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This raises one final consideration, pertinent to the models of inactivity used in humans.
Some evidence exists for enhanced vasoconstrictor function in models of inactivity, including exaggerated endothelin-1 responses (Thijssen et al. 2007b).
These impacts of each of the models of inactivity on the function and structure of these vessel beds will be considered separately below.
The relative impacts of different durations or models of inactivity, or different exercise volumes and intensities, has not been comprehensively studied to date.
The vasoconstrictor responses to l-NMMA and angiotensin II, and the dilator responses to SNP, were unaltered in both models of inactivity.
Despite the sparse and dispersed data, and the various models of inactivity that have been adopted, it remains likely that changes in conduit and resistance vessel structure and function may help to explain the increased cardiovascular mortality and morbidity associated with deconditioning.
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Similarly, pain increase has been suggested to contribute to low adherence rates, in accordance with a fear-avoidance model of inactivity [ 19].
Several models of physical inactivity of different duration demonstrated that these increases in shear rate associated with deconditioning were not due to increases in blood flow (Bleeker et al. 2005a, b, c; de Groot et al. 2006a, b; Olive et al. 2003).
Using strict bed rest as a model of physical inactivity seen during hospitalization, we aimed to determine if bed rest induced physical inactivity would reduce the incretin effect in healthy volunteers.
Using a multiple array analysis strategy [30], [31] we utilised the extensive animal models of muscle wasting, inactivity and inflammation from the Goldberg laboratory [32], [33].
Human models of short-term physical inactivity (4 8 weeks) demonstrate no change in blood pressure, obesity, BMI or cholesterol levels (Bleeker et al. 2005a, b, c; Demiot et al. 2007; Pawelczyk et al. 2001; Thijssen et al. 2007b).
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