Christian J. Cook

Possible stimuli for strength and power adaptation: acute hormonal responses

The metabolic response to resistance exercise, in particular lactic acid or lactate, has a marked influence upon the muscular environment, which may enhance the training stimulus (e.g. motor unit activation, hormones or muscle damage) and thereby contribute to strength and power adaptation. Hypertrophy schemes have resulted in greater lactate responses (%) than neuronal and dynamic power schemes, suggesting possible metabolic-mediated changes in muscle growth. Factors such as age, sex, training experience and nutrition may also influence the lactate responses to resistance exercise and thereafter, muscular adaptation. Although the importance of the mechanical and hormonal stimulus to strength and power adaptation is well recognised, the contribution of the metabolic stimulus is largely unknown. Relatively few studies for example, have examined metabolic change across neuronal and dynamic power schemes, and not withstanding the fact that those mechanisms underpinning muscular adaptation, in relation to the metabolic stimulus, remain highly speculative. Inconsistent findings and methodological limitations within research (e.g. programme design, sampling period, number of samples) make interpretation further difficult. We contend that strength and power research needs to investigate those metabolic mechanisms likely to contribute to weight-training adaptation. Further research is also needed to examine the metabolic responses to different loading schemes, as well as interactions across age, sex and training status, so our understanding of how to optimise strength and power development is improved.

Effectiveness of post-match recovery strategies in rugby players

Objectives: To examine the effectiveness of four interventions on the rate and magnitude of muscle damage recovery, as measured by creatine kinase (CK). Methods: 23 elite male rugby players were monitored transdermally before, immediately after, 36 hours after, and 84 hours after competitive rugby matches. Players were randomly assigned to complete one of four post-match strategies: contrast water therapy (CWT), compression garment (GAR), low intensity active exercise (ACT), and passive recovery (PAS). Results: Significant increases in CK activity in transdermal exudate were observed as a result of the rugby match (p<0.01). The magnitude of recovery in the PAS intervention was significantly worse than in the ACT, CWT, and GAR interventions at the 36 and 84 hour time points (p<0.05). Conclusions: An enhanced rate and magnitude of recovery was observed in the ACT, CWT, and GAR treatment groups when compared with the PAS group. Low impact exercise immediately post-competition, wearing compression garments, or carrying out contrast water therapy enhanced CK clearance more than passive recovery in young male athletes.

Glucocorticoid feedback increases the sensitivity of the limbic system to stress.

In the hypothalamus, corticotropin-releasing hormone (CRH) has a well-described role initiating the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Cortisol, released from the adrenal gland, exerts negative feedback on this axis. The role of extrahypothalamic CRH in stress responses is less well known. The purpose of this study was to measure the response of CRH in the amygdala to acute and repeated stress and to examine if cortisol had any effect on this response. Immunosensor-based microdialysis probes were used to measure CRH and cortisol in the amygdala and cortisol systemically in sheep exposed to a predator stress (a dog). Upon presentation of a dog, CRH increased in the amygdala of the sheep and then fell off. Cortisol levels rose both systemically and in the amygdala, and as they peaked, a second CRH response was observed. Repeated stress changed this response, with the magnitude of the first CRH peak decreasing while the second peak increased. Repeated stress also produced an exaggeration in both of the CRH peaks to presentation of a subsequent novel stress (a forelimb electric shock). Animals that had an escape route from the repeated dog stress did not show this exaggeration when faced subsequently with the novel stress. Administration of mifepristone, a glucocorticoid receptor antagonist, prior to the delivery of the repeat stress prevented subsequent changes in the CRH response. The data suggest that the amygdala shows a CRH response to presentation of a stressor acutely and repeatedly and that repeated stress can alter subsequent amygdala responsiveness to the same or a different stressor. This alteration appears dependent on circulatory glucocorticoids.

Two Emerging Concepts for Elite Athletes The Short-Term Effects of Testosterone and Cortisol on the Neuromuscular System and the Dose-Response Training Role of these Endogenous Hormones

The aim of this review is to highlight two emerging concepts for the elite athlete using the resistance-training model: (i) the short-term effects of testosterone (T) and cortisol (C) on the neuromuscular system; and (ii) the dose-response training role of these endogenous hormones. Exogenous evidence confirms that T and C can regulate long-term changes in muscle growth and performance, especially with resistance training. This evidence also confirms that changes in T or C concentrations can moderate or support neuromuscular performance through various short-term mechanisms (e.g. second messengers, lipid/protein pathways, neuronal activity, behaviour, cognition, motor-system function, muscle properties and energy metabolism). The possibility of dual T and C effects on the neuromuscular system offers a new paradigm for understanding resistance-training performance and adaptations.Endogenous evidence supports the short-term T and C effects on human performance. Several factors (e.g. workout design, nutrition, genetics, training status and type) can acutely modify T and/or C concentrations and thereby potentially influence resistance-training performance and the adaptive outcomes. This novel short-term pathway appears to be more prominent in athletes (vs non-athletes), possibly due to the training of the neuromuscular and endocrine systems. However, the exact contribution of these endogenous hormones to the training process is still unclear. Research also confirms a dose-response training role for basal changes in endogenous T and C, again, especially for elite athletes. Although full proof within the physiological range is lacking, this athlete model reconciles a proposed permissive role for endogenous hormones in untrained individuals. It is also clear that the steroid receptors (cell bound) mediate target tissue effects by adapting to exercise and training, but the response patterns of the membrane-bound receptors remain highly speculative.This information provides a new perspective for examining, interpreting and utilizing T and C within the elite sporting environment. For example, individual hormonal data may be used to better prescribe resistance exercise and training programmes or to assess the trainability of elite athletes. Possible strategies for acutely modifying the hormonal milieu and, thereafter, the performance/training outcomes were also identified (see above). The limitations and challenges associated with the analysis and interpretation of hormonal research in sport (e.g. procedural issues, analytical methods, research design) were another discussion point. Finally, this review highlights the need for more experimental research on humans, in particular athletes, to specifically address the concept of dual steroid effects on the neuromuscular system.

