Antioxidant response to exercise-induced oxidative stress and protection by vitamin E.
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Administration, Oral↗
Biomedical subjects
M A Fiatarone
Publications and source records attributed to M A Fiatarone.
Leg extensor power and functional performance in very old men and women.
1. Residents of a chronic care hospital (13 men of mean age 88.5 +/- 6 SD years and 13 women of mean age 86.5 +/- 6 SD years) who had multiple pathologies were assessed for leg extensor capability in several ways. 2. A custom-built rig was used to assess leg extensor power, that is, maximal power output over less than 1 s in a single extension of one leg. Performance measures were obtained by timing chair rises (from a standard chair 0.43 m high), stair climbing (four risers, total height 0.635 m) and a walk (6.1 m). For each measurement the best of several trials were recorded as definitive. 3. Leg extensor power was significantly correlated with all performance measures, but the performance measures were not related to each other except for chair rising and walking speed. 4. Women had significantly less extensor power than men, but their power explained more of the variance in performance, e.g. power accounted for 86% of the variance in walking speed. 5. There was no relation within the group between age and any of the variables measured. 6. Measurement of leg extensor power in frail elderly people may prove useful in focusing effective rehabilitation programmes.
Aged↗
Acute phase response in exercise. II. Associations between vitamin E, cytokines, and muscle proteolysis.
Cytokines such as interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and interleukin 6 (IL-6) mediate a variety of host responses to trauma and infection, including skeletal muscle proteolysis. This investigation assesses the influence of damaging eccentric exercise on in vitro production and plasma concentrations of cytokines and their relationship to muscle protein breakdown. In a double-blind placebo-controlled protocol, 21 male subjects took vitamin E supplements (800 IU/day) for 48 days, then ran downhill on an inclined treadmill. Twenty-four hours after this single session of eccentric exercise, endotoxin-induced secretion of IL-1 beta was augmented 154% (P less than 0.01) in cells obtained from the placebo subjects, but no significant exercise-related changes were observed in cells from the vitamin E-supplemented subjects. TNF-alpha secretion was also significantly increased 24 h after exercise, but the response was not inhibited by vitamin E. In contrast, IL-6 secretion did not change after exercise, but dietary vitamin E supplementation significantly reduced IL-6 secretion throughout the 12-day period of observation (P = 0.023). Urinary 3-methylhistidine excretion correlated with mononuclear cell secretion of both IL-1 beta (P less than 0.05) and prostaglandin E2 (P less than 0.05), supporting the concept that these mononuclear cell products contribute to the regulation of muscle proteolysis.
Acute-Phase Reaction↗
High-intensity strength training in nonagenarians. Effects on skeletal muscle.
Muscle dysfunction and associated mobility impairment, common among the frail elderly, increase the risk of falls, fractures, and functional dependency. We sought to characterize the muscle weakness of the very old and its reversibility through strength training. Ten frail, institutionalized volunteers aged 90 +/- 1 years undertook 8 weeks of high-intensity resistance training. Initially, quadriceps strength was correlated negatively with walking time (r = -.745). Fat-free mass (r = .732) and regional muscle mass (r = .752) were correlated positively with muscle strength. Strength gains averaged 174% +/- 31% (mean +/- SEM) in the 9 subjects who completed training. Midthigh muscle area increased 9.0% +/- 4.5%. Mean tandem gait speed improved 48% after training. We conclude that high-resistance weight training leads to significant gains in muscle strength, size, and functional mobility among frail residents of nursing homes up to 96 years of age.
Aged↗
Energy expenditure and subsequent nutrient intakes in overfed young men.
We investigated the mechanisms of body weight regulation in young men of normal body weight leading unrestricted lives. Changes in total and resting energy expenditure, body composition, and subsequent voluntary nutrient intakes in response to overeating by 4,230 +/- 115 (SE) kJ/day (1,011 +/- 27 kcal/day) for 21 days were measured in seven subjects consuming a typical diet. On average, 85-90% of the excess energy intake was deposited (with 87% of this amount in fat and 13% in protein on average). There was no detectable difference between individuals in susceptibility to energy deposition. The resting metabolic rate, averaged for fasting and fed states, increased during overfeeding (mean +/- SE, 628 +/- 197 kJ/day, P less than 0.01), but at least some of this amount was obligatory expenditure associated with nutrient assimilation. No significant increase in energy expenditure for physical activity or thermoregulation resulted from overfeeding. Thus energy expenditure did not substantially adapt to increased energy intake. However, significant decreases in voluntary energy intake (1,991 +/- 824 kJ/day, P less than 0.05) and fat intake (48 +/- 11 g/day, P less than 0.01) followed overeating, indicating that adaptive changes in nutrient intakes can contribute significantly to body weight regulation after overeating.
Adult↗
Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release.
