Hormonal deficiencies and the metabolic adaptations of rats to training

Gollnick, PD; Ianuzzo, C. D.

doi:10.1152/ajplegacy.1972.223.2.278

Cited by 57 publications

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“…3) demonstrate the effectiveness of the anti-GHRH antisera. Our results are consistent with the studies of Goldberg (19) and Gollnick and lanuzzo (20) who showed that muscle hypertrophy and increases in muscle SDH can occur either as a compensatory mechanism or in response to exercise in mature. hypophysectomized rats.…”

supporting

confidence: 93%

“…Hypophysectomy has been used previously in the mature rat to obliterate any possible effect of exercise on GH secretion (19,20), but this invasive surgical technique is technically more difficult in younger rats, results in reduced spontaneous physical activity, and requires the administration of other pituitary hormones to maintain health. As an alternative approach to attenuate GH secretion, we administered anti-GHRH antiserum.…”

mentioning

confidence: 99%

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Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

et al. 1994

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ABSTRACT. Exercise training improves maximal oxygen uptake and endurance times in adult human beings and other animals. The mechanism of this improvement results in part from anabolic effects of exercise and may be mediated by growth hormone (GH). Little is known about the role of GH in the adaptation to exercise in younger, stilldeveloping organisms. To examine this role, we began a 4-wk treadmill exercise training protocol in 14-d-old female rats. GH was suppressed by passive immunization with anti-GH releasing hormone antisera. There were four experimental groups: I) GH-control (normal GH secretory capacity), untrained (n = 21); 2) GH-suppressed, untrained (n = 13); 3) GH-control, trained (n = 14); and 4) GHsuppressed; trained (n = 11). At the end of the training period, maximal oxygen uptake and treadmill endurance running time were measured. Serum GH and IGF-I were assessed using RIA, and whole hind limb musculature succinate dehydrogenase (an indicator of mitochondria1 function) was measured with standard fluorometric technique. Body weight gain was markedly reduced in GHsuppressed rats (mean, 54% of GH-controls in untrained rats and 55% in trained; p < 0.05). No apparent effect of training on linear growth was observed. As expected, serum IGF-I was markedly reduced by GH suppression, but no exercise-induced increase occurred in IGF-I as a result of training in either the GH-control or GH-suppressed rats. In GH-control rats, maximal oxygen uptake and succinate dehydrogenase were 69% and 25% greater, respectively, in trained compared with untrained rats (p < 0.05). Despite GH inhibition, similar increases were found in the trained GH-suppressed rats (68% greater than controls for maximal oxygen uptake and 34% for succinate dehydrogenase, In mature human beings and animals of many species, increased physical activity leads, to improved functional capabilities often measured as increased Vozmax or exercise endurance time. A pivotal mechanism for the improved function is the unique, naturally occurring anabolic effects of exercise ( I ) , such as skeletal and cardiac muscle hypertrophy (2), increased capillarization and mitochondria (3), and increased bone density (4). Because exercise stimulates GH secretion (5) and because GH (either directly or in combination with IGF-I) is a potent growth factor for skeletal iind heart muscle (6-9), it is not surprising that many investigations in both human beings (10, I I) and other species (12)(13)(14) indicate that GH plays an important role in the adaptation to exercise. Despite this finding, the role of GH in exerciseinduced growth is not understood, and evidence exists that exogenous GH administration does not enhance the effect of exercise training on muscle growth or strength in young, welltrained adult males ( 15-17).Far less is known about responses to repeated bouts of physical activity in the younger, developing organism where overall body growth is rapid and secretory patterns of growth factors (such as GH) are in a state of flux (18). The purpose of this ...