Stress induces CRF release in the paraventricular nucleus, and both CRF and GABA release in the amygdala

In the hypothalamus, corticotropin-releasing factor (CRF) initiates the hypothalamic-pituitary-adrenal (HPA) axis response to stress, resulting in the release of glucocorticoids, including cortisol. Extrahypothalamic CRF, particularly in the limbic system, also appears to play a role in the stress response. To further define brain CRF response to stress, immunosensor-based microdialysis probes were used to measure the extracellular levels of CRF in the paraventricular nucleus of the hypothalamus (PVN) and in the amygdala of sheep during a predator (dog) exposure stress. In addition, gamma amino butyric acid (GABA) was measured in the amygdala and cortisol was measured in venous blood. Exposure to the predator stress increased CRF in the PVN and both CRF and GABA in the amygdala. These were followed in time by a rise in venous cortisol. Application of a CRF antagonist to the amygdala, immediately prior to stress, had a small effect on the subsequent observed stress responses. This treatment, however, significantly reduced the responses to a repeat stress administered 2 days later, compared to nontreated animals. Application of a GABA antagonist to the amygdala prior to stress had no effect on the subsequent observed stress response but increased the response to the stress repeated 2 days later. Perfusion with 4-aminopyridine, a neuronal depolarising agent, into the PVN induced a release of CRF accompanied shortly thereafter by a small increase in CRF in the amygdala, and 5-10 min later by an increase in venous cortisol. Perfusion into the amygdala increased the levels of both CRF and GABA but had no effect on either PVN CRF or venous cortisol. These data support roles for both the PVN and amygdala in stress responsiveness. It suggests further that actions at the amygdala can strongly influence subsequent responsiveness to a further stress, mediated in part by both CRF and GABA actions.

Optimal Loading for the Development of Peak Power Output in Professional Rugby Players

Bevan, HR, Bunce, PJ, Owen, NJ, Bennett, MA, Cook, CJ, Cunningham, DJ, Newton, RU, and Kilduff, LP. Optimal loading for the development of peak power output in professional rugby players. J Strength Cond Res 24(1): 43-47, 2010-The ability to develop high levels of muscular power is considered an essential component of success in many sporting activities; however, the optimal load for the development of peak power during training remains controversial. Our aim in the present study was to determine the optimal load required to observe peak power output during the ballistic bench throw (BBT) and squat jump (SJ) in professional rugby players. Forty-seven, professional, male, rugby players of (mean ± SD) mass 101.3 ± 12.8 kg and height 1.82 ± 0.08 m volunteered and gave informed consent for this study, which was approved by a university ethics committee. Players performed BBT at loads of 20, 30, 40, 50, and 60% of their predetermined 1 repetition maximum (1RM) and SJ at loads of 0, (body mass only), 20, 30, 40, 50, and 60% of their predetermined 1RM in a randomized and balanced order. Power output (PO) was determined by measurement of barbell displacement with subsequent calculation of velocity, force, and power. Relative load had a significant effect on PO for both the BBT (effect size &eegr;2: 0.297, p < 0.001) and SJ (Effect Size &eegr;2: 0.709, p < 0.001). Peak power output was produced when the athletes worked against an external load equal to 30% 1RM for the upper body and 0% 1RM for the lower body.

Digit Ratio (2D:4D): A Biomarker for Prenatal Sex Steroids and Adult Sex Steroids in Challenge Situations.

Digit ratio (2D:4D) denotes the relative length of the second and fourth digits. This ratio is considered to be a biomarker of the balance between fetal testosterone (T) and estrogen (E) in a narrow window of early ontogeny. Evidence for this assertion is derived from direct and indirect measures of prenatal hormonal exposure (in experimental animals, via amniotic fluid samples and in the study of sex-typical traits) in relation to 2D:4D. In contrast, the relationships between 2D:4D and levels of sex steroids in adults are less clear, as many correlational studies of 2D:4D and adult sex steroids have concluded that this association is statistically non-significant. Here, we suggest that in order to understand the link between 2D:4D and sex hormones, one must consider both fetal organizing and adult activating effects of T and E. In particular, we hypothesize that 2D:4D correlates with organizing effects on the endocrine system that moderate activating effects in adulthood. We argue that this is particularly evident in “challenging” conditions such as aggressive and sexual encounters, in which individuals show increased levels of T. We discuss this refinement of the 2D:4D paradigm in relation to the links between 2D:4D and sports performance, and aggression.

