The Effects of Magnetism On Strength Recovery From Combined Concentric and Eccentric Exercise

By Mike Croskery



Almost all types of strength training involve resistance exercises that require eccentric and concentric muscle contractions in order to stimulate strength gains (Fox, Bowers, & Foss, 1993), muscle hypertrophy (Fox et al., 1993; Tesch, 1988; Lüthi et al., 1986), neural adaptation (Sale, 1988), and metabolic adaptations (MacDougall, 1985) within the targeted muscle. It is the eccentric component of an exercise that is believed to cause the greatest amount of morphological change within the worked muscle (Armstrong, 1984; Clarkson & Tremblay, 1988; Fritz & Stauber, 1988; Stauber, Clarkson, Fritz, & Evans, 1990), strength loss (Fridén, Sjöström, & Ekblom, 1983; Newham, Jones, & Clarkson, 1987; Rödenburg, Bär, & De Boer, 1993) and muscle soreness (Abraham, 1977; Newham, 1988). These changes are believed to be due to muscle damage that is non-permanent and repairable (Fridén, 1984). In addition, muscle tissue has shown that an adaptation to this type of stress takes place during as well as after recovery that results in less damage and soreness in the targeted muscle after subsequent exercise bouts (Byrnes, Clarkson, White, and Frykman, 1985; Clarkson & Tremblay, 1988; Ebbeling & Clarkson, 1990).

The use of magnetism to aid in recovery from illness and injury has been practiced for thousands of years, from Aristotle who spoke of the powers of natural magnets to modern technology which uses a wide variety of applications of magnetic fields. However, it has only been recently that the medical community has begun to understand how magnetic therapy might work to aid the body in recovery. Researchers believe that magnetic therapy helps to stimulate the body to heal itself and decrease levels of pain by creating optimal healing conditions within the body or afflicted body part (Hacmac, 1991). Such conditions include: increasing blood flow and lymphatic function; changing the migration of calcium ions; returning pH balance to a more normal level; increasing or decreasing hormone production; and altering enzyme activities of certain systems (Hacmac, 1991).

Although some research performed primarily in Russia has suggested that magnetism aids in neural reparative processes (Krylov, Antonov, Eliseeva, Malikova, & Shevelev, 1991; Tkach, Abilova, & Gazalieva, 1989) and suppurative wound healing (Kuliev & Babaev, 1992), it appears that little, if any, direct research has been done on magnetism and muscle recovery.

Therefore, the following research project has been undertaken to determine if the use of natural magnets has an effect on strength recovery. The specific objective of this research project is to determine the effects of natural magnets on isokinetic concentric strength recovery over 5 days after combined maximal eccentric and concentric exercise. Examination of this relationship might provide insight into whether or not magnetic therapy decreases recovery time between exercise sessions. This could have potentially important benefits for maximizing athletic performance in shorter periods of time through altered training schedules and accelerated recovery.

In investigating such a relationship there are several uncontrollable variables which may be encountered and which could confound the results. Since a maximum contraction is subject to several different variables, especially in untrained individuals, there exists a variability that could contribute to the results of this study (MacDougall, Wenger, & Green, 1991). Furthermore, recovery is also based on several different factors such as hormone release, diet, genetic disposition, and other individual lifestyle habits. A variability could exist here that could be unique to each of the subjects (Fox et al., 1993). This could also affect the results of the study.

There are several limitations that have been placed on this investigation. This research project only examined natural magnets of a certain strength and for a certain duration. The amount of time that the magnets were applied was limited to a period of 8 hours. Only 6 untrained female subjects were used in this study for a period of 5 successive days due to the time constraints involved in this project and due to the availability of the subjects.

The following review of the literature examines the effects of concentric and eccentric contractions on skeletal muscle and strength recovery, as well as the effects of magnetism on human tissue and physiological systems. This review will form the basis of the discussion later in the paper.


