This study analyzed the postexercise blood pressure (BP) after resistance exercise (RE) on middle-aged type-2 diabetic (T2DM, n = 10, 46.6 +/- 13.1 years) and nondiabetic subjects (NDM, n = 10, 52.0 +/- 13.2 years). Participants performed (a) 1 repetition maximum (1RM) strength test; (b) 3 laps in an RE circuit of 6 exercises (16 repetitions at 43% 1RM); (c) 3 laps in an RE circuit (30 repetitions at 23% 1RM); and (d) a control session. The blood lactate concentration ([lac]) (YSI 2700S) and BP (Microlife BP3AC1-1) were measured pre-exercise, after exercise, and at each 15 minutes during the 120 minutes of recovery. Analysis of variance with Bonferroni as a post hoc evidenced that the 43% 1RM session elicited the highest [lac] response for both NDM (7.8 +/- 1.8 vs. 6.4 +/- 1.8 mmol x L(-1); p < 0.05) and T2DM (7.0 +/- 1.4 vs. 5.6 +/- 1.6 mmol x L(-1); p < 0.05). Also, the 43% 1RM session promoted a significant postexercise hypotension (PEH) of systolic blood pressure (SBP) and mean arterial pressure (MAP), whereas the 23% 1RM did not. The highest BP reductions for T2DM and NDM after 43% 1RM were, respectively, 9.5 +/- 11.1 and 11.0 +/- 7.1 mmHg for SBP and 6.4 +/- 7.8 and 7.7 +/- 7.9 mmHg for the MAP (p
This study compared the effects of resistance exercise (RE) intensities on blood glucose (GLUC) of individuals without (ND) and with type-2 diabetes (T2D). Nine individuals with T2D and 10 ND performed: (a) RE circuit at 23% of 1 maximal repetition (1RM) (RE_L); (b) RE circuit at 43% 1RM (RE_M); and (c) control (CON) session. Blood lactate (LAC) and GLUC were measured before, during, and postinterventions. Double product (DP) and rate of perceived exertion (RPE) were recorded. The area under the curve (AUC) revealed the effects of RE circuits in reducing GLUC in individuals with T2D (RE_L: 12,556 ± 3,269 vs. RE_M: 13,433 ± 3,054 vs. CON: 14,576 ± 3,922 mg.dl(-1).145 minutes; p < 0.05) with a lower AUC of GLUC in RE_L in comparison to RE_M. Similarly, for ND the RE_L reduced the AUC of GLUC when compared with RE_M and CON (RE_L: 10,943 ± 956 vs. RE_M: 12,156 ± 1,062 vs. CON: 11,498 ± 882 mg.dl(-1).145 minutes; p < 0.05). The AUC of GLUC was higher for T2D compared with ND on CON condition (p = 0.02). However, after RE circuits the difference between groups for AUC of GLUC was abolished. The RE_M for T2D was more stressful when compared with RE_L for LAC (CON: 1.3 ± 0.5 vs. RE_L: 5.5 ± 1.5 vs. RE_M: 6.8 ± 1.3 mmol·L(-1); p < 0.05), DP (CON: 8,415 ± 1,223 vs. RE_L: 15,980 ± 2,007 vs. RE_M: 18,047 ± 3,693 mmHg.bpm(-1); p < 0.05), and RPE (RE_L: 11 ± 2 vs. RE_M: 13 ± 2 Borg Scale; p < 0.05). We concluded that RE_L and RE_M were effective in reducing GLUC for individuals with T2D, with lower cardiovascular-metabolic and perceptual stress being observed for RE_L. These data suggest that acute RE sessions at light or moderate intensities are effective for controlling GLUC in individuals with T2D.
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