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No effect of ascorbate on cutaneous vasodilation and sweating in older men and those with type 2 diabetes exercising in the heat

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ABSTRACT

Aging and chronic disease such as type 2 diabetes (T2D) are associated with impairments in the body's ability to dissipate heat. To reduce the risk of heat‐related injuries in these heat vulnerable individuals, it is necessary to identify interventions that can attenuate this impairment. We evaluated the hypothesis that intradermal administration of ascorbate improves cutaneous vasodilation and sweating in older adults via nitric oxide synthase (NOS)‐dependent mechanisms during exercise in the heat and whether these improvements, if any, are greater in individuals with T2D. Older males with (n = 12, 61 ± 9 years) and without (n = 12, 64 ± 7 years) T2D performed two 30‐min bouts of cycling at a fixed rate of metabolic heat production of 500 W (~70% peak oxygen uptake) in the heat (35°C); each followed by a 20‐ and 40‐min recovery, respectively. Cutaneous vascular conductance (CVC) and sweat rate were measured at four intradermal microdialysis sites treated with either (1) lactated Ringer (Control), (2) 10 mmol/L ascorbate (an antioxidant), (3) 10 mmol/L L‐NAME (non‐selective NOS inhibitor), or (4) a combination of ascorbate + L‐NAME. In both groups, ascorbate did not modulate CVC or sweating during exercise relative to Control (all P > 0.05). In comparison to Control, L‐NAME alone or combined with ascorbate attenuated CVC during exercise (all P ≤ 0.05) but had no influence on sweating (all P > 0.05). We show that in both healthy and T2D older adults, intradermal administration of ascorbate does not improve cutaneous vasodilation and sweating during exercise in the heat. However, NOS plays an important role in mediating cutaneous vasodilation.

No MeSH data available.


Related in: MedlinePlus

Cutaneous vascular conductance evaluated at the last 5 min of the first (Ex 1) and second (Ex 2) 30‐min exercise in older healthy adults (Control, panel A) and those with type 2 diabetes (T2D, panel B). Cutaneous vascular conductance was evaluated at four skin sites treated with either 1) lactated Ringer (vehicle control site), 2) ascorbate, an antioxidant, 3) L‐NAME, a nitric oxide synthase inhibitor, or 4) ascorbate + L‐NAME. Data are expressed as mean ± 95% confidence interval. *, versus vehicle control site (P ≤ 0.05). †, versus Control group (P ≤ 0.05).
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phy213238-fig-0001: Cutaneous vascular conductance evaluated at the last 5 min of the first (Ex 1) and second (Ex 2) 30‐min exercise in older healthy adults (Control, panel A) and those with type 2 diabetes (T2D, panel B). Cutaneous vascular conductance was evaluated at four skin sites treated with either 1) lactated Ringer (vehicle control site), 2) ascorbate, an antioxidant, 3) L‐NAME, a nitric oxide synthase inhibitor, or 4) ascorbate + L‐NAME. Data are expressed as mean ± 95% confidence interval. *, versus vehicle control site (P ≤ 0.05). †, versus Control group (P ≤ 0.05).

Mentions: Main effects of treatment site, time, and group, as well as an interaction between time and group were detected for CVC (Fig. 1, Table 2, all P ≤ 0.05). There was an interaction between treatment site and group for ∆CVC (Fig. 2, P = 0.02). No main effects of treatment site and group and their interaction were measured for absolute maximal CVC (Table 2, all P > 0.05).


No effect of ascorbate on cutaneous vasodilation and sweating in older men and those with type 2 diabetes exercising in the heat
Cutaneous vascular conductance evaluated at the last 5 min of the first (Ex 1) and second (Ex 2) 30‐min exercise in older healthy adults (Control, panel A) and those with type 2 diabetes (T2D, panel B). Cutaneous vascular conductance was evaluated at four skin sites treated with either 1) lactated Ringer (vehicle control site), 2) ascorbate, an antioxidant, 3) L‐NAME, a nitric oxide synthase inhibitor, or 4) ascorbate + L‐NAME. Data are expressed as mean ± 95% confidence interval. *, versus vehicle control site (P ≤ 0.05). †, versus Control group (P ≤ 0.05).
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phy213238-fig-0001: Cutaneous vascular conductance evaluated at the last 5 min of the first (Ex 1) and second (Ex 2) 30‐min exercise in older healthy adults (Control, panel A) and those with type 2 diabetes (T2D, panel B). Cutaneous vascular conductance was evaluated at four skin sites treated with either 1) lactated Ringer (vehicle control site), 2) ascorbate, an antioxidant, 3) L‐NAME, a nitric oxide synthase inhibitor, or 4) ascorbate + L‐NAME. Data are expressed as mean ± 95% confidence interval. *, versus vehicle control site (P ≤ 0.05). †, versus Control group (P ≤ 0.05).
Mentions: Main effects of treatment site, time, and group, as well as an interaction between time and group were detected for CVC (Fig. 1, Table 2, all P ≤ 0.05). There was an interaction between treatment site and group for ∆CVC (Fig. 2, P = 0.02). No main effects of treatment site and group and their interaction were measured for absolute maximal CVC (Table 2, all P > 0.05).

View Article: PubMed Central - PubMed

ABSTRACT

Aging and chronic disease such as type 2 diabetes (T2D) are associated with impairments in the body's ability to dissipate heat. To reduce the risk of heat‐related injuries in these heat vulnerable individuals, it is necessary to identify interventions that can attenuate this impairment. We evaluated the hypothesis that intradermal administration of ascorbate improves cutaneous vasodilation and sweating in older adults via nitric oxide synthase (NOS)‐dependent mechanisms during exercise in the heat and whether these improvements, if any, are greater in individuals with T2D. Older males with (n = 12, 61 ± 9 years) and without (n = 12, 64 ± 7 years) T2D performed two 30‐min bouts of cycling at a fixed rate of metabolic heat production of 500 W (~70% peak oxygen uptake) in the heat (35°C); each followed by a 20‐ and 40‐min recovery, respectively. Cutaneous vascular conductance (CVC) and sweat rate were measured at four intradermal microdialysis sites treated with either (1) lactated Ringer (Control), (2) 10 mmol/L ascorbate (an antioxidant), (3) 10 mmol/L L‐NAME (non‐selective NOS inhibitor), or (4) a combination of ascorbate + L‐NAME. In both groups, ascorbate did not modulate CVC or sweating during exercise relative to Control (all P > 0.05). In comparison to Control, L‐NAME alone or combined with ascorbate attenuated CVC during exercise (all P ≤ 0.05) but had no influence on sweating (all P > 0.05). We show that in both healthy and T2D older adults, intradermal administration of ascorbate does not improve cutaneous vasodilation and sweating during exercise in the heat. However, NOS plays an important role in mediating cutaneous vasodilation.

No MeSH data available.


Related in: MedlinePlus