Training Adaptations – Dr Nicky Keay

Athletic Fatigue: Part 2

3 September 2017

A degree of athletic fatigue following a training session, as described in part 1, is required to set in motion mechanisms to drive beneficial adaptations to exercise. At what point does this process of functional over-reaching tip into non-functional over-reaching denoted by failure to improve sports performance? Or further still along the spectrum and time scale, the chronic situation of overtraining and decrease in performance? Is this a matter of time scale, or degree, or both?

: Integrated Periodisation of Training Load, Nutrition and Recovery keeps an individual on the green plateau, avoiding descent into the red zone, due to an excess or deficiency

Determining the tipping point between these fatigue situations is important for health and performance. A first step is always to exclude underlying organic disease states, be these of Endocrine, systemic inflammatory or infective aetiologies. Thereafter the crucial step is to assess whether the periodisation of training, nutrition and recovery are integrated over a training block and in the longer term over a training season.

What about the application of Endocrine markers to monitor training load? Although the recent studies described below are more applicable to research scenarios, they give some interesting insights into the interactive networks effects of the Endocrine system and the multifactorial nature of fatigue amongst individual athletes.

In the short term, during a 2 day rowing competition, increases in wakening salivary cortisol were noted followed by return towards baseline in subsequent 2 day recovery. Despite individual variability with salivary cortisol measurement, this does at least offer a noninvasive way to adjust training loads around competition time for elite athletes.

Over an 11 day stimulated training camp and recovery during the sport specific preparatory phase of the training season, blood metabolic and Endocrine markers were measured. In the case of an endurance based training camp in cyclists, a significant increase in urea (due to protein breakdown associated with high energy demand training) and decrease in insulin-like growth factor 1 (IGF1) from baseline were noted. Whereas for the strength-based athletes for ball sports, an increase in creatine kinase (CK) was seen, as a result of muscle damage. This study demonstrates how different markers of fatigue are specific to sport discipline and mode of training. Large inter-individual variability existed between the degree of change in markers and degree of fatigue.

In the longer term, for the case of overtraining syndrome potential Endocrine markers have been reviewed. Whilst basal levels of most measured hormones remained stable, a blunted submaximal exercise response of growth hormone (GH), prolactin and ACTH could be indicative of developing overtraining syndrome. Whilst this review is interesting, dynamic testing is not a practical approach and these findings are not specific to over training. Rather this blunted dynamic exercise response would indicate relative suppression of the neuroendocrine hypothalamic-pituitary axis which could potentially involve other stressors such as inadequate sleep or poor nutrition. Although basal levels may lie “within the normal range”, if both pituitary derived stimulating hormone and end endocrine gland hormone concentrations fall in the lower end of the normal ranges (eg low end of range TSH and T4) this is consistent with mild hypothalamic suppression observed over the range of training and fatigue conditions (functional/non-functional and overtraining) and/or Relative Energy Deficiency in Sports (RED-S).

Although the studies above are of research interest, non invasive monitoring, specific to an athlete is more practical for monitoring the effects of training. Several useful easily measurable metrics can give clues: resting heart rate, heart rate variability, power output. Tools on Strava and Training Peaks provide practical insights in monitoring training effectiveness via these metrics. A range of mobile apps makes it ever easier to augment a personal training log to include these training metrics, along with feel, sleep and nutrition. Such a log provides feedback on health and fitness for the individual athlete, in order to personalise training plans. Certainly adding the results from any standard basal blood tests will also help add to the picture, along the lines of building a longitudinal personal biological passport. After all, “normal ranges” are based on the general population, of which top level athletes may represent a subgroup. The more personalised the metics recorded over a long time scale, the more sensitive and useful the process to guide improvement in sport performance.

Context is key when considering athletic fatigue: temporal considerations and individual variation. Certainly the interactive network effects of the Endocrine system are important in determining the degree of adaptation to exercise and therefore sports performance. However the Endocrine system acts in conjunction with many other systems (metabolic, immune and inflammatory), in determining the effectiveness of training in improving sports performance. So it is not surprising that one metric or marker in isolation is not predictive of fatigue status in individual athletes.

For more discussion on Health, Hormones and Human Performance come to the British Association of Sport and Exercise Medicine annual conference

Presentations

References

Athletic Fatigue: Part 1

Endocrine system: balance and interplay in response to exercise training

Temporal considerations in Endocrine/Metabolic interactions Part 1

Fatigue, sport performance and hormones..more on the endocrine system Dr N Keay, British Journal of Sports Medicine 2017

Sport Performance and RED-S, insights from recent Annual Sport and Exercise Medicine and Innovations in Sport and Exercise Nutrition Conferences Dr N Keay, British Journal of Sports Medicine 2017

Capturing effort and recovery: reactive and recuperative cortisol responses to competition in well-trained rowers British Journal of Sports Medicine

Blood-Borne Markers of Fatigue in Competitive Athletes – Results from Simulated Training Camps Plos One

Hormonal aspects of overtraining syndrome: a systematic review BMC Sports Science, Medicine and Rehabilitation 2017

Clusters of Athletes – A follow on from RED-S blog series to put forward impact of RED-S on athlete underperformance Dr N Keay, British Association of Sport and Exercise Medicine 2017

Strava Fitness and Freshness Science4Performance 2017

From population based norms to personalised medicine: Health, Fitness, Sports Performance Dr N Keay, British Journal of Sports Medicine 2017

Sports Endocrinology – what does it have to do with performance? Dr N Keay, British Journal of Sports Medicine 2017

What has your gut microbiome ever done for you?

1 September 2017

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Our body acts as a host to vast array of micro-organisms. Often, we are only aware of these micro-organisms causing unwanted infection: for example when a cut on the skin becomes infected, or we suffer with a bout of infective gastro-intestinal upset. Actually, this perception of the micro-organisms, living both on and inside, only causing unwanted infections is very biased. The microbiome (all the micro-organisms, their genetic material and metabolites produced) plays a vital role in keeping us healthy.

Recent research demonstrates that elite level cyclists host distinct clusters of microbiome communities when compared to controls which contribute to more effective metabolic pathways.

The gut microbiota consist of the range of micro-organisms living in our gut, mainly the colon. Recent research reveals that the diversity and functions of the gut microbiota have far reaching impact on health. For example, there is an important interaction between these micro-organisms and mitochondria, which are the organelles in cells responsible for producing energy. This cross talk is of particular consideration for athletes who seek to optimise energy production for training and competition. The gut microbiota also interact with the immune system and central nervous system function, including behaviour. There is evidence that the gut microbiota even influences brain development.

