Activitats i programes d’educació ambiental

2.5.3.1 Delayed onset muscle soreness

Delayed onset muscle soreness (DOMS) is a very important problem for coaches and athletes because it causes chronic pain and diminishes muscle function and ability

to participate in sport (Ernst, 1998). DOMS commonly occurs between 24 and 72 hours after unaccustomed eccentric exercise (Appell, Soares, & Durate, 1992; Clarkson &

Sayers, 1999; Ebbeling & Clarkson, 1989; Howell, Chleboun, & Conaaster, 1993). The consequences of damage to muscle function include prolonged loss of muscle strength (Chleboun et al., 1995; Clarkson, Nosaka, & Braun, 1992; Clarkson & Sayers, 1999;

McHugh, Connolly, Eston, & Gleim, 2000; McHugh, Connolly, Eston, Gartman, &

Gleim, 2001), soreness sensation (Howell et al., 1993; McHugh et al., 2000; McHugh et al., 2001), decreased range of motion (Clarkson et al., 1992), increased muscle stiffness (Chleboun et al., 1995; Howell et al., 1993), increased resting metabolic rate (Dolezal, Potteiger, Jacobsen, & Benedict, 2000), and perturbed athletic performance (Harris, Wilcox, Smith, Quinn, & Lawson, 1990; Hone, Siler, & Schwane, 1990; Smith, 1992).

These changes might increase the risk of sports injury.

The sequence of DOMS events consists of the mechanical stress of exercise on muscle fibres (Appell et al., 1992; Armstrong, 1984; Cheung, Hume, & Maxwell, 2003;

Ebbeling & Clarkson, 1989; W. J. Evans & J. G. Cannon, 1991; Faulkner, Brooks, &

Opiteck, 1993), causing sarcomeres to rupture (Friden & Lieber, 1992) followed by calcium homeostasis disturbance. The damage of sarcoplasmic reticulum or muscle membrane can increase intracellular calcium and trigger calcium-sensitive pathways (Armstrong, 1990; Armstrong, Warren, & Warren, 1991). Calpain, the

calcium-activated neutral protease, plays a role in the ultrastructural muscle damage (Clarkson &

Sayers, 1999). The inflammatory response to damaged muscle fibres causes a transfer of fluid and cells to the damaged tissue (Smith, 1991). The increased fluid produces swelling after injury. Neutrophils and macrophages migrate to the inflammatory sites and play a role in both the damage and repair processes (Clarkson & Sayers, 1999).

The exact mechanisms to explain how soreness develops and why there is a delay in pain sensation is not fully understood (Cheung et al., 2003; Clarkson, 2000; Clarkson &

Hubal, 2002; deVries & Housh, 1996).

Several treatments which aim to prevent and/or reduce the severity of muscle damage have been investigated including acupuncture (Barles, Robinson, Allen, &

Baxter, 2000), ultrasound (Ciccone, Leggin, & Callamaro, 1991; Craig, Bradley, Walsh, Baxter, & Allen, 1999), cryotherapy (Eston & Peters, 1999), compression (Chleboun et

al., 1995; Kraemer et al., 2001), antiinflammatory drugs (Bourgeois, MacDougall, MacDonald, & Tarnopolsky, 1999), hyperbaric oxygen therapy (Mekjavic, Exner, Tesch, & Eiken, 2000), warm-up (High et al., 1989; Nosaka & Clarkson, 1997), stretching (High et al., 1989; Johansson et al., 1999; Lund, Vestergaard-Poulsen, Kanstrup, & Sejrsen, 1998a), and massage (Hasson et al., 1992; Lightfoot, Char, McDermont, & Goya, 1997; Rodenburg, Steenbeek, Schiereck, & Bar, 1994; Smith, Keating et al., 1994; Tiidus & Shoemaker, 1995; Weber, Servedio, & Woodall, 1994;

Wenos, Brilla, & Morrison, 1990). These treatments have been applied as a prophylactic and/or a therapeutic intervention. However, the benefits of these treatments are still inconclusive. From a clinical point of view, the treatment given prophylactically is more desirable for reducing or preventing injury, and consequently, for producing a reduction in further injuries, chronic pain, cost of injury treatment, and time lost from training activities.

Massage is one of the treatments commonly used to alleviate DOMS because it is thought to increase local blood and lymph flow, decrease oedema, and reduce pain.

Significant reductions in soreness perception of DOMS after massage have been reported (Bale & James, 1991; Rodenburg et al., 1994; Smith, Keating et al., 1994;

Tiidus & Shoemaker, 1995). Some studies explained the mechanism of DOMS

reduction by the increase of neutrophils (Smith, Keating et al., 1994), and the reduction of blood creatinine kinase (Rodenburg et al., 1994; Smith, Keating et al., 1994), while some researchers failed to explain the mechanism at all (Bale & James, 1991; Tiidus &

Shoemaker, 1995). Many researchers, however, reported that massage was not

beneficial in reducing DOMS (Hasson et al., 1992; Lightfoot et al., 1997; Weber et al., 1994; Wenos et al., 1990; Yackzan, Adams, & Francis, 1984). A summary of studies that have investigated the effects of massage on muscle soreness is presented in Table 2.7.

Table 2.7..The effects of massage on muscle soreness.

Reference Trial design

Samples Intervention Outcome measures Main results Smith et al.

a) 30-min of effleurage, shaking, petrissage, cross-fiber.

b) Control.

