Differential effect of oestrogen on post-exercise cardiac muscle myeloperoxidase and calpain activities in female rats.

The effects of oestrogen administration on 1 h post-exercise cardiac muscle myeloperoxidase (MPO) and calpain activities were determined in female rats. Rats were ovariectomized and implanted for 2 weeks with either oestrogen (25 mg 17-oestradiol) or placebo pellets or left with ovaries intact. Rats were then run for 1 h at 21 m min-1, 12% grade, killed 1 h post-exercise and cardiac muscle and blood samples were removed. Control animals from each group were killed without prior exercise. Serum oestrogen levels in the order of the highest to lowest were; ovariectomized oestrogen replaced rats > intact ovaries rats > ovariectomized placebo rats. Oestrogen induced significant (P < 0.05) elevations in cardiac MPO activity at rest and at 1 h post-exercise in ovariectomized rats. No significant elevations in cardiac MPO activity were evident in placebo ovariectomized or normal ovary rats at rest or post-exercise. Cardiac calpain activities were similar in all unexercised groups. Ovariectomized placebo and intact ovary rats had significantly (P < 0.05) elevated cardiac calpain activities 1 h post-exercise while calpain activity was not significantly elevated in hearts from ovariectomized oestrogen rats. These results demonstrate that oestrogen supplementation in ovariectomized rats induces elevations in cardiac muscle MPO activities at rest and at 1 h post-exercise. This is opposite to the effect of oestrogen in post-exercise skeletal muscle and implies a greater neutrophil infiltration into cardiac muscle caused by oestrogen. This effect cannot be explained by changes in 1 h post-exercise cardiac muscle calpain activity, the elevation of which was suppressed by oestrogen administration. Oestrogen influences cardiac calpain activity similarly to its effect in skeletal muscle. Thus, oestrogen administration to ovariectomized rats induces elevations in cardiac MPO activity while suppressing cardiac calpain activity.

Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats.

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17beta-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater (P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats (P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower (P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater (P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower (P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower (P < 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content (P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

Estrogen effect on post-exercise skeletal muscle neutrophil infiltration and calpain activity.

We hypothesized that estrogen administration would attenuate skeletal muscle neutrophil infiltration, indices of muscle membrane disruption, and muscle calpain activity shortly after the termination of exercise. Ovariectomized female rats were implanted with either an estogen pellet (25 mg beta-estradiol) or a placebo pellet. Two weeks postimplant, animals were killed either at rest or 1 h after running exercise (60 min at 21 m x min(-1), 12% grade). The 4 experimental groups (n = 12) used were: unexercised placebo (UP), unexercised estrogen (UE), exercised placebo (EP), and exercised estrogen (EE). Blood samples were analyzed for creatine kinase (CK) activity and estradiol content. Plantaris and gastrocnemius muscles were removed and histochemical determination of neutrophil content or biochemical determination of myeloperoxidase (MPO), glucose-6-phosphate dehydrogenase (G6PD), and calpain-like activity determined. Estrogen supplemented animals had 10-20-fold higher circulating estradiol levels than placebo animals. EP animals had significantly higher (P < 0.05) circulating CK activities than EE or unexercised animals. Muscle neutrophil concentrations were significantly (P < 0.01) elevated in EP and EE groups compared with unexercised controls, with EP muscle neutrophil levels also being over 60% greater (P < 0.05) than in EE animals. EP animals also had higher (P < 0.05) muscle MPO activities than unexercised or EE animals. Muscle G6PD activities were not significantly different between any groups. Muscle caplain-like activities were 80% higher (P < 0.01) in EP animals than EE animals with calpain-like activities in EE animals similar to unexercised groups. These results indicate that estrogen supplementation in ovariectomized rats attenuated 1-h post-exercise serum CK activities, muscle neutrophil infiltration, MPO activities, and calpain-like activities when compared with exercised, unsupplemented animals. This supports the possibility of a relationship between estrogen, calpain dependent production of neutrophil chemo-attractant peptides, and 1-h post-exercise skeletal muscle neutrophil infiltration.

