The purpose of this study was to determine what effects 26 wk of resistance training have on resting energy expenditure (REE), total free-living energy expenditure (TEE), activity-related energy expenditure (AEE), engagement in free-living physical activity as measured by the activity-related time equivalent (ARTE) index, and respiratory exchange ratio (RER) in 61- to 77-yr-old men (n = 8) and women (n = 7). Before and after training, body composition (four-compartment model), strength, REE, TEE (doubly labeled water), AEE (TEE - REE + thermic response to meals), and ARTE (AEE adjusted for energy cost of standard activities) were evaluated. Strength (36%) and fat-free mass (2 kg) significantly increased, but body weight did not change. REE increased 6.8%, whereas resting RER decreased from 0.86 to 0.83. TEE (12%) and ARTE (38%) increased significantly, and AEE (30%) approached significance (P = 0.06). The TEE increase remained significant even after adjustment for the energy expenditure of the resistance training. In response to resistance training, TEE increased and RER decreased. The increase in TEE occurred as a result of increases in both REE and physical activity. These results suggest that resistance training may have value in increasing energy expenditure and lipid oxidation rates in older adults, thereby improving their metabolic profiles.

We tested the hypothesis that older men (n = 9, 69 +/- 2 years) would experience greater resistance-training-induced myofiber hypertrophy than older women (n = 5, 66 +/- 1 years) following knee extensor training 3 days per week at 65-80% of one-repetition maximum for 26 weeks. Vastus lateralis biopsies were analyzed for myofiber areas, myosin heavy chain isoform distribution, and levels of mRNA for insulin-like growth factor 1 (IGF-1), IGFR1, and myogenin. Gender x Training interactions (p <.05) indicate greater myofiber hypertrophy for all three primary fiber types (I, IIa, IIx) and enhanced one-repetition maximum strength gain in men compared with women (p <.05). Covarying for serum IGF-1, dehydroepiandrosterone sulfate, or each muscle mRNA did not negate these interactions. In both genders, type IIx myofiber area distribution and myosin heavy chain type IIx distribution decreased with a concomitant increase in type IIa myofiber area distribution (p <.05). In summary, gender differences in load-induced myofiber hypertrophy among older adults cannot be explained by levels of circulating IGF-1 or dehydroepiandrosterone sulfate, or by expression of the myogenic transcripts examined.

The purpose of this study was to objectively compare the difficulty and determine the contribution of strength and muscle mass to the performance of physical tasks of daily living in a group of younger and older women. A cross-sectional design was used. Volunteer participants were from the community of Birmingham, AL; there were 21 older (aged 60-75 years) and 20 younger (23-34 years) healthy women in the study. Subjects were matched for height and weight. Their testing included total and regional body composition evaluation by use of dual-energy x-ray absorptiometry, isometric strength tests of elbow flexors and knee extensors, and integrated electromyography (IEMG) evaluation while the subjects were standing from and sitting into a chair, and while they were carrying a small load (weight relative to strength). A two-way analysis of variance and a two-way analysis of covariance with repeated measures, Pearson product correlation, and first-order partial correlations were used to analyze the data. A significant inverse correlation was observed between age and isometric strength of both the knee extensors and elbow flexors. Adjusting for upper leg lean tissue did not change the significant inverse correlation between age and knee extensor strength. However, after an adjustment for arm lean tissue, there was no significant correlation between elbow flexor strength and age. Older women experienced significantly greater difficulty in standing than younger women as measured by quadriceps normalized IEMG (i.e., IEMG during task/IEMG during maximum isometric strength test). This difference persisted even after the covariate upper leg lean tissue was added to the model. No significant difference was observed between younger and older women for difficulty (biceps normalized IEMG) during the carry task after the covariate arm lean tissue was added to the model. The older women in this study had less strength in the knee extensors and experienced greater difficulty standing from a chair than the younger women, even after the covariate upper leg lean tissue was added to the model. This suggests that other factors, in addition to loss of lean tissue, contribute to the age-related decline of muscular strength and the ability to perform tasks with the legs. In contrast, although elbow flexor strength declined, this appeared to be largely due to decreased arm lean tissue mass.

Abstract-The oxidation of low density lipoprotein (LDL) has been suggested as a key event in atherogenesis. Paradoxically, exercise, which imposes an oxidative stress, is an important deterrent of cardiovascular disease. In study 1 the oxidizability of LDL was enhanced in exercisers compared with sedentary controls. The lag time of isolated LDL subjected to copper-induced in vitro oxidation was significantly shortened in the exercisers compared with sedentary subjects. This increased sensitivity was not due to a decreased presence of vitamin E. Instead, these findings suggested that the LDL of exercisers may contain increased amounts of preformed lipid peroxides, which account for the increased oxidizability. In study 2, a groupϫsex ANOVA revealed that male exercisers had a significantly longer mean lag time than male sedentary subjects and that females had similar mean lag times regardless of exercise group. This remained the case when statistical adjustment was made for age, body mass index, blood lipid levels, LDL, and plasma ␣-tocopherol levels. Study 1 exercisers had been in training for a shorter time (Ͻ1 year) than study 2 exercisers (Ͼ2 years). These findings suggest that truly "chronic" exercise (aerobic intensity over several months) decreases the susceptibility of a male exerciser's LDL to undergo oxidation. Conversely, regular aerobic stress during an overall shorter time span creates a more oxidative environment in the body, thus increasing the susceptibility of LDL to undergo oxidation. The oxidative stress of aerobic exercise does not appear to adversely affect the oxidizability of LDL in women.