Review of Literature

Pertinent literature relating to the effects of concentric and eccentric exercise on skeletal muscle and strength recovery, as well as the effects of magnetism on human tissue and physiological systems, will be reviewed in this section.

Effects of Concentric and Eccentric Exercise on Muscle and Strength Recovery

Various types of muscle contractions can cause different types of changes within the worked muscle (Kroon & Naeije, 1991). Generally, traditional strength training exercise involves mainly a combination of eccentric and concentric muscle contractions and not primarily isometric or static contractions (Fox et al. 1993). The purpose of this section of the review of the literature is to examine the effects of eccentric and concentric type contractions on skeletal muscle.

Concentric exercise can cause decreases in concentric strength immediately following the exercise bout, but strength generally returns to normal levels following 24 hours of recovery (Golden & Dudley 1992; Kroon & Naeije, 1991). Concentric exercise does not appear to cause myofibrillar disruptions in the muscle (Newham, McPhail, Mills, & Edwards, 1983a) and perceptions of delayed onset muscle pain are significantly less and do not last as long as compared to eccentric exercise (Fox et al. 1993; Kroon & Naeije, 1991; Newham, Jones, & Edwards, 1983b). However, concentric contractions do not appear to cause adaptations within the specific muscle to unaccustomed eccentric exercise (Golden & Dudley, 1992). Reduced force generation and soreness after a bout of eccentric exercise several days following concentric exercise are just as great as when compared to the novel eccentric exercise (Golden & Dudley, 1992). It appears that the primary mechanism involved in short term (24 hours) strength performance decrements as a result of solely concentric contractions is due to metabolic fatigue (Ebbeling & Clarkson, 1989). It is therefore the recovery of the energy system involved in the contraction that determines the time period for return to maximal strength following concentric exercise.

Unaccustomed eccentric exercise can cause greater temporary damage to skeletal muscle fibers, muscle matrix (Ebbeling & Clarkson, 1990; Fridén, 1984; Fridén et al., 1983; Reichsman, Scordilis, Clarkson & Evans, 1991; Stauber et al., 1990) and connective tissue (Abraham, 1977; Fridén, 1983; Fritz & Stauber, 1988) than concentric contractions due to increases in tension per cross-sectional area of active muscle fibers (Ebbeling & Clarkson, 1989; Newham et al., 1983b). In addition, prolonged strength loss for longer than 24 hours (Clarkson, Nosaka, & Braun, 1992; Golden & Dudley, 1992; Kroon & Naeije, 1991; Newham et al., 1987; Rodenburg et al., 1993 ;), decreases in relaxed joint angle (Clarkson et al., 1992; Rodenburg et al. 1993), and delayed-onset muscle soreness (Newham, 1988; Newham et al., 1987; Stauber et al., 1990) are all associated with the effects of eccentric exercise.

Muscle tissue has shown an adaptation to this type of stress such that muscle damage, soreness, relaxed arm angle, and performance showed less of a decrease following subsequent exercise bouts both before and after full recovery (Clarkson et al., 1992; Clarkson & Tremblay, 1988; Donnelly, Clarkson, & Maughan, 1992; Ebbeling & Clarkson, 1990; Golden & Dudley, 1992; Newham et al., 1987; Nosaka, Clarkson, McGuiggin, & Byrne, 1991). This adaptation effect does not appear to be proportional to increases in volumes of eccentric work (Clarkson & Tremblay, 1988; Kroon & Naeije, 1991).

When not enough time is allowed for full recovery before the next bout of eccentric exercise, the adaptation that occurs appears to be related to changes in the connective tissue rather than changes within the muscle fibers (Ebbeling & Clarkson, 1989; Newham et al. 1987). Fridén (1983) has proposed three possible adaptations that can occur within the myofibrils when full recovery between exercise bouts takes place. These changes are increases in sarcomere length, the number of longitudinal sarcomeres, and synthesis of Z-band proteins (Ebbeling & Clarkson, 1989). Although adaptation to eccentric exercise has been shown to last up to 6 weeks (Nosaka et al., 1991), this would not be consistent for changes in myofibrillar proteins as the increases in structural integrity of the cellular components would not be expected to last for such a long period of time (Clarkson et al., 1992).

