Hormonal response to exercise in humans: influence of hypoxia and physical training

Kjær, Mette Mandrup; Bangsbo, Jens; Lortie, G.; Galbo, H.

doi:10.1152/ajpregu.1988.254.2.r197

Cited by 58 publications

(44 citation statements)

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“…Furthermore, and of relevance for the differential glucocorticoid responses to stress in the exercised rats, stressors that are physically demanding such as forced swimming evoke much larger increases in adrenaline than psychological challenges such as novel cage stress which are hardly physically demanding [59,60,61,62]. As mentioned, exercised animals show an enhanced adrenaline secretory capacity and indeed higher maximal adrenaline responses to various physically demanding challenges have been observed in exercised subjects [63,64,65,66,67,68,69]. Therefore, in aggregate it may be postulated that in exercised animals an enhanced adrenaline response upon a physically demanding challenge (e.g.…”

Section: Discussionmentioning

confidence: 99%

Voluntary Exercise Impacts on the Rat Hypothalamic-Pituitary-Adrenocortical Axis Mainly at the Adrenal Level

Droste

Chandramohan²,

Hill³

et al. 2007

Neuroendocrinology

132

143

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Introduction: Evidence is accumulating that the regular performance of exercise is beneficial for stress coping. However, the hypothalamic-pituitary-adrenocortical (HPA) axis of voluntarily exercising rats has never been comprehensively investigated. Methods: Therefore, male Sprague-Dawley rats were given access to a running wheel in their home cage for 4 weeks in which they ran 4–7 km per night. Results: After 4 weeks, the exercising animals showed significantly less body weight gain, less abdominal fat tissue, decreased thymus weight, and increased adrenal weight (relative to body weight). Furthermore, tyrosine hydroxylase (TH) mRNA levels were selectively increased in the right adrenal me- dulla indicating an increase in sympathoadrenomedullary capacity in exercising rats. No changes were observed in paraventricular corticotropin-releasing hormone (CRH), arginine-vasopressin (AVP) and oxytocin mRNA levels. Mineralocorticoid receptor (MR) mRNA levels in hippocampus and glucocorticoid receptor (GR) mRNA levels in frontal cortex, parvocellular paraventricular nucleus and anterior pituitary were unchanged, whereas GR mRNA levels were increased in distinct hippocampal cell layers. Early morning baseline levels of plasma ACTH and corticosterone were similar in both groups. Interestingly, the response to different stressful stimuli (e.g. forced swimming, novelty) revealed that the exercising rats showed stressor-specific changes in HPA hormone responses. Forced swimming evoked a markedly enhanced response in corticosterone levels in the exercising rats. In contrast, if rats were exposed to a novel environment, exercising rats showed a much lower response in corticosterone than the control animals. However, the response in ACTH to either stressor was comparable between groups. Thus, in exercising rats physically demanding stressors evoke enhanced glucocorticoid responses whereas mild psychologically stressful stimuli such as novelty result in an attenuated glucocorticoid response. Interestingly, this attenuated hormone response corresponded with the observation that the exercising rats showed less anxious behaviour in the novelty situation. Conclusions: The differential responses in plasma corticosterone levels to different types of stress in the face of comparable responses in ACTH levels underscore the existence of critical regulatory control mechanisms at the level of the adrenal gland. We have hypothesized that changes in the sympathoadrenomedullary input may play an important role in these distinct glucocorticoid responses to stress. Our previous studies have shown similar changes in voluntarily exercising mice. Therefore, we conclude that the effects of exercise on the organism are not species-specific. Thus, our observations may have translational implications for the human situation.

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Section: Discussionmentioning

confidence: 99%

Voluntary Exercise Impacts on the Rat Hypothalamic-Pituitary-Adrenocortical Axis Mainly at the Adrenal Level

Droste

Chandramohan²,

Hill³

et al. 2007

Neuroendocrinology

132

143

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“…In addition, hypoxia-stimulated glucose uptake is absent in mice expressing a dominant negative mutant AMPK, but contraction-stimulated glucose uptake is only partially reduced (ϳ50%) in these mice (37). No study has examined the effect of hypoxia on skeletal muscle AMPK activity, muscle energy balance, and glucose disposal during exercise in humans.It is critical, when comparing metabolism between hypoxic and normoxic exercise, that the intensity be normalized to both the absolute and relative workload, since the maximal rate of oxygen uptake (V O 2 peak ) is reduced in hypoxia (5,28,34). In other words, when exercise is performed under hypoxic conditions at the same absolute workload (with respect to power output) as normoxic conditions, the relative intensity of exercise (with respect to V O 2 peak ) is much higher compared with normoxic conditions.…”

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confidence: 99%

“…The hormonal response to hypoxic exercise, particularly catecholamines, is largely related to the relative rather than the absolute exercise intensity (28,34). At the same absolute intensity, hypoxic exercise increases glucose uptake (5,30,43), muscle glycogen breakdown (40), and plasma and muscle lactate levels (5,28,30,34) and increases the extent of muscle energy imbalance (25,40,47). However, it is not known whether the hypoxia effect on these metabolic variables is due to the hypoxic exercise being performed at a higher relative intensity.…”