Microbiome Mitochondria Feedback

On the other side of the coin, any disruption in the beneficial types of gut microbiota have been linked to chronic disease states including obesity, metabolic syndrome and mental health issues. What causes imbalances in gut microbiota to produce such problems? A possible aetiology is a poorly balanced diet, or the side effect of medication which does not support the growth and function of beneficial bacteria. Rather an overgrowth of potentially harmful bacteria is favoured: dysbiosis. In athletes there is a condition know as “leaky gut” which can result from endurance training. In this scenario, blood is diverted away from the gut during exercise to the exercising muscles. After stopping exercise, blood flow is restored to the gut resulting in a mild reperfusion injury. This results in a slightly “leaky gut” so that unwanted bacteria in the gut are able to pass into the body and provoke an inflammatory response. Equally this situation can also mean desirable nutrients in the gut as less well absorbed. Although a degree of inflammatory response supports desirable adaptations to exercise, clearly an over-response will be counter productive to improving sports performance.

The gut microbiota have been reported to regulate immune function. Athletes in heavy training can experience suppressed functional immunity so any strategies to support the gut microbiota will potentially be beneficial in preventing infection.

What can you do to support a beneficial gut microbiota to support health and sport performance?

Try to include at least one fermented food source in your diet every day to boost your probiotic bacteria. Try sourdough bread, yogurt, kefir (similar to yogurt), sauerkraut, kimchi (Korean fermented vegetables), tempeh and miso (fermented soya products) and kombucha (fermented teas). These products can be found in health food shops and are becoming more widely available in some supermarkets and lunch places.
Regularly eat pre-biotic foods like garlic, onion, leeks, chickpeas, beans and lentils. These provide fuel for your probiotic bacteria, enabling them to proliferate.
Have adequate fibre in your diet from a wide variety of plant foods: eg wholegrains, legumes, vegetables, fruits, nuts, seeds. Dietary fibre is fermented by your probiotic bacteria to produce short chain fatty acids (SCFAs) which play a key role in keeping your gut healthy.
Consume foods and drinks rich in polyphenols: eg berries, green tea, coffee, black tea, red wine, dark chocolate, apples. Polyphenols, found in many plant foods, have been shown to help increase probiotic bacteria in the gut.
Take a good quality, multi-species probiotic supplement during winter, heavy training blocks and when travelling abroad, especially for races. To find out more about the potential benefits of probiotic supplementation for athletes, see this blog by nutritional therapist Jo Scott-Dalgleish: http://www.endurancesportsnutritionist.co.uk/blog/probiotics-guide-endurance-athlete/

To find out more about the interaction between Health, Hormones and Human Performance come to the British Association of Sport and Exercise Medicine annual conference

References

Community characteristics of the gut microbiomes of competitive cyclists Microbiome August 2017

Ubiquitous Microbiome: impact on health, sport performance and disease

Endocrine system: balance and interplay in response to exercise training

Inflammation: Why and How Much? Dr N. Keay, British Association of Sport and Exercise Medicine 2017

Athletic Fatigue: Part 1

1 September 2017

Interpreting athletic fatigue is not easy. Consideration has to be given to context and time scale. What are the markers and metrics that can help identify where an athlete lies in the optimal balance between training, recovery and nutrition which support beneficial adaptations to exercise whilst avoiding the pitfalls of fatigue and maladaptation? This blog will discuss the mechanisms of athletic fatigue in the short term.

Screen Shot 2017-08-30 at 09.17.58 — Proposed causes of fatigue dependent on duration and intensity of training session

In the short term, during an endurance training session or race, the temporal sequence of athletic fatigue depends on duration and intensity. It is proposed that below lactate threshold (LT1), a central mechanism governs: increasing central motor drive is required to maintain skeletal muscular power output until neuromuscular fatigue cannot be overcome. From lactate threshold (LT1) to lactate turn point (LT2), a combination of central and peripheral factors (such as glycogen depletion) are thought to underpin fatigue. During high intensity efforts, above LT2 (which correspond to efforts at critical power), accumulation of peripheral metabolites and inability to restore homeostasis predominate in causing fatigue and ultimately inability to continue, leading to “task failure”. Of course there is a continuum and interaction of the mechanisms determining this power-duration relationship. As glycogen stores deplete this impacts muscle contractility by impairing release of calcium from the sarcoplasmic reticulum in skeletal muscle. Accumulation of metabolites could stimulate inhibitory afferent feedback to central motor drive for muscle contraction, combined with decrease in blood glucose impacting central nervous system (CNS) function.

Even if you are a keen athlete, it may not be possible to perform a lactate tolerance or VO2 max test under lab conditions. However a range of metrics, such as heart rate and power output, can be readily collected using personalised monitoring devices and then analysed. These metrics are related to physiological markers. For example heart rate and power output are surrogate markers of plasma lactate concentration and thus can be used to determine training zones.

A training session needs to provoke a degree of training stress, reflected by some short term fatigue, to set in motion adaptations to exercise. At a cellular level this includes oxidative stress and exerkines released by exercising tissues, backed up by Endocrine responses that continue to take effect after completing training during recovery and sleep. Repeated bouts of exercise training, followed by adequate recovery, result in a stepwise increase in fitness. Adequate periodised nutrition to match variations in demand from training also need to be factored in to prevent the Endocrine system dysfunction seen in Relative Energy Deficiency in Sports (RED-S), which impairs Endocrine response to training and sports performance. Integrated periodisation of training/recovery/nutrition is essential to support beneficial multi-system adaptations to exercise on a day to day time scale, over successive training blocks and encompassing the whole training and competition season. Psychological aspects cannot be underestimated. At what point does motivation become obsession?

In Part 2 the causes of athletic fatigue over a longer time scale will be discussed, from training blocks to encompassing whole season.

For more discussion on Health, Hormones and Human Performance come to the British Association of Sport and Exercise Medicine annual conference

Presentations

References

Endocrine system: balance and interplay in response to exercise training

Power–duration relationship: Physiology, fatigue, and the limits of human performance European Journal of Sport Science 2016

Strava Ride Statistics Science4Performance 2017

Sleep for health and sports performance Dr N Keay, British Journal of Sports Medicine 2017

Relative Energy Deficiency in Sports (RED-S) Practical Considerations for Endurance Athletes

Sports Endocrinology – what does it have to do with performance? Dr N Keay, British Journal of Sports Medicine 2017

Optimal Health: For All Athletes! Part 4 – Mechanisms Dr N Keay, British Association of Sport and Exercise Medicine 2017

Addiction to Exercise – what distinguishes a healthy level of commitment from exercise addiction? Dr N Keay, British Journal of Sports Medicine 2017

Endocrine system: balance and interplay in response to exercise training

12 June 2017

The process of homeostasis maintains a steady internal milieu. So how is it possible for adaptations to occur? What are the internal mechanisms that determine a good outcome versus a negative one?

