TIME COURSE AND RECOVERY FROM ECCENTRIC EXERCISE INDUCED MUSCLE DAMAGE ASSESSED BY sEMG ANALYSIS AND ULTRASONOGRAPHY P. Sbriccoli 1,2, F. Felici1, A. Aliotta2, V Castellano2 and M. Marchetti 1,2 1. Department of Human Physiology and Pharmacology, University “La Sapienza”, Rome, Italy 2. I.R.C.C.S. S. Lucia, Rome, Italy It is generally accepted that eccentric exercise (EC) can elicit temporary repairable damage to skeletal muscle (Ebbeling and Clarkson, 1989). This is accompanied by a delayed onset of muscle soreness (DOMS), which becomes evident 24-48 hours after exercise, and to a marked loss in voluntary strength (MVC) (Felici et al., 1997). As a consequence of the myofibrillar disruption EC induced (Friden and Lieber, 1992), an increase of the plasmatic level of creatin chinase (CK) (Ebbeling and Clarkson, 1989) and of other cytokines (Blais et al., 1999) is also observed. Beside the muscle fibres disruption, which mainly affects Type IIB fibres (Friden and Lieber, 1992), some morphological changes occur, such as hyperaemia-induced swelling and oedema (Chleboun et al., 1998) of the injured muscles, which can be investigated by means of magnetic resonance (MR) and ultrasonography (US) (Nosaka and Clarkson, 1996). The effects of EC induced muscle damage on surface electromyographic (sEMG) activity have already been investigated (Felici et al., 1997; Day et al., 1998). In both studies the sEMG spectral analysis showed a shift towards the lower frequencies of sEMG power spectra immediately evident after EC, and this phenomenon was assumed by the authors as an indirect early marker of selective damage of Type IIB fibres (Felici et al., 1997). The aim of this study was to further investigate the sEMG modifications induced by EC, and to give an enzymatic and US correlate to sEMG changes. The evolution and recovery from EC induced muscle damage was also assessed. Ten healthy subjects participated to this study. They were subdivided at random into two groups: five subjects were submitted to the eccentric exercise (EC Group), performed on the biceps brachii of their non dominant arm, the other arm acting as control; five subjects were tested without performing EC (CON Group). The experimental protocol consisted of three phases: 1) Isometric exercise: after measuring the MVC of the biceps brachii of both arms during isometric contractions the sEMG and the force signal were recorded while contracting at 80% MVC for 20 seconds (three attempts). 2) EC (on the first day only): two bouts of 35 eccentric maximum contractions were performed by the non-dominant arm (left in all subjects). 3) An US assessment on both biceps brachii and CK-LDH plasma levels evaluation was done. Isometric tests were performed before EC, 1 hour after, and then three times a week for one month. Ultrasonographic and CK-LDH measures were executed before EC, 1 hour, 48 hours and 96 hours after EC; then they were repeated weekly for 1 month. On sEMG signals it was performed a time and frequency domain analysis, and the Root Mean Square (RMS) and the Median Frequency (MDF) were computed over the whole constant force phase. The MDF initial frequencies were considered as representative of the initial state of muscle activation, and the rate of frequency decay over time was assumed as an indirect index of muscle fatigue. US was assessed by means of the measurement of muscle belly thickness and local muscle blood flow. One hour after EC the mean MVC was reduced by 40% on average with respect to the control values. The MVC gradually returned to the baseline in about two weeks. On the control arm, it was only observed a tendency towards an increase of the MVC, although non significant (13%). The spectral analysis showed a significant decrease of the initial frequency content, and of the normalised slopes of MDF (22-31% less than the pre-EC values, respectively). On the control arm no change was observed. The sEMG amplitude (RMS) was also decreased after EC. These myoelectric modifications, only observed in the EC arm, were consistent in all subjects immediately after EC, 24 hours before the beginning of CK-LDH increases. The latter reached their peak 48-72 hours after EC. The US assessment provided clear modifications with respect to the pre-EC data with the same CK-LDH temporal pattern: an increase of muscle belly thickness and an increase in local muscle blood flow in the EC arm. A complete recovery of all considered parameters was achieved in about three weeks. On the CON group no significant changes were detected. In conclusion the sEMG is confirmed as an early indicator of muscle damage. Nevertheless, both sEMG and US may be used to follow the time-course and recovery from muscle damage provoked by EC. REFERENCES Blais C.Jr et al. (1999): J Appl Physiol 87(3) : 1197-1201 Chleboun G.S. et al., (1998) : Med Sci Sports Exerc 30(4): 529-535 Day S.H . et al., (1998): Muscle Nerve 21: 961, 963 Ebbeling CB, Clarkson P.M. (1989): Sports Med 7: 207-234 Felici F. et al., (1997): J Electromyogr Kinesiol 7(3): 193-202 Friden J., Lieber R. (1992): Med Sci Sports Exerc 24(5): 521-530 Nosaka K., Clarkson P.M. (1998): Med Sci Sports Exerc 28(8): 953-961

Time course and recovery from eccentric exercise induced muscle damage assessed by sEMG analysis and ultrasonography

