OBJECTIVETo determine the effects of exercise order on acute glycemic responses in individuals with type 1 diabetes performing both aerobic and resistance exercise in the same session.RESEARCH DESIGN AND METHODSTwelve physically active individuals with type 1 diabetes (HbA1c 7.1 ± 1.0%) performed aerobic exercise (45 min of running at 60% V̇o2peak) before 45 min of resistance training (three sets of eight, seven different exercises) (AR) or performed the resistance exercise before aerobic exercise (RA). Plasma glucose was measured during exercise and for 60 min after exercise. Interstitial glucose was measured by continuous glucose monitoring 24 h before, during, and 24 h after exercise.RESULTSSignificant declines in blood glucose levels were seen in AR but not in RA throughout the first exercise modality, resulting in higher glucose levels in RA (AR = 5.5 ± 0.7, RA = 9.2 ± 1.2 mmol/L, P = 0.006 after 45 min of exercise). Glucose subsequently decreased in RA and increased in AR over the course of the second 45-min exercise bout, resulting in levels that were not significantly different by the end of exercise (AR = 7.5 ± 0.8, RA = 6.9 ± 1.0 mmol/L, P = 0.436). Although there were no differences in frequency of postexercise hypoglycemia, the duration (105 vs. 48 min) and severity (area under the curve 112 vs. 59 units ⋅ min) of hypoglycemia were nonsignificantly greater after AR compared with RA.CONCLUSIONSPerforming resistance exercise before aerobic exercise improves glycemic stability throughout exercise and reduces the duration and severity of postexercise hypoglycemia for individuals with type 1 diabetes.

OBJECTIVEIn type 1 diabetes, small studies have found that resistance exercise (weight lifting) reduces HbA1c. In the current study, we examined the acute impacts of resistance exercise on glycemia during exercise and in the subsequent 24 h compared with aerobic exercise and no exercise.RESEARCH DESIGN AND METHODSTwelve physically active individuals with type 1 diabetes (HbA1c 7.1 ± 1.0%) performed 45 min of resistance exercise (three sets of seven exercises at eight repetitions maximum), 45 min of aerobic exercise (running at 60% of Vo2max), or no exercise on separate days. Plasma glucose was measured during and for 60 min after exercise. Interstitial glucose was measured by continuous glucose monitoring 24 h before, during, and 24 h after exercise.RESULTSTreatment-by-time interactions (P < 0.001) were found for changes in plasma glucose during and after exercise. Plasma glucose decreased from 8.4 ± 2.7 to 6.8 ± 2.3 mmol/L (P = 0.008) during resistance exercise and from 9.2 ± 3.4 to 5.8 ± 2.0 mmol/L (P = 0.001) during aerobic exercise. No significant changes were seen during the no-exercise control session. During recovery, glucose levels did not change significantly after resistance exercise but increased by 2.2 ± 0.6 mmol/L (P = 0.023) after aerobic exercise. Mean interstitial glucose from 4.5 to 6.0 h postexercise was significantly lower after resistance exercise versus aerobic exercise.CONCLUSIONSResistance exercise causes less initial decline in blood glucose during the activity but is associated with more prolonged reductions in postexercise glycemia than aerobic exercise. This might account for HbA1c reductions found in studies of resistance exercise but not aerobic exercise in type 1 diabetes.

Aging is associated with an attenuated physiological ability to dissipate heat. However, it remains unclear if age-related impairments in heat dissipation only occur above a certain level of heat stress and whether this response is altered by aerobic fitness. Therefore, we examined changes in whole body evaporative heat loss (HE) as determined using whole body direct calorimetry in young (n = 10; 21 ± 1 yr), untrained middle-aged (n = 10; 48 ± 5 yr), and older (n = 10; 65 ± 3 yr) males matched for body surface area. We also studied a group of trained middle-aged males (n = 10; 49 ± 5 yr) matched for body surface area with all groups and for aerobic fitness with the young group. Participants performed intermittent aerobic exercise (30-min exercise bouts separated by 15-min rest) in the heat (40°C and 15% relative humidity) at progressively greater fixed rates of heat production equal to 300 (Ex1), 400 (Ex2), and 500 (Ex3) W. Results showed that HE was significantly lower in middle-aged untrained (Ex2: 426 ± 34; and Ex3: 497 ± 17 W) and older (Ex2: 424 ± 38; and Ex3: 485 ± 44 W) compared with young (Ex2: 472 ± 42; and Ex3: 558 ± 51 W) and middle-aged trained (474 ± 21; Ex3: 552 ± 23 W) males at the end of Ex2 and Ex3 (P < 0.05). No differences among groups were observed during recovery. We conclude that impairments in HE in older and middle-aged untrained males occur at exercise-induced heat loads of ≥400 W when performed in a hot environment. These impairments in untrained middle-aged males can be minimized through regular aerobic exercise training.

