To investigate the role of sympathoadrenergic activity on glucose production (Ra) during exercise, eight healthy males bicycled 20 min at 41 +/- 2 and 74 +/- 4% maximal O2 uptake (VO2max; mean +/- SE) either without (control; Co) or with blockade of sympathetic nerve activity to liver and adrenal medulla by local anesthesia of the celiac ganglion (Bl). Epinephrine (Epi) was in some experiments infused during blockade to match (normal Epi) or exceed (high Epi) Epi levels during Co. A constant infusion of somatostatin and glucagon was given before and during exercise. At rest, insulin was infused at a rate maintaining euglycemia. During intense exercise, insulin infusion was halved to mimic physiological conditions. During exercise, Ra increased in Co from 14.4 +/- 1.0 to 27.8 +/- 3.0 mumol.min-1.kg-1 (41% VO2max) and to 42.3 +/- 5.2 (74% VO2max; P < 0.05). At 41% VO2max, plasma glucose decreased, whereas it increased during 74% VO2max. Ra was not influenced by Bl. In high Epi, Ra rose more markedly compared with control (P < 0.05), and plasma glucose did not fall during mild exercise and increased more during intense exercise (P < 0.05). Free fatty acid and glycerol concentrations were always lower during exercise with than without celiac blockade. We conclude that high physiological concentrations of Epi can enhance Ra in exercising humans, but normally Epi is not a major stimulus. The study suggests that neither sympathetic liver nerve activity is a major stimulus for Ra during exercise. The Ra response is enhanced by a decrease in insulin and probably by unknown stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the role of liver nerve activity on hepatic glucose production during exercise, liver-transplant subjects (LTX, n = 7, 25-62 yr, 4-18 mo postoperative) cycled for 40 min, 20 min at 52 +/- 3% (SE) maximal O2 consumption (VO2max) and 20 min at 83 +/- 1% VO2max, respectively. Kidney-transplant (KTX) and healthy control subjects (C) matched for sex and age exercised at the same %VO2max as LTX. VO2max was lower in both LTX (1.59 +/- 0.12 l/min) and KTX (1.59 +/- 0.07) than in C (2.60 +/- 0.26). At rest plasma renin and insulin were higher and plasma adrenocorticotropic hormone and cortisol lower in transplant corticosteroid-treated subjects compared with C. In LTX, hepatic glucose production (Ra) increased from 11.9 +/- 0.9 (rest) to 17.6 +/- 1.8 and 25.5 +/- 1.8 mumol.min-1.kg-1 at 52 and 82% VO2max, respectively. Peripheral glucose uptake was similar to Ra, and glucose remained at basal postabsorptive levels. During exercise the Ra increase as well as norepinephrine, insulin, and growth hormone responses were similar in LTX compared with both KTX and C. The increase in epinephrine was smaller in LTX than in C, the only group showing an increase in cortisol. The increase in plasma renin activity during exercise was attenuated in KTX compared with LTX and C. During exercise blood lactate rose more and plasma glycerol and free fatty acid levels were lower in LTX and KTX compared with C.(ABSTRACT TRUNCATED AT 250 WORDS)
To establish whether or not hypoxia influences the training-induced adaptation of hormonal responses to exercise, 21 healthy, untrained subjects (2) years, mean (SE)] were studied in three groups before and after 5 weeks' training (cycle ergometer, 45 min.day-1, 5 days.week-1). Group 1 trained at sea level at 70% maximal oxygen uptake (VO2max), group 2 in a hypobaric chamber at a simulated altitude of 2500 m at 70% of altitude VO2max, and group 3 at a simulated altitude of 2500 m at the same absolute work rate as group 1. Arterial blood was sampled before, during and at the end of exhaustive cycling at sea level (85% of pretraining VO2max). VO2max increased by 12 (2)% with no significant difference between groups, whereas endurance improved most in group 1 (P < 0.05). Training-induced changes in response to exercise of noradrenaline, adrenaline, growth hormone, beta-endorphin, glucagon, and insulin were similar in the three groups. Concentrations of erythropoietin and 2,3-diphosphoglycerate at rest did not change over the training period. In conclusion, within 5 weeks of training, no further adaptation of hormonal exercise responses takes place if intensity is increased above 70% VO2max. Furthermore, hypoxia per se does not add to the training-induced hormonal responses to exercise.
Effects of endurance training on maximal inspiratory pressure and fatigue were evaluated after 5 weeks. Twelve male and 9 female untrained subjects were matched in the three groups for sex and maximal oxygen uptake (VO2 max). Training was performed at 70% VO2max; 45 min day-1; 5 days week-1 (n = 7); and at the same relative (n = 7) and absolute (n = 7) work loads in a pressure chamber corresponding to 2500 m (560 mmHg). Work load was increased every week to maintain the training heart rate. Maximal respiratory pressure was measured at the mouth before and 30, 60 and 120 s after maximal exercise. With no significant difference between the three groups of subjects, VO2max increased from 2.96 (1.98-4.47) (median and range for 21 subjects) to 3.33 (2.50-4.72) 1 min-1 (p < 0.001) and ventilation (VE max) from 109 (57-147) to 123 (73-148) 1 min-1 (p < 0.001), while maximal heart rate decreased from 193 (180-211) to 192 (169-207) beats min-1 (p < 0.01). Maximal inspiratory pressure (87 (56-115) mmHg), inspiratory muscle fatigue (18 (-2-43)%, p < 0.001), and arterial oxygen tension during exercise (12.4 (9.9-15.6)kPa) were similar before and after training. The results demonstrate that training at simulated altitude at 2500 m does not increase VE max or VO2 max above the increases obtained from training at sea level. Furthermore, VEmax and VO2 max increased approximately 13% despite unchanged maximal inspiratory pressure and inspiratory muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
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