Dietary nitrate does not enhance running performance in elite cross-country skiers.

PURPOSE The objective of this study is to examine the effects of acute ingestion of dietary nitrate on endurance running performance in highly trained cross-country skiers. Dietary nitrate has been shown to reduce the oxygen cost of submaximal exercise and improve tolerance of high-intensity exercise, but it is not known if this holds true for highly trained endurance athletes. METHODS Ten male junior cross-country skiers (V˙O(2max)) ≈ 70 mL·kg·min) each completed two trials in a randomized, double-blind design. Participants ingested potassium nitrate (614-mg nitrate) or a nitrate-free placebo 2.5 h before two 5-min submaximal tests on a treadmill at 10 km·h (≈55% of V˙O(2max)) and 14 km·h (≈75% of V˙O(2max)), followed by a 5-km running time trial on an indoor track. RESULTS Plasma nitrite concentrations were higher after nitrate supplementation (325 ± 95 nmol·L) compared with placebo (143 ± 59 nmol·L, P < 0.001). There was no significant difference in 5-km time-trial performance between nitrate (1005 ± 53 s) and placebo treatments (996 ± 49 s, P = 0.12). The oxygen cost of submaximal running was not significantly different between placebo and nitrate trials at 10 km·h (both 2.84 ± 0.34 L·min) and 14 km·h (3.89 ± 0.39 vs. 3.77 ± 0.62 L·min). CONCLUSIONS Acute ingestion of dietary nitrate may not represent an effective strategy for reducing the oxygen cost of submaximal exercise or for enhancing endurance exercise performance in highly trained cross-country skiers.

High and low rigor temperature effects on sheep meat tenderness and ageing

Immediately after electrical stimulation, the paired m. longissimus thoracis et lumborum (LT) of 40 sheep were boned out and wrapped tightly with a polyethylene cling film. One of the paired LTs was chilled in 15°C air to reach a rigor mortis (rigor) temperature of 18°C and the other side was placed in a water bath at 35°C and achieved rigor at this temperature. Wrapping reduced rigor shortening and mimicked meat left on the carcass. After rigor, the meat was aged at 15°C for 0, 8, 26 and 72 h and then frozen. The frozen meat was cooked to 75°C in an 85°C water bath and shear force values obtained from a 1×1 cm cross-section. The shear force values of meat for 18 and 35°C rigor were similar at zero ageing, but as ageing progressed, the 18 rigor meat aged faster and became more tender than meat that went into rigor at 35°C (P<0.001). The mean sarcomere length values of meat samples for 18 and 35°C rigor at each ageing time were significantly different (P<0.001), the samples at 35°C being shorter. When the short sarcomere length values and corresponding shear force values were removed for further data analysis, the shear force values for the 35°C rigor were still significantly greater. Thus the toughness of 35°C meat was not a consequence of muscle shortening and appears to be due to both a faster rate of tenderisation and the meat tenderising to a greater extent at the lower temperature. The cook loss at 35°C rigor (30.5%) was greater than that at 18°C rigor (28.4%) (P<0.01) and the colour Hunter L values were higher at 35°C (P<0.01) compared with 18°C, but there were no significant differences in a or b values.

The relationship between changes in interstitial creatine kinase and game-related impacts in rugby union

Aim: The primary purpose of this study was to investigate the relationship between the pre-game to post-game changes in creatine kinase concentration (Δ[CK]) and impact-related game statistics in elite rugby union players. Methods: Twenty-three elite male rugby union players each provided interstitial fluid samples obtained via electrosonophoresis (ESoP) 210 min before and within a maximum time of 30 min after up to five rugby union games. Specific game statistics that were deemed to be important in determining the relationship between impact and [CK] were obtained from AnalyRugby software for each individual player. Regression equations to predict Δ[CK] from game statistics were created using a backwards random-effects maximum likelihood regression. Results: The Δ[CK] (mean (SD)) from pre-game to post-game was 926.8 (204.2) IU. Game time and time defending were significantly correlated to Δ[CK] in both the forwards and backs. The predicted Δ[CK] (mean (95% confidence limit)) was 1439.8 (204.9) IU for the forwards and 545.3 (78.0) IU for the backs and was significantly correlated with the actual Δ[CK] (r = 0.69 and r = 0.74). Conclusions: CK increased from pre-game to post-game in a position-specific manner. A large proportion of the Δ[CK] can be explained by physical impact and thus can be predicted using a prescribed number of game statistics. As the Δ[CK] is an indicator of muscle damage, the prediction of Δ[CK] provides a theoretical basis for recovery strategies and adjustment of subsequent training sessions after rugby union games.