The aim of the study was to examine several physiological responses to a climbing-specific task to identify determinants of endurance in sport rock climbing. Finger strength and endurance of intermediate rock climbers (n = 11) and non-climbers (n = 9) were compared using climbing-specific apparatus. After maximum voluntary contraction (MVC) trials, two isometric endurance tests were performed at 40% (s = 2.5%) MVC until volitional exhaustion (continuous contractions and intermittent contractions of 10 s, with 3 s rest between contractions). Changes in muscle blood oxygenation and muscle blood volume were recorded in the flexor digitorum superficialis using near infra-red spectroscopy. Statistical significance was set at P < 0.05. Climbers had a higher mean MVC (climbers: 485 N, s = 65; non-climbers 375 N, s = 91) (P = 0.009). The group mean endurance test times were similar. The force-time integral, used as a measure of climbing-specific endurance, was greater for climbers in the intermittent test (climbers: 51,769 N x s, s = 12,229; non-climbers: 35,325 N x s, s = 9724) but not in the continuous test (climbers: 21,043 N x s, s = 4474; non-climbers: 15,816 N x s, s = 6263). Recovery of forearm oxygenation during rest phases (intermittent test) explained 41.1% of the variability in the force-time integral. Change in total haemoglobin was significantly greater in non-climbers (continuous test) than climbers (P = 0.023--40% test timepoint, P = 0.014--60% test timepoint). Pressor responses were similar between groups and not related to the force-time integral for either test. We conclude that muscle re-oxygenation during rest phases is a predictor of endurance performance.

The effect of cimetidine and ranitidine on doxepin pharmacokinetics was studied in 6 healthy volunteers. Each subject completed 3 study phases: Treatment A, 9 consecutive doses of 50 mg doxepin (once daily); Treatment B, same as Treatment A but co-administration of cimetidine 600 mg b.i.d. starting after the sixth doxepin dose and continuing until approximately 2 days following discontinuation of doxepin administration; Treatment C, identical to Treatment B but with ranitidine 150 mg b.i.d. instead of cimetidine. Unlike ranitidine, cimetidine co-administration resulted in a significant increase in steady state plasma levels of doxepin (4.7, 9.0 and 4.5 ng/ml during Treatments A, B and C respectively) but not desmethyldoxepin (4.1, 4.6 and 4.2 ng/ml during Treatments A, B and C respectively). Elimination half-lives of doxepin and desmethyldoxepin were prolonged by cimetidine co-administration (19.6 and 26.2 h respectively), but remained unchanged during the ranitidine treatment phase (13.3 and 18.4 h) as compared to the control phase i.e. Treatment A (13.2 and 19.0 h). These results show that cimetidine, unlike ranitidine, significantly inhibits the biotransformation of doxepin. This data has clinical implications when the co-administration of tricylic antidepressants and H2-receptor antagonists are indicated.

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