The precise mechanisms involved in decreases in strength performance which can last longer than 7 days (Clarkson et al., 1992; Golden & Dudley, 1992; Kroon & Naeije, 1991; Newham et al., 1987; Rodenburg et al. 1993), are not completely understood. Many different theories examining the reason for this extended strength loss tend to focus on the protein disruption and degradation within the muscle fibers (Ebbeling & Clarkson, 1989). Although soreness within the exercised muscle is associated with eccentric exercise, it appears that this is not solely the reason for decreases in strength, nor does it appear to be related (Ebbeling & Clarkson, 1989; Kroon & Naeije, 1991; Newham et al., 1987). Loss of sarcollemal integrity due to forced lengthening, particularly in fast twitch type II fibers (Armstrong, 1990; Ebbeling & Clarkson, 1989; Fridén et al., 1983) appears to be one of the reasons for loss of force generation (Clarkson et al., 1992; Ebbeling & Clarkson, 1989). Clarkson et al. (1992) has proposed that damage to the sarcoplasmic reticule could contribute to this as well.

It is believed that decreased calcium levels within the damaged sarcoplasmic reticulum results in less calcium being available for the excitatory action potential that is necessary for muscle contraction (Clarkson et al., 1992; Ebbeling & Clarkson, 1989; Newham et al., 1983b;). In addition, Kroon and Naeije (1991) have reported changes in the potassium gradient of the damaged muscle fiber membranes due to eccentric exercise. These changes could also explain an altered electrical excitability of the fibers and would therefore also result in lowered strength performance (Kroon & Naeije, 1991). Increased extracellular calcium due to a damaged sarcoplasmic reticulum from eccentric exercise (Armstrong, 1984; Newham et al., 1983a) could also be partly responsible for decreases in force generation due to increases in muscle damage (Baracos, Greenburg, & Goldberg, 1986). This appears to be due to increases in proteolytic enzymes triggered by the high calcium levels (Busch, Stromer, Goll, & Suzuki, 1972). It is these enzymes that are believed to be the cause that muscle damage is generally greatest approximately 3 days later than immediately following the eccentric exercise bout (Fridén et al. 1983; Newham, 1988).

Full recovery of strength from intense eccentric exercise is a slow process (Clarkson & Tremblay, 1988). Full strength recovery from novel, unaccustomed eccentric exercise has been shown to take between 5 and 10 days and sometimes even longer (Clarkson et al. 1992; Ebbeling & Clarkson 1990; Newham et al., 1987). The length of time it takes for maximal voluntary contraction to return to normal appears to be a function of the volume and intensity of the exercise performed. However, specific training appears to cause strength performance to return to initial levels faster following eccentric contractions compared to no training at all (Clarkson & Tremblay, 1988; Ebbeling & Clarkson, 1989; Newham et al., 1987; Nosaka et al., 1991). This adaptation, believed to be partially stimulated by fiber necrosis and damage, can occur after either partial or full recovery of the muscle (Ebbeling & Clarkson, 1989; Milne, 1988).

The process of recovery involves several different physiological responses and factors (Ebbeling & Clarkson, 1989; Vander, Sherman, & Luciano, 1990). Upon damage to the muscle, an increase in lysosomal activity is noted (Armstrong, Ogilvie, & Schwane, 1983), perhaps this is due to an increase in prostaglandin production as a result of high calcium levels (Baracos et al., 1986). During the next four days the lethally damaged fibers are phagocytosed by the lysosomes (Armstrong, 1986) while mononuclear cells, believed to be satellite cells, become evident between the third and fifth days (Armstrong, 1986; Armstrong et al., 1983). Between the third and twelfth days, the satellite cells appear to generate into new myofibrils to replace necrosed myofibrils while the number of cells within the basal lamina decrease (Armstrong, 1986; White & Esser, 1989). By the fourteenth day, the muscles appear normal once again.

