Background: Adventure tourism has led to an unprecedented number of individuals being exposed to altitude, including those with subclinical cardiometabolic disorders. The disproportionate hemodynamic challenge associated with small-muscle static activities is potentially dangerous at altitude as these may compound the risk for cardiac events. We thus examined the cardiovascular response to, and during recovery from, static exercise performed at altitude. Methods: Eighteen individuals completed this study at three altitudes (sea level; ∼1,500 m; ∼3,000 m) in central Nepal. At each altitude, individuals performed two handgrip contractions for 2 minutes at the same intensity (30% maximal voluntary contraction [MVC]), with two distinct recovery periods: during control recovery was completed quietly at rest, while during ischemic challenge recovery was conducted with a cuff occluding the upper limb. Results: Oxygen saturation decreased during ascent to 1,500 m (−2%) and 3,000 m (−8%), compared with sea level. Handgrip MVC was not affected by altitude, although heart rate at rest (∼70 beat/min), during static exercise (range ∼90–95 beat/min), and during recovery in both conditions (each ∼70 beat/min) was significantly increased by ∼15% at 3,000 m, but not 1,500 m. The magnitude of the muscle metaboreflex during recovery from static exercise was unaffected by altitude; however, the rate-pressure product was significantly elevated by ∼10% during and following static exercise at 3,000 m. Conclusions: A significant increase in the rate-pressure product during static exercise was observed at altitude, which persisted during recovery. Individuals at risk for cardiac events should use awareness of static contractions while at altitude, especially considering that stress induced by static exercise is additive to that of dynamic activities such as hiking.