Type 1 diabetes (T1DM) is known to cause both peripheral and autonomic neuropathy through mechanisms affecting thinly myelinated afferents. These same afferents may also play a role in the exercise pressor reflex suggesting that T1DM could alter this reflex as well. The purpose of this study was to establish the effects of type 1 diabetes on the pressor and cardioaccelerator responses evoked by statically contracting the hindlimb muscles at different time points of the disease and identify possible mechanisms responsible for these changes. We injected (i.p.) 50 mg/kg of Streptozotocin (STZ) or the vehicle (CTL) in either sex and waited 1wk (STZ: BW=267±12 g, glucose=438±24 mg/dL, HbA1C=6.5±0.3%; CTL: BW=328±16 g, glucose=167±10 mg/dL, HbA1C=4.4±0.1%), 3wks (STZ: BW=293±10 g, glucose=465±22 mg/dL, HbA1C=10±0.3%; CTL: BW=329±22 g, glucose=212±26 mg/dL, HbA1C=4.8±0.4%), or 6wks (STZ: BW=380±16 g, glucose=546±35 mg/dL, HbA1C=12±0.4%) before performing experiments. In unanaesthetized, decerebrate rats, we statically contracted the hindlimb muscles for 30s and measured changes in mean arterial pressure (MAP) and heart rate (HR). We then injected either α,β‐methylene ATP (20μg/kg; 200μl), a P2X receptor agonist, or lactic acid (24mM; 200μl), an ASIC3 channel agonist, into the arterial supply of the hindlimb and measured the evoked pressor and cardioaccelerator responses for each group. We found that the pressor (STZ: ΔMAP=25±5 mmHg, n=4; CTL: ΔMAP=13±2 mmHg, n=7; p=0.01) but not cardioaccelerator (STZ: ΔHR=23±9 bpm, n=4; CTL: ΔHR=13±3 bpm, n=7; p=0.10) response to static contraction was exaggerated 1wk after injecting STZ. Likewise, the pressor (STZ: ΔMAP=32±5 mmHg, n=8; CTL: ΔMAP=17±3 mmHg, n=6; p=0.02) but not cardioaccelerator (STZ: ΔHR=22±5 bpm, n=8; CTL: ΔHR=15±2 bpm, n=6; p=0.27) response to static contraction was exaggerated 3wks after injecting STZ. Conversely, both the pressor (6wks STZ: ΔMAP=5±2 mmHg, n=7) and cardioaccelerator (6wks STZ: ΔHR=1±2 bpm, n=7) responses to static contraction were significantly attenuated 6wks after injecting STZ compared to 1wk (MAP: p=0.02; HR: p=0.01) and 3wks after injecting STZ (MAP: p<0.01; HR: p<0.01). The developed tensions from contraction were similar within each comparison. Furthermore, we found that injecting lactic acid, but not α,β‐methylene ATP, into the arterial supply of the hindlimb evoked a greater pressor (STZ: ΔMAP=31±5 mmHg, n=9; CTL: ΔMAP=20±3 mmHg, n=13; p=0.04) and cardioaccelerator (STZ: ΔHR=13±3 bpm, n=9; CTL: ΔHR=3±2 bpm, n=13; p<0.01) response 1wk after STZ injection compared to CTL. We conclude that the exercise pressor reflex is exaggerated in the early stages of T1DM but attenuated in the late stages of this disease. Additionally, ASIC3 channels but not P2X receptors may play a role in this exaggerated reflex 1wk after STZ injection.