Changes in the external environment, such as exercise training, challenge homeostasis, producing spatial and temporal responses in the internal environment. These cause interactions between muscle, bone and gut, modulated by the Endocrine system. The degree and nature of these responses dictate whether a positive adaptation occurs. An excessive response, or a response not in tune with the networks of the Endocrine system, can hinder adaptation or produce a maladaptive response. The balance and interplay of internal responses are crucial in determining the outcome to exercise training in the individual.

F=MA

Local responses in exercising tissues

Exercising tissues release exerkines (metabolites, nucleic acids, peptides) which are packaged in exosomes and microvesicles. The content of these vesicle packages increases with intensity of endurance exercise in a dose-dependent manner. These exerkines have autocrine and paracrine effects, which modulate systemic adaptations to endurance exercise in the tissues themselves and those in the vicinity.

The range of these molecular responses from exercising tissues has been identified applying multi-omics (epigenomic, transcriptomic and proteomic analyses). Furthermore variance in trainability has been shown to be correlated with the integrated responses of tissue molecular signalling pathways to endurance exercise.

In a similar manner, the degree of inflammatory response and production of reactive oxygen and nitrogen species (RONS) to exercise mediate favourable adaptations. Inter-individual variations in redox status has been shown to determine the ability to adapt to exercise training. However, unlimited increase in response does not necessarily produce a better outcome. An over response to exercise in these signalling pathways, hinders adaptation.

Exercise promotes bone adaptation in terms of bone material, structure and muscle action. Paracrine crosstalk occurs between muscle and bone. Muscle myokines and insulin like growth factor 1 (IGF1) favour bone formation, whilst inflammatory molecules, such as interleukin 6 (Il-6) released during muscle contractions, favour bone reabsorption. The balance between these opposing processes determines whether bone remodelling is effective, or whether bone stress reactions occur over a pathological continuum. These responses and adaptations occur on the background of lifespan Endocrine environment, which impacts the outcome.

Gut microbiota

The gut microbiota support the regulation of inflammation at the local and systemic level. Furthermore the communication between the gut microbiota and mitochondria has been described as an important interaction in facilitating adaptive responses to exercise. Mitochondria are organelles crucial for production of ATP, as well as RONS. The gut microbiota are involved in mitochondrial biogenesis by regulating key mitochondrial transcriptional factors and enzymes . Furthermore, the metabolites of the gut microbiota such as short chain fatty acids, modulate the inflammatory effects of mitochondrial oxidative stress. Conversely genetic variants in the mitochondrial genome could impact mitochondrial function and thus the gut microbiota in terms of composition and activity.

The gut microbiota have a role in regulating intestinal permeability. Leaky gut is where epithelial integrity is lost at the tight junctions between cells in the gut lining. Leaky gut can occur in gut dysbiosis and also following endurance exercise where re-perfusion injury produces acute hyper-permeability. In these instances, increased gut permeability augments the antigen load and causes increased systemic inflammation and potentially can trigger autoimmune disease. This demonstrates that an excessive inflammatory response to exercise can hinder positive adaptation

Metabolic adaptations

Metabolic flexibility, the ability to respond and adapt to changes in metabolic demand, is enhanced with exercise training through these autocrine, paracrine and Endocrine mechanisms. Metabolic flexibility supports energy availability and fuel selection during exercise. Exercise mimetics, such as artificial metabolic modulators, have been reported to up-regulate gene expression to shift metabolism to fat oxidation in exercising muscle. This would potentially extend the limit of endurance exercise. However this “short cut” to adaptation favouring improved sport performance is illegal, with such molecular ligands on the World Anti-Doping Agency (WADA) banned list.

Hierarchy of control

There is a hierarchy of control in modulating multi-system adaptations to exercise. The Endocrine system is key. Exercise per se produces an Endocrine response, for example exercise is a key stimulus for growth hormone release via the hypothalamus, the neuroendocrine gatekeeper. Growth hormone supports the anabolic response to exercise. In addition, the Endocrine milieu during the lifespan has an impact on response and adaptations to exercise. Any disruption in the Endocrine system hinders adaptive changes. Endocrine dysfunction may occur as a result of non-integrated periodisation of exercise/nutrition and recovery as seen in relative energy deficiency in sports (RED-S). Dysfunction can also occur due to an Endocrine pathology.

Conclusion

Changes in external stimuli, such as exercise and nutrition, produce internal responses on autocrine, paracrine and Endocrine levels. These molecular signalling pathways drive adaptive changes through integrated, network effects. However any imbalances in these interactive responses can hinder desired adaptive changes and even result in negative maladaptive outcomes to exercise training.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Keay N, Logobardi S, Ehrnborg C, Cittadini A, Rosen T, Healy ML, Dall R, Bassett E, Pentecost C, Powrie J, Boroujerdi M, Jorgensen JOL, Sacca L. Growth hormone (GH) effects on bone and collagen turnover in healthy adults and its potential as a marker of GH abuse in sport: a double blind, placebo controlled study. Journal of Endocrinology and Metabolism. 85 (4) 1505-1512. 2000.

Sport Endocrinology presentations

Sports Endocrinology – what does it have to do with performance? Dr N.Keay, British Journal of Sport Medicine

Balance of recovery and adaptation for sports performance Dr N.Keay, British Association of Sport and Exercise Medicine

Inflammation: Why and How Much? Dr N.Keay, British Association of Sport and Exercise Medicine

Clusters of Athletes – A follow on from RED-S blog series to put forward impact of RED-S on athlete underperformance Dr N.Keay, British Association of Sport and Exercise Medicine

Optimal Health: For All Athletes! Part 4 – Mechanisms Dr N.Keay, British Association of Sport and Exercise Medicine

The potential of endurance exercise-derived exosomes to treat metabolic diseases Nature Reviews Endocrinology

Exosomes as Mediators of the Systemic Adaptations to Endurance Exercise Cold Spring Harbor Perspectives in Medicine

Genomic and transcriptomic predictors of response levels to endurance exercise training
Journal of Physiology

Adaptations to endurance training depend on exercise-induced oxidative stress: exploiting redox inter-individual variability Acta Physiologica

Mechanical basis of bone strength: influence of bone material, bone structure and muscle action Journal of Musculoskeletal and Neuronal Interactions

The Crosstalk between the Gut Microbiota and Mitochondria during Exercise Frontiers in Physiology

Leaky Gut As a Danger Signal for Autoimmune Diseases Frontiers in Immunology

Metabolic Flexibility in Health and Disease Cell Metabolism

Hormones and Sports Performance

PPARδ Promotes Running Endurance by Preserving Glucose Cell Metabolism

Clusters of Athletes

2 April 2017

At some time, most athletes experience periods of underperformance. What are the potential causes and contributing factors?

classification

Effective training improves sports performance through a process of adaptation that occurs, at both the cellular and system levels, during the recovery phase. Training overload must be balanced with sufficient subsequent recovery. A long-term improvement in form is expected, following a temporary dip in performance, due to short-term fatigue.

