Vitamin D and the Athlete: Current Perspectives and New Challenges

Abstract

The last decade has seen a dramatic increase in general interest in and research into vitamin D, with many athletes now taking vitamin D supplements as part of their everyday dietary regimen. The most recognized role of vitamin D is its regulation of calcium homeostasis; there is a strong relationship between vitamin D and bone health in non-athletic individuals. In contrast, data have consistently failed to demonstrate any relationship between serum 25[OH]D and bone health, which may in part be due to the osteogenic stimulus of exercise. Vitamin D may interact with extra-skeletal tissues such as muscle and the immune system to modulate recovery from damaging exercise and infection risk. Given that many athletes now engage in supplementation, often consuming extreme doses of vitamin D, it is important to assess whether excessive vitamin D can be detrimental to health. It has been argued that toxic effects only occur when serum 25[OH]D concentrations are greater than 180 nmol·l⁻¹, but data from our laboratory have suggested high-dose supplementation could be problematic. Finally, there is a paradoxical relationship between serum 25[OH]D concentration, ethnicity, and markers of bone health: Black athletes often present with low serum 25[OH]D without physiological consequences. One explanation for this could be genetic differences in vitamin D binding protein due to ethnicity, resulting in greater concentrations of bioavailable (or free) vitamin D in some ethnic groups. In the absence of any pathology, screening may be unnecessary and could result in incorrect supplementation. Data must now be re-examined, taking into consideration bioavailable or "free" vitamin D in ethnically diverse groups to enable new thresholds and target concentrations to be established; perhaps, for now, it is time to "set vitamin D free".

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Administration of Caffeine in Alternate Forms

Abstract

There has been recent interest in the ergogenic effects of caffeine delivered in low doses (~ 200 mg or ~ 3 mg/kg body mass) and administered in forms other than capsules, coffee and sports drinks, including chewing gum, bars, gels, mouth rinses, energy drinks and aerosols. Caffeinated chewing gum is absorbed quicker through the buccal mucosa compared with capsule delivery and absorption in the gut, although total caffeine absorption over time is not different. Rapid absorption may be important in many sporting situations. Caffeinated chewing gum improved endurance cycling performance, and there is limited evidence that repeated sprint cycling and power production may also be improved. Mouth rinsing with caffeine may stimulate nerves with direct links to the brain, in addition to caffeine absorption in the mouth. However, caffeine mouth rinsing has not been shown to have significant effects on cognitive performance. Delivering caffeine with mouth rinsing improved short-duration, high-intensity, repeated sprinting in normal and depleted glycogen states, while the majority of the literature indicates no ergogenic effect on aerobic exercise performance, and resistance exercise has not been adequately studied. Studies with caffeinated energy drinks have generally not examined the individual effects of caffeine on performance, making conclusions about this form of caffeine delivery impossible. Caffeinated aerosol mouth and nasal sprays may stimulate nerves with direct brain connections and enter the blood via mucosal and pulmonary absorption, although little support exists for caffeine delivered in this manner. Overall, more research is needed examining alternate forms of caffeine delivery including direct measures of brain activation and entry of caffeine into the blood, as well as more studies examining trained athletes and female subjects.

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Assessing the Role of Muscle Protein Breakdown in Response to Nutrition and Exercise in Humans

Abstract

Muscle protein breakdown (MPB) is an important metabolic component of muscle remodeling, adaptation to training, and increasing muscle mass. Degradation of muscle proteins occurs via the integration of three main systems—autophagy and the calpain and ubiquitin-proteasome systems. These systems do not operate independently, and the regulation is complex. Complete degradation of a protein requires some combination of the systems. Determination of MPB in humans is technically challenging, leading to a relative dearth of information. Available information on the dynamic response of MPB primarily comes from stable isotopic methods with expression and activity measures providing complementary information. It seems clear that resistance exercise increases MPB, but not as much as the increase in muscle protein synthesis. Both hyperaminoacidemia and hyperinsulinemia inhibit the post-exercise response of MPB. Available data do not allow a comprehensive examination of the mechanisms behind these responses. Practical nutrition recommendations for interventions to suppress MPB following exercise are often made. However, it is likely that some degree of increased MPB following exercise is an important component for optimal remodeling. At this time, it is not possible to determine the impact of nutrition on any individual muscle protein. Thus, until we can develop and employ better methods to elucidate the role of MPB following exercise and the response to nutrition, recommendations to optimize post exercise nutrition should focus on the response of muscle protein synthesis. The aim of this review is to provide a comprehensive examination of the state of knowledge, including methodological considerations, of the response of MPB to exercise and nutrition in humans.

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Protection Before Impact: the Potential Neuroprotective Role of Nutritional Supplementation in Sports-Related Head Trauma

Abstract

Even in the presence of underreporting, sports-related concussions/mild traumatic brain injuries (mTBI) are on the rise. In the absence of proper diagnosis, an athlete may return to play prior to full recovery, increasing the risk of second-impact syndrome or protracted symptoms. Recent evidence has demonstrated that sub-concussive impacts, those sustained routinely in practice and competition, result in a quantifiable pathophysiological response and the accumulation of both concussive and sub-concussive impacts sustained over a lifetime of sports participation may lead to long-term neurological impairments and an increased risk of developing neurodegenerative diseases. The pathophysiological, neurometabolic, and neurochemical cascade that initiates subsequent to the injury is complex and involves multiple mechanisms. While pharmaceutical treatments may target one mechanism, specific nutrients and nutraceuticals have been discovered to impact several pathways, presenting a broader approach. Several studies have demonstrated the neuroprotective effect of nutritional supplementation in the treatment of mTBI. However, given that many concussions go unreported and sub-concussive impacts result in a pathophysiological response that, too, may contribute to long-term brain health, protection prior to impact is warranted. This review discusses the current literature regarding the role of nutritional supplements that, when provided before mTBI and traumatic brain injury, may provide neurological protection.

