Jeffrey M. Anderson

Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’

Sudden cardiac death (SCD) is the leading cause of death in athletes during sport. Whether obtained for screening or diagnostic purposes, an ECG increases the ability to detect underlying cardiovascular conditions that may increase the risk for SCD. In most countries, there is a shortage of physician expertise in the interpretation of an athletes ECG. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from abnormal findings suggestive of pathology. On 13–14 February 2012, an international group of experts in sports cardiology and sports medicine convened in Seattle, Washington, to define contemporary standards for ECG interpretation in athletes. The objective of the meeting was to develop a comprehensive training resource to help physicians distinguish normal ECG alterations in athletes from abnormal ECG findings that require additional evaluation for conditions associated with SCD.

Testosterone physiology in resistance exercise and training: the up-stream regulatory elements.

Testosterone is one of the most potent naturally secreted androgenicanabolic hormones, and its biological effects include promotion of muscle growth. In muscle, testosterone stimulates protein synthesis (anabolic effect) and inhibits protein degradation (anti-catabolic effect); combined, these effects account for the promotion of muscle hypertrophy by testosterone. These physiological signals from testosterone are modulated through the interaction of testosterone with the intracellular androgen receptor (AR). Testosterone is important for the desired adaptations to resistance exercise and training; in fact, testosterone is considered the major promoter of muscle growth and subsequent increase in muscle strength in response to resistance training in men. The acute endocrine response to a bout of heavy resistance exercise generally includes increased secretion of various catabolic (breakdown- related) and anabolic (growth-related) hormones including testosterone. The response of testosterone and AR to resistance exercise is largely determined by upper regulatory elements including the acute exercise programme variable domains, sex and age. In general, testosterone concentration is elevated directly following heavy resistance exercise in men. Findings on the testosterone response in women are equivocal with both increases and no changes observed in response to a bout of heavy resistance exercise. Age also significantly affects circulating testosterone concentrations. Until puberty, children do not experience an acute increase in testosterone from a bout of resistance exercise; after puberty some acute increases in testosterone from resistance exercise can be found in boys but not in girls. Aging beyond 35–40 years is associated with a 1–3% decline per year in circulating testosterone concentration in men; this decline eventually results in the condition known as andropause. Similarly, aging results in a reduced acute testosterone response to resistance exercise in men. In women, circulating testosterone concentration also gradually declines until menopause, after which a drastic reduction is found. In summary, testosterone is an important modulator of muscle mass in both men and women and acute increases in testosterone can be induced by resistance exercise. In general, the variables within the acute programme variable domains must be selected such that the resistance exercise session contains high volume and metabolic demand in order to induce an acute testosterone response.

Hydration and Muscular Performance Does Fluid Balance Affect Strength, Power and High-Intensity Endurance?

Significant scientific evidence documents the deleterious effects of hypohydration (reduced total body water) on endurance exercise performance; however, the influence of hypohydration on muscular strength, power and high-intensity endurance (maximal activities lasting >30 seconds but <2 minutes) is poorly understood due to the inconsistent results produced by previous investigations. Several subtle methodological choices that exacerbate or attenuate the apparent effects of hypohydration explain much of this variability. After accounting for these factors, hypohydration appears to consistently attenuate strength (by ≈2%), power (by ≈3%) and high-intensity endurance (by ∼10%), suggesting alterations in total body water affect some aspect of force generation. Unfortunately, the relationships between performance decrement and crucial variables such as mode, degree and rate of water loss remain unclear due to a lack of suitably uninfluenced data. The physiological demands of strength, power and high-intensity endurance couple with a lack of scientific support to argue against previous hypotheses that suggest alterations in cardiovascular, metabolic and/or buffering function represent the performance-reducing mechanism of hypohydration. On the other hand, hypohydration might directly affect some component of the neuromuscular system, but this possibility awaits thorough evaluation. A critical review of the available literature suggests hypohydration limits strength, power and highintensity endurance and, therefore, is an important factor to consider when attempting to maximise muscular performance in athletic, military and industrial settings.

Resistance Exercise Biology Manipulation of Resistance Exercise Programme Variables Determines the Responses of Cellular and Molecular Signalling Pathways

Recent advances in molecular biology have elucidated some of the mechanisms that regulate skeletal muscle growth. Logically, muscle physiologists have applied these innovations to the study of resistance exercise (RE), as RE represents the most potent natural stimulus for growth in adult skeletal muscle. However, as this molecular-based line of research progresses to investigations in humans, scientists must appreciate the fundamental principles of RE to effectively design such experiments. Therefore, we present herein an updated paradigm of RE biology that integrates fundamental RE principles with the current knowledge of muscle cellular and molecular signalling. RE invokes a sequential cascade consisting of: (i) muscle activation; (ii) signalling events arising from mechanical deformation of muscle fibres, hormones, and immune/inflammatory responses; (iii) protein synthesis due to increased transcription and translation; and (iv) muscle fibre hypertrophy. In this paradigm, RE is considered an ‘upstream’ signal that determines specific downstream events. Therefore, manipulation of the acute RE programme variables (i.e. exercise choice, load, volume, rest period lengths, and exercise order) alters the unique ‘fingerprint’ of the RE stimulus and subsequently modifies the downstream cellular and molecular responses.

