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P M Tiidus

Publications and source records attributed to P M Tiidus.

28 records · Page 2Linked to original sources
PubMed1996

Lack of antioxidant adaptation to short-term aerobic training in human muscle.

The effects of 8 wk of 35 min of aerobic cycle training (3 times/wk) on indexes of male and female human vastus lateralis muscle antioxidant status were investigated. Training resulted in significant elevations in whole body maximal O2 consumption and muscle citrate synthase activity. Despite this, muscle superoxide dismutase, catalase, and glutathione peroxidase activities were not significantly altered by the training protocol. In addition, training did not affect muscle vitamin E (alpha- and gamma-tocopherol) concentrations. Glutathione status determined as the concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), total glutathione (GSH + 2 x GSSG), and GSH/GSSG ratio was unaffected by the training protocol. There were no significant differences between males and females in any indexes of muscle antioxidant status. These results indicate that the moderate aerobic training typically performed by regularly exercising humans did not positively alter endogenous antioxidant status. This suggests that short-term aerobic training increases capacity for flux through the citric acid cycle without necessarily increasing the ability to handle potential free radicals generated by the enhanced electron flux.

Adaptation, Physiological↗
PubMed1996

Effect of vitamin E deprivation and exercise training on induction of HSP70.

To investigate the effect of dietary vitamin E deprivation and chronic exercise on the relative content of selected isoforms of the heat-shock protein 70 (HSP70) family in rat hindlimb muscle, vitamin E was withheld for 16 wk from female rats that underwent treadmill run training during the final 8 wk. As indicated by increased (P < 0.05) content of the stress-inducible isoform (HSP72), training did stress the exercising muscles. However, vitamin E deficiency did not alter HSP72 content in nontrained rats and was associated with a lesser induction (P < 0.01) in some muscles of trained animals. The constitutive isoform, which exhibited similar levels in muscles of varying fiber types, was demonstrated to be largely refractory to exercise, with an equivocal response to vitamin E deprivation. HSP72 content was correlated to type I myosin heavy chain (MHC-I) content but only in muscles of sedentary normal-diet rats. After training, HSP72 content in a muscle essentially devoid of MHC-I (superficial vastus lateralis) reached levels comparable to those in a muscle high in MHC-I (soleus).

Animals↗
PubMed1995

Effleurage massage, muscle blood flow and long-term post-exercise strength recovery.

Manual massage is commonly assumed to enhance long term muscle recovery from intense exercise, partly due to its ability to speed healing via enhanced muscle blood flow. We tested these assumptions by daily (for four days) massaging the quadriceps muscles of one leg on subjects who had previously completed an intense bout of eccentric quadriceps work with both legs. Immediate post-exercise isometric and dynamic quadriceps peak torque measures had declined to approximately 60-70% of pre-exercise values in both legs. Peak torques for both the massage and control leg tended to slowly return toward pre-exercise values through the subsequent four days (96 hrs). There was no significant difference between the isometric and dynamic peak torques between massage and control legs up to 96 hours post-exercise. Leg blood flow was estimated by determining femoral artery and vein mean blood velocities via pulsed Doppler ultrasound velocimetry. Massage of the quadriceps muscles did not significantly elevate arterial or venous mean blood velocity above resting levels, while light quadriceps muscle contractions did. The perceived level of delayed onset muscle soreness tended to be reduced in the massaged leg 48-96 hours post-exercise. It was concluded that massage was not an effective treatment modality for enhancing long term restoration of post-exercise muscle strength and its use for this purpose in athletic settings should be questioned.

Adult↗
PubMed1995

Can estrogens diminish exercise induced muscle damage?

Estrogens are female sex hormones that may also protect against peroxidative damage of membrane lipids and low density lipoproteins (LDL). Studies have reported that female rats have greater protection against free radical induced lipid peroxidation and muscle damage consequent to exercise than do male rats. It has been suggested that the lower susceptibility to exercise induced oxidative stress and muscle membrane disruption of female rats may be due primarily to the antioxidant and membrane stabilizing properties of estrogens. Studies on humans have indicated that the lower incidence of atherosclerosis seen in premenopausal females in comparison to males is due at least in part to the ability of estrogens to diminish LDL peroxidation. However, there is little evidence as to the potential of estrogens to protect human females from free radical induced peroxidation and muscle damage due to exercise. This paper reviews the evidence for membrane stabilization potential of estrogens and their possible mechanisms, and speculates as to the potential significance of this for human exercise.

Animals↗
PubMed1995

Vitamin E status and response to exercise training.

Vitamin E is an important intramembrane antioxidant and membrane stabiliser. Over the past 40 years, vitamin E supplementation has been advocated for athletes in the hope of improving performance, minimising exercise-induced muscle damage and maximising recovery. However, there is currently a lack of conclusive evidence that exercise performance or recovery would benefit in any significant way from dietary vitamin E supplementation. Exceeding current recommended intakes of vitamin E even by several orders of magnitude will result in relatively modest increases in tissue or serum vitamin E concentrations. Most evidence suggests that there is no discernible effect of vitamin E supplementation on performance, training effect or rate of postexercise recovery in either recreational or elite athletes. There is very little evidence, particularly involving humans, that exercise or training will significantly alter tissue or serum vitamin E levels. While there is some evidence that certain indices of tissue peroxidation may be reduced following dietary vitamin E supplementation, the physiological and performance consequences in humans of these relatively minor effects are unknown. Although there appears to be little reason for vitamin E supplementation among athletes, it does not appear that the practice of supplementation is harmful.