Massage and ultrasound as therapeutic modalities in exercise-induced muscle damage.

Although both massage and ultrasound treatment are used in clinical settings to enhance muscle functional recovery following exercise-induced muscle damage, there is a paucity of experimental evidence for their efficacy. Theoretically both massage and ultrasound could affect some physiological factors associated with enhancement of postexercise muscle recovery. However, the actual physiological mechanisms by which massage or ultrasound could influence postexercise muscle damage and repair are unknown. Most experimental evidence suggests that massage has little influence on muscle blood flow, clearance of "noxious" substances, recovery of postexercise muscle strength, or delayed soreness sensation. However, more data is needed before conclusions can be drawn as to the ability of massage to influence postexercise inflammatory response or various other physiological changes that characterize exercise-induced muscle damage and repair. There is even less information on the ability of ultrasound to influence physiological or functional factors associated with postexercise muscle damage. The few experiments that have been done tend to be contradictory and have yet to consider the range of ultrasound treatment parameters for therapeutic effectiveness in treating postexercise damage and influencing repair processes. Much more research is needed to determine whether either treatment modality can have any therapeutic effect on exercise-induced muscle damage and recovery of postexercise muscle function.

Failure of manual massage to alter limb blood flow: measures by Doppler ultrasound.

The ability of manual massage to alter muscle blood flow through three types of massage treatments in a small (forearm) and a large (quadriceps) muscle mass was tested in 10 healthy individuals. A certified massage therapist administered effleurage, petrissage, and tapotement treatments to the forearm flexors (small muscle mass) and quadriceps (large muscle mass) muscle groups in a counterbalanced manner. Limb blood flow was determined from mean blood velocity (MBV) (pulsed Doppler) and vessel diameter (echo Doppler). MBV values were obtained from the continuous data sets prior to treatment, and at 5, 10, and 20 s and 5 min following the onset of massage. Arterial diameters were measured immediately prior to and following the massage treatments; these values were not different and were averaged for the blood flow calculations. The MBV (e.g., 5.77 +/- 0.4 and 9.73 +/- 0.7 cm.s-1) and blood flows (39.1 +/- 6.4 and 371 +/- 30 ml.min-1) for brachial and femoral arteries, respectively, were not altered by any of the massage treatments in either the forearm or quadriceps muscle groups (P > 0.05). Mild voluntary handgrip (approximately 35% maximal voluntary isometric contraction) and knee extension (15 cm) contractions resulted in peak blood velocities (15.2 +/- 1.2 and 28.1 +/- 3.1 cm.s-1) and blood flow (126 +/- 19 and 1087 +/- 144 ml.min-1) for brachial and femoral arteries, respectively, which were significantly elevated from rest (P < 0.05). The results indicate that manual massage does not elevate muscle blood flow irrespective of massage type or the muscle mass receiving the treatment. Further, the results indicate that if an elevated muscle blood flow is the desired therapeutic effect, then light exercise would be beneficial whereas massage would not.

Manual massage and recovery of muscle function following exercise: a literature review.

There is currently little scientific evidence that manual massage has any significant impact on the short- or long-term recovery of muscle function following exercise or on the physiological factors associated with the recovery process. In addition, delayed onset muscle soreness may not be affected by massage. Light exercise of the affected muscles is probably more effective than massage in improving muscle blood flow (thereby possibly enhancing healing) and temporarily reducing delayed onset muscle soreness. This paper reviews current scientific evidence on the use of manual massage to affect: 1) muscle damage caused by eccentric muscle action; 2) retention and recovery of muscle strength and performance following "eccentric-mechanical" muscle damage; 3) reduction of delayed onset muscle soreness following "eccentric-mechanical" muscle damage; and 4) recovery of muscle strength and performance following anaerobic exercise. Because manual massage does not appear to have a demonstrated effect on the above, its use in athletic settings for these purposes should be questioned.

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.

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.