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The Interaction of Exercise, Stress, and Inflammation on Growth

  • Ashley Peckett
  • Brian W. Timmons
  • Michael C. Riddell
Chapter

Abstract

The body’s main stress axis, the hypothalamic-pituitary–adrenal (HPA) axis, has profound effects on growth and immune function that can impact health well into adulthood. In the short term, elevations in cortisol, the main stress hormone in humans, promote a catabolic state to allow for short-term defense against stressors that may be psychological or physiological in nature. In the long term, however, elevations in glucocorticoids from either endogenous or exogenous sources promote reductions in bone mass, bone density, stature, muscle mass, and an increase in central adipose gain in children and adolescents. These deleterious effects can also set the stage for numerous chronic diseases. Exercise is a potent activator of the HPA axis in humans and in rodents, yet regular exercise is not associated with chronic elevations in circulating GCs or the detrimental effects of elevated GCs, likely because of several adaptations to the HPA axis. In some cases of excessive exercise and overtraining, the detrimental effects of chronic elevations in GC levels that impact normal growth can be observed. The cellular, molecular, and physiological interactions of exercise, stress, and immune function in the context of normal and abnormal growth are highlighted in this chapter.

Keywords

Glucocorticoid Receptor Regular Exercise Growth Hormone Release Urinary Free Cortisol Level Stressed Mother 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

ACTH

Adrenocorticotropic hormone

ASCs

Adipose stromal cells

ATF-4

Activating transcription factor 4

ATGL

Adipose triglyceride lipase

11β-HSD

11β-Hydroxysteroid dehydrogenase

CRH

Corticotrophin-releasing hormone

CYP

Cytochrome P450

4EBP1

eIF4E-binding protein 1

foxO

Forkhead box O

GC

Glucocorticoid

GH

Growth hormone

GRs

Glucocorticoid receptors

HPA

Hypothalamic–pituitary–adrenal

HSL

Hormone-sensitive lipase

IGF-1

Insulin-like growth factor-1

LH

Luteinizing hormone

LPL

Lipoprotein lipase

MAFbx

Muscle atrophy Fbox

MCSF

Macrophage colony-stimulating factor

MC2R

Melanocortin-2 receptor

MRs

Mineralocorticoid receptors

mTOR

Mammalian target of rapamycin

MuRF1

Muscle ring finger 1

NE

Norepinephrine

NPY

Neuropeptide Y

PEPCK

Phosphoenolpyruvate carboxykinase

PNMT

Phenylethanolamine N-methyltransferase

PVN

Paraventricular nucleus

RANKL

Receptor activator for nuclear factor κ B ligand

REDD1

Regulated in development and DNA damage responses

SES

Socioeconomic status

StAR

Steroidogenic acute regulatory protein

S6K1

S6 kinase 1

UFC

Urinary free cortisol

UPS

Ubiquitin–proteasome system

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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Ashley Peckett
    • 1
  • Brian W. Timmons
    • 2
  • Michael C. Riddell
    • 1
  1. 1.Physical Activity and Chronic Disease Unit, School of Kinesiology and Health ScienceMuscle Health Research Centre, York UniversityTorontoCanada
  2. 2.Children’s Exercise & Nutrition Centre, McMaster Children’s HospitalMcMaster UniversityHamiltonCanada

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