However, when an athlete experiences a stagnation of performance, what are the potential underlying causes? How should these be addressed to prevent an acute situation developing into a more chronic spiral of decreasing performance?

Depending on clinical presentation, the first step is to exclude medical conditions. Potential infective causes include Epstein Barr virus (particularly in young athletes), Lyme disease and Weil’s disease. Systemic inflammatory conditions should be considered. Endocrine and metabolic causes include pituitary, gonadal, adrenal, thyroid dysfunction, blood sugar control, and malabsorption.

If medical conditions are excluded, attention should turn to the athlete’s energy balance in the context of adherence to the current training plan. Potential causes of underperformance, the inability to improve in training and competition, are illustrated in the diagram above.

Athletes in the upper right quadrant fail to live up to performance expectations, in spite of maintaining a good energy balance while adhering to the prescribed training plan. However, they may represent non-functional overreaching, where overload is not balanced with sufficient recovery. In other words, the periodisation of training and recovery is not optimised. The balance between chronic training load (fitness) and acute training load (fatigue) provides a useful metric for assessing form. Heart rate variability (HRV) can be another potentially useful measure in detecting aerobic, endurance fatigue. If the training plan is not producing the expected improvements, then this plan needs revising. Don’t forget that sleep is essential to facilitate endocrine driven adaptations to exercise training.

Athletes in the lower right quadrant are of more concern. Inadequate energy balance, especially during periods of increased training load or intentional weight loss, can be a cause of underperformance, despite the athlete being able to adhere to the training plan. This would correspond to being at risk of developing relative energy deficiency in sport (RED-S) on the amber warning in the risk stratification laid out by the International Olympic Committee.

Both of these groups are able to adhere to a training plan, but suboptimal training and recovery periodisation and/or insufficient energy intake can produce a situation of underperformance. Intervention is required to prevent them moving into the clusters on the left, representing a more chronic underperformance scenarios that are therefore more difficult to rectify.

Athletes in the upper left quadrant exhibit overtraining syndrome: a prolonged maladaptation process accompanied by a decrease in performance (not merely stagnation) and inability to adhere to training plan. The metric of decreased HRV and inability of heart rate to accelerate in response to exercise have been suggested as markers of overtraining.

Those athletes in the lower left quadrant fall into the RED-S category, where multiple interacting Endocrine networks are impacted by an energy deficient state. RED-S not only impairs sports performance, but impacts both current and future health. For example low endogenous levels of sex steroids and insulin-like growth factor 1 (IGF1) disrupt formation of bone microarchitecture and bone mineralisation, resulting in increased risk of recurrent stress fracture in addition to potentially irreversible bone loss in the longer term. In cases of recurrent injury and underperformance amongst athletes it is imperative to exclude Endocrine dysfunction and then consider whether RED-S is the fundamental cause.

There are many potential causes of underperformance in athletes. Once medical conditions have been excluded, the main aim should be to prevent acute situations becoming chronic and therefore more difficult to resolve.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Sport Endocrinology Dr N. Keay, British Journal of Sport Medicine 2017

Sport Performance and RED-S, insights from recent Annual Sport and Exercise Medicine and Innovations in Sport and Exercise Nutrition Conferences Dr N.Keay, British Journal of Sport Medicine 2017

Relative Energy Deficiency in Sport CPD module for British Association of Sport and Exercise Medicine

Optimal Health: For All Athletes! Part 4 – Mechanisms, Dr N. Keay, British Association of Sport and Exercise Medicine

Balance of recovery and adaptation for sports performance Dr N. Keay, British Association of Sport and Exercise Medicine

Sleep for health and sports performance Dr N. Keay, British Journal of Sport Medicine

Optimal health: including female athletes! Part 1 Bones Dr N.Keay, British Journal of Sport Medicine

Inflammation: why and how much? Dr N. Keay, British Association of Sport and Exercise Medicine

Fatigue, Sport Performance and Hormones… Dr N.Keay, British Journal of Sport Medicine

Part 3: Training Stress Balance—So What? Joe Friel

Heart Rate Variability (HRV) Science for Sport

Relative Energy Deficiency in sport (REDs) Lecture by Professor Jorum Sundgot-Borgen, IOC working group on female athlete triad and IOC working group on body composition, health and performance. BAEM Spring Conference 2015.

Prevention, Diagnosis, and Treatment of the Overtraining Syndrome: Joint Consensus Statement of the European College of Sport Science and the American College of
Sports Medicine. Joint Consensus Statement. Medicine & Science in Sports & Exercise 2012

Sports Endocrinology

25 March 2017

SportsEndocrinologyWordCloud

The Endocrine system comprises various glands distributed throughout the body that secrete hormones to circulate in the blood stream. These chemical messengers, have effects on a vast range of tissue types, organs and therefore regulate metabolic and physiological processes occurring in systems throughout the body.

The various hormones produced by the Endocrine system do not work in isolation; they have interactive network effects. The magnitude of influence of a hormone is largely determined by its circulating concentration. This in turn is regulated by feedback loops. For example, too much circulating hormone will have negative feedback effect causing the control-releasing system to down regulate, which will in turn bring the level of the circulating hormone back into range. Ovulation in the menstrual cycle is a rare example of a process induced by positive hormonal feedback.

In the control system of hormone release, there are interactions with other inputs in addition to the circulating concentration of the hormone. The hypothalamus (gland in the brain) is a key gateway in the neuro-endocrine system, coordinating inputs from many sources to regulate output of the pituitary gland, which produces the major stimulating hormones to act on the Endocrine glands throughout the body.

growthhormone

The Endocrine system displays complex dynamics. There are temporal variations in secretion of hormones both in the long term during an individual’s lifetime and on shorter timescales, as seen in the diurnal variation of some hormones such as cortisol, displaying a circadian rhythm of secretion. The most fascinating and complex control system is found in the hypothalamic-pituitary-ovarian axis. Variation in both frequency and amplitude of gonadotrophin releasing factor (GnRH) secretion from the hypothalamus dictates initiation of menarche and the subsequent distinct pattern of cyclical patterns of the sex steroids, oestrogen and progesterone.