Those fibers that are not lethally injured by eccentric exercise undergo an increase in the protein structures of the myofibers resulting in a strengthening of the fiber (Fridén, 1983). The increase in protein content is both a combination of protein degradation and synthesis that occurs within the target cell area (Houston, 1985). Degradation seems to be at least partially controlled by the lysosomes, as previously mentioned, while protein synthesis seems to be stimulated by a different procedure. It appears that protein synthesis is mainly stimulated by a combination of hormonal and neurohumoural factors (Borer, 1994; Cooper, 1994). While growth factors responsible for increasing protein synthesis can be released as a result of trauma to the muscle cell (Yamada, Buffinger, DiMario, & Strohman, 1989), tension placed upon the exercised muscle may expose the growth factor receptor sites to stimulate protein synthesis (McNeely, 1994).

Recovery and adaptation of connective tissue is believed to play a role in the restoration of previous strength levels by providing structural stability for the regenerating muscle cells (Fritz & Stauber, 1988). It appears that by-products of collagen breakdown stimulate the monocytes to travel from the blood into the muscle resulting in phagocytosis of muscle cells (Armstrong et al., 1983). Although proteoglycans are localized around the muscle matrix from 1 to 3 days following exercise, by the fifth day proteoglycan localization is essentially back to normal levels (Fritz & Stauber, 1988). This could potentially indicate that reparative processes are well under way.

In summary, concentric exercise results in no myofibrillar disruptions and strength performance generally returns to normal after 24 hours. This time frame appears to be due to the energy systems involved. However, no adaptation effect is seen with concentric training. Eccentric exercise results in muscle damage and fiber necrosis as well as decreased levels of force generation that can vary depending on the volume, intensity, and training history of the particular muscle. It appears that the decreases in force generation can be partially contributed to by the damage and disruption of the sarcollema and sarcoplasmic reticulum as well as by changes in the excitability of the muscle fibers. Muscle damage is greatest several days after the exercise bout and appear to be at least partly due to altered calcium levels within the muscle. Strength recovery and muscle adaptation occurs due to a combination of lysosomal activity, cell regeneration, connective tissue recovery, and protein synthesis and degradation.

Effects of Magnetism on Tissue and Physiological Systems

The therapeutic use of natural magnets to help in reduction of pain and general life disruption appears to be increasing in popularity (Hacmac, 1991). However, there seems to be lack of research on the effects of magnetism on muscle recovery. Although there has been some research performed using electromagnetism to investigate nervous tissue regeneration and wound healing (Krylov et al. 1991; Kuliev and Babaev 1992; Poslavskii, Parfenov, Korochkin, Zdanovitch, & Abshilava, 1989; Tkach , Abalova, & Gazalieva, 1989; Trok et al., 1992), there has generally been a void in the research area concerning the effects of magnetism on muscle tissue.

Some physiological functions that have been reported due to magnetic fields include increased blood flow, changes in the migration of calcium ions, alteration of pH balance, increased or decreased hormone production, and an alteration of enzyme activity and biochemical processes (Hacmac, 1991). These effects are related to where the magnet is placed on the body, the strength of the field, the uniformity of the field, the direction of the magnetic field, and the operation time (Hayashi et al., 1976).

Ardizzone (1992a) has proposed a mechanism initiated by magnetism that allows increased blood flow through vasodilation . Ions such as sodium and chloride in the blood pass perpendicularly into the magnetic field imposed by the magnetic pads placed on the surface of the skin. The voltages in the magnetic field attract or repel the ions in alternate directions. The ions eventually encounter the walls of the blood vessels and it is this resistance combined with the electrical current created by the magnetic field which causes an increase in temperature and, consequently, vasodilation. The alternating configuration of the poles on the therapeutic magnet results in constant movement of the ions in the blood and therefore a uniform heat distribution.

