Neural Adaptations to Repeated Bouts of Eccentric and Concentric Exercise

Malachy P. McHugh,*,# Declan A.J. Connolly,^ Roger G. Eston,* Ian J. Kremenic,# Gilbert W. Gleim#

*School of Sport, Health and Physical Education Sciences, U. of Wales, Bangor, U.K.; ^Human Performance Laboratory, Department of Physical Education, U. of Vermont, U.S.A.; #NISMAT, Lenox Hill Hospital, New York, USA.

INTRODUCTION

Muscle damage occurs following a single bout of unfamiliar eccentric exercise. Following recovery, a repeated bout of eccentric exercise results in reduced damage. It has been suggested that neural adaptations may explain this repeated bout effect (RBE) (Nosaka & Clarkson 1995). Muscle damage has been attributed to the high tension generated by the smaller number of active fibers during eccentric versus concentric contractions (Moritani, Muramatsu & Muro 1988). The damage is seen predominantly in fast-twitch fibers (Fridén, Sjostrom, & Ekblom 1983), which appear to be selectively recruited for eccentric contractions (Nardone, Romano & Schieppati 1989). Increased motor unit recruitment and a shift to slow-twitch fiber activation could decrease myofibrillar stresses and potentially avoid damage. The purpose of this study was to examine surface EMG amplitude and frequency signals during repeated bouts of eccentric exercise for evidence of changes in recruitment patterns that might explain the RBE.

METHODS

The response of the hamstring muscle group to sub-maximal, isokinetic, eccentric (ECC) exercise at 2.6 rad./s was studied in ten subjects (6 men, 4 women). Following testing of isometric (ISOM) hamstring strength, subjects performed 6 sets of 10 repetitions of ECC hamstring contractions to a target force equal to 60% of ISOM strength, with a 1 min rest between sets (Bout 1). ISOM strength was re-tested immediately following this protocol and again on each of the next three days. Subjects were also asked to report hamstring pain with walking each day(0="no pain", 10="walking with limp"). This four day protocol was repeated two weeks later (Bout 2). The same target force was used for Bout 1 and Bout 2. Additionally, a control group (6 men, 4 women) performed repeated bouts (two weeks apart) of isokinetic concentric (CONC) hamstring exercise at 2.6 rad./s (6 sets of 10 reps at 60% of ISOM strength) with ISOM strength tests on the following three days.

EMG signals were recorded from surface electrodes placed over the biceps femoris (BF), semitendinosus (ST) and semimembranosus (SM) muscles during ECC and CONC exercise bouts and ISOM strength tests. For EMG amplitude measurements, the area under the rectified EMG signal was integrated (IEMG). For EMG frequency measurements, Fast Fourier Transforms (FFT) were performed on the raw EMG signal and the median frequency (MF) was calculated. Changes in strength, pain, IEMG and MF during isometric tests were analyzed using a mixed model ANOVA; Group (ECC-CONC) x Time (pre-post-day1-day2-day3) x Bout (1-2), with repeat measures on the last two factors. For ECC and CONC bouts IEMG for the three muscles was totaled and expressed relative to the work performed for a given set of contractions (IEMG/work). A Group x Set (1-6) x Bout ANOVA was used to examine changes in IEMG/work and MF during ECC and CONC Bouts 1 and 2.

RESULTS

Isometric Strength and Pain: ECC exercise resulted in significant strength loss (16%) and sensation of pain (3/10) over the three days following Bout 1, contrasted with a slight increase in strength (6%) and no pain (0/10) following Bout 2 (ISOM strength, p=0.009; pain, p=0.013). IEMG activity was maintained during ISOM tests on days 1,2 and 3 following ECC Bout 1 despite significant strength loss. ISOM strength was not significantly decreased immediately post Bout 1 or 2, either for ECC or for CONC exercise (i.e. exercise bouts were non-fatiguing).

IEMG/work: For initial contractions, ECC IEMG/work was 36% of ISOM IEMG/work while CONC IEMG/work was 87% of ISOM (p=0.001). IEMG/work increased from set 1 to 6 during ECC exercise (33% Bout 1, 24% Bout 2) with no change during CONC exercise (p=0.0001). IEMG/work during ECC exercise tended to be greater (15%) in Bout 2 vs. Bout 1, whereas during CONC exercise, IEMG/work tended to be lower (7%) in Bout 2 (p=0.08). The increase in IEMG during ECC Bout 1 was inversely correlated to strength loss over the subsequent three days (r=-0.73, p=0.02).

Median Frequency (MF): MF was significantly higher in all three muscles during ECC exercise compared to ISOM tests (76Hz vs 65Hz, p=0.001) but was not different between CONC and ISOM (60Hz vs 64Hz, p=0.11). MF increased from set 1 to 6 during ECC Bout 1 (10%) and Bout 2 (12%) but did not change during CONC exercise (p=0.0001). Lower MF during ISOM test pre- ECC Bout 1 was correlated to greater strength loss over the subsequent three days (r=-0.66, p=0.04). MF during ISOM tests was increased immediately following ECC (9% Bout 1, 10% Bout 2) and CONC exercise (9% Bout 1, 8% Bout 2) but returned to baseline on the following 3 days (p=0.001).

DISCUSSION

Changes in strength and pain following ECC Bout 1 compared to Bout 2 provided clear evidence of an RBE. Greater IEMG/work for eccentric Bout 2 vs. Bout 1 (15%) suggests that the RBE may have been due to a neural adaptation. The higher MF for sub-maximal ECC contractions compared to maximal ISOM contractions indicated selective recruitment of fast twitch fibers. The increase in IEMG and MF during non-fatiguing ECC exercise indicated increased recruitment of fast-twitch fibers. The ability to increase recruitment during ECC exercise (Bout 1) appeared to protect against strength loss over the subsequent three days. Low EMG frequency during maximum contractions has been shown to reflect a high proportion of slow twitch fibers (Wretling, Gerdle & Henriksson-Larson 1987). The association between lower MF during maximum ISOM contractions and greater strength loss following ECC exercise suggests that subjects with a greater proportion of slow-twitch fibers experienced more muscle damage. Strength loss following ECC Bout 1 with no change in IEMG activity during the ISOM tests on days 1,2 and 3 suggests mechanical disruption, rather than neural inhibition, of the affected muscle.

In conclusion, these data offer new insights into the neural basis of muscle damage and identify specific factors which may provide protection against damage.

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