Abstract
Lifelong overexpression of heat shock protein (HSP) 72 in skeletal muscle is known to protect against age-related oxidative stress and muscle damage. This study aimed to ascertain whether exhaustive exercise-induced damage can be prevented by lifelong overexpression of HSP72. Transgenic mice that were heterozygous for a porcine HSP70.2 gene ([+]HSP72) and transgene-negative littermate controls ([-]HSP72) were subjected to an exhaustive exercise protocol. Mice were divided into four groups, including control, HSP72, exhaustive exercise and HSP72 exhaustive exercise groups. Eighty-two min after completion of the exhaustive exercise, animals were sacrificed and different tissues, including brain, heart, liver, lung, kidney and muscle were isolated. Then the levels of HSP72, matrix metalloproteinase (an indicator for inflammatory myopathies), pathological observations and p-P-38 MAP kinase (p-P-38) expressions were determined in all tissues. When exhaustive exercise group or HSP72 exhaustive exercise group underwent an exhaustive exercise test, the latency values (the mean duration of exhaustive exercise onset) for the occurrence of exhaustive exercise was found to be different significantly (82 ± 3 and 110 ± 3 min, respectively). HSP72 exhaustive exercise group underwent a exhaustive exercise test, and had a longer exercise time. Furthermore HSP72 exhaustive exercise group showed significantly increased matrix metalloproteinase levels and p-P-38 expression, whereas morphological damage was significantly decreased compared to exhaustive exercise group. The results suggest that the improvement of inflammation and damage induced by exhaustive exercise in HSP72 overexpressing transgenic mice may be associated with p-P-38 expression.