Male Cyclists: Bones, Body composition, Nutrition, Performance

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There has been much recent coverage regarding female runners suffering with health and performance issues due to relative energy deficiency in sports (RED-S). What about male athletes? A recent article about male cyclists who explained how they developed RED-S, did not receive as sympathetic a response as articles concerning female athletes. Yet multiple Endocrine network disruption in RED-S, associated with suboptimal health and performance, is equally applicable to male and female athletes.

Although competitive road cycling is excellent for cardiovascular (CV) fitness, why are male cyclists at particular risk of impaired bone health and RED-S? Cycling is a non-weight bearing type of exercise, as is swimming, so does not provide much osteogenic (bone building) stimulus. The additional element in road cycling is that, in the short term, low body weight, with associated low body fat, confers a performance advantage. However this can lead to restrictive nutrition and RED-S, that have adverse effects on health and performance, over the longer term.

A recent study looking at bone acquisition in adolescent males found that bone mass, microarchitecture and makers of bone formation were more favourable in footballers compared with cyclists and swimmers. Swimmers had the lowest Vitamin D, presumably as this is generally an indoor sport (unless you live in Australia where outdoor 50m pools abound). Another study found reduction in femoral neck bone mineral accumulation in adolescent male cyclists compared against increases over the same time frame seen in controls.

What about adult male road cyclists? When runners and cyclists were matched for age and body weight, there were no significant differences in hormone or nutrition status, yet cyclists were 7 times more likely to have osteopenia of the lumbar spine than runners. Similar results were found in another study where competitive male road cyclists were found to have reduced lumbar spine bone mineral density (BMD) for age, despite normal levels of testosterone and insulin-like growth factor 1 (IGF1), although intriguingly an inverse correlation with lumbar spine BMD and IGF1 was found. It appears that the biomechanical stress patterns on the spine in cycling are not oesteogenic in nature, which contrasts with rowing where, although also seated, the biomechanical load exerted through the spine does provide an osteogenic effect.

In addition to the non-load bearing nature of cycling on the skeleton, restrictive nutrition can contribute to suboptimal bone health. Reducing energy availability by restricting energy intake whilst increasing training load can be a strategy, especially during pre-season training to reduce body weight and body fat. Essentially, cycling up a steep incline demands less power through the pedals if your body weight is low. Nevertheless, reducing energy availability runs the risk of developing RED-S, associated Endocrine dysfunction and suboptimal bone health, on top of the non-beneficial mechanical osteogenic effect of cycling. On a practical note, with long training rides in the saddle it can be physically and practically difficult to fuel optimally. Recent research in female athletes shows that within day energy deficits magnify hormonal disruption. Could this be a factor in male cyclists where consistent fuelling is either actively avoided and/or practically difficult?

The psychological element of disordered eating has been described amongst elite male cyclists. Male cyclists, in particular, collect many metrics associated with training and racing which could be a manifestation of a drive to perfectionism. Determination and attention to detail are laudable qualities for athletes, but there is a fine line when the balance swings to behaviours and attitudes that can be detrimental to health and performance. Even starting off with good intentions can lead to problems as seen with the growing emergence of orthorexia: “clean eating”, which, ironically, becomes detrimental to health and performance with exclusion of food groups such as carbohydrates.

Exclusively practising a non weight bearing sport such as cycling although great for CV fitness, is not so good for bone health. Does this matter? Potentially injury is more likely in bike spills, which occur both in training and competition even for the most experienced bike handler. Combined with the drive for low body weight in competitive road cycling, health and performance issues can be compounded with RED-S. What are the solutions for the cyclist to support favourable body composition and bone health, which ultimately also optimises performance? A further planned study, following a current pilot study of competitive road cyclists, aims to investigate the potential beneficial effects of strength and conditioning to load the skeleton combined with a review of nutrition. See details of next study to see if you wish to participate.

For more discussion on the Endocrine aspects of Sports and Exercise Science and Medicine, BASEM Spring conference 22 March 

References

Cumulative Endocrine Dysfunction in Relative Energy Deficiency in Sport (RED-S)

Optimal health: including male athletes! Part 2 Relative Energy Deficiency in sports BJSM 2017

Too healthy to ride? How clean living could slow you down Cycling Weekly 2017

Body Composition for Health and Sports Performance

Longitudinal Adaptations of Bone Mass, Geometry, and Metabolism in Adolescent Male Athletes: The PRO-BONE Study JBMR 2017

Bone Related Health Status in Adolescent Cyclists Plos 2011

Participation in road cycling vs running is associated with lower bone mineral density in men Metabolism 2008

Evaluation of the Bone Status in High-Level Cyclists Journal of Clinical Densitometry 2012

Effect of exercise training programme on bone mineral density in novice college rowers BJSM 1995

Energy Intake and Energy Expenditure of Elite Cyclists During Preseason Training Int J Sports Med 2005
Kings and Queens of the Mountains Science4Performance 2017

Cumulative Endocrine Dysfunction in Relative Energy Deficiency in Sport (RED-S)

Perfectionism and Risk for Disordered Eating among Young French Male Cyclists of High Performance Perceptual and Motor Skills 2004

Kings and Queens of the Mountains Science4Performance 2017

Addiction to Exercise – what distinguishes a healthy level of commitment from exercise addiction? BJSM 2017

Optimal Health: For All Athletes! Part 4 – Mechanisms BASEM 2017

 

 

 

 

 

Endocrine system: balance and interplay in response to exercise training

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