Ardizzone (1992b) has also proposed that magnetic fields can possibly create a situation within the nervous system that results in a shifting of the membrane resting potential to higher levels. This effect would result in the fiber being less likely to depolarize. This appears to have large applications for decreasing the conditions associated with chronic pain due to the effect on the nervous system C-fibers and pain transmission.

In summary, magnetism appears to be mainly effective on the nervous system by resulting in nervous tissue regeneration and decreasing levels of pain. There has been some research to support the notion of its effectiveness on soft tissue wounds, but little or no research concerning its effects on muscle tissue. Magnetism is believed to stimulate healing by creating an optimal environment within the body to heal itself (Hacmac, 1991).



Informed consent consistent with the University of Ottawa’s Faculty of Health Science Human Research Ethics Committee was obtained from 6 healthy untrained female university students who were between the ages of 20 years and 23 years. Untrained was defined as not having participated in any predominately strength training for the biceps brachii during the previous 9 weeks. The subjects were all volunteers who had decided that they were interested in participating. No compensation or reward was offered to the subjects.


The magnetic pads used in this experiment were thin, light, and flexible, yet large enough to easily cover the whole biceps brachii complex. The magnetic pads were of the New Ardizzone Design configuration with an energy product of 1.4 mgoE (Ardizzone, 1992a). A non-adhesive, 2" wide elastic bandage was used to secure the magnetic pad to the front of the upper arm. The non-magnetic pad appeared physically the same as the magnetic pad. Assessment of strength performance and exercise sessions were conducted on an isokinetic dynamometer, specifically the KinCom (Chattecx, Chattanooga, TN; version 3.2).


The experiment was conducted over a period of 5 successive days. The first day required that the subject become familiar with the KinCom Isokinetic Dynamometer in order to decrease any learning effects acquired during the experiment with the required movements. A specific warm-up for the forearm flexors was made part of this initiation session using the "Warm-up" option given by the KinCom in the Evaluation stage. All testing, initiation periods, and training sessions took place under trained supervision according to the safety procedures involved with the KinCom.

After the warm-up and initiation period, the subject’s maximal concentric force produced by elbow flexion at 120ş per second for each arm was established over 5 trials. Maximal force was obtained by noting the peak force in the averaged force curves produced during the trials by using the Overlay option during the evaluation stage. There was a 15 second rest period between each trial which is consistent with standard isokinetic testing procedures (Sale, 1991). Upon completion of the maximal testing period, the subjects then performed 3 sets of 10 repetitions of maximal concentric and eccentric contractions at 120ş per second and 90ş per second respectively for each arm utilizing the Training feature on the KinCom. Rest periods between sets were set at 180 seconds. 30 total repetitions were chosen based on the literature of Clarkson & Tremblay (1988) so as to minimize any muscle soreness that would occur while still causing a training effect. Verbal encouragement was given during the testing and training periods to bring about true maximal contractions.

Upon completion of the exercise bout, each subject was provided with two seemingly identical magnetic pads that were labeled for the left and right arms. Two elastic bandages were also distributed to each subject in order to secure the magnetic pads to the front of the upper arms. One pad was an actual magnetic pad while the other pad was not magnetized. The administration of the pads was performed in a double blind fashion so that neither the subject nor the administrator knew which pad was magnetized and which one was not. The subjects were instructed to wear the appropriate magnetic pads on the front portion of each of their upper arms for a period of 8 hours each day either during the evening or during their sleep period for the duration of the research.

From the second through to the fifth day, the subjects reconvened at an agreed upon time in order to re-test maximal concentric strength following the same procedures as previously outlined. The subjects were reminded to wear the appropriate magnetic pads for the appropriate arm for 8 hours that night as previously discussed. On the fifth day, the magnetic pads and elastic bandages were returned and the magnetized and non-magnetized pads were identified and recorded. The subjects were thanked and appreciation expressed for their participation in this research project.