So what have the Endocrine system and hormone production got to do with athletes and sport performance?

Exercise training stimulates release of certain hormones that support favourable adaptive changes. For example, exercise is a major stimulus of growth hormone, whose action positively affects body composition in terms of lean mass, bone density and reduction of visceral fat.
Disruption of hormones secreted from the Endocrine system can impair sport performance and have potential long term adverse health risks for athletes. This picture is seen in the female athlete triad (disordered eating, amenorrhoea and low bone mineral density) and relative energy deficiency in sport (RED-S) with multi-system effects. In this situation there is a mismatch between dietary energy intake (including diet quality) and energy expenditure through training. The net result is a shift to an energy saving mode in the Endocrine system, which impedes both improvement in sport performance and health. RED-S should certainly be considered among the potential causes of sport underperformance, suboptimal health and recurrent injury, with appropriate medical support being provided.
Caution! Athletic hypothalamic amenorrhoea, as seen in female athletes (in female athlete triad and RED-S) is a diagnosis of exclusion. Other causes of secondary amenorrhoea (cessation of periods >6 months) should be excluded such as pregnancy, polycystic ovary syndrome (PCOS), prolactinoma, ovarian failure and primary thyroid dysfunction.
Unfortunately the beneficial effects of some hormones on sport performance are misused in the case of doping with growth hormone, erythropoeitin (EPO) and anabolic steroids. Excess administered exogenous hormones not only disrupt the normal control feedback loops, but have very serious health risks, which are seen in disease states of excess endogenous hormone secretion.

So the Endocrine system and the circulating hormones are key players not only in supporting health, but in determining sport performance in athletes.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Sport Performance and RED-S, insights from recent Annual Sport and Exercise Medicine and Innovations in Sport and Exercise Nutrition Conferences Dr N. Keay, British Journal of Sports Medicine 17/3/17

Teaching module on RED-S for British Association of Sport and Exercise Medicine as CPD for Sports Physicians

Optimal Health: Including Female Athletes! Part 1 – Bones Dr N. Keay, British Journal of Sport Medicine 26/3/17

Optimal Health: Including Male Athletes! Part 2 – REDs Dr N. Keay, British Journal of Sport Medicine 4/4/17

Optimal health: especially young athletes! Part 3 Consequences of Relative Energy Deficiency in sports Dr N. Keay, British Association of Sport and Exercise Medicine 13/4/17

Optimal health: for all athletes! Part 4 Mechanisms Dr N. Keay, British Association of Sport and Exercise Medicine 13/4/17

Enhancing sport performance: part 1 Dr N. Keay, British Association of Sport and Exercise Medicine

Enhancing sports performance: part 3

From population based norms to personalised medicine: Health, Fitness, Sports Performance Dr N. Keay, British Journal of Sport Medicine

Sleep for health and sports performance Dr N. Keay, British Journal of Sport Medicine

Balance of recovery and adaptation for sports performance Dr N. Keay, British Association of Sport and Exercise Medicine

Clusters of athletes Dr N. Keay, British Association of Sport and Exercise Medicine

Inflammation: why and how much? Dr N. Keay, British Association of Sport and Exercise Medicine

Fatigue, Sport Performance and Hormones…Dr N. Keay, British Journal of Sport Medicine

Wallace J, Cuneo R, Keay N, Sonksen P. Responses of markers of bone and collagen turover to exercise, growth hormone (GH) administration and GH withdrawal in trained adult males. Journal of Endocrinology and Metabolism 2000. 85 (1): 124-33.

Keay N. The effects of growth hormone misuse/abuse. Use and abuse of hormonal agents: Sport 1999. Vol 7, no 3, 11-12.

Wallace J, Cuneo R, Baxter R, Orskov H, Keay N, Sonksen P. Responses of the growth hormone (GH) and insulin-like factor axis to exercise,GH administration and GH withdrawal in trained adult males: a potential test for GH abuse in sport. Journal of Endocrinology and Metabolism 1999. 84 (10): 3591-601.

Keay N, Logobardi S, Ehrnborg C, Cittadini A, Rosen T, Healy ML, Dall R, Bassett E, Pentecost C, Powrie J, Boroujerdi M, Jorgensen JOL, Sacca L. Growth hormone (GH) effects on bone and collagen turnover in healthy adults and its potential usefulness as in the detection of GH abuse in sport: a double blind, placebo controlled study. Endocrine Society Conference 1999.

Wallace J, Cuneo R, Keay N. Bone markers and growth hormone abuse in athletes. Growth hormone and IGF Research, vol 8: 4: 348.

Keay N, Fogelman I, Blake G. Effects of dance training on development,endocrine status and bone mineral density in young girls.Current Research in Osteoporosis and bone mineral measurement 103, June 1998.

Keay N, Effects of dance training on development, endocrine status and bone mineral density in young girls, Journal of Endocrinology, November 1997, vol 155, OC15.

Keay N, Fogelman I, Blake G. Bone mineral density in professional female dancers. British Journal of Sports Medicine, vol 31 no2, 143-7, June 1997.

Keay N. Bone mineral density in professional female dancers. IOC World Congress on Sports Sciences. October 1997.

Keay N, Bone Mineral Density in Professional Female Dancers, Journal of Endocrinology, November 1996, volume 151, supplement p5.

Sport Performance and Relative Energy Deficiency in Sport

11 March 2017

The Holy Grail of any training program is to improve performance and achieve goals.

Periodisation of training is essential in order to maximise beneficial adaptations for improved performance. Physiological adaptations occur after exercise during the rest period, with repeated exercise/rest cycles leading to “super adaptation”. Adaptations occur at the system level, for example cardiovascular system, and at the cellular level in mitochondria. An increase in mitochondria biogenesis in skeletal muscle occurs in response to exercise training, as described by Dr Andrew Philip at a recent conference at the Royal Society of Medicine (RSM). This cellular level adaptation translates to improved performance with a right shift of the lactate tolerance curve.