Normal electrocardiographic findings: recognising physiological adaptations in athletes

Electrocardiographic changes in athletes are common and usually reflect benign structural and electrical remodelling of the heart as a physiological adaptation to regular and sustained physical training (athletes heart). The ability to identify an abnormality on the 12-lead ECG, suggestive of underlying cardiac disease associated with sudden cardiac death (SCD), is based on a sound working knowledge of the normal ECG characteristics within the athletic population. This document will assist physicians in identifying normal ECG patterns commonly found in athletes. The ECG findings presented as normal in athletes were established by an international consensus panel of experts in sports cardiology and sports medicine.

Maximal Power at Different Percentages of One Repetition Maximum: Influence of Resistance and Gender

National Collegiate Athletic Association Division I athletes were tested to determine the load at which maximal mechanical output is achieved. Athletes performed power testing at 30, 40, 50, 60, and 70% of individual 1 repetition maximum (1RM) in the squat jump, bench press, and hang pull exercises. Additionally, hang pull power testing was performed using free-form (i.e., barbell) and fixed-form (i.e., Smith machine) techniques. There were differences between genders in optimal power output during the squat jump (30–40% of 1RM for men; 30–50% of 1RM for women) and bench throw (30% of 1RM for men; 30–50% of 1RM for women) exercises. There were no gender or form interactions during the hang pull exercise; maximal power output during the hang pull occurred at 30–60% of 1RM. In conclusion, these results indicate that (a) gender differences exist in the load at which maximal power output occurs during the squat jump and bench throw; and (b) although no gender or form interactions occurred during the hang pull exercise, greater power could be generated during fixed-form exercise. In general, 30% of 1RM will elicit peak power outputs for both genders and all exercises used in this study, allowing this standard percentage to be used as a starting point in order to train maximal mechanical power output capabilities in these lifts in strength trained athletes.

Abnormal electrocardiographic findings in athletes: recognising changes suggestive of cardiomyopathy

Cardiomyopathies are a heterogeneous group of heart muscle diseases and collectively are the leading cause of sudden cardiac death (SCD) in young athletes. The 12-lead ECG is utilised as both a screening and diagnostic tool for detecting conditions associated with SCD. Fundamental to the appropriate evaluation of athletes undergoing ECG is an understanding of the ECG findings that may indicate the presence of an underlying pathological cardiac disorder. This article describes ECG findings present in cardiomyopathies afflicting young athletes and outlines appropriate steps for further evaluation of these ECG abnormalities. The ECG findings defined as abnormal in athletes were established by an international consensus panel of experts in sports cardiology and sports medicine.

Abnormal electrocardiographic findings in athletes: recognising changes suggestive of primary electrical disease

Cardiac channelopathies are potentially lethal inherited arrhythmia syndromes and an important cause of sudden cardiac death (SCD) in young athletes. Other cardiac rhythm and conduction disturbances also may indicate the presence of an underlying cardiac disorder. The 12-lead ECG is utilised as both a screening and a diagnostic tool for detecting conditions associated with SCD. Fundamental to the appropriate evaluation of athletes undergoing ECG is an understanding of the ECG findings that may indicate the presence of a pathological cardiac disease. This article describes ECG findings present in primary electrical diseases afflicting young athletes and outlines appropriate steps for further evaluation of these ECG abnormalities. The ECG findings defined as abnormal in athletes were established by an international consensus panel of experts in sports cardiology and sports medicine.

Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism

Hypohydration (decreased total body water) exacerbates the catabolic hormonal response to endurance exercise with unclear effects on anabolic hormones. Limited research exists that evaluates the effect of hypohydration on endocrine responses to resistance exercise; this work merits attention as the acute postexercise hormonal environment potently modulates resistance training adaptations. The purpose of this study was to examine the effect of hydration state on the endocrine and metabolic responses to resistance exercise. Seven healthy resistance-trained men (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three identical resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via controlled water deprivation and exercise-heat stress. Cortisol, epinephrine, norepinephrine, testosterone, growth hormone, insulin-like growth factor-I, insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding resistance exercise, immediately postexercise, and during 60 min of recovery. Body mass decreased 0.2 +/- 0.4, 2.4 +/- 0.4, and 4.8 +/- 0.4% during EU, HY25, and HY50, respectively, supported by humoral and urinary changes that clearly indicated subjects achieved three distinct hydration states. Hypohydration significantly 1) increased circulating concentrations of cortisol and norepinephrine, 2) attenuated the testosterone response to exercise, and 3) altered carbohydrate and lipid metabolism. These results suggest that hypohydration can modify the hormonal and metabolic response to resistance exercise, influencing the postexercise circulatory milieu.

Abnormal electrocardiographic findings in athletes

Cardiomyopathies are a heterogeneous group of heart muscle diseases and collectively are the leading cause of sudden cardiac death (SCD) in young athletes. The 12-lead ECG is utilised as both a screening and diagnostic tool for detecting conditions associated with SCD. Fundamental to the appropriate evaluation of athletes undergoing ECG is an understanding of the ECG findings that may indicate the presence of an underlying pathological cardiac disorder. This article describes ECG findings present in cardiomyopathies afflicting young athletes and outlines appropriate steps for further evaluation of these ECG abnormalities. The ECG findings defined as abnormal in athletes were established by an international consensus panel of experts in sports cardiology and sports medicine.