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![Absolute carbohydrate (CHO) (A) and fat (B) energy expenditure (kcal) responses [individual and group (solid line)] during 30 min of exercise at 5 different exercise intensities relative to the lactate threshold (LT). P 0.002 and P 0.50, respectively.](profile/Glenn-Gaesser-2/publication/237109659/figure/fig1/AS:413465790435328@1475589334113/Absolute-carbohydrate-CHO-A-and-fat-B-energy-expenditure-kcal-responses.png)
Absolute carbohydrate (CHO) (A) and fat (B) energy expenditure (kcal) responses [individual and group (solid line)] during 30 min of exercise at 5 different exercise intensities relative to the lactate threshold (LT). P 0.002 and P 0.50, respectively.
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Context 1
... absolute fat and CHO responses during exercise at the five different exercise intensities are shown in Fig. 1. CHO expenditure increased with increasing exercise intensity in all 10 subjects (P 0.002, Fig. 1A). The relationship between fat expenditure during exercise and exercise intensity was not significant (P 0.50) or directionally consistent (5 subjects increased fat expenditure, 5 subjects decreased fat expenditure with increasing ...
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... absolute fat and CHO responses during exercise at the five different exercise intensities are shown in Fig. 1. CHO expenditure increased with increasing exercise intensity in all 10 subjects (P 0.002, Fig. 1A). The relationship between fat expenditure during exercise and exercise intensity was not significant (P 0.50) or directionally consistent (5 subjects increased fat expenditure, 5 subjects decreased fat expenditure with increasing exercise intensity) (Fig. 1B). When CHO expenditure during exercise was modeled as the percentage of total ...
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... CHO expenditure increased with increasing exercise intensity in all 10 subjects (P 0.002, Fig. 1A). The relationship between fat expenditure during exercise and exercise intensity was not significant (P 0.50) or directionally consistent (5 subjects increased fat expenditure, 5 subjects decreased fat expenditure with increasing exercise intensity) (Fig. 1B). When CHO expenditure during exercise was modeled as the percentage of total energy expenditure during exercise, percentage CHO increased with increasing exercise intensity in 8 of 10 subjects (P 0.009, data not shown). Figure 2 presents the same analysis for CHO expen- diture and fat expenditure vs. exercise intensity during 3.5 h of ...
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... point in energy utilization during escalating exercise intensities (4, 5), standardized against the subject-specific LT. Unexpectedly, we report that abso- lute energy utilization from CHO increased progres- sively according to a linear model, with increasing exercise intensity, whereas fat utilization was not af- fected under the same conditions (Fig. 1). An increase was also evident when CHO utilization during exercise was examined relative to total energy utilized during exercise. In addition, the present data reveal the novel insight that, during recovery from exercise, fat utiliza- tion correlated strongly with increasing exercise inten- sity (Fig. 2). Thus the present data do not ...
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... CHO metabo- lism (4, 5) because elevated lactate can inhibit free fatty acid mobilization (18). Our data suggest that, although the blood lactate rise itself exhibits a thresh- old followed by a curvilinear increase with increasing exercise intensity (29), a simple linear relationship is evident between CHO energy utilized and exercise intensity (Fig. 1). Accordingly, the time course of the blood lactate response to exercise does not appear to correspond to (and thus may not mediate) substrate ...
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... the percentage of fat energy utilized de- creased with increasing exercise intensity, total (abso- lute) fat utilization during exercise was not affected by exercise intensity. The mean slope of the 10 subjects tends to support only a slight increase in fat expendi- ture with increasing exercise intensity (Fig. ...
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.
