Exercising in the cold inhibits growth hormone secretion by reducing the rise in core body temperature

Wheldon, Adam; Savine, Richard; Sönksen, Peter H.; Holt, Richard

doi:10.1016/j.ghir.2006.02.005

Cited by 20 publications

(8 citation statements)

References 39 publications

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“…Supporting a role of body temperature is the observation that the GH response to exercise is greatly attenuated during exercise in cold conditions [37] and is proportional to core temperature [39]. Against an effect of lactate are the observations that infusion of sodium L-lactate does not increase GH secretion [18] (although this experimental model differs significantly from an exercise-induced metabolic acidosis), and furthermore there is a linear increase in GH secretion with increased exercise intensity that can be observed before the lactate threshold is reached [24].…”

Section: The Gh Response To Exercisementioning

confidence: 99%

The physiology of growth hormone and sport

Widdowson

Healy

Sönksen

et al. 2009

Growth Hormone & IGF Research

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Section: The Gh Response To Exercisementioning

confidence: 99%

The physiology of growth hormone and sport

Widdowson

Healy

Sönksen

et al. 2009

Growth Hormone & IGF Research

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“…Supporting a role of body temperature is the observation that the GH response to exercise is greatly attenuated during exercise in cold conditions (148) and is proportional to core temperature (150). Against an effect of lactate are the observations that infusion of sodium L-lactate does not increase GH secretion (127) (although this experimental model differs significantly from an exercise-induced metabolic acidosis), and as described above there is a linear increase in GH secretion with increased exercise intensity that can be observed before the lactate threshold is reached (133).…”

Section: A the Acute And Long-term Effects Of Exercise On The Gh/ Igmentioning

confidence: 99%

The Growth Hormone/Insulin-Like Growth Factor-I Axis in Exercise and Sport

2007

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The syndrome of adult GH deficiency and the effects of GH replacement therapy provide a useful model with which to study the effects of the GH/IGF-I axis on exercise physiology. Measures of exercise performance including maximal oxygen uptake and ventilatory threshold are impaired in adult GH deficiency and improved by GH replacement, probably through some combination of increased oxygen delivery to exercising muscle, increased fatty acid availability with glycogen sparing, increased muscle strength, improved body composition, and improved thermoregulation. In normal subjects, in addition to the long-term effects of GH/IGF-I status, there is evidence that the acute GH response to exercise is important in regulating substrate metabolism after exercise. Administration of supraphysiological doses of GH to athletes increases fatty acid availability and reduces oxidative protein loss, particularly during exercise, and increases lean body mass. Despite a lack of evidence that these metabolic effects translate to improved performance, GH abuse by athletes is widespread. Tests to detect GH abuse have been developed based on measurement in serum of 1) indirect markers of GH action, and 2) the relative proportions of the two major naturally occurring isoforms (20 and 22kDa) of GH. There is evidence that exercise performance and strength are improved by administration of GH and testosterone in combination to elderly subjects. The potential benefits of GH in these situations must be weighed against potential adverse effects. (Endocrine Reviews 28: 603-624, 2007)

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“…Indeed, after exercise GH levels increase 5.1-fold in humans [ 18 ] and GH secretion is correlated to exercise intensity [ 15 , 19 ]. Proposed mechanisms for such increase are: acidosis [ 20 ]; central adrenergic outflow [ 21 ], core body temperature [ 22 ] and cholinergic mediation [ 23 ]. Interestingly, obese patients present a blunted spontaneous GH secretion as well as in response to exercise attributed to a decrease in pulsatile GH release and a shorter half-life of endogenous GH [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release

Ignacio

Silvestre

Cavalcanti-de-Albuquerque

et al. 2015

PLoS ONE

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Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response.

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Exercising in the cold inhibits growth hormone secretion by reducing the rise in core body temperature

Cited by 20 publications

References 39 publications

The physiology of growth hormone and sport

The physiology of growth hormone and sport

The Growth Hormone/Insulin-Like Growth Factor-I Axis in Exercise and Sport

Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release

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