Effects of innervation state on Hsp25 content and phosphorylation in inactive rat plantaris muscles.

AIM: Previous reports suggest a role for neuromuscular activity levels and/or connectivity in modulating Hsp25 expression and phosphorylation (pHsp25) in skeletal muscles. However, pHsp25 has only been studied in denervated muscles and/or muscles exposed to high levels of residual neuromuscular activity. Spinal cord isolation (SI) provides a model in which the muscle is exposed to nearly complete inactivity with maintenance of the nerve-muscle connection. To parcel out the roles of innervation state and activity-independent neural factors, we compared Hsp25 and pHsp25 in the plantaris of control (Con), SI, and denervated (Den, inactivity without neural connectivity) rats. METHODS: Hsp25 and pHsp25 protein levels (soluble and insoluble fractions) were measured with Western blot analysis after 1, 3, 8, 14, or 28 days of SI or Den. pHsp25 was normalized to non-pHsp25 at each time point. RESULTS: Hsp25 was unchanged (days 1, 3 and 14) or increased (days 8 and 28) in the soluble fraction, and decreased (day 1) or increased (days 3, 8 and 14) in the insoluble fraction in Den compared with Con rats. pHsp25 was reduced after 1 and 28 days of Den, but near control levels on days 3, 8, and 14 in the soluble fraction. In the insoluble fraction, pHsp25 levels were lower in Den than Con rats on all days. In both fractions, Hsp25 was lower in SI than Con rats. pHsp25 levels were lower in the soluble fraction and higher in the insoluble fraction in SI than Con rats. CONCLUSION: These results suggest that an intact innervation, even in the absence of muscle activation and/or loading, is critical for Hsp25 phosphorylation in the insoluble fraction. However, the time-dependent decrease in Hsp25 with SI suggests a role for minimal levels of muscle activation and/or loading in maintaining Hsp25 expression during sustained inactivity.

Alterations in bilateral force judgment following strenuous eccentric exercise.

This study investigated the effects of strenuous eccentric exercise on bilateral force-matching ability. After unilaterally performing 50 maximal eccentric elbow actions, participants were evaluated for bilateral force-matching ability. Participants were asked to match a reference force held by the control (CNT) arm with their exercised (EXD) arm. The experimental condition was then reversed. Constant error (bias) of the EXD arm was increased through 5 days postexercise, when it underestimated the CNT force in all trials. In contrast, an overestimation of the EXD force by the CNT arm resulted in an increased constant and variable error (variability around the bias) through 5 days postexercise, when the EXD arm served as the force reference. Strenuous eccentric exercise severely compromises bilateral force-matching ability, regardless of whether the EXD attempted to match the reference force or served as the force reference, indicating central or peripheral alterations to force judgment.

Creatine kinase release and clearance using MM variants following repeated bouts of eccentric exercise.

PURPOSE: This study investigated the release and clearance of plasma CK-MM (muscle) isoforms following two bouts of eccentric exercise to determine whether enhanced enzyme clearance could in part explain the blunted creatine kinase (CK) response to a second bout of exercise. METHODS: Nonweight trained college-aged male subjects performed both bouts of 50 forced lengthening contractions of the forearm flexor muscles separated by 6 d either with the same arm (CON; N = 4) or with one arm followed by the contralateral arm (EXP; N = 4). Range of motion, arm circumference, maximal isometric strength, perceived muscle soreness, total CK (TCK), and MM variants were assessed. Each MM isoform was measured as a percentage of TCK activity and in absolute activity (IU.L-1) following isoelectric separation and densitometry. The MM1:MM3 ratio, calculated from absolute concentrations, was used to indicate periods of release and clearance. RESULTS: Non-CK criterion measures indicated that similar damage occurred in both arms for EXP (P > 0.05), whereas CON exhibited a blunted response on bout 2 (P < 0.01). Postbout 1, TCK peaked at 96 h for CON (3530 +/- 927 IU.L-1) and EXP (6683 +/- 433 IU.L-1) (P < 0.01). Postbout 2, CON TCK showed no additional increase; however, a second rise in EXP TCK reached its highest point by day 5 (3602 +/- 1190 IU.L-1). Expectedly, %MM1 and the MM1: MM3 ratio were increased after bout 1 in both groups (P < 0.01). New CK release was observed postbout 2 in both groups as indicated by an increase in %MM1 (P < 0.01), despite no increase in TCK after bout 2 for CON and a smaller CK response for EXP. CONCLUSION: Accelerated clearance of CK seems to be one factor contributing to the blunted response of this enzyme following a repeated bout of exercise.

The effects of oral contraceptives on delayed onset muscle soreness following exercise.

Several authors have suggested that estrogen may serve to protect skeletal muscle from exercise-induced damage. The present study examined the effects of regularly ingesting estrogen, in the form of oral contraceptives, on postexercise muscle damage following a bench-stepping regimen. Women currently ingesting oral contraceptives (OC) were compared with eumennorheic controls (CG). All subjects performed a 50-min stepping exercise during the midluteal phase of their menstrual cycle. Muscle damage was evaluated on 2, 3, and 5 days postexercise using several established indirect indicators: perceived soreness, strength and range of motion changes, girth measurements, and creatine kinase (CK) activity. Subjects on OC reported significantly lower quadriceps soreness (p < 0.05) relative to the CG (peak soreness = 4.0 and 7.8, respectively, on a scale of 1-10 where 1 is normal and 10 is very, very sore). These results indicate that oral contraceptive use attenuates soreness following an exhaustive stepping activity but cannot support a relationship between estrogen ingestion and other indices of exercise-induced muscle damage.