Statistical Methods

Descriptive statistics (means and standard deviations) were calculated for the subjects’ profiles using the computer program Kwikstat. A Repeated Measures Analysis was used for this research project. A Neuman-Keuls Multiple Comparisons post hoc procedure was performed to determine where the significant differences, if any, occurred.


Descriptive statistics and data for the magnetized and non-magnetized arms of the subjects are given in Table 1. There was no significant difference at the 0.05 significance level for maximal concentric strength between the magnetized and non-magnetized arms.

TABLE 1. Descriptive statistics and data for the magnetized and non-magnetized arms over the five day period (n = 6). Results are in Newtons (N).

Non-Magnetized Arm

Mean Force Production (N)

Standard Deviation

Minimum Force Value (N)

Maximum Force Value (N)

Day 1





Day 2





Day 3





Day 4





Day 5





Magnetized Arm


Day 1





Day 2





Day 3





Day 4





Day 5





Both the magnetized and non-magnetized arms experienced a statistically significant drop (at the 0.05 level) in maximal concentric strength on day 2 (as compared to day 1) when the subjects could only produce 83% and 81% respectively of their maximum strength. As illustrated in Figure 1, this was followed by a slow recovery from day 2 to day 5 where the subjects only reached 87% of their maximal strength for the magnetized arm and 86% for the non-magnetized arm. There was no significant differences at the 0.05 significance level between the magnetized and non-magnetized arms when they were compared to each other.

FIGURE 1. Percentage of maximum strength for both magnetized and non-magnetized arms throughout the five days. Note the large drop in performance for day 1 and the slow recovery to day 5 which did not return to baseline levels.

In addition, there were no significant changes in concentric strength recovery between the time period of day 2 through to day 5 between both the magnetized and non-magnetized arms.

The magnetized arm showed a greater increase in strength performance of approximately 8% of maximum from day 3 to day 5, whereas the non-magnetized arm increased only 5% of maximum. However, these changes were statistically insignificant at the 0.05 level. Furthermore, the magnetized arm had the lowest values of strength performance the second day after the study, whereas the non-magnetized arm results showed lowest values occurring the day after the exercise. Again, these values were not significant at the 0.05 level.


The primary finding of this research project was that there were no significant differences in strength recovery between the magnetized and the non-magnetized arms. Although little research appears to have been done previously which either supports or refutes this finding there are several possible explanations that can be offered based on the known mechanisms of strength recovery. Such explanations arise from research examining the process of muscle recovery and repair from eccentric exercise.

The patterns of strength loss and slow recovery for the magnetized and non-magnetized arms found in this project were consistent with the findings of previous research which studied the effects of eccentric exercise on strength performance (Clarkson et al., 1992; Ebbeling & Clarkson, 1990; Newham et al., 1987; Rodenburg et al. 1993). Studies in which the effects of concentric contractions and eccentric contractions were examined showed that eccentric contractions resulted in prolonged strength loss (Golden & Dudley, 1992; Kroon & Naeije, 1991). Therefore, the significant drop in strength and prolonged strength loss which the subjects in this research project showed beginning on the first day and continuing to the fourth day following the exercise session can most likely be attributed to the effects of the eccentric portion of the exercise and not the concentric portion.

Eccentric contractions appear to result in muscle damage combined with a loss of concentric strength (Ebbeling & Clarkson, 1989; Fridén et al., 1983). Since this experiment involved maximal eccentric contractions which resulted in decreases of concentric force production, it can be reasonably assumed that there was also some degree of muscle damage. As previously reviewed, it is this muscle damage that appears to trigger certain responses to stimulate the muscle to recover.

There were no significant differences between the magnetized and the non-magnetized arms and therefore no differences in the recovery patterns of the two arms. In addition, the lack of significance also indicates that there was no dominance effect between the two arms for this experiment. There are a number of potential explanations that will be discussed concerning why magnetism did not affect strength recovery in this study.