The degree of this response is probably genetically determined, though further research would be required to establish causal links, bearing in mind the ethical considerations laid out in the recent position statement from the Australian Institute of Sport (AIS) on genetic testing in sport. Dr David Hughes, Chief Medical Officer of the AIS, explored this ethical stance at a fascinating seminar in London. Genetic testing in sport may be a potentially useful tool for supporting athletes, for example to predict risk of tendon injury or response to exercise and therefore guide training. However, genetic testing should not be used to exclude or include athletes in talent programmes. Although there are polymorphisms associated with currently successful endurance and power athletes, these do not have predictive power. There are many other aspects associated with becoming a successful athlete such as psychology. There is no place for gene doping to improve performance as this is both unethical and unsafe.

To facilitate adaptation, exercise should be combined with periodised rest and nutrition appropriate for the type of sport, as described by Dr Kevin Currell at the conference on “Innovations in sport and exercise nutrition”. Marginal gains have a cumulative effect. However, as discussed by Professor Asker Jeukendrup, performance is more than physiology. Any recommendations to improve performance should be given in context of the situation and the individual. In my opinion women are often underrepresented in studies on athletes and therefore further research is needed in order to be in a position to recommend personalised plans that take into account both gender and individual variability. As suggested by Dr Courtney Kipps at the Sport and Exercise Conference (SEM) in London, generic recommendations to amateur athletes, whether male or female, taking part in marathons could contribute to women being at risk of developing exercise associated hyponatraemia.

For innovation in sport to occur, complex problems approached with an open mind are more likely to facilitate improvement as described by Dr Scott Drawer at the RSM. Nevertheless, there tends to be a diffusion from the innovators and early adapters through to the laggards.

Along the path to attaining the Holy Grail of improved performance there are potential stumbling blocks. For example, overreaching in the short term and overtraining in the longer term can result in underperformance. The underlying issue is a mismatch between periodisation of training and recovery resulting in maladapataion. This situation is magnified in the case of athletes with relative energy deficiency in sport (RED-S). Due to a mismatch of energy intake and expenditure, any attempt at increase in training load will not produce the expected adaptations and improvement in performance. Nutritional supplements will not fix the underlying problem. Nor will treatments for recurrent injuries. As described by Dr Roger Wolman at the London SEM conference, short term bisphosphonante treatment can improve healing in selected athletes with stress fractures or bone marrow lesions. However if the underlying cause of drop in performance or recurrent injury is RED-S, then tackling the fundamental cause is the only long term solution for both health and sport performance.

Network effects of interactions lead to sport underperformance. Amongst underperforming athletes there will be clusters of athletes displaying certain behaviours and symptoms, which will be discussed in more detail in my next blog. In the case of RED-S as the underlying cause for underperformance, the most effective way to address this multi-system issue is to raise awareness to the potential risk factors in order to support athletes in attaining their full potential.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Teaching module RED-S British Association Sport and Exercise Medicine

From population based norms to personalised medicine: Health, Fitness, Sports Performance Dr N. Keay, British Journal of Sport Medicine 22/2/17

Balance of recovery and adaptation for sports performance Dr N. Keay, British Association Sport and Exercise Medicine 21/1/17

Sleep for health and sports performance Dr N. Keay, British Journal of Sport Medicine 7/7/17

Fatigue, Sport Performance and Hormones… Dr N. Keay, British Journal of Sport Medicine

Annual Sport and Exercise Medicine Conference, London 8/3/17

Bisphosphonates in the athlete. Dr Roger Wolman, Consultant in Rheumatology and Sport and Exercise Medicine, Royal National Orthopaedic Hospital

Collapse during endurance training. Dr Courtney Kipps, Consultant in Sport and Exercise Medicine. Consultant to Institute of Sport, medical director of London and Blenheim Triathlons

Innovations in Sport and Exercise Nutrition. Royal Society of Medicine 7/3/17

Identifying the challenges: managing research and innovations programme. Dr Scott Drawer, Head of Performance, Sky Hub

Exercise and nutritional approaches to maximise mitochondrial adaptation to endurance exercise. Dr Andrew Philip, Senior Lecturer, University of Birmingham

Making technical nutrition data consumer friendly. Professor Asker Jeukendrup, Professor of Exercise Metabolism, Loughborough University

Innovation and elite athletes: what’s important to the applied sport nutritionists? Dr Kevin Currell, Director of Science and Technical Development, The English Institute of Sport

Genetic Testing and Research in Sport. Dr David Hughes, Chief Medical Officer Australian Institute of Sport. Seminar 10/3/17

Effects of adaptive responses to heat exposure on exercise performance

Over Training Syndrome, Ian Craig, Webinar Human Kinetics 8/3/17

The Fatigued Athlete BASEM Spring Conference 2014

Mountjoy M, Sundgot-Borgen J, Burke L, Carter S, Constantini N, Lebrun C, Meyer N, Sherman R, Steffen K, Budgett R, Ljungqvist A. The IOC consensus statement: beyond the Female Athlete Triad-Relative Energy Deficiency in Sport (RED-S).Br J Sports Med. 2014 Apr;48(7):491-7.

Inflammation: why and how much?

19 February 2017

Inflammation: optimal or overreaction

Systemic autoimmune disease is a chronic overreaction of the inflammatory system. Exercise training is structured to provoke the optimal level of inflammation for adaptation to facilitate sport performance. This blog describes some of the recent significant advances in the understanding of the underlying mechanisms of inflammation and its interactions with the endocrine system, immunity and the microbiome, in relation to autoimmune disease. Applying this knowledge to the adaptive inflammatory effects of training in sport represents a potentially hugely beneficial area of future research.

The ubiquitous microbiome

There has been much discussion on the key role of the microbiome, eloquently described by Professor Tim Spector, Professor of Genetic Epidemiology, King’s College, London at recent conferences at the Royal Society of Medicine and The Royal College of Physicians. The microbiome is the DNA of all the microbes in our body. The diversity of the microbiota community in the gut wall of the colon appears to have the most profound effects in terms of disease prediction and indeed a better indicator of developing autoimmune conditions (such as inflammatory bowel disease and rheumatoid arthritis) and metabolic conditions (such as obesity and diabetes mellitus) than our own DNA. So how does the diversity of the gut microbiome have such a profound impact?

It appears that in order to promote diversity of the gut micobiota, prebiotics such as inulin found in fibrous foods should be ingested and then “fertilised” with probiotics found in fermented foods. Enhancing the diversity of the gut microbiome supports the production of short-chain fatty acids which have far reaching influences on epigenetic and immune regulation, the brain, gut hormones and the liver. Furthermore, the diurnal rhythmic movement of the gut microbiota have been shown to regulate host circadian epigenetic, transcriptional and metabolite oscillations which impacts host physiology and disease susceptibility.