Several host defense responses and metabolic reactions that occur during infection have been observed after exercise. We hypothesized that these reactions, known as the "acute phase response," contribute to the breakdown and clearance of damaged tissue after exercise. This hypothesis was tested with 21 male volunteers representing two ranges of age (22-29 and 55-74 yr), who ran downhill on an inclined treadmill to accentuate damaging eccentric muscular contractions. The subject groups were further divided in a double-blind placebo-controlled protocol, which examined the influence of 48 days of dietary vitamin E supplementation before the exercise. All subjects were monitored for 12 days after exercise for changes in circulating leukocytes, superoxide release from neutrophils, lipid peroxidation, and efflux of the intramuscular enzyme creatine kinase (CK) into the circulation. Among those receiving placebo, the less than 30-yr-old subjects responded to exercise with a significantly greater neutrophilia and higher plasma CK concentrations than the greater than 55-yr-old subjects. Dietary supplementation with vitamin E tended to eliminate the differences between the two age groups, primarily by increasing the responses of the greater than 55-yr-old subjects. At the time of peak concentrations in the plasma, CK correlated significantly with superoxide release from neutrophils. The association of enzyme efflux with neutrophil mobilization and function supports the concept that neutrophils are involved in the delayed increase in muscle membrane permeability after damaging exercise.
Acute-Phase Reaction↗
The effect of exercise on natural killer cell activity in young and old subjects.
Alterations in immune function have been commonly reported in elderly persons. We have examined the effect of age on the responsiveness of natural killer (NK) cells to in vitro stimulation with recombinant interleukin-2 (rIL-2) and in vivo stimulation with exercise in 17 healthy subjects (8 young and 9 old). The old subjects were found to have NK cell numbers and function that were not significantly different from the young subjects at baseline. They also responded as well as the young subjects to rIL-2 stimulation of NK cells in vitro. In response to maximal bicycle ergometry exercise, there was a marked rise in NK activity in the old (7.52 +/- 1.71 LU/10(6) pre-exercise vs 15.20 +/- 3.27 LU/10(6) post-exercise, p less than .03) and the young (6.29 +/- .48 LU 10(6) vs 14.56 +/- 1.86 LU 10(6), p less than .005) subjects. Lymphocytes bearing the NK marker Leu 11a also rose significantly post-exercise in both old and young subjects. We conclude that healthy elderly subjects increase their NK activity in response to the acute stressor, exercise, at least as effectively as do young subjects.
Adult↗
Increased interleukin 1 beta in human skeletal muscle after exercise.
Interleukin 1 beta (IL-1 beta) is a protein released from blood monocytes and related cells in response to infectious or inflammatory stimuli. Although IL-1 beta is elevated in the circulation for only a few hours after an acute inflammatory challenge or exercise, it has been proposed to mediate anabolic and catabolic processes that can last for several days. In this report, eccentric exercise was used as a noninfectious inflammatory stimulus. IL-1 beta was found in muscle tissue up to 5 days after exercise using specific immunohistochemical tissue staining. Increased IL-1 beta immunoreactivity was observed in muscle tissue from four human subjects who performed the exercise, but not in tissue obtained at the same time intervals from two subjects who did not exercise. Little immunohistochemical evidence of interleukin-1 alpha or tumor necrosis factor alpha was observed before or after exercise. These results implicate IL-1 beta in the metabolic adaptations of muscle tissue, which occur in response to noninfectious stresses.
Adult↗
Psychoimmunologic and endorphin function in the aged.
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Adult↗
Endogenous opioids and the exercise-induced augmentation of natural killer cell activity.
Based on prior observations that both beta-endorphin and exercise stimulate natural killer (NK) cell activity, we have examined the hypothesis that the release of endogenous opioids during the stress of acute exercise may mediate this NK cell augmentation. Eight healthy young women underwent a maximal bicycle ergometer exercise test with prior in vivo administration of a placebo and an opioid antagonist, naloxone (100 micrograms/kg), in a randomized, blind protocol. Exercise after the placebo injection was accompanied by a dramatic rise in NK activity, as well as an increase in the percentage of lymphocytes bearing the NK cell surface markers Leu 11a and Leu 19. Significant stimulation of NK activity was observed with beta-endorphin in vitro before exercise, but after exercise, beta-endorphin had a nonsignificant inhibitory effect. When these experiments were carried out in the presence of naloxone in vivo, the rise in NK activity after exercise was no longer significant. Naloxone did not significantly alter the rise in Leu 11a+ or Leu 19+ cell after exercise, as compared with the placebo. Finally, when naloxone was given to the subjects beforehand, exercise no longer completely blocked the in vitro beta-endorphin stimulation of NK cells. In conclusion, our observations that the exercise-induced augmentation of NK activity and the lack of effect of beta-endorphin in vitro on NK activity after exercise are both significantly attenuated by prior administration of naloxone suggest that the opioid system may play a major role in the modulation of NK cells during physiologic stress.
Adult↗