As previously discussed, strength recovery involves a combination of lysosomal activity, cell regeneration, connective tissue recovery, and protein synthesis and degradation. These processes appear to be regulated by the physiological environment and condition of the muscle itself (Armstrong, 1990; Ebbeling & Clarkson, 1989). Magnetism can increase blood flow, change the migration of calcium ions, increase or decrease hormone production, and alter enzyme and biochemical processes (Hacmac, 1991). However, any changes caused by magnetism in this study do not appear to affect strength recovery over the 5 days.

An increase in blood flow would not necessarily mean a decrease in recovery time. Although blood carries necessary proteins, hormones, and monocytes to the injured muscle as well as carrying away waste products, improving the rate at which this transport occurs would not necessarily accelerate muscle recovery. This is due to the fact that the exchange between metabolic end products, hormones and nutrients is regulated more by membrane transport and diffusion than by bulk flow (Vander et al., 1990).

Certain key processes in muscle recovery such as protein synthesis, protein degradation, and satellite cell activation and growth do not rely upon blood flow. This statement is based on research which has shown that muscle growth and regeneration can take place in a culture environment (Bischoff, 1989; Vandenburgh, Hatfaludy, Karlisch, & Shansky, 1989).

Although an increase in extracellular calcium ions has been shown to induce muscle damage (Baracos, 1986), the exact mechanism and how this occurs remains elusive to researchers in the field (Armstrong, 1990). Hacmac (1991) has stated that magnetism can change the migration of calcium ions. Whether or not magnetism can change the concentration of calcium ions in damaged muscle remains to be determined; however, in this experiment the magnets were not worn until several hours after the exercise. Perhaps any potential protective benefits which may have been provided to the muscle by changing the migration of calcium ions may have occurred too late for any significant protection to be evident. More over, it must be re-stated that the effects of magnetism on calcium migration in injured muscle has not been researched. Therefore, no conclusive statement can be offered as to how this might have improved or decreased recovery time.

Literature exists on magnetism and pineal gland functioning (Sandyk, 1992). However, the type of magnetism used in this experiment is not similar to the type reviewed by Sandyk in 1992. Furthermore, since this particular experiment involved applying the magnet only to the upper arms, any potential effects to the pineal gland would have been negligible due to the location of the magnetic field.

Since no specific research oriented towards the effects of magnetism on connective tissue has been done, no conclusions can be offered as to its relationship to strength recovery. Studies investigating the effects of magnetism on osteoarthritis tend to focus more on relief of symptoms than on physiological changes within the joints (Trock et al., 1993). It is interesting to note that a study in 1989 by Sanders-Shamis, Bramlage, Weisbrode, and Gabel investigated the effects of electromagnetism on bone healing in horses. The study concluded that the type of magnetic fields used in the study did not have an effect on the repair of an osseous defect.

In conclusion, this research project investigated the effects of natural magnets on strength recovery. For the purposes of this study strength recovery was measured by examining changes in the isokinetic concentric strength of forearm flexors following maximal eccentric and concentric exercise. The results of this examination indicated that natural magnets as used in this study had no significant effects on strength recovery over a period of 5 days.

Recommendations for Future Research

There are many novel areas related to magnetism which researchers might explore considering the lack of information on the effects of magnetism on muscle recovery. With respect to this study, it would be interesting for future investigations to examine the effects of using stronger magnets, extending the time period for wearing the magnets, or extending the actual time period of the investigation. This last recommendation is based on the fact that strength levels had not returned to normal at the end of the 5 days. A more complete examination into the physiological effects of magnetism on muscle tissue would expand our knowledge and understanding of this possible useful subject.

To conclude, it appears that research literature concerning natural magnets and their effects on muscle tissue and strength recovery is particularly lacking in pertinent information. Further study of either a specific aspect or a combination of the ideas expressed here would lead to new insight into the effects of magnetism on muscle tissue and strength recovery.


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