Betablocking medication

Beta-blockers, unless contraindicated, are now standardised prescription in the UK and the USA following myocardial infarction (Brand, et al., 1995;

Blood lactate

RPE 11 13 15 RPE 11 13 15

Figure 3.6. RPE, %VO2 max, %HRmax and blood lactate in trained (open boxes) and untrained (black circles) individuals.

(Adapted from the summary of findings of: Berry, et al., 1989; Boutcher, et al., 1989; Briswalter and Delignieres, 1997; Ekblom and Goldbarg, 1971; Held, et al, 1997; Held and Marti, 1999; Hetzler, et al, 1991; Hill, et al, 1987; Kang, et al, 1996; Seip, et al, 1991; Swaine, et al., 1995;Travilos and Marisi, 1996.)

Department of Health: National Service Framework for Coronary Heart Disease, 2000). These guidelines recommend that patients be prescribed beta-blockers for at least 12 months following myocardial infarction. This means that most post-MI patients attending cardiac rehabilitation will require an exercise prescription that respects the effects of beta-blockade, including: an altered cardio-respiratory response, changes in physical performance capability, slowed oxygen kinetics and potential side effects such as postural hypotension (Hughson and Smyth, 1983; Reents, 2000).

The year 1979 appears to be a watershed for research published on the potential interactions between beta-blockade and perceived exertion. Three studies (Davies and Sargeant, 1979; Sjoberg, et al., 1979; van Herwarden, 1979) reported that the use of beta-blockade did not affect perceived exertion. One study did report an increase in RPE with the administration of beta-blockade (Pearson, et al., 1979). However, this study involved healthy participants, where the other studies involved either hypertensive or myocardial infarction patients. The validity of studying the effects of beta-blockade on normoten-sive and non-cardiac diseased patients is thus questioned.

Wilcox, et al. (1984) reported that in the acute stages of first administering beta-blockers, RPE was modulated upward for a given exercise intensity. It is therefore important to consider the wash-in period of these medications during research and during the practice of exercise prescription when patients are either first given medication or have medication changed. The review by Eston and Connolly (1996) was very clear to point out that studies on RPE

a. Heart rate (beats.min-1)

210 190 170 150 130 110 90 70 50

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75 65

75 65

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c. Blood lactate (mmol.l-1)

14 12 10 8 6 4 2 0

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d. Differentiated and whole body ratings of perceived exertion

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_BRPE Legs

♦ RPE-Breath " ARPE-Overall

Figure 3.7. Heart rate (a), oxygen uptake (b), blood lactate, (c) RPE and (d) responses to an incremental maximal cycle ergometer test.

These data correspond with the studies referenced in Figure 3.6. Take note of the RPE values of 12 to 13, at testing stages 4 to 5, corresponding to the point where blood lactate has risen in an accelerating fashion (the lactate threshold). For this individual this point was at 80% of HRmax and 64% VO2max.

(Buckley JP and Whyte G (Oct. 2003) Unpublished data: British Olympic Medical Institute, London.)

and beta-blockade involved three different types of participants: healthy individuals, patients with hypertension and patients with angina or a previous myocardial infarction. A further consideration is that a variety of makes and types of beta-blockade (e.g. atenolol, bisoprolol, celiprolol, metoprolol, practolol, propranolol) were used in the four studies noted above.

The majority of studies have shown that beta-blockade does not interact with RPE, but with two key exceptions: (1). When the exercise lasts for more than 60 minutes and (2). When exercise is performed at higher relative intensities (>~65% VO2 max) (Eston and Connolly, 1996; Noble and Robertson, 1996; Head, et al., 1997; Borg, 1998; Liu, et al., 2000). The latter exception appears to have been a function of the type of beta-blocker prescribed, and with some brands RPE is unchanged for a given %VO2 max, regardless of intensity.These levels of intensity (>65% max) and duration (>60 minutes) represent more advanced limits of exercise prescription for cardiovascular patients (ACSM, 1994, 2000; BACR, 1995; AACVPR, 2004). The majority of patients in phase III and IV rehabilitation programmes will exercise at the low to moderate level of exercise. Other interactions between RPE and beta-blockade have also been dependent on whether the ratings were measured as overall, central (cardio-pulmonary) or peripheral/local (muscle) sensations (see Figure 3.7) and whether or not the beta-blocker was a car-dioselective drug. It has been shown that non-selective compared to cardios-elective beta-blocking medications have more influence in reducing blood flow to pulmonary tissues and skeletal muscle (British National Formulary, 2004), but that all types dampen fat metabolism (Eston and Connolly, 1996; Head, et al., 1997; Lamont, et al., 1997). Thus, there could be an increased perception of pulmonary effort due to an increased demand on carbohydrate and decreased supply of oxygen and free fatty acids to the skeletal muscle. Muscle fatigue during prolonged low-to-moderate intensity exercise is linked to reductions in carbohydrate reserves (Newsolme, et al., 1992). Cardioselective beta-blockers (e.g. atenolol) have less effect on blocking beta-receptors in pulmonary tissue and skeletal muscle. It can therefore be seen why both the effect of reduced fatty acid metabolism and non-cardioselective beta-blockade may cause an increased local/peripheral perception of effort. Furthermore, during prolonged (>60 minutes) and/or higher intensity (>65%VO2 max) exercise there will be an increased susceptibility to an earlier onset of muscle fatigue due to increased reliance on limited carbohydrate substrates.

Duration of exercise has been regarded as a modulator of RPE whether under beta-blockade or not, from the effects of reductions in carbohydrate energy substrates, increased body temperature and the psychological concept of duration-fatigue (Potteiger and Weber, 1994; Kang, et al., 1996; Head, et al., 1997; Utter, et al., 1997,1999; Borg, 1998).

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