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confidence: 99%

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Wadley¹,

Lee²,

Canny³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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221 phosphorylation, free AMP content, and glucose clearance were more influenced by the absolute than by the relative exercise intensity, being greatest in 73% Normoxia with no difference between 51% Normoxia and 72% Hypoxia. In contrast to this, increases in muscle glycogen use, muscle lactate content, and plasma catecholamine concentration were more influenced by the relative than by the absolute exercise intensity, being similar in 72% Hypoxia and 73% Normoxia, with both trials higher than in 51% Normoxia. In conclusion, increases in muscle AMPK signaling, free AMP content, and glucose disposal during exercise are largely determined by the absolute exercise intensity, whereas increases in plasma catecholamine levels, muscle glycogen use, and muscle lactate levels are more closely associated with the relative exercise intensity. metabolic regulation; glucose kinetics; contraction AMP-ACTIVATED PROTEIN KINASE (AMPK) is a serine/threonine protein kinase that responds to cellular energy status by inhibiting ATP-consuming pathways and activating ATP-producing pathways (27). The catalytic ␣-subunits of AMPK (␣1 and ␣2) are expressed in skeletal muscle and are activated allosterically by increased AMP levels following phosphorylation of the upstream kinase LKB1 (17,27,48,53,58). Skeletal muscle AMPK activity is increased during contractions and exercise in rodents (18, 19, 38, 50) and humans (8, 9, 14, 57).It has been suggested that skeletal muscle glucose uptake during exercise is regulated by AMPK (53). This is largely based on studies using the nucleoside intermediate 5Ј-aminoimidazole-4-carboxamide ribonucleoside (AICAR). AICAR activates AMPK in rat skeletal muscle and increases glucose uptake (2, 19, 54) and GLUT4 translocation (32). Further support for AMPK in the regulation of glucose uptake during exercise is the finding that AICAR and contraction stimulation of glucose uptake are not additive (2, 19). However, in some circumstances, AMPK activation and glucose uptake during exercise are not tightly coupled. For example, during lowintensity exercise (9, 56) and during moderate-intensity exercise following short-term exercise training (35), skeletal muscle AMPK␣2 activity does not increase despite large increases in glucose disposal during exercise. In addition, AMPK dominant negative mice and AMPK␣2 null mice have partially reduced and normal contraction-stimulated glucose uptake, respectively (24, 37).Hypoxic exercise may be a useful experimental model to tease out the role of AMPK in skeletal muscle glucose uptake during exercise, as some studies suggest that hypoxia and contractions involve the same pathway to activate skeletal muscle glucose uptake (6). Indeed, both hypoxia and muscle contraction increase glucose uptake in isolated rat muscle, alter muscle energy status, and activate AMPK (18). However, others find that hypoxia has an additive effect on glucose uptake during contractions in perfused rat hindlimbs (12, 13). In addition, hypoxia-stimulated glucose uptake is absent in mice expressing a dom...

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“…The similar effects in HT and NT might also be related to the fact that the stimulation of the b-adrenergic receptors involved in oxidative adaptations to endurance training (Booth and Baldwin 1996) was identical for HT and NT during training. A previous study (Kjaer et al 1988) reported that epinephrine and norepinephrine responses to exercise were similar in untrained subjects whether the exercise was performed at the same relative work rate in hypoxia or in normoxia. Finally, if one considers heart rate as an indicator of the metabolic load for muscle tissues in exercise, it is interesting to note that HT and NT displayed the same heart rates during the training sessions (Table 2).…”

Section: Discussionmentioning

confidence: 89%

Effects of training in normoxia and normobaric hypoxia on time to exhaustion at the maximum rate of oxygen uptake

et al. 2004

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The effects of endurance training in normoxia or in hypoxia on time to exhaustion ( T(lim)) at the work rate corresponding to peak oxygen uptake (VO(2peak)) were examined at sea level in 13 healthy subjects. Before and after training the subjects performed the following: (1) incremental exercises up to exhaustion to determine peak oxygen uptake in normoxia (VO(2peak)N), the percentage of this value at the 4 mmol l(-1) blood lactate concentration (VO(2)4%N) and the work rate corresponding to VO(2peak)N (Pa(peak)N), (2) a 5-min 90% Pa(peak)N exercise followed by a 10-min passive recovery to determine the maximal blood lactate concentration (La(max)) measured during the recovery, and (3) a T(lim) at Pa(peak)N. Training consisted of pedalling 2 h a day, 6 days a week, for 4 weeks. Five subjects trained in normobaric hypoxia [HT; partial pressure of inhaled oxygen ( P(I)O(2)) 89 mmHg] and eight subjects trained at the same relative work rates in normoxia (NT; P(I)O(2) 141 mmHg). The training-induced improvement of all the measured parameters were closely matched between the HT and the NT ( P>0.05). Training increased T(lim) by 59.7% [164(40) s]. The value of T(lim) was related to VO(2)4%N and to La(max) before and after training. Also, the training-induced improvement of T(lim) was related to the concomitant decrease in La(max). It is concluded that: (1) endurance training including continuous high-intensity exercises improves T(lim) for exercises performed at the same relative (higher absolute) work rate after training, (2) intermittent hypoxic training has no potentiating effect on T(lim) as compared with training in normoxia, and (3) the intra-individual training-induced improvement of T(lim) was associated with metabolic alteration in relation to lactate accumulation.

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Hormonal response to exercise in humans: influence of hypoxia and physical training

Cited by 58 publications

References 0 publications

Voluntary Exercise Impacts on the Rat Hypothalamic-Pituitary-Adrenocortical Axis Mainly at the Adrenal Level

Voluntary Exercise Impacts on the Rat Hypothalamic-Pituitary-Adrenocortical Axis Mainly at the Adrenal Level

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Effects of training in normoxia and normobaric hypoxia on time to exhaustion at the maximum rate of oxygen uptake

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