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supporting

confidence: 93%

mentioning

confidence: 99%

Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

et al. 1994

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“…Associated with these changes, the authors also observed a significant improvement in running time to exhaustion when compared with an untrained control group (186±18 min vs. 29±3 min). Similar findings have subsequently been observed by other groups using guinea pigs (Barnard et al, 1970), rats (Gollnick & Ianuzzo, 1972) and later humans (Morgan et al, 1971). Using a single-leg cycling design, Morgan et al (1971) observed that an increase in mitochondrial protein content was largely due to increases in mitochondrial size (i.e.…”

Section: Exercise-induced Mitochondrial Biogenesissupporting

confidence: 81%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

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PGC-1α is regarded as a key regulator of mitochondrial biogenesis due to its central role in regulating the activity of key transcription factors associated with encoding mitochondrial components. Additionally, PGC-1α has shown to mediate adaptations that increase fat metabolism and angiogenesis, contributing to the overall oxidative phenotype of the muscle. While it is well established that exercise is a potent stimulator of PGC-1α, recent evidence indicates that heat and cold exposures may also influence mitochondrial biogenesis through the up-regulation of PGC-1α. This highlights the potential use of these modalities in conjunction with exercise to enhance training adaptations. As such, the purpose of this review is to describe the possible mechanisms and pathways by which exercise, as well as hot and cold exposures may influence mitochondrial biogenesis. It is clear that changes in intracellular calcium, oxidative stress and phosphorylation potential are major up-regulators of PGC-1α during exercise. Moreover, there is evidence implicating calcium signalling, in addition to β-adrenergic activation in cold-induced mitochondrial biogenesis, while PGC-1α during heat exposure is likely triggered by changes in phosphorylation potential and nitric oxide signalling. However, these mechanisms appear to change considerably when cold/heat is administered following exercise, and seem to be dependent on the experimental models used (i.e. in vitro vs. in vivo, rodent vs. human). Understanding the effects heat/cold exposure and its interaction with exercise may lead to the optimisation and development of temperature-related interventions to enhance training adaptations, or aid in the treatment of mitochondrial related diseases.

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“…Electronmicroscopy of hypothyroid muscle suggests an increase in the number of mitochondria (41), while the yield ofmitochondrial protein has been reported to be both normal (4) or decreased (6,8). Most authors, however, agree that the activities of those muscle enzymes that serve as markers of mitochondria are reduced in hypothyroidism (4)(5)(6)(7)(8)(9). This reduction seems more pronounced in red muscle (7)(8)(9) and its net effect on mixed muscles is not clear.…”

Section: P Nmrmentioning

confidence: 99%

“…Furthermore, the activities of several key mitochondrial enzymes are reduced (4)(5)(6)(7)(8)(9). The latter is more pronounced in slow twitch, red muscles compared with fast, white muscles (7,8).…”

Section: Introductionmentioning

confidence: 99%

Effects of thyroid hormones on skeletal muscle bioenergetics. In vivo phosphorus-31 magnetic resonance spectroscopy study of humans and rats.

et al. 1988

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The pathophysiology of the myopathy in dysthyroid states is poorly understood. We therefore tested the effects of thyroid hormones on muscle bioenergetics in humans and rats, using in vivo 31P NMR. Two hypothyroid patients had: low phosphocreatine to inorganic phosphate ratio (PCr/Pi) at rest, increased PCr depletion during exercise and delayed postexercise recovery of PCr/Pi. Eight thyroidectomized rats did not show abnormalities at rest, but muscle work induced by nerve stimulation resulted in a significantly (P < 0.0001) lower PCr/ Pi (3545% of control) at each of the three stimulation frequencies tested (0.25, 0.5, and 1.0 Hz). Recovery rate was markedly slowed to one-third of normal values. Thyroxine therapy reversed these abnormalities in both human and rat muscle. Five patients and six rats with hyperthyroidism did not differ from normal controls during rest and exercise but had an unusually rapid recovery after exercise. The bioenergetic abnormalities in hypothyroid muscle suggest the existence of a hormone-dependent, reversible mitochondrial impairment in this disorder. The exercise intolerance and fatigue experienced in hypothyroid muscle may be due to such a bioenergetic impairment. The changes in energy metabolism in hyperthyroid muscle probably do not cause the muscular disease in this disorder.

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Hormonal deficiencies and the metabolic adaptations of rats to training

Cited by 57 publications

References 0 publications

Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Effects of thyroid hormones on skeletal muscle bioenergetics. In vivo phosphorus-31 magnetic resonance spectroscopy study of humans and rats.

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