Nitric oxide synthase (NOS) contributes to sweating and cutaneous vasodilation during exercise in younger adults. We hypothesized that endothelial NOS (eNOS) and neuronal NOS (nNOS) mediate NOS-dependent sweating, whereas eNOS induces NOS-dependent cutaneous vasodilation in younger adults exercising in the heat. Further, aging may upregulate inducible NOS (iNOS), which may attenuate sweating and cutaneous vasodilator responses. We hypothesized that iNOS inhibition would augment sweating and cutaneous vasodilation in exercising older adults. Physically active younger (n = 12, 23 ± 4 yr) and older (n = 12, 60 ± 6 yr) adults performed two 30-min bouts of cycling at a fixed rate of metabolic heat production (400 W) in the heat (35°C). Sweat rate and cutaneous vascular conductance (CVC) were evaluated at four intradermal microdialysis sites with: 1) lactated Ringer (control), 2) nNOS inhibitor (nNOS-I, NPLA), 3) iNOS inhibitor (iNOS-I, 1400W), or 4) eNOS inhibitor (eNOS-I, LNAA). In younger adults during both exercise bouts, all inhibitors decreased sweating relative to control, albeit a lower sweat rate was observed at iNOS-I compared with eNOS-I and nNOS-I sites (all P < 0.05). CVC at the eNOS-I site was lower than control in younger adults throughout the intermittent exercise protocol (all P < 0.05). In older adults, there were no differences between control and iNOS-I sites for sweating and CVC during both exercise bouts (all P > 0.05). We show that iNOS and eNOS are the main contributors to NOS-dependent sweating and cutaneous vasodilation, respectively, in physically active younger adults exercising in the heat, and that iNOS inhibition does not alter sweating or cutaneous vasodilation in exercising physically active older adults.

We examined whether older individuals experience greater levels of hyperthermia and cardiovascular strain during an extreme heat exposure compared to young adults. During a 3-hour extreme heat exposure (44°C, 30% relative humidity), we compared body heat storage, core temperature (rectal, visceral) and cardiovascular (heart rate, cardiac output, mean arterial pressure, limb blood flow) responses of young adults (n = 30, 19–28 years) against those of older adults (n = 30, 55–73 years). Direct calorimetry measured whole-body evaporative and dry heat exchange. Body heat storage was calculated as the temporal summation of heat production (indirect calorimetry) and whole-body heat loss (direct calorimetry) over the exposure period. While both groups gained a similar amount of heat in the first hour, the older adults showed an attenuated increase in evaporative heat loss (p < 0.033) in the first 30-min. Thereafter, the older adults were unable to compensate for a greater rate of heat gain (11 ± 1 ; p < 0.05) with a corresponding increase in evaporative heat loss. Older adults stored more heat (358 ± 173 kJ) relative to their younger (202 ± 92 kJ; p < 0.001) counterparts at the end of the exposure leading to greater elevations in rectal (p = 0.043) and visceral (p = 0.05) temperatures, albeit not clinically significant (rise < 0.5°C). Older adults experienced a reduction in calf blood flow (p < 0.01) with heat stress, yet no differences in cardiac output, blood pressure or heart rate. We conclude, in healthy habitually active individuals, despite no clinically observable cardiovascular or temperature changes, older adults experience greater heat gain and decreased limb perfusion in response to 3-hour heat exposure.