Aerobic exercises such as running, walking and cycling are known to elicit a PEH (post-exercise hypotensive) response in both trained and UT (untrained) subjects. However, it is not known whether swim exercise produces a similar effect in normotensive individuals. The complex acute physiological responses to water immersion suggest swimming may affect BP (blood pressure) differently than other forms of aerobic exercises. We tested the hypothesis that an acute bout of swimming would fail to elicit a PEH BP response compared with an equivalent bout of stationary cycling, regardless of training state. We studied 11 UT and ten triathlon-trained young healthy normotensive [SBP/DBP (systolic BP/diastolic BP) <120/80 mmHg)] men and women (age 23±1 years) who underwent 30 min of intensity-matched cycling and swimming sessions to assess changes in BP during a 75-min seated recovery. CO (cardiac output), SV (stroke volume), TPR (total peripheral resistance), HR (heart rate), HRV (HR variability) and core and skin temperature were also assessed. In UT subjects, PEH was similar between cycling (−3.1±1 mmHg) and swimming (−5.8±1 mmHg), with the greater magnitude of PEH following swimming, reflecting a significant fall in SV between modalities ( P <0.05). Trained individuals did not exhibit a PEH response following swimming (0.3±1 mmHg), yet had a significant fall in SBP at 50 min post-cycling exercise (−3.7±1 mmHg) ( P <0.05). The absence of PEH after swimming in the trained group may reflect a higher cardiac sympathetic outflow [as indicated by the LF (low-frequency) spectral component of HRV) (25 and 50 min) ( P <0.05)] and a slower return of vagal tone, consistent with a significant increase in HR between modalities at all time points ( P <0.05). These results suggest that training may limit the potential for an effective post-exertional hypotensive response to aerobic swimming.

The β 2 -adrenergic agonist, clenbuterol, has powerful muscle anabolic and lipolytic effects and is used by athletes to improve exercise performance; however, its use in conjunction with different forms of exercise training has received limited attention. Since previous studies have reported that chronic use of other β 2 -adrenergic agonists has deleterious effects on cardiac muscle structure and function, the aim of the present study was to determine whether chronic clenbuterol administration would reduce the exercise capabilities of rats subjected to long-term treadmill sprint running, endurance swimming or voluntary wheel running training. The effect of clenbuterol treatment on exercise performance in rats was evaluated in three separate studies. Different groups of male rats were assigned to an endurance swimming (2 h/day, 5/7 days, 18 weeks) group, a treadmill sprint running (8×1 min bouts, 1.05 m/s, 20 weeks) group, or a voluntary wheel running (16 weeks) group. In each study, rats were allocated into either a treated group that received clenbuterol (2 mg·kg -1 ·day -1 ) in their drinking water or an untreated control group. In each of the three studies, treated rats exhibited a reduction in exercise performance compared with untreated rats. Treated rats ran ∼ 57% less total distance than untreated rats in the voluntary running programme and were unable to complete the swimming and sprinting protocols performed by the untreated rats. In each of the studies, the treated rats exhibited cardiac hypertrophy, with absolute heart mass increased by ∼ 19% and heart mass relative to body mass increased by ∼ 20%. The hearts of sedentary rats treated with clenbuterol exhibited extensive collagen infiltration surrounding blood vessels and in the wall of the left ventricle. The results indicate strongly that chronic clenbuterol administration deleteriously affects exercise performance in rats, potentially due to alterations in cardiac muscle structure and function.