Haemodynamic changes in human masseter and temporalis muscles induced by different levels of isometric contraction
Introduction
In a contracting muscle, there is a rise in intramuscular pressure proportional to its percentage maximum voluntary contraction (Sjogaard et al., 1988). This causes mechanical compression of the blood vessels, which competes against local metabolic, neurogenic and systemic humoral factors that induce vasodilation. The exact level of sustained contraction necessary for the induction of a metabolic debt in normal human jaw muscles is not known. It is speculated that above 50% maximum voluntary contraction, the extravascular compression is a dominant factor and very little compensatory vasodilation is produced during an isometric task (Johnson, 1989). Moreover, at 70% or more of maximum voluntary contraction, there is almost no blood flow through the contracting muscle and therefore isometric contractions cannot be sustained for longer than 1–2 min. Of course, the level of isometric contraction that can arrest intramuscular blood flow varies among different muscles from around 60% for the forearm (Humphreys and Lind, 1963) down to 20% for the quadriceps (Edwards et al., 1972).
Sustained voluntary clenching for 90 s in the intercuspal position by healthy humans at approx. 25% maximum voluntary contraction or higher produces a relative blood-flow impairment with a large postcontraction hyperaemia in the jaw closers (Rasmussen et al., 1977, Moller et al., 1979, Moller, 1981). Monteiro et al. (1989) studied jaw-muscle blood flow in 10 healthy humans using a 133xenon clearance technique and reported a clear and substantial postcontraction hyperaemia following both a 10% and 50% sustained isometric contraction. These limited data suggest a powerful effect on muscle blood flow at very low force. However, further investigations using improved methods for measuring blood flow are necessary to determine more accurately the effects of low levels of contraction on muscle blood flow.
Recently a non-invasive method using near-infrared spectroscopy has been demonstrated for studying the haemodynamics of skeletal muscles (Hampson and Piantadosi, 1988, Wilson et al., 1989, Chance et al., 1992). Its principal limitation is that absolute concentrations of deoxygenated Hb cannot be determined: this is because the path length of the reflected light is unknown as the system uses reflected light rather than the transillumination typical of pulse oximetry of the finger or earlobe. Nevertheless, changes in blood volume (or Hb level) within a contracting muscle are usually expressed as arbitrary units of perfusion with respect to the muscle’s resting baseline condition. Using this technique, Wilson et al. (1989) isolated the canine gracilis muscle and demonstrated that absorption at 760–850 nm correlated closely with venous Hb oxygen saturation when the muscle was electrically stimulated to contract. Chance et al. (1992) successfully used this device to assess changes in total Hb in the exercizing quadriceps muscle of competitive rowers. Finally, using this method, clear differences in haemodynamics were found between chronically painful and non-painful masticatory muscles in the recovery phase of a sustained contraction (Delcanho et al., 1996). Using the near-infrared method, they studied 10 women with a history of chronic jaw-muscle pain and eight matched healthy women controls without muscle pain. They found an increase in haemoglobin in both groups in the postcontraction phase following a 30-s isometric contraction, but the participants with chronic muscle pain had a significantly lower response than the control group. Their results support the concept that individuals with chronic muscle pain have a slower intramuscular reperfusion during the recovery phase after sustained isometric contractions. In order to investigate this clinical difference further, more knowledge is needed on what are the rate-limiting effects on intramuscular blood flow in normal individuals.
Our aim now was to investigate how the contraction level of the masseter and temporalis changes the intramuscular blood flow and what differences exist in the haemodynamic changes between these two muscles. The null hypothesis was that there are no differences in the haemodynamic characteristics of the masseter or temporalis following 5, 15, 25 and 100% of maximum isometric contraction sustained for 30 s in normal individuals. A brief abstract on the findings has been published elsewhere (Kim et al., 1996).
Section snippets
Participants
Twenty individuals (10 men and 10 women) aged 22–42 years participated in the study. Their mean age was 29.1±5.3 years (men, 30.5±5.6 years; women, 27.6±4.8 years). Their mean height was 170.2±9.3 cm (men, 174.0±7.2; women, 166.4±9.8). Their mean weight was 63.6±13.1 kg (men, 73.5±9.9; women, 53.7±6.8). The participants were recruited by local newspaper advertisements and most worked, or were students, at the UCLA Medical Center. After a screening questionnaire, those deemed as suitable were
Actual bite forces
There were no significant differences in age between male and female participants. The mean maximum bite force measured by the load cell was 228.9±96.9 N (men, 221.8±78.5 N; women, 235.9±116.5 N). The mean bite forces were not statistically different between male and female participants. Table 1 shows the actual mean bite forces produced during the various trials. These results also showed no sex differences at any bite force. Fig. 1 shows representative raw data from one of the participants in
Discussion
There are three major findings in this study. First, that very low levels of voluntary contraction (as little as 5% maximum voluntary contraction) induced a postcontraction hyperaemia in both the masseter and temporalis. Second, that this postcontraction hyperaemia had a curvilinear relation with the contraction effort. Thirdly, that the contraction-induced haemodynamic responses were clearly different between the masseter and temporalis. Overall these findings allow us to reject our null
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Cited by (0)
- 1
Postdoctoral Resident, UCLA School of Dentistry (currently in Private Practice, Seoul, South Korea).
- 2
Visiting Scholar from Okayama University Dental School, Okayama, Japan.
- 3
Visiting Scholar from Faculty of Dentistry, Kyushu University, Fukuoka, Japan.
- 4
Visiting Associate Professor from Faculty of Dentistry, Kyushu University, Fukuoka, Japan.