Cardiovascular response to handgrip
The time to fatigue during static handgrip was similar following all four interventions (p > 0.05). Hemodynamic measurements before, during, and after handgrip and post-exercise circulatory arrest are presented in Fig. 2. Heart rate was significantly lower at baseline and throughout the protocol following caloric restriction, whereas bedrest was associated with a higher HR. At the same relative forces, HR gradually increased during static handgrip, reached its peak at fatigue, and immediately returned to baseline values during post-exercise circulatory arrest following each intervention. The contraction-induced increases in HR were diminished with caloric restriction (calorie * time interaction p < 0.001). Systolic and diastolic BP (SBP and DBP) increased progressively during static handgrip, peaked at fatigue, and decreased but remained elevated compared to baseline during post-handgrip circulatory arrest. The increase in DBP (Fig. 2) and SBP (Figs. 2 and 3) during handgrip were greatly attenuated with caloric restriction independent of bedrest. Responses were well maintained during post-exercise ischemia.
Fig. 2 Systemic neural and hemodynamic responses to static handgrip and post-exercise muscle ischemia. Data are presented as mean ± SEM. The x-axis during exercise corresponds to the % of time to fatigue. C1 and C2, minutes 1 and 2 of arm cuff occlusion. MSNA is adjusted to minute values and expressed as bursts/min. The main effects calorie, posture, and time are significantly different for HR. Following caloric restriction, the responses of all variables during exercise are attenuated (calorie * time interaction). Values during 2 min of occlusion are similar
Fig. 3 The change in SBP at the point of maximum fatigue. Data are presented as mean ± SEM. The maximum SBP response to static handgrip to fatigue was significantly attenuated following caloric restriction, independent of bedrest