Effects of continuous versus intermittent exercise, obesity, and gender on growth hormone secretion

Abstract

Context: Obesity attenuates spontaneous GH secretion and the GH response to exercise. Obese individuals often have low fitness levels, limiting their ability to complete a typical 30-min bout of continuous exercise. An alternative regimen in obese subjects may be shorter bouts of exercise interspersed throughout the day.

Objective: The objective of the study was to examine whether intermittent and continuous exercise interventions evoke similar patterns of 24-h GH secretion and whether responses are attenuated in obese subjects or affected by gender.

Design: This was a repeated-measures design in which each subject served as their own control.

Setting: This study was conducted at the University of Virginia General Clinical Research Center.

Subjects: Subjects were healthy nonobese (n = 15) and obese (n = 14) young adults.

Interventions: Subjects were studied over 24 h at the General Clinical Research Center on three occasions: control, one 30-min bout of exercise, and three 10-min bouts of exercise.

Main outcome measures: Twenty-four hour GH secretion was measured.

Results: Compared with unstimulated 24-h GH secretion, both intermittent and continuous exercise, at constant exercise intensity, resulted in severalfold elevation of 24-h integrated serum GH concentrations in young adults. Basal and pulsatile modes of GH secretion were attenuated both at rest and during exercise in obese subjects.

Conclusions: The present data suggest that continuous and intermittent exercise training should be comparably effective in increasing 24-h GH secretion.

Figure 1

Design of the present study. CHO, Cholesterol.

Figure 2

Twenty-four-hour serum GH concentration profiles sampled every 10 min in a nonobese and obese man and woman during three study sessions each (control; a 30 min continuous bout of exercise, 1 × 30 min; three 10 min intermittent bouts of exercise, 3 × 10 min). Asterisks denote significant pulse onsets. The overlying interrupted curves are predicted (fit) by the deconvolution model (methods). Sampling began at 0700 h (time 0). Exercise was performed at 0900–0930 h (single exercise bout) and at 0920–0930, 1320–1330, and 1720–1730 h (three 10 min bouts). Standardized meals were fed at 1000, 1400, and 1800 h. Lights were put out at 2300 h.

Figure 3

IGHC (0700–0700 h) across three exercise conditions (control; a 30 min continuous bout of exercise, 1 × 30 min; three 10 min intermittent bouts of exercise, 3 × 10 min) in nonobese and obese men and women. Data are means ± se. ANOVA revealed the following: significant main effects for obesity status (P < 0.001) and condition (P = 0.003). Within each condition, 24-h IGHC in nonobese subjects exceeded that of obese individuals (P < 0.002 for all comparisons). Both exercise conditions resulted in augmented 24-h IGHC compared with the control condition (P = 0.004 for 1 × 30 min vs. C and P = 0.002 for 3 × 10 min vs. C). There were no differences observed between exercise conditions (P = 0.82), no main effect for gender, and no interactions. Capital letters give differences between exercise conditions and lower-case letters differences among subjects (e.g. A and B indicate that 1 × 30 min and 3 × 10 min were different than control; a and b indicate that within each condition nonobese subjects differed from obese subjects).

Figure 4

Linear-mixed regression models examining the linear and nonlinear effects of VO₂ (milliliters per kilogram per minute) on pulsatile GH (micrograms per liter per 24 h) at rest and during exercise in females. The solid line represents the predicted values and the dashed lines represent the simultaneous 95% confidence intervals. There were significant linear trends in the relationship between VO_2peak and log(pulsatile GH) under both the control and exercise conditions (P < 0.001 and P = 0.008 at rest and exercise, respectively). The linear trend was not condition dependent.

Figure 5

Linear-mixed regression models examining the linear and nonlinear effects of VO₂ (milliliters per kilogram per minute) on pulsatile GH (micrograms per liter per 24 h) at rest and during exercise in males. The solid line represents the predicted values and the dashed lines represent the simultaneous 95% confidence intervals. There were significant linear trends in the relationship between VO_2peak and log(pulsatile GH) under both the control and exercise conditions (P = 0.016 and P = 0.025 at rest and exercise, respectively). The linear trend was not condition dependent.

Figure 6

Linear-mixed regression models examining the linear and nonlinear effects of BMI on pulsatile GH (micrograms per liter per 24 h) at rest and during exercise in females. The solid line represents the predicted values and the dashed lines represent the simultaneous 95% confidence intervals. There were significant linear trends in the relationship between BMI and log(pulsatile GH) under both the control and exercise conditions (P < 0.001 at rest and exercise). The linear trend was not condition dependent.

Figure 7

Linear-mixed regression models examining the linear and nonlinear effects of BMI on pulsatile GH (micrograms per liter per 24 h) at rest and during exercise in males. The solid line represents the predicted values and the dashed lines represent the simultaneous 95% confidence intervals. There were significant linear trends in the relationship between BMI and log(pulsatile GH) under both the control and exercise conditions (P < 0.001 at rest and exercise). The linear trend was not condition dependent.