In inflammatory conditions such as autoimmune disease, a decrease in the diversity of “good” microbiota has been described. Furthermore, if a decrease in beneficial microbiota is the primary event, then this can lead to an increase in the likelihood of developing autoimmune disease. What is the mechanism of this dynamic interaction between the microbiome and immunity?

Immunity and inflammation

In recent research, the protein receptor marker of microbiota in the gut has been shown to modulate intestinal serotonin transporter activity. Serotonin (5-hydroxytryptamine 5-HT) has shown to be an essential intestinal physiological neuromodulator that is also involved in inflammatory bowel disease. In addition, an increase in inflammatory cytokines such as interleukin 6 and tumour necrosis factor alpha, is know to be associated with low levels of cerebral serotonin and dopamine. The causal link between disrupted immune function and increased inflammation, as in autoimmune disease, is an unfavourable microbiome. Development of autoimmune disease is often multifactorial, for example, a change in the microbiome might trigger gene expression with adverse effects. Indeed gene expression (independent of sex steroids) has been shown to account for increased prevalence of autoimmune disease in women.

Depression of serotonin levels

Low levels of the neurotransmitter serotonin are know to be linked to depression. Hence prescription of selective serotonin uptake inhibitors to those suffering with depression. However recent research has now revealed a dynamic interaction between peripheral and cerebral effects of the microbiome on immunity and mood, mediated via the circadian release of key hormones such as serotonin. Serotonin is synthesised from precursor tryptophan in the gastrointestinal tract and central nervous system. Low mood in autoimmune disease could be due to psychological factors: knowing that this is a chronic condition with reduced life expectancy. Reduced serotonin, may be a further biochemical reason. Potentially lack of sleep due to pain in autoimmune disease would also suppress serotonin levels.

Applications for microbiome/immunity/inflammation interactions

How will these findings from recent research help in optimising inflammatory mediated adaptations to exercise training and support the understanding and treatment of autoimmune disease? It has been suggested that serotonin could be a treatment for rheumatoid arthritis, as 5HT appears to have a peripheral immuno-regulatoty role in the pathophysiology of this autoimmune disease. Optimising the microbiome, with prebiotics and probiotics, may improve disease activity and improve response to treatment with biologics.

Is the nature of an autoimmune disease such as rheumatoid arthritis (RA) changing? Deformed hands with swollen joints were a perennial favourite for medical examinations. However as described recently at a conference at Royal College of Physicians, although joint destruction is still a feature of RA, this seems to be accompanied by less joint swelling and involvement of greater range of joints. Are the triggers changing rather than a change in the nature of disease? How do nutrition and medication impact the microbiome?

For athletes, apart from periodising energy requirements and micronutrients to support training, encouraging a diverse microbiome will potentially support adaptive changes to training.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Balance of recovery and adaptation for sports performance. Dr N. Keay, British Association of Sports and Exercise Medicine

Sleep for health and sports performance. Dr N. Keay, British Journal of Sport and Exercise Medicine

Conference Royal Society of Medicine. “Food: the good, the bad and the ugly” 1/2/17

“Food, microbes and health” Professor Tim Spector, Professor of Genetic Epidemiology, King’s College, London

“Nutrition and the gut: food as trigger for disease; food as medicine” Dr Charlie Lees, Chair Scottish Society of Gastroenterology IBD Interest Group. European Crohn’s and Colitis Organisation Committe

“Nutrition and its effect on the immune system” Dr Liam O’Mahony, Head of Molecular Immunology, swiss Institute of Allergy and Asthma Research

Advanced Medicine Conference. Royal College of Physicians 13-16 February 2017

” The gut microbiome clinical and physiological tolerance” Professor Tim Spector, Professor of Genetic Epidemiology, King’s College, London

“Rheumatoid arthritis-ensuring everyone gets the best treatment” Dr Neil Snowden

Microbiota Diurnal Rhythmicity Programs Host Transcriptome Oscillations Cell Volume 167, Issue 6, p1495–1510.e12, 1 December 2016

Intestinal Serotonin Transporter Inhibition by Toll-Like Receptor 2 Activation. A Feedback Modulation. Eva Latorre , Elena Layunta, Laura Grasa, Marta Castro, Julián Pardo, Fernando Gomollón, Ana I. Alcalde †, José E. Mesonero. Published: December 29, 2016

A gene network regulated by the transcription factor VGLL3 as a promoter of sex-biased autoimmune diseases. Yun Liang, Lam C Tsoi, Xianying Xing, Maria A Beamer, William R Swindell, Mrinal K Sarkar, Celine C Berthier, Philip E Stuart, Paul W Harms, Rajan P Nair, James T Elder, John J Voorhees, J Michelle Kahlenberg & Johann E Gudjonsson
Nature Immunology 18, 152–160 (2017)

Serotonin Is Involved in Autoimmune Arthritis through Th17 Immunity and Bone Resorption. Yasmine Chabbi-Achengli, Tereza Coman, Corinne Collet, Jacques Callebert, Michelangelo Corcelli, Hilène Lin, Rachel Rignault, Michel Dy, Marie-Christine de Vernejoul, Francine Côté. The American Journal of Pathology. April 2016 Volume 186, Issue 4, Pages 927–937

Sleep for Health and Sports Performance

22 December 2016

“Sleep.. chief nourisher in life’s feast,” Macbeth.

In my blog for British Association of Sport and Exercise Medicine, I described improving sport performance by balancing the adaptive changes induced by training together with the recovery strategies to facilitate this, both in the short and long term. alec0120-12x17

A recovery strategy which is vital in supporting both health and sport performance, during all stages of the training cycle is sleep.

Sufficient sleep is especially important in young athletes for growth and development and in order to support adaptive changes stimulated by training and to prevent injury. Amongst teenage athletes, studies have shown that a lack of sleep is associated with higher incidence of injury. This may be partly due to impaired proprioception associated with reduced sleep. Sleep is vital for consolidating neurological function and protein synthesis, for example in skeletal muscle. Sleep and exercise are both stimuli for growth hormone release from the anterior pituitary, which mediates some of these adaptive effects.

Lack of sleep can also interfere with functioning of the immune system due to disruption of the circadian rhythm of secretion in key areas of the Endocrine system. Athletes in heavy training, with high “stress” loads and associated elevated cortisol can also experience functional immunosuppression. So a combination of high training load and insufficient sleep can compound to disrupt efficient functioning of the immune system and render athletes more susceptible to illness and so inability to train, adapt and recover effectively. Lack of sleep disrupts carbohydrate metabolism and recently found to suppress expression of genes regulating cholesterol transport. In overreaching training, lack of sleep could be either a cause or a symptom of insufficient recovery. Certainly sleep deprivation impairs exercise performance capacity (especially aerobic exercise) although whether this is due to a psychological, physical or combination effect is not certain.

