levels in professional football players

Strenuous exercise causes a rise in circulating levels of creatine kinase (CK), and well-trained athletes liberate smaller amounts than do untrained individuals. Plasma CK, aspartate aminotransferase, and lactate dehydrogenase were measured in a group of 23 professional football players 48 hours after competition. All players were asymptomatic for myalgias or chest discomfort despite elevations of CK levels. Physicians should be aware of these elevations in muscle enzymes postexertion and interpret each in conjunction with the athlete's symptoms.     

Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase

Strategies to prevent and treat obesity aim to decrease energy intake and/or increase energy expenditure. Regarding the increase of energy expenditure, two key intracellular targets may be considered (1) mitochondrial oxidative phosphorylation, the major site of ATP production, and (2) AMP-activated protein kinase (AMPK), the master regulator of cellular energy homeostasis. Experiments performed mainly in transgenic mice revealed a possibility to ameliorate obesity and associated disorders by mitochondrial uncoupling in metabolically relevant tissues, especially in white adipose tissue (WAT), skeletal muscle (SM), and liver. Thus, ectopic expression of brown fat-specific mitochondrial uncoupling protein 1 (UCP1) elicited major metabolic effects both at the cellular/tissue level and at the whole-body level. In addition to expected increases in energy expenditure, surprisingly complex phenotypic effects were detected. The consequences of mitochondrial uncoupling in WAT and SM are not identical, showing robust and stable obesity resistance accompanied by improvement of lipid metabolism in the case of ectopic UCP1 in WAT, while preservation of insulin sensitivity in the context of high-fat feeding represents the major outcome of muscle UCP1 expression. These complex responses could be largely explained by tissue-specific activation of AMPK, triggered by a depression of cellular energy charge. Experimental data support the idea that (1) while being always activated in response to mitochondrial uncoupling and compromised intracellular energy status in general, AMPK could augment energy expenditure and mediate local as well as whole-body effects; and (2) activation of AMPK alone does not lead to induction of energy expenditure and weight reduction.     

Structure and nucleotide polymorphisms in pig uncoupling protein 2 and 3 genes

Uncoupling proteins (UCPs) are mitochondrial membrane transporters, acting as an uncoupler in oxidative phosphorylation. In this study, we designed 11 primer sets based on the human and mouse UCP2, UCP3 sequences and successfully amplified full regions of porcine UCP2 and UCP3 by polymerase chain reactions (PCR). Comparison of the UCP2 and UCP3 genic structures revealed a highly conservative region was putatively presented, showing the second transmembrane domain may be the UCPs' cardinal function region. Altogether 23 nucleotide polymorphisms of UCP2 and UCP3 genes were discovered in Yorkshire, Wuzhishan, and Lepinghua pigs. These polymorphisms included 3 missense mutations, 16 intronic substitutions, and 4 intronic deletions. The substitution of Ala-55-Val in UCP2 is actually the most common mutation in human. We also calculated genotypic frequencies of five polymorphisms in three pig breeds.     

Occlusion training increases muscular strength in division IA football players

The purpose of this study was to investigate the effectiveness of 4 weeks of low-intensity resistance training with blood-flow occlusion on upper and lower body muscular hypertrophy and muscular strength in National Collegiate Athletic Association Division IA football players. There were 32 subjects (average age 19.2 ± 1.8 years) who were randomized to an occlusion group or control group. The athletes performed 4 sets of bench press and squat in the following manner with or without occlusion: 30 repetitions of 20% predetermined 1 repetition maximum (1RM), followed by 3 sets of 20 repetitions at 20% 1RM. Each set was separated by 45 seconds. The training duration was 3 times per week, after the completion of regular off-season strength training. Data collected included health history, resting blood pressure, pretraining and posttraining bench press and squat 1RM, upper and lower chest girths, upper and lower arm girths, thigh girth, height, and body mass. The increases in bench press and squat 1RM (7.0 and 8.0%, respectively), upper and lower chest girths (3 and 3%, respectively), and left upper arm girth were significantly greater in the experiment group (p < 0.05). Occlusion training could provide additional benefits to traditional strength training to improve muscular hypertrophy and muscular strength in collegiate athletes.     