Sbriccoli P;F Felici;I Bazzucchi;
2000-01-01

Abstract

TIME COURSE AND RECOVERY FROM ECCENTRIC EXERCISE INDUCED MUSCLE DAMAGE ASSESSED BY sEMG ANALYSIS AND ULTRASONOGRAPHY P. Sbriccoli 1,2, F. Felici1, A. Aliotta2, V Castellano2 and M. Marchetti 1,2 1. Department of Human Physiology and Pharmacology, University “La Sapienza”, Rome, Italy 2. I.R.C.C.S. S. Lucia, Rome, Italy It is generally accepted that eccentric exercise (EC) can elicit temporary repairable damage to skeletal muscle (Ebbeling and Clarkson, 1989). This is accompanied by a delayed onset of muscle soreness (DOMS), which becomes evident 24-48 hours after exercise, and to a marked loss in voluntary strength (MVC) (Felici et al., 1997). As a consequence of the myofibrillar disruption EC induced (Friden and Lieber, 1992), an increase of the plasmatic level of creatin chinase (CK) (Ebbeling and Clarkson, 1989) and of other cytokines (Blais et al., 1999) is also observed. Beside the muscle fibres disruption, which mainly affects Type IIB fibres (Friden and Lieber, 1992), some morphological changes occur, such as hyperaemia-induced swelling and oedema (Chleboun et al., 1998) of the injured muscles, which can be investigated by means of magnetic resonance (MR) and ultrasonography (US) (Nosaka and Clarkson, 1996). The effects of EC induced muscle damage on surface electromyographic (sEMG) activity have already been investigated (Felici et al., 1997; Day et al., 1998). In both studies the sEMG spectral analysis showed a shift towards the lower frequencies of sEMG power spectra immediately evident after EC, and this phenomenon was assumed by the authors as an indirect early marker of selective damage of Type IIB fibres (Felici et al., 1997). The aim of this study was to further investigate the sEMG modifications induced by EC, and to give an enzymatic and US correlate to sEMG changes. The evolution and recovery from EC induced muscle damage was also assessed. Ten healthy subjects participated to this study. They were subdivided at random into two groups: five subjects were submitted to the eccentric exercise (EC Group), performed on the biceps brachii of their non dominant arm, the other arm acting as control; five subjects were tested without performing EC (CON Group). The experimental protocol consisted of three phases: 1) Isometric exercise: after measuring the MVC of the biceps brachii of both arms during isometric contractions the sEMG and the force signal were recorded while contracting at 80% MVC for 20 seconds (three attempts). 2) EC (on the first day only): two bouts of 35 eccentric maximum contractions were performed by the non-dominant arm (left in all subjects). 3) An US assessment on both biceps brachii and CK-LDH plasma levels evaluation was done. Isometric tests were performed before EC, 1 hour after, and then three times a week for one month. Ultrasonographic and CK-LDH measures were executed before EC, 1 hour, 48 hours and 96 hours after EC; then they were repeated weekly for 1 month. On sEMG signals it was performed a time and frequency domain analysis, and the Root Mean Square (RMS) and the Median Frequency (MDF) were computed over the whole constant force phase. The MDF initial frequencies were considered as representative of the initial state of muscle activation, and the rate of frequency decay over time was assumed as an indirect index of muscle fatigue. US was assessed by means of the measurement of muscle belly thickness and local muscle blood flow. One hour after EC the mean MVC was reduced by 40% on average with respect to the control values. The MVC gradually returned to the baseline in about two weeks. On the control arm, it was only observed a tendency towards an increase of the MVC, although non significant (13%). The spectral analysis showed a significant decrease of the initial frequency content, and of the normalised slopes of MDF (22-31% less than the pre-EC values, respectively). On the control arm no change was observed. The sEMG amplitude (RMS) was also decreased after EC. These myoelectric modifications, only observed in the EC arm, were consistent in all subjects immediately after EC, 24 hours before the beginning of CK-LDH increases. The latter reached their peak 48-72 hours after EC. The US assessment provided clear modifications with respect to the pre-EC data with the same CK-LDH temporal pattern: an increase of muscle belly thickness and an increase in local muscle blood flow in the EC arm. A complete recovery of all considered parameters was achieved in about three weeks. On the CON group no significant changes were detected. In conclusion the sEMG is confirmed as an early indicator of muscle damage. Nevertheless, both sEMG and US may be used to follow the time-course and recovery from muscle damage provoked by EC. REFERENCES Blais C.Jr et al. (1999): J Appl Physiol 87(3) : 1197-1201 Chleboun G.S. et al., (1998) : Med Sci Sports Exerc 30(4): 529-535 Day S.H . et al., (1998): Muscle Nerve 21: 961, 963 Ebbeling CB, Clarkson P.M. (1989): Sports Med 7: 207-234 Felici F. et al., (1997): J Electromyogr Kinesiol 7(3): 193-202 Friden J., Lieber R. (1992): Med Sci Sports Exerc 24(5): 521-530 Nosaka K., Clarkson P.M. (1998): Med Sci Sports Exerc 28(8): 953-961
2000
951-790-156-9
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14244/6013
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