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Imbalance of synaptic actin dynamics as a key to the Fragile X syndrome?

Abstract

Our experiences and memories define who we are and evidence accumulates that memory formation is dependent on functional and structural adaptations of synaptic structures in our brain. Especially dendritic spines, the postsynaptic compartments of synapses, show a strong structure-to-function relationship and a high degree of structural plasticity. Although the molecular mechanisms are not completely understood, it is known that these modifications are highly dependent on the actin-cytoskeleton, the major cytoskeletal component of the spine. Given the crucial involvement of actin in these mechanisms, dysregulations of spine actin dynamics (reflected by alterations in dendritic spine morphology) can be found in a variety of neurological disorders ranging from schizophrenia to several forms of autism spectrum disorders like the Fragile X Syndrome (FXS). FXS is caused by a single mutation leading to an inactivation of the X-linked fragile X mental retardation 1 gene and loss of its gene product, the RNA-binding protein Fragile X Mental Retardation Protein 1 (FMRP) which normally can be found both pre- and postsynaptically. FMRP is involved in mRNA transport as well as regulation of local translation at the synapse and although hundreds of FMRP-target mRNAs could be identified only very few interactions between FMRP and actin-regulating proteins were reported and validated. In this review we want to give an overview about recent work by our lab and others providing evidence that dysregulated actin dynamics might indeed be at the very base of a deeper understanding of neurological disorders ranging from cognitive impairment to the autism spectrum.

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Fat feeding facilitates hot bodies, but is resistance futile?

Abstract

High-fat diets (HFD) result in metabolic dysregulation and cardiometabolic abnormalities which contribute to the development of obesity and cardiovascular disease.

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Anatomic Relationship between the Hook of the Hamate and the Distal Transverse Carpal Ligament: Implications for Ultrasound Guided Carpal Tunnel Release

ABSTRACTObjectiveDuring ultrasound guided carpal tunnel release (USCTR), osseous landmarks may supplement direct visualization of the distal transverse carpal ligament (dTCL) to ensure a complete release. The purpose of this study was to determine the relationship between the apex of the hook of the hamate (aHH) and the dTCL within the transverse safe zone (TSZ) of the carpal tunnel.DesignTwenty unembalmed cadaveric specimens were dissected to determine the aHH-dTCL distance and the aHH-SPA distance (the distance between the aHH and the superficial palmar arch) at the ulnar and radial limits of the TSZ (the distance between the hook of the hamate or ulnar artery to the median nerve).ResultsThe aHH-dTCL distance averaged 11-12 mm across the TSZ (maximum 18.2 mm), whereas the aHH-SPA distance was significantly greater on the radial side of the TSZ compared to the ulnar side (22.6 ± 3.6 mm versus 14.0 ± 4.0 mm).ConclusionsThe dTCL lies approximately 11-12 mm distal to the aHH across the TSZ, with an upper limit of 18.2 mm. Along with direct sonographic visualization of the dTCL, the aHH can be used with other osseous landmarks to estimate the position of the dTCL during USCTR. Objective During ultrasound guided carpal tunnel release (USCTR), osseous landmarks may supplement direct visualization of the distal transverse carpal ligament (dTCL) to ensure a complete release. The purpose of this study was to determine the relationship between the apex of the hook of the hamate (aHH) and the dTCL within the transverse safe zone (TSZ) of the carpal tunnel. Design Twenty unembalmed cadaveric specimens were dissected to determine the aHH-dTCL distance and the aHH-SPA distance (the distance between the aHH and the superficial palmar arch) at the ulnar and radial limits of the TSZ (the distance between the hook of the hamate or ulnar artery to the median nerve). Results The aHH-dTCL distance averaged 11-12 mm across the TSZ (maximum 18.2 mm), whereas the aHH-SPA distance was significantly greater on the radial side of the TSZ compared to the ulnar side (22.6 ± 3.6 mm versus 14.0 ± 4.0 mm). Conclusions The dTCL lies approximately 11-12 mm distal to the aHH across the TSZ, with an upper limit of 18.2 mm. Along with direct sonographic visualization of the dTCL, the aHH can be used with other osseous landmarks to estimate the position of the dTCL during USCTR. Please send correspondence to: Jay Smith, M.D. Department of PM&R, W14 Mayo Building, 200 1st ST, SW, Rochester, MN 55905, Email: smith.jay@mayo.edu Acknowledgement of Funding Sources Funding provided by Mayo Clinic Institutional Funds. This project was supported by Grant Number UL1 TR000135 from the National Center for Advancing Translational Sciences (NCATS). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Neither funding source had a role in the study design, the collection, analysis and interpretation of data, the writing of the report or the decision to submit for publication. Declaration of Conflicting Interests Dr. Smith is Co-Founder and Chief Medical Officer for Sonex Health, LLC. Dr. Kakar is on the Medical Advisory Board for Sonex Health, LLC and is a consultant for Arthrex, Inc. and Skeletal Dynamics, LLC. Previous Presentation Results were presented in abbreviated form as a poster at the American Academy of Physical Medicine and Rehabilitation in October 2016. They have not been published, nor are they under consideration for publication elsewhere. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

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