Validity and reliability of agility tests in junior Australian football players

Young, W, Farrow, D, Pyne, D, McGregor, W, and Handke, T. Validity and reliability of agility tests in junior Australian football players. J Strength Cond Res 25(12): 3399-3403, 2011-The importance of sport-specific stimuli in reactive agility tests (RATs) compared to other agility tests is not known. The purpose of this research was to determine the validity and reliability of agility tests. Fifty junior Australian football players aged 15-17 years, members of either an elite junior squad (n = 35) or a secondary school team (n = 15), were assessed on a new RAT that involved a change of direction sprint in response to the movements of an attacking player projected in life size on a screen. These players also underwent the planned Australian Football League agility test, and a subgroup (n = 13) underwent a test requiring a change of direction in response to a left or right arrow stimulus. The elite players were significantly better than the school group players on the RAT (2.81 ± 0.08 seconds, 3.07 ± 0.12 seconds; difference 8.5%) but not in the arrow stimulus test or planned agility test. The data were log transformed and the reliability of the new RAT estimated using typical error (TE) expressed as a coefficient of variation. The TE for the RAT was 2.7% (2.0-4.3, 90% confidence interval) or 0.07 seconds (0.5-1.0), with an intraclass correlation coefficient (ICC) of 0.33. For the test using the arrow stimulus, the TE was 3.4% (2.4-6.2), 0.09 (0.06-0.15) seconds, and ICC was 0.10. The sport-specific stimulus provided by the new RAT is a crucial component of an agility test; however, adoption of the new RAT for routine testing is likely to require more accessible equipment and several familiarization trials to improve its reliability.     

Activation of AMP-activated protein kinase is required for berberine-induced reduction of atherosclerosis in mice: the role of uncoupling protein 2

Aims

Berberine, a botanical alkaloid purified from Coptidis rhizoma, is reported to activate the AMP-activated protein kinase (AMPK). Whether AMPK is required for the protective effects of berberine in cardiovascular diseases remains unknown. This study was designed to determine whether AMPK is required for berberine-induced reduction of oxidative stress and atherosclerosis in vivo.

Methods

ApoE (ApoE^-/-) mice and ApoE^-/-/AMPK alpha 2^-/- mice that were fed Western diets were treated with berberine for 8 weeks. Atherosclerotic aortic lesions, expression of uncoupling protein 2 (UCP2), and markers of oxidative stress were evaluated in isolated aortas.

Results

In ApoE^-/- mice, chronic administration of berberine significantly reduced aortic lesions, markedly reduced oxidative stress and expression of adhesion molecules in aorta, and significantly increased UCP2 levels. In contrast, in ApoE^-/-/AMPK alpha 2^-/- mice, berberine had little effect on those endpoints. In cultured human umbilical vein endothelial cells (HUVECs), berberine significantly increased UCP2 mRNA and protein expression in an AMPK-dependent manner. Transfection of HUVECs with nuclear respiratory factor 1 (NRF1)-specific siRNA attenuated berberine-induced expression of UCP2, whereas transfection with control siRNA did not. Finally, berberine promoted mitochondrial biogenesis that contributed to up-regulation of UCP2 expression.

Conclusion

We conclude that berberine reduces oxidative stress and vascular inflammation, and suppresses atherogenesis via a mechanism that includes stimulation of AMPK-dependent UCP2 expression.     