Intervention performed 2 hr after biceps and triceps eccentric exercise.

c) Flexion angle of elbow.

10-minute effleurage on leg 3 days before, immediately after, and repeated on day 2 and 3 after quadriceps eccentric exercise.

Table 2.7 (continued) The effects of massage on muscle soreness.

Reference Trial design

Samples Intervention Outcome measures Main results

Farr et al.

30 min leg massage (effleurage & petrissage) 2 hr after 40 min treadmill walk.

a) Swedish massage (7 min of effleurage, 1 min of tapotement, 12 min of petrissage).

b) control (placebo lotion applied and rest for 20 min).

Intervention performed 2 hr after hamstrings eccentric

24 hr postexercise on the left calf muscle.

Table 2.7 (continued) The effects of massage on muscle soreness.

Reference Trial design

Samples Intervention Outcome measures Main results

Hasson et

b) Placebo massage (n=5).

c) Control (n=5)

c) Upper body ergometry.

d) Control

CCT = controlled clinical trial; RCT = randomised controlled trial; CT = counterbalance trial; S = significant; NS = non-significant; DOMS = delayed onset muscle soreness; F = female; M = male; CK = creatine kinase; DDS = Differential Descriptor Scale; POMS = Profile of Mood States; ↑ = increase; ↓ = decrease.

The inconclusive data on the effects of massage on DOMS may be due to the

limitations of previous research. The majority of studies used small sample sizes, which limited the statistical power of the studies (Bale & James, 1991; Hasson et al., 1992;

Lightfoot et al., 1997; Smith, Keating et al., 1994; Tiidus & Shoemaker, 1995; Weber et al., 1994; Wenos et al., 1990). Some studies used another limb as a control group that

could have introduced intrasubject bias (Tiidus & Shoemaker, 1995; Wenos et al., 1990). One study used a combination of treatments making it difficult to establish the effectiveness of each of the treatments alone (Rodenburg et al., 1994). Two studies were reported only in abstract form (Hasson et al., 1992; Wenos et al., 1990). The different genders of participants might affect the results (Lightfoot et al., 1997; Tiidus &

Shoemaker, 1995) because of the different patterns of DOMS between males and females as reported in the literature (MacIntyre, Reid, Lyster, & McKenzie, 2000). The wide variation of massage techniques, duration of massage application, area of the body massaged, and outcome measures also affect the conclusions that can be drawn from the studies.

The unclear mechanisms of massage may also lead to inappropriate massage application. In practice, massage is often applied immediately after exercise in order to enhance blood circulation. The effects of massage on blood circulation are still

questionable as described previously. The eccentric exercise, which induced muscle damage, does not produce waste products that require extra blood flow. Research which investigated the effects of massage immediately after exercise found a decrease of DOMS 48 hours after exercise but did not find any change in blood circulation (Tiidus & Shoemaker, 1995). Some studies have not found any effects of massage immediately after exercise (Weber et al., 1994; Wenos et al., 1990).

Some researchers have speculated that massage may reduce DOMS sensation by decreasing muscle oedema. However, in studies by Hasson et al. (1992) and Lightfoot et al. (1997), leg volume and soreness sensation did not change after massage

immediately after exercise and/or 24 hours after exercise. Massage performed two hours post-exercise was reported to benefit DOMS by reducing an inflammatory

process (Smith, Keating et al., 1994). The neutrophil values in the massage group were significantly higher than in the control group at eight and 24 hours. The authors

speculated that the elevation of the neutrophil counts was the result of the mechanical action of massage by the shearing of the neutrophils from the vessel walls. The increased blood flow from the proposed physiological mechanism of massage might prevent the migration of the neutrophils from the circulation into the injury sites. Thus, the neutrophil values would be elevated in the blood count. Two studies used the

protocol of Smith et al. (1994) to examine the effects of massage application two hours after eccentric exercise (Farr et al., 2002; Hilbert et al., 2003). Farr et al. (2002) and Hilbert et al. (2003) reported that massage performed two hours post-exercise was effective in reducing soreness sensation. It is important to note that Farr et al.’s study investigated massage on one leg and used the other leg as the control group. Therefore, it is likely that massage might provide a psychological advantage as only soreness sensation - the subjective measure reported by the participants - was reduced after massage application. However, there was no benefit of massage for preventing muscle strength and function loss (as determined by isometric and isokinetic tests and jumping height, respectively) (Farr et al., 2002; Hilbert et al., 2003). Interestingly, both research studies did not find any change in neutrophil count.

It is hypothesized, that if the mechanical effect of massage can increase muscle flexibility and reduce muscle stiffness, enhance local microcirculation and lymph flow, and increase muscle compliance, massage should be applied before eccentric exercise in order to lower the initial mechanical overload of eccentric exercise. A theoretical model of the expected mechanism of massage on the severity of DOMS is presented in Figure 2.2.

Figure 2.2 Theoretical model of the expected mechanisms of massage on the severity of muscle soreness.

Massage

⇓

↓ Mechanical overload on sarcomeres during lengthening actions (eccentric exercise)

⇓

↓ Sarcoplasmic reticulum ruptures

⇓

↓ Intracellular calcium & trigger calcium-sensitive degradative pathways

⇓

↓ Ultrastructural damage

2.5.4 Summary of the evidence for massage improving performance, enhancing