Abstract

Advanced glycation end-products (AGEs) accumulate with aging and have been associated with tissue modifications and metabolic disease. Regular exercise has several health benefits, and the purpose of this study was to investigate the effect of regular long-term exercise and diet on skin autofluorescence (SAF) as a measure of glycation and on Achilles tendon structure. In connection with the 2017 European Masters Athletics Championships Stadia, high-level male athletes (n = 194) that had regularly trained for more than 10 years were recruited, in addition to untrained controls (n = 34). SAF was non-invasively determined using an AGE Reader. Achilles tendon thickness and vascular Doppler activity were measured by ultrasonography, and diet was assessed by a questionnaire. There was no significant difference in SAF between the athletes and controls. However, greater duration of exercise was independently associated with lower SAF. Diet also had an effect, with a more “Western” diet in youth being associated with increased SAF. Furthermore, our data demonstrated that greater Achilles tendon thickness was associated with aging and training. Together, our data indicate that long-term exercise may yield a modest reduction in glycation and substantially increase Achilles tendon size, which may protect against injury.

Highlights

  • As part of the normal aging process, collagen-rich connective tissues, such as skin, cornea, cartilage, arteries, and tendon, undergo progressive and irreversible changes that are associated withNutrients 2019, 11, 1409; doi:10.3390/nu11061409 www.mdpi.com/journal/nutrientsNutrients 2019, 11, 1409 tissue injury and several lifestyle diseases [1]

  • There was no difference in skin autofluorescence (SAF) between the athletes and controls, more training years was independently associated with lower SAF

  • Our data indicate that long-term exercise is associated with lower glycation and greater Achilles tendon size, which may protect against injury

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Summary

Introduction

As part of the normal aging process, collagen-rich connective tissues, such as skin, cornea, cartilage, arteries, and tendon, undergo progressive and irreversible changes that are associated withNutrients 2019, 11, 1409; doi:10.3390/nu11061409 www.mdpi.com/journal/nutrientsNutrients 2019, 11, 1409 tissue injury and several lifestyle diseases [1]. As part of the normal aging process, collagen-rich connective tissues, such as skin, cornea, cartilage, arteries, and tendon, undergo progressive and irreversible changes that are associated with. A major component of age-related impairment of these connective tissues are long-lived protein modifications derived from the formation of advanced glycation end-products (AGEs). AGEs are formed through a non-enzymatic reaction between reducing sugars and free amino groups of proteins, lipids, or nucleic acids that accumulate with age in long-lived molecules, including the collagen of skin and tendon [2,3]. The Achilles tendon is frequently injured during physical activity, either in the form of chronic pain (tendinopathy) or more rarely as an acute rupture [7,8]. Modification by AGEs can directly affect the collagen fibrils that make up connective tissues by cross-linking and swelling [9,10], and it has been demonstrated to reduce collagen fibril sliding [11,12] and cause impaired mechanics and fragility of connective tissues [13,14,15]

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