Regulation of mitochondrial uncoupling respiration during exercise in rat heart: role of reactive oxygen species (ROS) and uncoupling protein 2

The physiological significance of cardiac mitochondrial uncoupling protein 2 (UCP2)-mediated uncoupling respiration in exercise is unknown. In the current study, mitochondrial respiratory function, UCP2 mRNA level, UCP2-mediated respiration (UCR), and reactive oxygen species (ROS) generation, as well as manganese superoxide dismutase (MnSOD) activity were determined in rat heart with or without endurance training after an acute bout of exercise of different duration. In the untrained rats, state 4 respiration and UCR-independent respiration rates were progressively increased with exercise time and were 64 and 70% higher, respectively, than resting rate at 150 min, whereas UCR was elevated by 86% with no significant change in state 3 respiration. UCP2 mRNA level showed a 5- and 4-fold increase, respectively, after 45 and 90 min of exercise, but returned to resting level at 120 and 150 min. Mitochondrial ROS production and membrane potential (Deltapsi) increased progressively until 120 min, followed by a decrease to the resting level at 150 min. MnSOD mRNA abundance showed a 2-fold increase at 120 min but MnSOD activity did not change with exercise. Training significantly increased mitochondrial ATP synthetase activity, ADP to oxygen consumption (P/O) ratio, respiratory control ratio, and MnSOD activity, whereas exercise-induced state 4 respiration, UCR, ROS production, and Deltapsi were attenuated in the trained rats. We conclude that (1) UCP2 mRNA expression and activity in rat heart can be upregulated during prolonged exercise, which may reduce cross-membrane Deltapsi and thus ROS production; and (2) endurance training can blunt exercise-induced UCP2 and UCR, and improve mitochondrial efficiency of oxidative phosphorylation due to increased removal of ROS.     

The uncoupling protein from brown-adipose-tissue mitochondria. Chymotrypsin-induced structural and functional modifications

Mitoplasts prepared from brown adipose tissue mitochondria were treated with chymotrypsin and the fragments derived from the 32-kDa uncoupling protein identified by immunoblotting. Extensive proteolysis of the uncoupling protein occurred, the polypeptide pattern being affected by binding of the inhibitory nucleotide GDP. Chymotrypsin modifies the nucleotide binding site, lowering its affinity from 1.7 microM to 21 microM but without decreasing its binding capacity. Nucleotide bound to the modified site can still inhibit the permeation of H+ and Cl- through the protein. The ion conducting pathway itself is also sensitive to chymotrypsin, Cl- and H+ transport being partially inhibited in parallel. The ability of fatty acids to increase the H+ permeability of the protein is also inhibited in parallel with the basal H+ permeability. The results confirm that the transport of H+ and Cl-, and the fatty acid regulation of H+ permeation all share a common structural element within the 32-kDa protein.     

Role of intrahelical arginine residues in functional properties of uncoupling protein (UCP1)

The functional role of the four intrahelical arginines in uncoupling protein (UCP1) from brown adipose tissue were studied in mutants where they were replaced by noncharged residues. Wild-type and mutant UCP1 were expressed in Saccharomyces cerevisiae. As measured in isolated UCP1, nucleotide binding was largely lost in mutants of R83, R182, and R276 occurring in three repeated domains and common to mitochondrial carrier family, whereas mutation of the UCP typical R91 shows normal binding capacity but > 20-fold lower binding affinity and a near loss of pH dependency of binding. In reconstituted UCP1, fatty acid dependent H(+) transport is retained in all four mutants, but inhibition by nucleotide changes according to the binding ability of UCP1. Cl(-) transport is inhibited only by mutations of arginines in the first domain (R83 and R91). Also in isolated mitochondria H(+) transport and respiration with all four mutants is similar to wt, and inhibition by GDP is found only in R91T. The three "regular" arginines are suggested to influence the nucleotide binding site indirectly via a charge network and the "extra" R91 directly via an ion bond with the previously characterised pH sensor E190. The mutants were also used to assess intrahelical control of UCP1. In the yeast cells expressing UCP1, the aerobic growth could be reduced by fatty acid addition only with the nucleotide insensitive mutants. This demonstrates an intracellular control of UCP1 by nucleotides and fatty acids.