Sufficient sleep quality and quantity is required for cognitive function, motor learning, and memory consolidation. All skills that are important for sports performance, especially in young people where there is greater degree of neuroplasticity with potential to develop neuromuscular skills. In a fascinating recorded lecture delivered by Professor Jim Horne at the Royal Society of Medicine, the effects of prolonged wakefulness were described. Apart from slowing reaction time, the executive function of the prefrontal cortex involved in critical decision making is impaired. Important consequences not only for athletes, but for doctors, especially for those of us familiar with the on call system in hospitals back in the bad old days. Sleep pattern pre and post concussive events in teenage athletes is found to be related to degree and duration of concussive symptoms post injury. The explanation of how sleep deprivation can cause these functional effects on the brain has been suggested in a study where subtle changes in cerebral neuronal structural properties were recorded. It is not known whether these changes have long term effects.

So given that sleep is essential not only for health and fitness, but to support sports performance, what strategies to maximise this vital recovery process? Use of electronic devices shortly before bedtime suppresses secretion of melatonin (neurotransmitter and hormone), which is a situation not conducive for sleep. Tryptophan is an amino acid precursor in the synthesis of melatonin and serotonin (neurotransmitter) both of which promote sleep. Recent research demonstrates that protein intake before bed can support skeletal and muscle adaptation from exercise and also recovery from tendon injury. Conversely there is recent report that low levels of serotonin synthesis may contribute to the pathogenesis of autoimmune inflammatory disease such as rheumatoid arthritis. This highlights the subtle balance between degree of change required for positive adaptation and a negative over-response, as in inflammatory conditions. This balance is different for each individual, depending on the clinical setting. So maybe time to revisit the warm milky drink before bed? Like any recovery strategy, sleep can also be periodised to support exercise training, with well structured napping during the day as described by Dr Hannah Macleod, member of gold winning Olympic Hockey team.

In conclusion, when you are planning your training cycle, don’t forget that periodised recovery to compliment your schedule should be factored in, with sleep a priority recovery and adaptation strategy.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

References

Balance of recovery and adaptation for sports performance Dr N. Keay, British Association of Sport and Exercise Medicine

Sleep, Injury and Performance

Keay N. The effects of growth hormone misuse/abuse. Use and abuse of hormonal agents: Sport 1999. Vol 7, no 3, 11-12.

Sleep and sporting performance

Young people: neuromuscular skills for sports performance

Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

“Sleepiness and critical decision making”. Recorded lecture Professor Jim Horne, Royal Society of Medicine 16/11/16

What Does Sleep Deprivation Actually Do To The Brain?

Pre-Sleep Protein Ingestion to Improve the Skeletal Muscle Adaptive Response to Exercise Training

Exercise and fitness in young people – what factors contribute to long term health? Dr N. Keay, British Journal of Sports Medicine

Serotonin Synthesis Enzyme Lack Linked With Rheumatoid Arthritis

“Science in Elite Sport” Dr Hannah Macleod, University of Roehampton, 6/12/16

Balance of Recovery and Adaptation for Sport Performance

11 December 2016

There has been much recent discussion about the optimal balance of recovery strategies to enable effective return to training, and adaptive processes which occur as the result of training to improve sporting performance.

I have been reading the scientific reports to try and gain an understanding of this balance between recovery and adaptation. However, my investigations were put into context after attending two fascinating meetings last week where insightful talks were given by Dr Hannah Macleod Olympic gold medallist and presentations at the King’s Sport and Exercise Medicine Conference.

The scientific principle behind exercise training, of any sort, is that improvement in exercise performance follows from the cycle of overload exercise, followed by recovery phase during which adaptive changes occur in musculoskeletal, cardiovascular, metabolic and neurological systems to improve exercise performance capacity. If sufficient recovery is not taken before next training session, then rather than a progressive stepwise upward improvement in performance capacity, a downward progression occurs. In order to avoid this overreaching and overtraining scenario, rather to improve performance, training cycle as described by Dr Macleod often consists of 3 weeks “on”, followed by “rest” week together with well structured napping.

Theoretically, if the amount of recovery needed could be shortened, then more training could be done and thus potentially more adaptive advantages gained. However, by shortening recovery time with various strategies, this might actually curtail and reduce the very adaptive changes being sought. Considering recovery and adaptive responses of skeletal muscle to exercise, there are recent apparently contradictory reports on the benefits of ice baths. To ice bath or not to? Certainly for muscle injury RICE (rest, ice, compression, elevation) regime is well established. Does the same apply for skeletal muscle recovery and adaptation post exercise? The most recent study on 9 non-elite athletic males revealed that post resistance exercise there was no difference in the inflammatory markers or cellular stress markers in skeletal muscle whether recovery was either active or with cold water immersion. Nevertheless a previous study 2015 by the same group had reported attenuated gains in muscle mass and strength with cold water immersion recovery during 3 months of resistance training in 24 non-elite athletic males. The main issue seems to be that it all depends on the part of the long term training cycle and the type of sport in which the athlete is involved. For example, during pre-season training, where long term adaptations are being sought, then an ice bath might potentially attenuate adaptive responses gained from strength training. On the other hand, in the acute clinical setting, post match in a multi-day competition, an ice bath may be of benefit during the course of this competition period. Certainly Dr Macleod described having a compressive ice system on the team bus post match during the Olympics in Rio where 8 matches were played over 14 days. So recovery, especially from any impact injuries, was far more important than considerations of longer term performance in resistance training post Olympics. Not to mention the psychological beneficial effect to athletes with reduced perception of fatigue and muscle soreness and feeling in control of all factors possible.

Finally I would also suggest that just as there is variation between individuals in the positive adaptive responses to exercise, probably genetically determined, there may also be individual variation in the extent and benefits of recovery strategies. For example, in a clinical setting, an over-response of the inflammatory pathways can actually cause harm, such as in autoimmune disease. Another point is that I have restricted this blog to discuss cellular responses of skeletal muscle to resistance exercise and competition. Clearly there are other mechanisms involved in exercise training adaptations such as the neuroendocrine system, together with other types of exercise training and other recovery strategies.

In conclusion, just as training is periodised, it would appear that recovery strategies should also be periodised in conjunction with the phase of the training /competition cycle and type of sport. Apart from the scientific rational, the psychological aspects for athletes also has to be considered.