Heat shock protein 90 does not contribute to cutaneous vasodilatation in older adults during heat stress.

OBJECTIVES: Heat shock protein 90 (HSP90) contributes to cutaneous vasodilatation during exercise in the heat through nitric oxide synthase (NOS)-dependent mechanisms in young adults. We hypothesized that similar responses would be observed in older middle-aged adults.

METHODS: In nineteen habitually-active older middle-aged (56±5 years) men (n=9) and women (n=10), cutaneous vascular conductance (CVC) was measured at four forearm skin sites continuously treated with 1) lactated Ringers solution (Control), 2) 10 mM L-NAME (NOS inhibitor), 3) 178 μM geldanamycin (HSP90 inhibitor), or 4) 10 mM L-NAME and 178 μM geldanamycin combined. Participants rested in an upright semi-recumbent position in the heat (35°C) for 70 min, followed by a 50-min bout of moderate-intensity cycling (~55% peak oxygen uptake) and a 30-min recovery period in the heat.

RESULTS: In both men and women, we observed no significant effects of HSP90 inhibition on CVC throughout rest, exercise, and recovery in the heat (all P>0.27). Conversely, NOS inhibition and dual NOS and HSP90 inhibition attenuated CVC relative to Control throughout the protocol (all P<0.05).

CONCLUSIONS: While NOS mediates cutaneous vasodilatation during rest, exercise, and recovery in the heat, HSP90 does not measurably influence this response in habitually-active older middle-aged men or women under these conditions. This article is protected by copyright. All rights reserved.