Fig 5 - uploaded by Glenn A Gaesser
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Individual and group (solid line) relationships between epinephrine and CHO expenditure during exercise (A) and norepinephrine and CHO expenditure during exercise (B). P 0.002 and P 0.004, respectively.
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Context 1
... individual relationships between CHO expendi- ture and Epi during exercise and between CHO expen- diture and NE during exercise are shown in Fig. 5. We evaluated this relationship because both peak Epi and peak NE occurred during exercise and only CHO ex- penditure during exercise was related to exercise in- tensity. Within-subject regression revealed that CHO expenditure during exercise increased significantly with increasing Epi and NE during exercise (P 0.002 and P 0.004, ...
Context 2
... is that increased SNS activity associated with incremental exercise may re- sult in increased CHO utilization. At first glance, our data seem to support this view, because there was a progressive increase in Epi and NE with increasing exercise intensity (Fig. 3) and a similar relationship between Epi and NE and CHO expenditure during exercise (Fig. 5). Indeed, an individual's hormonal and metabolic responses to exercise are generally intensity dependent (11). Moreover, both NE and Epi appear to augment muscle lactate output during muscle contrac- tions (11) and may, thus, in part govern the magnitude of the lactate response (24,37). With increasing exer- cise intensity, SNS activity ...
Citations
Resistance exercise induces a host of endocrine responses that potentiate its effects on body composition and metabolism. Excess adiposity negatively affects some hormonal responses to exercise in sedentary men. This study compared the resistance exercise (RE)-associated growth hormone (GH), insulin-like growth factor-1 (IGF-1), and testosterone responses in lean vs. obese physically active men.
Ten healthy physically active obese males (body fat % 36.2 ± 4.03, age 24.6 ± 3.7 years, mass 104.5 ± 15.5 kg, height 178.8 ± 6.0 cm) were compared to ten lean counterparts (body fat % 12.7 ± 2.9, age 24.6 ± 3.7 years, mass 77.1 ± 6.4 kg, height 177.2 ± 4.8 cm). The muscular endurance RE protocol consisted of six sets of ten repetitions per leg of stepping onto an elevated platform (20 % of participant's height) while wearing a weighted-vest (50 % of participant's lean mass). Pre-, immediately post-exercise (IP), and three more blood samples were collected during the one-hour recovery.
When accounting for baseline differences there were no group by time interactions for GH (p = 0.33); or LH (p = 0.52). Lean presented a trend towards significance for higher IGF-1 IP (p = 0.08) than obese. Testosterone IP was similar in obese and lean, but lower in obese than lean at 30 min into recovery (p < 0.01). AUC were lower in obese than lean for all hormones (p < 0.05 for all).
These findings suggest that excess adiposity does not appear to negatively affect the immediate GH and T responses to RE in active males; but possibly negatively affects IGF-1. However, the baseline and integrated concentrations during recovery appear negatively affected by excess adiposity.
In subjects with obesity, the implementation of long-term exercise intervention increases lean tissue mass and lowers adipose tissue mass. However, data indicate a blunted lipolytic response, and/or skeletal muscle protein synthesis, when subjects with obesity are exposed to acute endurance or resistance exercise, respectively. Therefore, subjects with obesity seem to display a suboptimal physiological response to acute exercise stimuli. It might be hypothesized that hormonal disturbances contribute, at least in part, to these abnormal physiological reactions in the obese. This review discusses the impact of acute endurance and resistance exercise on endocrine hormones directly related to lipolysis and/or skeletal muscle protein synthesis (insulin, [nor]epinephrine, cortisol, growth hormone, testosterone, triiodothyronine, atrial natriuretic peptide, insulin-like growth factor-1), as well as the impact of long-term endurance and resistance exercise intervention on these hormonal responses to acute endurance and resistance exercise. In the obese, some endocrinological disturbances during acute endurance and resistance exercise have been identified: a blunted blood growth hormone, atrial natriuretic peptide and epinephrine release, and greater cortisol and insulin release. These hormonal disturbances might contribute to a suppressed lipolytic response, and/or suppressed skeletal muscle protein synthesis, as a result of acute endurance or resistance exercise, respectively. In subjects with obesity, the impact of acute endurance and resistance exercise on other endocrine hormones (norepinephrine, testosterone, triiodothyronine, insulin-like growth factor-1) remains elusive. Furthermore, whether long-term endurance and resistance exercise intervention might reverse these hormonal disturbances during acute endurance and resistance exercise in these individuals remains unknown.