Animals↗
PubMed1994

Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training.

The effects of endurance training on tissue antioxidant and oxidative enzyme activities were determined in heart, liver, and five skeletal muscles of female rats. Rats were fed either normal (+E) or vitamin E free (-E) diets for 16 wk. For the final 8 wk, subgroups of +E and -E diet animals were trained by treadmill running at 40 m.min-1, 15% grade for 60 min.d-1. No significant differences in training abilities were observed between diet groups. Endurance training significantly increased citrate synthase (CS) activity in all skeletal muscles for both the +E and -E diet animals with no significant difference in degree of response between diet groups. Neither vitamin E deprivation, training, or their combination generally affected the activities of the antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPX) in skeletal muscles, heart, or liver of the animals. These results suggest that despite an anticipated increase in free radical induced tissue "oxidative stress" brought about by a combination of vitamin E deprivation and endurance training, antioxidant enzyme adaptations were not evident and the response of citrate synthase to training was not impaired in female rats.

Adaptation, Physiological↗
PubMed1993

Vitamin E status does not affect the responses to exercise training and acute exercise in female rats.

Responses of vitamin E-depleted female rats to acute exercise and chronic exercise training were tested. Rats were fed either a control diet (+E rats) or a vitamin E-depleted diet (-E rats). After 8 wk, subgroups of the +E and -E rats performed treadmill exercise for 45 min at 28 m/min, 15% grade, and were immediately killed. Vitamin E concentrations were 80-90% lower in liver, heart and muscles in -E rats as determined by HPLC. There was no difference between +E and -E rats in blood lactate concentration, creatine kinase, lipid peroxidation indices, hematocrit or hemoglobin concentration following acute exercise. Remaining rats were either trained for a further 8 wk at 40 m/min, 15% incline for up to 60 min/d or served as untrained controls. No differences in training tolerance were seen between diet groups, with 64% of +E rats and 71% of -E rats consistently completing 60 min of daily training. The training induced similar adaptive elevations in succinate dehydrogenase activity (31-107%) in various hind limb muscles of both +E and -E rats. Trained +E rats had lower vitamin E concentrations in some but not all tissues when compared with untrained +E controls. These results suggest that consumption of a vitamin E-free diet for 8 wk did not result in differences in blood indices associated with exercise stress or in the ability to perform a submaximal acute exercise test when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of intensity and duration of muscular exercise on delayed soreness and serum enzyme activities.

The purposes of this study were to: 1) determine the time course of changes in serum enzyme activities and muscular soreness following muscular exercise, 2) quantify the relative amounts and importance of intensity and duration of muscular exercise in inducing elevated serum enzyme activities and muscular soreness in untrained individuals, and 3) determine the correlation between magnitude of soreness sensation and level of post-exercise serum enzyme activity. It was determined that the highest serum enzyme activities and muscular soreness sensation occurred 8-24 h and 48 h post-exercise, respectively. Intensity and duration of exercise were varied by adjusting the percent 10-repetition maximum (% 10RM) and number of contractions (NR) performed. Increasing intensity and duration of exercise resulted in corresponding increases in serum enzyme activities and muscular soreness. High-intensity, short-duration exercise (80% 10RM, 170 NR) resulted in greater serum enzyme activities and muscular soreness than long-duration, low-intensity exercise (30% 10RM, 545 NR). Most subjects experiencing high levels of muscular soreness were unable to lift resistances of 90% 1RM, 48 h post-exercise. These findings indicate that a positive relationship exists among exercise performed, serum enzyme activity 24 h post-exercise, and muscular soreness. Increased intensity and duration of exercise produced increased serum enzyme activities and muscular soreness, with intensity having the more pronounced effect.

Adult↗
PubMedDate not supplied

Estrogen administration, postexercise tissue oxidative stress and vitamin C status in male rats.

Estrogen can putatively act as an antioxidant and protect tissues from exercise-induced oxidative stress. To test the in vivo efficacy of estrogen, the effects of 2 weeks of daily estrogen (40 microg x kg(-1) body weight beta-estradiol 3-benzoate) injection on indices of immediate postexercise oxidative stress and antioxidant status were determined in adult male rats, with and without 8 weeks of prior dietary vitamin E deprivation. The treadmill running protocol (60 min at 21 m x min(-1), 12% grade) induced significant oxidative stress as indicated by muscle glutathione status. Estrogen administration had little effect on postexercise tissue glutathione status, superoxide dismutase and glutathione peroxidase activity, and vitamin E levels. Estrogen administration induced significant reductions in muscle, liver, and heart vitamin C concentrations following exercise, as well as in unexercised male rats. Tissue vitamin C loss was not directly mediated through liver glycogen or glutathione status. Thus, estrogen administration generally did not appear to influence postexercise tissue indices of oxidative stress or antioxidant status and may have contributed to a decline in overall antioxidant protection by inducing losses in tissue vitamin C content.

Animals↗